tag:blogger.com,1999:blog-38505027672501398702024-03-27T07:23:28.630-07:00sarnatscatTV REPAIR PARTShttp://www.blogger.com/profile/03272638773780329095noreply@blogger.comBlogger5125tag:blogger.com,1999:blog-3850502767250139870.post-36210128881991261272024-03-27T07:22:00.000-07:002024-03-27T07:22:28.385-07:00William Llewellyn’s, ANABOLICS,<p> William Llewellyn’s,
ANABOLICS, E-Book Edition
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SPORT SUPPLEMENT REFERENCE GUIDE - Kindle Edition
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William Llewellyn’s
SPORT SUPPLEMENT REFERENCE GUIDE
ISBN-13: 978-0-9679304-8-0
ISBN-10: 0-9679304-8-0
Underground Anabolics
ISBN-13: 978-0967930497
ISBN-10: 0967930499
WILLIAM LLEWELLYN’S
ANABOLICS
E-Book Edition
DISCLAIMER: This information was gathered from sources including, but not
limited to medical journals, pharmaceutical reports, laboratory reports,
textbooks, as well as interviews with medical experts, athletes, and steroid
distributors. Neither the author nor publisher assumes any liability for the
information presented. This book is intended to provide a compendium of
information for the reader. None of the information is meant to be applied and is
for entertainment purposes only. It is not intended to provide nor replace medical
advice. Readers are advised that the substances described in this reference book
are to be used only under a physician’s care and may be prohibited in certain
jurisdictions. Readers should consult with appropriate medical authorities before
using any drug, and proper legal authorities on the status of substances described
herein. Neither the publisher nor author advocate readers engage in any illegal
activities. Copyright © 2011 and published by Molecular Nutrition, LLC in Jupiter, FL 33458. All rights
reserved.None of the content in this publication may be reproduced, stored in a retrieval system, resold,
redistributed, or transmitted in any form or by any means (digital, electronic, mechanical, photocopy,
recorded, or otherwise) without the prior written permission of the publisher. William Llewellyn’s
ANABOLICS are trademarks used herein under license. Molecular Nutrition LLC, 5500 Military Trail,
Ste. 22-308, Jupiter, FL 33458 www.mnbody.com
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As longtime advocates of the legitimate medical use of anabolic/androgenic
steroids, we have launched HRT-Rx, a national referral service to help patients
find progressive HRT/Anti-Aging physicians. Network doctors are the type that
regularly work with testosterone medications, and understand the value of
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New Service (HRT-Labs):
We have also partnered with a laboratory that can run extensive blood tests
including hormone levels, liver/kidney enzymes, and general health markers.
The service is available in all 50 states and can be accessed at www.HRTLabs.com.
Table of Contents
PART I: ANABOLIC OVERVIEW
An Introduction to Testosterone
Direct and Indirect Anabolic Effects
Free vs. Bound Testosterone
Estrogen Aromatization
DHT Conversion
Brief History of Anabolic/Androgenic Steroids
Synthetic AAS Development
Synthetic AAS Chemistry
Steroid Nomenclature
Clinical Applications
Side Effects
Acute Steroid Safety: Studies with Real-World Dosages
The Endocrinology of Muscle Growth
PART II: PRACTICAL APPLICATION
Steroid Cycles
Sample Steroid Cycles
PCT: Post Cycle Therapy
OCT: Off Cycle Therapy
Injection Protocols
Steroid Frequently Asked Questions
Understanding Blood Tests
Harm Reduction/Safer Use Guidelines
Sterilizing Injectable AAS
Counterfeit Steroids
Counterfeit Steroid Identification
Country Specifics
Underground Steroids
Designer Steroids
Anabolic Steroid Possesion and the Law
Acquiring AAS (Best Practices)
PART III: DRUG PROFILES
ANABOLIC/ANDROGENIC STEROIDS (Listed by Common Brand)
Agovirin Depot (testosterone isobutyrate)
Anadrol® - 50 (oxymetholone)
Anadur® (nandrolone hexyloxyphenylpropionate)
Anavar (oxandrolone)
Andractim® (dihydrotestosterone)
Andriol® (testosterone undecanoate)
Androderm® (testosterone)
AndroGel® (testosterone)
Andronaq (testosterone suspension)
Cheque Drops® (mibolerone)
Deca-Durabolin® (nandrolone decanoate)
Delatestryl®(testosterone enanthate)
Depo®-Testosterone (testosterone cypionate)
Deposterona (testosterone blend)
Dianabol®(methandrostenolone, methandienone)
Drive® (boldenone/methylandrostenediol blend)
Durabolin® (nandrolone phenylpropionate)
Dynabol® (nandrolone cypionate)
Dynabolon®(nandrolone undecanoate)
Equipoise® (boldenone undecylenate)
Finajet (trenbolone acetate)
Halotestin® (fluoxymesterone)
Laurabolin® (nandrolone laurate)
Masteron® (drostanolone propionate)
Megagrisevit-Mono® (clostebol acetate)
Metandren (methyltestosterone)
Methandriol (methylandrostenediol)
Metribolone (methyltrienolone)
Miotolan® (furazabol)
Myagen (bolasterone)
Nebido (testosterone undecanoate)
Nilevar® (norethandrolone)
Omnadren® 250 (testosterone blend)
Orabolin® (ethylestrenol)
Oral Turinabol (4-chlorodehydromethyltestosterone)
Oreton (testosterone propionate)
Parabolan® (trenbolone hexahydrobenzylcarbonate)
Primobolan® (methenolone acetate)
Primobolan® Depot (methenolone enanthate)
Proviron® (mesterolone)
Sten (testosterone cypionate & propionate)
Striant® (testosterone)
Sustanon® 100 (testosterone blend)
Sustanon® 250 (testosterone blend)
Synovex® (testosterone propionate & estradiol)
Testoderm® (testosterone)
Testolent (testosterone phenylpropionate)
Testopel® (testosterone)
Testoviron® (testosterone propionate/enanthate blend)
Trenabol® (trenbolone enanthate)
Winstrol® (stanozolol)
ANABOLIC AGENTS (NON-STEROID)
Arachidonic Acid (eicosa-5,8,11,14-enoic acid)
Kynoselen®
Lutalyse® (diniprost)
ANTI-ESTROGENS
Arimidex® (anastrozole)
Aromasin® (exemestane)
Clomid® (clomiphene citrate)
Cytadren® (aminoglutethimide)
Evista (raloxifene)
Fareston® (toremifene citrate)
Faslodex® (fulvestrant)
Femara® (letrozole)
Fertodur® (cyclofenil)
Lentaron® (formestane)
Nolvadex® (tamoxifen citrate)
Teslac® (testolactone)
ANTI-PROLACTIN
Dostinex® (cabergoline)
Parlodel® (bromocriptine mesylate)
APPETITE STIMULANTS
Periactin (cyproheptadine hydrochloride)
CARDIOVASCULAR SUPPORT
Lipid Stabil
TM
Lovaza® (omega-3 ethyl esters)
DIURETICS
Aldactone® (spironolactone)
Dyrenium® (triamterene)
Hydrodiuril® (hydrochlorthiazide)
Lasix® (furosemide)
ENDURANCE/ERYTHROPOIETIC DRUGS
Aranesp® (darbepoetin alfa)
Epogen® (epoetin alfa)
Provigil® (modafinil)
FAT LOSS AGENTS – SYMPATHOMIMETICS
Adipex-P (phentermine hydrochloride)
Albuterol (albuterol sulfate)
Clenasma (clenbuterol hydrochloride)
Ephedrine (ephedrine hydrochloride)
Meridia® (sibutramine hydrochloride monohydrate)
Zaditen® (ketotifen fumarate)
FAT LOSS AGENTS – THYROID
Cytomel® (liothyronine sodium)
Synthroid® (levothyroxine sodium)
FAT LOSS AGENTS – OTHER
DNP (2,4-dinitrophenol)
Lipostabil N
GROWTH HORMONES & RELATED
Geref®(sermorelin acetate)
Human Growth Hormone (somatropin)
Increlex® (mecasermin)
Protropin® (somatrem)
HYPOGLYCEMICS
Glucophage
Insulin
HYPOTENSIVES
BP Stabil
TM
Catapres
LIVER DETOXIFICATION
Essentiale forte N
LIV-52®
Liver Stabil
TM
REDUCTASE INHIBITORS
Avodart® (dutasteride)
Proscar® (finasteride)
TESTOSTERONE STIMULATING DRUGS
HCG (human chorionic gonadotropin)
Drug Profiles Bibliography
Drug Profiles Bibliography
GLOSSARY
Part I
Anabolic Overview
An Introduction to Testosterone
Anabolic steroids are a class of medications that contain a
synthetically manufactured form of the hormone
testosterone, or a related compound that is derived from
(or similar in structure and action to) this hormone. In
order to fully grasp how anabolic steroids work, it is,
therefore, important to understand the basic functioning
of testosterone.
Testosterone is the primary male sex hormone. It is
manufactured by the Leydig's cells in the testes at varying
amounts throughout a person's life span. The effects of
this hormone become most evident during the time of
puberty, when an increased output of testosterone will
elicit dramatic physiological changes in the male body.
This includes the onset of secondary male characteristics
such as a deepened voice, body and facial hair growth,
increased oil output by the sebaceous glands,
development of sexual organs, maturation of sperm, and
an increased libido. Indeed the male reproductive system
will not function properly if testosterone levels are not
significant. All such effects are considered the
masculinizing or “androgenic” properties of this
hormone.
Increased testosterone production will also cause growth
promoting or “anabolic” changes in the body, including
an enhanced rate of protein synthesis (leading to muscle
accumulation). Testosterone is the reason males carry
more muscle mass than women, as the two sexes have
vastly contrasting amounts of this hormone. More
specifically, the adult male body will manufacture
between 2.5 and 11mg per day
1 while females only
produce about 1/4mg. The dominant sex hormone for
women is estrogen, which has a significantly different
effect on the body. Among other things, a lower androgen
and higher estrogen level will cause women to store more
body fat, accumulate less muscle tissue, have a shorter
stature, and become more apt to bone weakening with age
(osteoporosis).
The actual mechanism in which testosterone elicits these
changes is somewhat complex. When free in the blood
stream, the testosterone molecule is available to interact
with various cells in the body. This includes skeletal
muscle cells, as well as skin, scalp, kidney, bone, central
nervous system, and prostate tissues. Testosterone binds
with a cellular target in order to exert its activity, and
will, therefore, effect only those body cells that posses
the proper hormone receptor site (specifically the
androgen receptor). This process can be likened to a lock
and key system, with each receptor (lock) only being
activated by a particular type of hormone (key). During
this interaction, the testosterone molecule will become
bound to the intracellular receptor site (located in the
cytosol, not on the membrane surface), forming a new
“receptor complex.” This complex (hormone + receptor
site) will then migrate to the cell's nucleus, where it will
attach to a specific section of the cell's DNA, referred to
as the hormone response element. This will activate the
transcription of specific genes, which in the case of a
skeletal muscle cell will ultimately cause (among other
things) an increase in the synthesis of the two primary
contractile proteins, actin and myosin (muscular growth).
Carbohydrate storage in muscle tissue may be increased
due to androgen action as well.
Once this messaging process is completed, the complex
will be released, and the receptor and hormone will
disassociate. Both are then free to migrate back into the
cytosol for further activity. The testosterone molecule is
also free to diffuse back into circulation to interact with
other cells. The entire receptor cycle, including hormone
binding, receptor-hormone complex migration, gene
transcription and subsequent return to cytosol is a slow
process, taking hours, not minutes, to complete. For
example, in studies using a single injection of
nandrolone, it is measured to be 4 to 6 hours before free
androgen receptors migrate back to the cytosol after
activation. It is also suggested that this cycle includes the
splitting and formation of new androgen receptors once
returned to cytosol, a possible explanation for the many
observations that androgens are integral in the formation
of their own receptor sites.
2
In the kidneys, this same process works to allow
androgens to augment erythropoiesis (red blood cell
production).
3
It is this effect that leads to an increase in
red blood cell concentrations, and possibly increased
oxygen transport capacity, during anabolic/androgenic
steroid therapy. Many athletes mistakenly assume that
oxymetholone and boldenone are unique in this ability,
due to specific uses or mentions of this effect in drug
literature. In fact, stimulation of erythropoiesis occurs
with nearly all anabolic/androgenic steroids, as this effect
is simply tied with activation of the androgen receptor in
kidney cells. The only real exceptions might be
compounds such as dihydrotestosterone and some of its
derivatives,
4 which are rapidly broken down upon
interaction with the 3alpha-hydroxysteroid
dehydrogenase enzymes (kidney tissue has a similar
enzyme distribution to muscle tissue, see
“anabolic/androgenic dissociation” section), and
therefore display low activity in these tissues.
CELLULAR DIAGRAM: Testosterone freely diffuses
through the plasma membrane and binds with an
intracellular androgen receptor. The hormonereceptor complex then enters the cell nucleus to bind
with a specific segment of DNA (the Hormone
Response Element), activating the transcription of
specific genes.
Adipose (fat) tissues are also androgen responsive, and
here these hormones support the lipolytic (fat mobilizing)
capacity of cells.
5 This may be accomplished by an
androgen-tied regulation of beta-adrenergic receptor
concentrations or general cellular activity (through
adenylate cyclase).
6 We also note that the level of
androgens in the body will closely correlate (inversely)
with the level of stored body fat. As the level of
androgenic hormones drops, typically the deposition of
body fat will increase.
7 Likewise as we enhance the
androgen level, body fat may be depleted at a more active
rate. The ratio of androgen to estrogen action is in fact
most important, as estrogen plays a counter role by acting
to increase the storage of body fat in many sites of
action.
8 Likewise, if one wished to lose fat during steroid
use, estrogen levels should be kept low. This is clearly
evidenced by the fact that non-aromatizing steroids have
always been favored by bodybuilders looking to increase
the look of definition and muscularity while aromatizing
compounds are typically relegated to bulking phases of
training due to their tendency to increase body fat
storage. Aromatization is discussed in more detail in a
following section (see: Estrogen Aromatization).
As mentioned, testosterone also elicits androgenic
activity, which occurs by its activating receptors in what
are considered to be androgen responsive tissues (often
through prior conversion to dihydrotestosterone. See:
DHT Conversion). This includes the sebaceous glands,
which are responsible for the secretion of oils in the skin.
As the androgen level rises, so does the release of oils. As
oil output increases, so does the chance for pores
becoming clogged (we can see why acne is such a
common side effect of steroid use). The production of
body and facial hair is also linked to androgen receptor
activation in skin and scalp tissues. This becomes most
noticeable as boys mature into puberty, a period when
testosterone levels rise rapidly, and androgen activity
begins to stimulate the growth of hair on the body and
face. Some time later in life, and with the contribution of
a genetic predisposition, androgen activity in the scalp
may also help to initiate male-pattern hair loss. It is a
misconception that dihydrotestosterone is an isolated
culprit in the promotion of hair loss, however; as in
actuality it is the general activation of the androgen
receptor that is to blame (see: DHT Conversion). The
functioning of sex glands and libido are also tied to the
activity of androgens, as are numerous other regions of
the central nervous/neuromuscular system.
1. Role of androgens in growth and development of the fetus, child, and adolescent. Rosenfield R.L. Adv
Pediatr. 19 (1972) 172-213
2. Metabolism of Anabolic Androgenic Steroids, Victor A. Rogozkin, CRC Press 1991
3. Androgens and Erythropoeisis. J Clin Pharmacol. Feb-Mar 1974 p94-101
4. Effects of various modes of androgen substitution therapy on erythropoiesis. Jockenhovel F, Vogel E,
Reinhardt W, Reinwein D. Eur J Med Res 1997 Jul
28;2(7):293-8
5. Testosterone increases lipolysis and the number of beta-adrenoceptors in male rat adipocytes. Xu XF, De
Pergola G, Bjorntorp P. Endocrinology 1991 Jan;128(1):379-82
6. The effects of androgens on the regulation of lipolysis in adipose precursor cells. Endocrinol 126 (1990)
1229-34
7. Visceral fat accumulation in men is positively associated with insulin, glucose, and C-peptide levels, but
negatively with testosterone levels. Seidell JC, Bjorntorp L, Sjostrom L, et al.Metabolism 39 (1990) 897-
901
8. Effects of testosterone and estrogens on deltoid and trochanter adipocytes in two cases of transsexualism.
Vague J, Meignen J.M. and Negrin J.F. Horm. Metabol. Res. 16 (1984) 380-381
Direct and Indirect Anabolic Effects
Although testosterone has been isolated, synthesized, and actively experimented
with for many decades now, there is still some debate today as to exactly how
steroids affect muscle mass. At this point in time, the primary mode of anabolic
action with all anabolic/androgenic steroids is understood to be direct activation
of the cellular androgen receptor and increases in protein synthesis. As follows,
if we are able to increase our androgen level from an external source by
supplementing testosterone or a similar anabolic steroid, we can greatly enhance
the rate in which protein is retained by the muscles. This is clearly the primary
cause for muscle growth with all anabolic/androgenic steroids. As our hormone
levels increase, so does androgen receptor activation, and ultimately the rate of
protein synthesis.
But other indirect mechanisms could possibly affect muscle growth outside of
the normally understood androgen action on protein synthesis. An indirect
mechanism is one that is not brought about by activation of the androgen
receptor, but the affect androgens might have on other hormones, or even the
release of locally acting hormones or growth promoters inside cells (perhaps
mediated by other membrane bound receptors). We must remember also that
muscle mass disposition involves not only protein synthesis, but also other
factors such as tissue nutrient transport and protein breakdown. We need to look
at androgenic interaction with these factors as well to get a complete picture.
Concerning the first possibility, we note that studies with testosterone suggest
that this hormone does not increase tissue amino acid transport.
9 This fact
probably explains the profound synergy bodybuilders have noted in recent years
with insulin, a hormone that strongly increases transport of nutrients into muscle
cells. But regarding protein breakdown, we do see a second important pathway
in which androgens might affect muscle growth.
Anti-Glucocorticoid Effect of Testosterone
Testosterone (and synthetic anabolic/androgenic steroids) may help to increase
mass and strength by having an anti-catabolic effect on muscle cells. Considered
one of the most important indirect mechanisms of androgen action, these
hormones are shown to affect the actions of another type of steroid hormone in
the body, glucocorticoids (cortisol is the primary representative of this group).
10
Glucocorticoid hormones actually have the exact opposite effect on the muscle
cell than androgens, namely sending an order to release stored protein. This
process is referred to as catabolism, and represents a breaking down of muscle
tissue. Muscle growth is achieved when the anabolic effects of testosterone are
more pronounced overall than the degenerative effects of cortisol. With intense
training and a proper diet, the body will typically store more protein than it
removes, but this underlying battle is always constant.
When administering anabolic steroids, however, a much higher androgen level
can place glucocorticoids at a notable disadvantage. With their effect reduced,
fewer cells will be given a message to release protein, and more will be
accumulated in the long run. The primarily mechanism believed to bring this
effect out is androgen displacement of glucocorticoids bound to the
glucocorticoid receptor. In fact, in-vitro studies have supported this notion by
demonstrating that testosterone has a very high affinity for this receptor,
11 and
further suggesting that some of its anabolic activity is directly mediated through
this action.
12
It is also suggested that androgens may indirectly interfere with
DNA binding to the glucocorticoid response element.
13 Although the exact
underlying mechanism is still in debate, what is clear is that steroid
administration inhibits protein breakdown, even in the fasted state, which seems
clearly indicative of an anti-catabolic effect.
Testosterone and Creatine
In addition to protein synthesis, a rise in androgen levels should also enhance the
synthesis of creatine in skeletal muscle tissues.
14 Creatine, as creatine phosphate
(CP), plays a crucial role in the manufacture of ATP (adenosine triphosphate),
which is a main store of energy for the muscles. As the muscle cells are
stimulated to contract, ATP molecules are broken down into ADP (adenosine
diphosphate), which releases energy. The cells will then undergo a process using
creatine phosphate to rapidly restore ADP to its original structure, in order to
replenish ATP concentrations. During periods of intense activity, however, this
process will not be fast enough to compensate and ATP levels will become
lowered. This will cause the muscles to become fatigued and less able to effort a
strenuous contraction. With increased levels of CP available to the cells, ATP is
replenished at an enhanced rate and the muscle is both stronger and more
enduring. This effect will account for some portion of the early strength
increases seen during steroid therapy. Although perhaps not technically
considered an anabolic effect as tissue hypertrophy is not a direct result,
androgen support of creatine synthesis is certainly still looked at as a positive
and growth-supporting result in the mind of the bodybuilder.
Testosterone and IGF-1
It has also been suggested that there is an indirect mechanism of testosterone
action on muscle mass mediated by Insulin-Like Growth Factor. To be more
specific, studies note a clear link between androgens and tissue release of,
15 and
responsiveness to, this anabolic hormone. For example, it has been demonstrated
that increases in IGF-1 receptor concentrations in skeletal muscle are noted
when elderly men are given replacement doses of testosterone.
16
In essence, the
cells are becoming primed for the actions of IGF-1, by testosterone. Alternately
we see marked decreases in IGF-1 receptor protein levels with androgen
deficiency in young men. It also appears that androgens are necessary for the
local production and function of IGF-1 in skeletal muscle cells, independent of
circulating growth hormone, and IGF-1 levels.
17 Since we do know for certain
that IGF-1 is at least a minor anabolic hormone in muscle tissue, it seems
reasonable to conclude that this factor, at least at some level, is involved in the
muscle growth noted with steroid therapy.
Direct and Indirect Steroids?
In looking over the proposed indirect effects of testosterone, and pondering the
effectiveness of the synthetic anabolic/androgenic steroids, we must resist the
temptation to believe we can categorize steroids as those which directly, and
those which indirectly, promote muscle growth. The belief that there are two
dichotomous groups or classes of steroids ignores the fact that all commercial
steroids promote not only muscle growth but also androgenic effects. There is no
complete separation of these traits at this time, making clear that all activate the
cellular androgen receptor. I believe the theory behind direct and indirect steroid
classifications originated when some noted the low receptor binding affinity of
seemingly strong anabolic steroids like oxymetholone and
methandrostenolone.
18
If they bind poorly, yet work well, something else must
be at work. This type of thinking fails to recognize other factors in the potency
of these compounds, such as their long half-lives, estrogenic activity, and weak
interaction with restrictive binding proteins (see: Free vs. Bound Testosterone).
While there may possibly be differences in the way various compounds could
foster growth indirectly, such that advantages might even be found with certain
synergistic drug combinations, the primary mode of action with all of these
compounds is the androgen receptor. The notion that steroid X and Y must never
be stacked together because they both compete for the same receptor when
stimulating growth, while X and Z should be combined because they work via
different mechanisms, should likewise not be taken too seriously. Such
classifications are based on speculation only, and upon reasonable investigation
are clearly invalid.
MECHANISM OF ACTION DIAGRAM: The mechanism of anabolic
action due to the administration of anabolic/androgenic steroids. AAS
causes not only direct stimulation of the androgen receptor, but also
supports muscle growth by increasing the levels of free androgens,
increasing androgen receptor density, inhibiting corticosteroid action,
increasing GH/IGF-1, and suppressing IGF-1 binding proteins.
9. Testosterone injection stimulates net protein synthesis but not tissue amino acid transport. Fernando A,
Tipton K, Doyle D et al. Am J. Physiol (Endocrinology and Metabolism) 38:E864-71,1998.
10. Glucorticoid antagonism by exercise and androgenic-anabolic steroids. Hickson RC, Czerwinski SM,
Falduto MT, Young AP. Med Sci Sports Exerc 22 (1990) 331-40
11. Binding of glucorticoid antagonists to androgen and glucorticoid hormone receptors in rat skeletal
muscle. Danhaive PA, Rousseau GG. J Steroid Biochem Mol Biol 24 (1986) 481-71
12. Evidence for a sex-dependent anabolic response to androgenic steroids mediated by muscle glucorticoid
receptors in the rat. Danhaive PA, Rousseau GG. J. Steroid Biochem Mol Biol. 29 (1988) 575-81
13. Glucorticoid antagonism by exercise and androgenic-anabolic steroids. Hickson RC, Czerwinski SM,
Falduto MT, Young AP. Med Sci Sports Exerc 22 (1990) 331-40
14. The source of excess creatine following methyl testosterone. Samuels L. T., Sellers D. M., McCaulay C.
J. J. Clin. Endocrinol. Metab. 6 (1946) 655-63
15. Ontogeny of growth hormone, insulin-like growth factor, estradiol and cortisol in the growing lamb:
effect of testosterone. Arnold AM, Peralta JM,Tonney MI. J Endocrinol 150 (1996) 391-9
12.Jun;130(6):3677-83. 81, 2001.
16. Testosterone administration to elderly men increases skeletal muscle strength and protein synthesis. Am
J Physiol 269 (1995) E820-6
17. Testosterone deficiency in young men: marked alterations in whole body protein kinetics, strength, and
adiposity. Mausas N, Hayes V, Welch S et al. J Clin Endocrin Metab 83 (1998) 1886-92
18. Endocrinology 114(6):2100-06 1984 June,“Relative Binding Affinity of Anabolic-Androgenic
Steroids…”, Saartok T; Dahlberg E; Gustafsson JA
Free vs. Bound Testosterone
A very small amount of testosterone actually exists in a free state, where
interaction with cellular receptors is possible. The majority will be bound to the
proteins SHBG (sex hormone binding globulin, also referred to as sex steroid
binding globulin and testosterone-estradiol binding globulin) and albumin,
which temporarily prevent the hormone from exerting activity. Steroid hormones
actually bind much more avidly to SHBG than albumin (with approximately
1,000 times greater affinity), however albumin is present in a level 1,000 times
greater than SHBG. Therefore, the activity of both binding proteins in the body
is relatively equal. The distribution of testosterone in men is typically 45% of
testosterone bound to SHBG, and about 53% bound to albumin. The remaining
2% of the average blood concentration exists in a free, unbound state. In women,
the percentage of free testosterone is lower, measured to be approximately 1%.
A binding protein called ABP (androgen binding protein) also helps to mediate
androgen activity in the reproductive system, although since it is found
exclusively in these tissues, it is not relevant to muscle growth.
The level of free testosterone available in the blood is likewise an important
factor mediating its activity, as only a small percentage is really active at any
given time. It must also be noted that as we alter testosterone to form new
anabolic/androgenic steroids, we also typically alter the affinity in which the
steroid will bind to plasma proteins. This is an important consideration, as the
higher percentage we have of free hormone, the more active the compound
should be on a milligram for milligram basis. And the variance can be
substantial between different compounds.
For example, Proviron® (1-methyl dihydrotestosterone) binds with SHBG many
times more avidly than testosterone,
19 while mibolerone (7,17 dimethylnandrolone) and bolasterone (7,17 dimethyl-testosterone) show virtually no
affinity for this protein at all (clearly the reason these steroids are such potent
androgens).
The level of SHBG present in the body is also variable, and can be altered by a
number of factors. The most prominent seems to be the concentration of
estrogen and thyroid hormones present in the blood. We generally see a
reduction in the amount of this plasma binding protein as estrogen and thyroid
content decreases, and a rise in SHBG as they increase. A heightened androgen
level due to the administration of anabolic/androgenic steroids has also been
shown to lower levels of this protein considerably. This is clearly supported by a
1989 German study, which noted a strong tendency for SHBG reduction with the
oral anabolic steroid stanozolol (Winstrol®).
20 After only 3 days of
administering a daily dose of .2mg/kg body-weight (about 18mg for a 200lb
man), SHBG was lowered nearly 50% in normal subjects. Similar results have
been obtained with the use of injectable testosterone enanthate; however,
milligram for milligram, the effect of stanozolol was much greater in
comparison. The form of administration may have been important in reaching
this level of response. Although the injectable was not tried in the German study,
we can refer to others comparing the effect of oral vs. transdermal estrogen.
21
These show a much greater response in SHBG levels when the drug is given
orally. This is perhaps explained by the fact that SHBG is produced in the liver.
Therefore, we cannot assume that injectable Winstrol® (or injectable steroids in
general) will display the same level of potency in this regard.
Lowering the level of plasma binding proteins is also not the only mechanism
that allows for an increased level of free testosterone. Steroids that display a high
affinity for these proteins may also increase the level of free testosterone by
competing with it for binding. Obviously if testosterone finds it more difficult to
locate available plasma proteins in the presence of the additional compound,
more will be left in an unbound state. A number of steroids including
dihydrotestosterone, Proviron®, and Oral-Turinabol
(chlorodehydromethyltestosterone) display a strong tendency for this effect. If
the level of free-testosterone can be altered by the use of different
anabolic/androgenic steroids, the possibility also exists that one steroid can
increase the potency of another through these same mechanisms. For example,
Proviron® is a poor anabolic, but its extremely high affinity for SHBG might
make it useful by allowing the displacement of other steroids that are more
active in these tissues.
We must not let this discussion lead us into thinking that binding proteins serve
no valuable function. In fact they play a vital role in the transport and
functioning of endogenous androgens. Binding proteins act to protect the steroid
against rapid metabolism, ensure a more stable blood hormone concentration,
and facilitate an even distribution of hormone to various body organs. The recent
discovery of a specific receptor for Sex Hormone Binding Globulin (SHBG-R)
located on the membrane surface of steroid responsive body cells also suggests a
much more complicated role for this protein than solely hormone transport.
However, it remains clear that manipulating the tendency of a hormone to exist
in an unbound state is an effective way to alter drug potency.
19. Endocrinology 114(6):2100-06 1984 June,“Relative Binding Affinity of Anabolic-Androgenic
Steroids…”, Saartok T; Dahlberg E; Gustafsson JA
20. Sex Hormone-Binding Globulin Response to the Anabolic Steroid Stanozolol: Evidence for Its
Suitability as a Biological Androgen Sensitivity Test. J Clin Endocrinol Metab 68:1195,1989
21. Twenty two weeks of transdermal estradiol increases sex hormone-binding globulin in surgical
menopausal women. Eur J Obstet Gynecol Reprod Biol 73: 149-52,1997
Estrogen Aromatization
Testosterone is the primary substrate used in the male body for the synthesis of
estrogen (estradiol), the principal female sex hormone. Although the presence of
estrogen may seem quite unusual in men, it is structurally very similar to
testosterone. With a slight alteration by the enzyme aromatase, estrogen is
produced in the male body. Aromatase activity occurs in various regions of the
male body, including adipose,
22
liver,
23 gonadal,
24 central nervous system,
25 and
skeletal muscle
26
tissues. In the context of the average healthy male, the amount
of estrogen produced is generally not very significant to one's body disposition,
and may even be beneficial in terms of cholesterol values (See Side Effects:
Cardiovascular System). However, in larger amounts it does have potential to
cause many unwanted effects including water retention, female breast tissue
development (gynecomastia), and body fat accumulation. For these reasons,
many focus on minimizing the build-up or activity of estrogen in the body with
aromatase inhibitors such as Arimidex and Cytadren, or anti-estrogens such as
Clomid or Nolvadex, particularly at times when gynecomastia is a worry or the
athlete is attempting to increase muscle definition.
We must, however, not be led into thinking that estrogen serves no benefit. It is
actually a desirable hormone in many regards. Athletes have known for years
that estrogenic steroids are the best mass builders, but it is only recently that we
are finally coming to understand the underlying mechanisms why. It appears that
reasons go beyond the simple size, weight, and strength increases that one would
attribute to estrogen-related water retention, with this hormone actually having a
direct effect on the process of anabolism. This is manifest through increases in
glucose utilization, growth hormone secretion,and androgen receptor
proliferation.
Glucose Utilization and Estrogen
Estrogen may play a very important role in the promotion of an anabolic state by
affecting glucose utilization in muscle tissue. This occurs via an altering of the
level of available glucose 6-phosphate dehydrogenase, an enzyme directly tied to
the use of glucose for muscle tissue growth and recuperation.
27 28 More
specifically, G6PD is a vital part of the pentose phosphate pathway, which is
integral in determining the rate nucleic acids and lipids are to be synthesized in
cells for tissue repair. During the period of regeneration after skeletal muscle
damage, levels of G6PD are shown to rise dramatically, which is believed to
represent a mechanism for the body to enhance recovery when needed.
Surprisingly, we find that estrogen is directly tied to the level of G6PD that is to
be made available to cells in this recovery window.
The link between estrogen and G6PD was established in a study demonstrating
levels of this dehydrogenase enzyme to rise after administration of testosterone
propionate. The investigation further showed that the aromatization of
testosterone to estradiol was directly responsible for this increase, and not the
androgenic action of this steroid.
29 The non-aromatizable steroids
dihydrotestosterone and fluoxymesterone were tested alongside testosterone
propionate, but failed to duplicate the effect of testosterone. Furthermore, the
positive effect of testosterone propionate was blocked when the aromatase
inhibitor 4-hydroxyandrostenedione (formestane) was added, while 17-beta
estradiol administration alone caused a similar increase in G6PD to tesosterone
propionate. The inactive estrogen isomer alpha estradiol, which is unable to bind
the estrogen receptor, failed to do anything. Further tests using testosterone
propionate and the anti-androgen flutamide showed that this drug also did
nothing to block the positive action of testosterone, establishing it as an effect
independent of the androgen receptor.
Estrogen and GH/IGF-1
Estrogen may also play an important role in the production of growth hormone
and IGF-1. IGF-1 (insulin-like growth factor) is an anabolic hormone released in
the liver and various peripheral tissues via the stimulus of growth hormone (See
Drug Profiles: Growth Hormone). IGF-1 is responsible for the anabolic activity
of growth hormone such as increased nitrogen retention/protein synthesis and
cell hyperplasia (proliferation). One of the first studies to bring this issue to our
attention looked at the effects of the anti-estrogen tamoxifen on IGF-1 levels,
demonstrating it to have a suppressive effect.
30 A second, perhaps more
noteworthy, study took place in 1993, which looked at the effects of testosterone
replacement therapy on GH and IGF-1 levels alone, and compared them to the
effects of testosterone combined again with tamoxifen.
31 When tamoxifen was
given, GH and IGF-1 levels were notably suppressed, while both values were
elevated with the administration of testosterone enanthate alone. Another study
has shown 300 mg of testosterone enanthate weekly to cause a slight IGF-1
increase in normal men. Here the 300 mg of testosterone ester caused an
elevation of estradiol levels, which would be expected at such a dose. This was
compared to the effect of the same dosage of nandrolone decanoate; however,
this steroid failed to produce the same increase. This result is quite interesting,
especially when we note that estrogen levels were actually lowered
32 when this
steroid was given. Yet another demonstrated that GH and IGF-1 secretion is
increased with testosterone administration on males with delayed puberty, while
dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1
secretion.
33
Estrogen and the Androgen Receptor
It has also been demonstrated that estrogen can increase the concentration of
androgen receptors in certain tissues. This was shown in studies with rats, which
looked at the effects of estrogen on cellular androgen receptors in animals that
underwent orchiectomy (removal of testes, often done to diminish endogenous
androgen production). According to the study, administration of estrogen
resulted in a striking 480% increase in methyltrienolone (a potent oral androgen
often used to reference receptor binding in studies) binding in the levator ani
muscle.
34 The suggested explanation is that estrogen must either be directly
stimulating androgen receptor production, or perhaps diminishing the rate of
receptor breakdown. Although the growth of the levator ani muscle is commonly
used as a reference for the anabolic activity of steroid compounds, it is
admittedly a sex organ muscle, and different from skeletal muscle tissue in that it
possesses a much higher concentration of androgen receptors. This study,
however, did look at the effect of estrogen in fast-twitch skeletal muscle tissues
(tibialis anterior and extensor digitorum longus) as well, but did not note the
same increase as the levator ani. Although discouraging at first glance, the fact
that estrogen can increase androgen receptor binding in any tissue remains an
extremely significant finding, especially in light of the fact that we now know
androgens to have some positive effects on muscle growth that are mediated
outside of muscle tissue.
Estrogen and Fatigue
“Steroid Fatigue” is a common catchphrase these days, and refers to another
important function of estrogen in both the male and female body, namely its
ability to promote wakefulness and a mentally alert state. Given the common
availability of potent third-generation aromatase inhibitors, bodybuilders today
are (at times) noticing more extreme estrogen suppression than they had in the
past. Often associated with this suppression is fatigue. Under such conditions,
the athlete, though on a productive cycle of drugs, may not be able to maximize
his or her gains due to an inability to train at full vigor. This effect is sometimes
also dubbed “steroid lethargy.” The reason is that estrogen plays an important
supporting role in the activity of serotonin. Serotonin is one of the body's
principle neurotransmitters, vital to mental alertness and the sleep/wake cycle.
35
36
Interference with this neurotransmitter is also associated with chronic fatigue
syndrome,
37 38 so we can see how vital it is to fatigue specifically. Estrogen
suppression in menopause has also been associated with fatigue,
39 as has the
clinical use of newer (more potent) aromatase inhibitors like anastrozole,
40
letrozole,
41 exemestane,
42 and fadrozole
43
in some patients. These things may be
important to consider when planning your next cycle. Although not everyone
notices this problem when estrogen is low, for those that do, a little testosterone
or estrogen can go a long way in correcting this. It is also of note that the use of
strictly non-aromatizable steroids sometimes causes this effect as well, likely
due to the suppression of natural testosterone production (cutting off the main
substrate used by the male body to make estrogen).
Anti-Estrogens and the Athlete
So what does this all mean to the bodybuilder looking to gain optimal size?
Basically I think it calls for a cautious approach to the use of estrogen
maintenance drugs if mass is the key objective (things change, of course, if we
are talking about cutting). Obviously, anti-estrogens should be used if there is a
clear need for them due to the onset of estrogenic side effects, or at the very
least, the drugs being administered should be substituted for non-estrogenic
compounds. Gynecomastia is certainly an unwanted problem for the steroid user,
as are noticeable fat mass gains. But if these problems have not presented
themselves, the added estrogen due to a cycle of testosterone or Dianabol, for
example, might indeed be aiding in the buildup of muscle mass, or keeping you
energetic. An individual confident they will notice, or are not prone to getting,
estrogenic side effects, may therefore want to hold off using estrogen
maintenance drugs so as to achieve the maximum possible gains in tissue mass.
22. Aromatization of androgens by muscle and adipose tissue in vivo. Longcope C, Pratt JH, Schneider SH,
Fineberg SE. J Clin Endocrinol Metab 1978 Jan;46(1):146-52
23. The aromatization of androstenedione by human adipose and liver tissue. J Steroid Biochem. 1980
Dec;13(12):1427-31.
24. Aromatase expression in the human male. Brodie A, Inkster S, Yue W. Mol Cell Endocrinol 2001 Jun
10;178(1-2):23-8
25. A review of brain aromatase cytochrome P450. Lephart ED. Brain Res Brain Res Rev 1996 Jun;22(1):1-
26
26. Aromatization by skeletal muscle. Matsumine H, Hirato K, Yanaihara T, Tamada T, Yoshida M. J Clin
Endocrinol Metab 1986 Sep;63(3):717-20
27. Pentose Cycle Activity in Muscle from Fetal, Neonatal and Infant Rhesus Monkeys. Arch Biochem
Biophys 117:275-81 1966
28. The pentose phosphate pathway in regenerating skeletal muscle. Biochem J 170: 17 1978
29. Aromatization of androgens to estrogens mediates increased activity of glucose 6-phosphate
dehydrogenase in rat levator ani muscle. Endocrinol
106(2):440-43 1980
30.
Influence of tamoxifen, aminoglutethimide and goserelin on human plasma IGF-1 levels in breast cancer
patients. J steroid Biochem Mol Bio 41:541-3,1992
31. Activation of the somatotropic axis by testosterone in adult males: Evidence for the role of
aromatization. J Clin. Endocrinol Metab 76:1407-12 1993
32. Testosterone administration increases insulin-like growth factor-I levels in normal men. J Clin
Endocrinol Metab 77(3):776-9 1993
33. Androgen-stimulated pubertal growth:the effects of testosterone and dihydrotestosterone on growth
hormone and insulin-like growth factor-I in the treatment of short stature and delayed puberty. J Clin
Endocrinol Metab 76(4)996-1001 1993
34. Modulation of the cytosolic androgen receptor in striated muscle by sex steroids. Endocrinology. 1984
Sep;115(3):862-6.
35. Effect of estrogen-serotonin interactions on mood and cognition. Zenab Amin et al. Behav Cogn
Neurosci Reviews 4(1) 2005:43-58
36. Serotonin and the sleep/wake cycle: special emphasis on miscodialysis studies. Chiara M Portas et al.
Progress in Neurology 60(200) 13-35.
37. Reduction of serotonin transporters of patients with chronic fatigue syndrome. Neuroreport 2004 Dec
3;15(17):2571-4
38. Association between serotonin transporter gene polymorphism and chronic fatigue syndrome. Narita M
et al. Biochem Biophys Res Commun 2003 Nov 14;311(2)264-6
39. Premenstrual Syndrome. Dickerson LM et al. Am Fam Physician 2003 Apr 15;67(8):1743-52
40. Phase II trial of anastrozole in women with asymptomatic mullerian cancer. Gynecol Oncol. 2003
Dec;91(3):596-602.
41. Letrozole. A review of its use in postmenopausal women with advanced breast cancer. Drugs. 1998
Dec;56(6):1125-40. Review.
42. Exemestane: a review of its clinical efficacy and safety. Breast. 2001 Jun;10(3):198-208.
43. A study of fadrozole, a new aromatase inhibitor, in postmenopausal women with advanced metastatic
breast cancer. J Clin Oncol. 1992 Jan;10(1):111-6.
DHT Conversion
As we see from our discussion with estrogen, in considering the physiological
effects of any steroid, we must look at all of its active metabolites, and not just
the initial compound. This includes not only estrogenic products, but androgenic
metabolites as well. With this in mind, it is important to note that the potency of
testosterone is considerably increased in many androgen responsive tissues when
it converts to dihydrotestosterone. More commonly referred to by the three-letter
abbreviation DHT, this hormone is, in fact, measured to be approximately three
to four times stronger than testosterone. It is the most potent steroid found
naturally in the human body, and important to discuss if we are to understand the
full activity of testosterone, as well as other anabolic/androgenic steroids that
undergo a similar conversion.
Testosterone is converted to dihydrotestosterone upon interaction with the 5-
alpha reductase enzyme. More specifically, this enzyme removes the C4-5
double-bond of testosterone by the addition of two hydrogen atoms to its
structure (hence the name dihydro testosterone). The removal of this bond is
important, as in this case it creates a steroid that binds to the androgen receptor
much more avidly than its parent steroid. 5-alpha reductase is present in high
amounts in tissues of the prostate, skin, scalp, liver, and various regions of the
central nervous system, and as such represents a mechanism for the body to
increase the potency of testosterone specifically where strong androgenic action
is needed. In these areas of the body little testosterone will actually make its way
to the receptor without being converted to dihydrotestosterone, making DHT by
far the active form of androgen here.
DHT and Androgenic Side Effects
In some regards this local potentiation of testosterone's activity may be
unwelcome, as higher androgenic activity in certain tissues may produce a
number of undesirable side effects. Acne, for example, is often triggered by
dihydrotestosterone activity in the sebaceous glands, and the local formation of
dihydrotestosterone in the scalp is typically blamed for triggering male pattern
hair loss. You should know that it is a terrible misconception among
bodybuilders that dihydrotestosterone is an isolated culprit when it comes to
these side effects. All anabolic/androgenic steroids exert their activities, both
anabolic and androgenic, through the same cellular androgen receptor.
Dihydrotestosterone is no different than any other steroid except that it is a more
potent activator of this receptor than most, and can be formed locally in certain
androgen-sensitive tissues. All steroids can cause androgenic side effects in
direct relation to their affinity for this receptor, and DHT has no known unique
ability in this regard.
Benefits of DHT
While a lot of attention is being paid to the negative side effects of the androgen
dihydrotestosterone, you should know that there are some known benefits to the
strong androgenic activity brought about by this hormone as well. For example,
DHT plays an important role in the organization and functioning of the central
nervous system. Many neural cells contain active androgen receptors, and it is
thought that there may even be a specific importance of dihydrotestosterone in
this area of the body. Studies have shown DHT to have a profoundly greater
impact in these cells compared to testosterone. More specifically, animal models
demonstrated that both testosterone and DHT would result in increased androgen
receptor proliferation in neural cells three and seven hours after being
administered, however only DHT was able to sustain this increase at the twentyone hour mark.
44 Although some might contend that this difference is simply
due to DHT forming a more stable and lasting complex with the androgen
receptor, others suggest that DHT and testosterone might even be affecting
neural cells differently, such that the dihydrotestosterone-receptor complex and
testosterone-receptor complex might be activating the transcription of different
target genes.
The strong interaction between the central nervous system and skeletal muscles,
collectively referred to as the neuromuscular system, is of key importance to the
athlete. There appears to be little doubt that the ability of the body to adapt to
training, and to activate nerve endings in muscle tissue, is reliant on the
interactions of the neuromuscular system. Inhibiting the formation of DHT
during a testosterone cycle may therefore inadvertently interfere with strength
and muscle mass gains. This would explain why bodybuilders commonly report
a drop in steroid potency when they add the 5-alpha reductase inhibitor
finasteride to a testosterone cycle. Many complain strength and even muscle
mass gains slow significantly when this medication is added, which would not
make sense if testosterone and androgen receptor activation in muscle tissue
were solely responsible for growth. Clearly more is involved, and we cannot
look at dihydrotestosterone simply as a side-effect hormone.
44. Neural androgen receptor regulation: effects of androgen and antiandrogen. Lu S, Simon NG, Wang Y,
Hu S. J Neurobiol 1999 Dec;41(4):505-12
Brief History of Anabolic/Androgenic Steroids
While it had been clear for many centuries that the testicles were crucial for the
male body to properly develop, it was not until modern times that an
understanding of testosterone began to form. The first solid scientific
experiments in this area, which eventually led to the discovery and replication of
testosterone (and related androgens), were undertaken in the 1800s. During this
century a number of animal experiments were published, most of which involved
the removal and/or implantation of testicular material from/in a subject.
Although very crude in design by today's standards, these studies certainly laid
the foundation for the modern field of endocrinology (the study of hormones).
By the turn of the century, scientists were able to produce the first experimental
androgen injections. These were actualized either through the filtering of large
quantities of urine (for active hormones), or by extracting testosterone from
animal testicles. Again, the methods were rough but the final results proved to be
very enlightening.
Chemists finally synthesized the structure of testosterone in the mid-1930’s,
sparking a new wave of interest in this hormone. With the medical community
paying a tremendous amount of attention to this achievement, the possible
therapeutic uses for a readily available synthetic testosterone quickly became an
extremely popular focus. Many believed the applications for this type of a
medication would be extremely far-reaching, with uses ranging from the
maintenance of an androgen deficiency, to that of a good health and well-being
treatment for the sickly or elderly. During the infancy of such experimentation,
many believed they had crossed paths with a true “fountain of youth.”
Dihydrotestosterone and nandrolone, two other naturally occurring steroids,
were also isolated and synthesized in the early years of steroid development. To
make things even more interesting, scientists soon realized that the androgenic,
estrogenic, and anabolic activity of steroid hormones could be adjusted by
altering their molecular structure. The goal of many researchers thereafter
became to manufacture a steroid with extremely strong anabolic activity, but will
display little or no androgenic/estrogenic properties. This could be very
beneficial, because side effects will often become pronounced when steroid
hormones are administered in supraphysiological amounts. A “pure” anabolic
would theoretically allow the patient to receive only the beneficial effects of
androgens (lean muscle mass gain, increased energy and recuperation, etc.),
regardless of the dosage. Some early success with the creation of new structures
convinced many scientists that they were on the right track. Unfortunately none
of this progress led researchers their ultimate goal. By the mid-1950’s, well over
one thousand testosterone, nandrolone, and dihydrotestosterone analogues had
been produced, but none proved to be purely anabolic compounds.
The failure to reach this goal was primarily due to an initial flawed
understanding of testosterone's action. Scientists had noticed high levels of DHT
in certain tissues, and believed this indicated an unusual receptor affinity for this
hormone. This led to the belief that the human body had two different androgen
receptors. According to this theory, one receptor site would respond only to
testosterone (eliciting the beneficial anabolic effects), while the other is activated
specifically by the metabolite, dihydrotestosterone. With this understanding,
eliminating the conversion of testosterone to DHT was thought capable of
solving the problem of androgenic side effects, as these receptors would have
little or none of this hormone available for binding. More recently, however,
scientists have come to understand that only one type of androgen receptor exists
in the human body. It is also accepted that no anabolic/androgenic steroid can
possibly be synthesized that would participate only with receptors in tissues
related to anabolism. DHT, which was once thought not to bind to the same
receptor as testosterone, is now known to do so at approximately three to four
times the affinity of its parent, and the unusual recovery of DHT from androgen
responsive tissues is now attributed to the distribution characteristics of the 5areductase enzyme.
Synthetic AAS Development
In order to develop products that would be effective therapeutically, chemists
needed to solve a number of problems with using natural steroid hormones for
treatment. For example, oral dosing was a problem, as our basic steroids
testosterone, nandrolone, and dihydrotestosterone are ineffective when
administered this way. The liver would efficiently break down their structure
before reaching circulation, so some form of alteration was required in order for
a tablet or capsule to be produced. Our natural steroid hormones also have very
short half-lives in the body, so when administered by injection, an extremely
frequent and uncomfortable dosing schedule is required if a steady blood level is
to be achieved. Therefore, extending steroid activity was a major goal for many
chemists during the early years of synthetic AAS development. Scientists also
focused on the nagging problems of possible excess estrogenic buildup in the
blood, particularly with testosterone, which can become very uncomfortable for
patients undergoing therapy.
Methylated Compounds and Oral Dosing
Chemists realized that by replacing the hydrogen atom at the steroid's 17th alpha
position with a carbon atom (a process referred to as alkylation), its structure
would be notably resistant to breakdown by the liver. The carbon atom is
typically added in the form of a methyl group (CH3), although we see oral
steroids with an added ethyl
(C2H5) grouping as well. A steroid with this alteration is commonly descirbed
as a C-17 alpha alkylated oral, although the terms of methylated or ethylated oral
steroid are also used. The alkyl group cannot be removed metabolically, and
therefore inhibits reduction of the steroid to its inactive 17-ketosteroid form by
occupying one of the necessary carbon bonds. Before long, pharmaceutical
companies had utilized this advance (and others) to manufacture an array of
effective oral steroids including methyltestosterone, Dianabol, Winstrol®,
Anadrol 50®, Halotestin®, Nilevar, Orabolin, and Anavar. The principle
drawback to these compounds is that they place a notable amount of stress on the
liver, which in some instances can lead to actual damage to this organ.
Because the alkyl group cannot be removed, it mediates the action of the steroid
in the body. Methyltestosterone, for example, is not simply an oral equivalent of
testosterone, as the added alkylation changes the activity of this steroid
considerably. One major change we see is an increased tendency for the steroid
to produce estrogenic side effects, despite the fact that it actually lowers the
ability of the hormone to interact with aromatase.
45 Apparently with 17-
alkylation present on a steroid, aromatization (when possible) produces a more
active form of estrogen (typically 17alpha-methyl or 17alpha-ethyl estradiol).
These estrogens are more biologically active than estradiol due to their longer
half-life and weaker tendency to bind with serum proteins. In some instances,
17alpha-alkylation will also enhance the ability of the initial steroid compound
to bind with and activate the estrogen or progesterone receptor.
46 An
enhancement of estrogenic properties is also obvious when we look at
methandrostenolone, which is an alkylated form of boldenone (Equipoise®), and
Nilevar, which is an alkylated form of the mild anabolic nandrolone. Dianabol is
clearly more estrogenic than Equipoise®, a drug not noted for producing strong
side
effects of this nature. The same holds true for the comparison of Nilevar to
Deca-Durabolin, a compound that we also know to be extremely mild in this
regard.
C17 alpha alkylation also typically lowers the affinity in which the steroid binds
to the androgen receptor, as is noted with the weak relative binding affinity of
such popular agents as Dianabol and Winstrol (stanozolol). However, since this
alteration also greatly prolongs the half-life of a steroid, as well as increases the
tendency for it to exist in an unbound state, it creates a more potent
anabolic/androgenic agent in both cases. This explains why Dianabol and
stanozolol are notably effective in relatively lower weekly doses (often 140 mg
weekly will produce notable growth) compared to injectables such as
testosterone and nandrolone, which often need to reach doses of 300-400 mg
weekly for a similar level of effect.
Non-Alkylated Orals
In an attempt to solve the mentioned problems with liver toxicity we see with
c17-alpha alkylated compounds, a number of other orals with different chemical
alterations (such as Primobolan®, Proviron®, AndriolË, and Anabolicum Vister)
were created. Primobolan® and Proviron® are alkylated at the one position
(methyl), a trait which also slows ketosteroid reduction. Andriol® uses a 17beta
carboxylic acid ester (used with injectable compounds, discussed below),
however, here the oil-dissolved steroid is sealed in a capsule and is intended for
oral administration. This is supposed to promote steroid absorption through
intestinal lymphatic ducts, bypassing the first pass through the liver. In addition
to 1 methylation, Primobolan® also utilizes a 17 beta ester (acetate) to further
protect against reduction to inactive form (here there is no lymphatic system
absorption). Anabolicum Vister uses 17beta enol ether linkage to protect the
steroid, which is very similar to esterification as the ether breaks off to release a
steroid base (boldenone in this case). While all of these types of compounds do
not place the same stress on the liver, they are also much less resistant to
breakdown than 17 alkylated orals, and are ultimately less active milligram for
milligram.
Esters and Injectable Compounds
You may notice that many injectable steroids will list long chemical names like
testosterone cypionate and testosterone enanthate, instead of just testosterone. In
these cases, the cypionate and enanthate are esters (carboxylic acids) that have
been attached to the 17-beta hydroxyl group of the testosterone molecule, which
increase the active life span of the steroid preparation. Such alterations will
reduce the steroid's level of water solubility, and increase its oil solubility. Once
an esterified compound has been injected, it will form a deposit in the muscle
tissue (depot) from which it will slowly enter circulation. Generally the larger
the ester chain, the more oil soluble the steroid compound will be, and the longer
it will take for the full dosage to be released. Once free in circulation, enzymes
will quickly remove the ester chain and the parent hormone will be free to exert
its activity (while the ester is present the steroid is inert).
There are a wide number of esters, which can provide varying release times,
used in medicine today. To compare, an ester like decanoate can extend the
release of active parent drug into the blood stream for three to four weeks, while
it may only be extended for a few days with an acetate or propionate ester. The
use of an ester allows for a much less frequent injection schedule than if using a
water-based (straight) testosterone, which is much more comfortable for the
patient. We must remember when calculating dosages, that the ester is figured
into the steroid's measured weight. 100 mg of testosterone enanthate, therefore,
contains much less base hormone than 100 mg of a straight testosterone
suspension (in this case it equals 72mg of testosterone). In some instances, an
ester may account for roughly 40% or more of the total steroid weight, but the
typical measure is somewhere around 15% to 35%. Below are the free base
equivalents for several popular steroid compounds.
It is also important to stress the fact that esters do not alter the activity of the
parent steroid in any way. They work only to slow its release. It is quite common
to hear people speak about the properties of different esters, almost as if they can
magically alter a steroid's effectiveness. This is really nonsense. Enanthate is not
more powerful than cypionate (perhaps a few extra milligrams of testosterone
released per injection, but nothing to note), nor is Sustanon some type of
incredible testosterone blend. Personally, I have always considered Sustanon a
very poor buy in the face of cheaper 250 mg enanthate ampules. Your muscle
cells see only testosterone; ultimately there is no difference. Reports of varying
levels of muscle gain, androgenic side effects, water retention, etc. are only
issues of timing. Faster releasing testosterone esters will produce estrogen
buildup faster simply because there is more testosterone free in the blood from
the start of the cycle. The same is true when we state that Durabolin® is a milder
nandrolone for women compared to Deca. It is simply easier to control the blood
level with a faster acting drug. Were virilization symptoms to become apparent,
hormone levels will drop much faster once we stop administration. This should
not be confused with the notion that the nandrolone in Durabolin® acts
differently in the body than that released from a shot of Deca-Durabolin®.
It is also worth noting that while the ester is typically hydrolyzed in general
circulation, some will be hydrolyzed at the injection site where the steroid depot
first contacts blood. This will cause a slightly higher concentration of both free
steroid and ester in the muscle where the drug had been administered. On the
plus side, this may equate to slightly better growth in this muscle, as more
hormone is made available to nearby cells. Many bodybuilders have come to
swear by the use of injection sites such as the deltoids, biceps, and triceps, truly
believing better growth can be achieved if the steroid is injected directly into
these muscles. The negative to this is that the ester itself may be irritating to the
tissues at the site of injection once it is broken free. In some instances it can be
so caustic that the muscle itself will become swollen and sore due to the
presence of the ester, and the user may even suffer a lowgrade fever as the body
fights off the irritant (the onset of such symptoms typically occurs 24-72 hours
after injection). This effect is more common with small chain esters such as
propionate and acetate, and can actually make a popular steroid such as Sustanon
(which contains testosterone propionate) off-limits for some users who
experience too much discomfort to justify using the drug. Longer chain esters
such as decanoate and cypionate are typically much less irritating at the site of
injection, and therefore are preferred by sensitive individuals.
Anabolic/Androgenic Dissociation
Although never complete, scientists had some success in their quest to separate
the androgenic and anabolic properties of testosterone. A number of synthetic
anabolic steroids had been developed as a result, with many being notably
weaker and stronger than our base androgen. In order to first assess the anabolic
and androgenic potential of each newly developed steroid, scientists had
generally used rats as a model. To judge androgenic potency the typical
procedure involved the post-administration measure (% growth) of the seminal
vesicles and ventral prostate. These two tissues will often respond unequally to a
given steroid, however, so an average of the two figures is used. Anabolic
activity was most commonly determined by measuring the growth of the levator
ani, a sex organ (not skeletal) muscle. This tissue may not be the most ideal one
to use though, as it contains more androgen receptor than most skeletal muscles
(the AR is still less abundant here than in target tissues such as the ventral
prostate).
47 48
In integrating both measures, the anabolic index is used, which
relates the ratio of anabolic to androgenic response for a given steroid. An
anabolic index greater than one indicates a higher tendency for anabolic effect,
and therefore classifies the drug as an anabolic steroid. A measure lower than
one in turn assesses the steroid as androgenic. There is some variance between
experimental results and the actual real world experiences with humans, but
(with a few exceptions) designations based on the anabolic index are generally
accepted. Below are discussed a few factors that greatly affect
anabolic/androgenic dissociation.
Nandrolone and 19-norandrogens
The section of this book dealing with DHT conversion is important, because it
helps us understand the anabolic steroid nandrolone and many of its derivatives.
Nandrolone is identical to testosterone except it lacks a carbon atom in the 19th
position, hence its other given name 19-nortestosterone. Nandrolone is very
interesting because it offers the greatest ratio of anabolic to androgenic effect of
the three natural steroids (see: Synthetic AAS Chemistry).This is because it is
metabolized into a less potent structure (dihydronandrolone) in androgen target
tissues with high concentrations of the 5-alpha reductase enzyme, which is the
exact opposite of what happens with testosterone. Apparently the removal of the
c4-5 double bond, which normally increases the androgen receptor binding
capability of testosterone, causes an unusual lowering of this ability with
nandrolone.Instead of becoming three to four times more potent, it becomes
several times weaker. This is a very desirable trait if you want to target anabolic
effects over androgenic. This characteristic also carries over to most synthetic
steroids derived from nandrolone, making this an attractive base steroid to use in
the synthesis of new, primarily anabolic, steroids.
5-alpha Irreducible Steroids
When we look at the other mild anabolic steroids Primobolan®, Winstrol®, and
Anavar, none of which are derived from nandrolone, we see another interesting
commonality. These steroids are DHT derivatives that are unaffected by 5alphareductase, and therefore become neither weaker nor stronger in androgen
responsive target tissues with high concentrations of this enzyme. In essence,
they have a very balanced effect between muscle and androgen tissues, making
them outwardly less androgenic than testosterone. This is why these steroids are
technically classified as anabolics, and are undeniably less troublesome than
many other steroids in terms of promoting androgenic side effects. However, if
we wanted to look for the absolute least androgenic steroid, the title would still
go to nandrolone (or perhaps one of its derivatives). Female bodybuilders should
likewise take note that despite the recommendations of others, steroids like
Anavar, Winstrol and Primo are not the least risky steroids to use. This is of
great importance, as male sex hormones can produce many undesirable and
permanent side effects when incorrectly taken by females (See: Side Effects,
Virilization).
3-alpha Hydroxysteroid Dehydrogenase
The 3-alpha hydroxysteroid dehydrogenase enzyme is also important, because it
can work to reduce the anabolic potency of certain steroids considerably. As
follows, not all potent binders of the androgen receptor are, as a rule, great
muscle-building drugs, and this enzyme is an important factor.
Dihydrotestosterone is a clear example. Just as the body converts testosterone to
DHT as a way to potentiate its action in certain tissues (skin, scalp, prostate,
etc.), it also has ways of countering the strong activity of DHT, in other tissues
where it is unneeded. This is accomplished by the rapid reduction of DHT to its
inactive active metabolites, namely androstanediol, before it reaches the
androgen receptor. This activity occurs via interaction with the 3-alpha
hydroxysteroid dehydrogenase enzyme. This enzyme is present in high
concentrations in certain tissues, including skeletal muscle, and DHT is much
more open to alteration by it than other steroids that possess a c4-5 double-bond
(like testosterone).
49 This causes dihydrotestosterone to be an extremely poor
anabolic, despite the fact that it actually exhibits a much higher affinity for the
cellular androgen receptor than most other steroids. Were it able to reach the
cellular androgen receptor without first being metabolized by 3a-HSD, it
certainly would be a formidable muscle-building steroid. Unfortunately this is
not the case, explaining why injectable dihydrotestosterone preparations (no
longer commercially produced) were never favorite drugs among athletes
looking to build mass. This trait is also shared by the currently popular oral
androgen Proviron®, which is, in essence, just an oral form of DHT (1-methyl
dihydrotestosterone to be specific) and known to be an extremely poor tissue
builder.
Anabolics and Potency
One must remember that being classified as an anabolic just means that the
steroid is more inclined to produce muscle growth than androgenic side effects.
Since both effects are mediated through the same receptor, and growth is not
produced by androgen receptor activation in muscle tissue alone (other CNS
tissues, for example, are integral to this process as well), we find that a reduction
in the androgenic activity of a compound will often coincide with a similar
lowering of its muscle-building effectiveness. If we are just looking at overall
muscle growth, androgenic steroids (usually potent due to their displaying a high
affinity to bind with the androgen receptor in all tissues) are typically much
more productive muscle-builders than anabolics, which usually bind with lower
affinity in many tissues. In fact, with all of the analogues produced throughout
the years, the base androgen testosterone is still considered to be one of the most
effective bulking agents. The user must simply endure more side effects when
acquiring his or her new muscle with this type of drug. Individuals wishing to
avoid the stronger steroids will, therefore, make a trade-off, accepting less
overall muscle gain in order to run a more comfortable cycle.
RBA Assay:
Another way of evaluating the potential ratio of anabolic to androgenic activity
is the practice of comparing the relative binding affinity (RBA) of various
steroids for the androgen receptor in rat skeletal muscle versus prostate. When
we look at the detailed study published in 1984, we see some recognizable (and
expected) trends. Aside from dihydrotestosterone and Proviron® (mesterolone),
which undergo rapid enzymatic reduction in muscle tissue to inactive
metabolites, the remaining anabolic/androgenic steroids seem to bind with near
equal affinity to receptors in both tissues. They seem to be relatively “balanced”
in effect. This study also discusses the unique activity of testosterone and
nandrolone compounds, which are good substrates for the 5a-reductase enzyme
found in androgen target tissues (such as the prostate), and seem to provide the
most notable variance between anabolic and androgenic effect in humans due to
this local metabolism. When it comes to real-world use in humans, anabolic
steroids do not always behave in 100% uniformity with their anabolic and
androgenic profiles as determined by animal models, so all such figures need to
be taken with a small grain of salt.
RBA of various anabolic/androgenic steroids as competitors for human
SHBG binding of DHT, and for receptor binding of methyltrienolone in
cytosol from rabbit, rat skeletal muscle and prostate. Source:
Endocrinology 114(6):2100-06 1984 June, “Relative Binding Affinity of
Anabolic-Androgenic Steroids…”, Saartok T; Dahlberg E; Gustafsson JA.
2_A10_Section_I_II-edits3.qxd 11/11/10 10:53 PM Page 19
45. A comparative study of the metabolic fate of testosterone, 17alpha-methyltestosterone, 19-nortestosterone, 17alpha-methyl-19-nor-testosterone and 17alpha-methyl-estr-5(10)-ene-17beta-ol-3-one in
normal males. Dimick D, Heron M, et al. Clin Chim Acta 6(1961) 63-71.
46. Unique steroid congeners for receptor studies. Ojasoo T, Raynaud J. Cancer Research 38 (1978) 4186-98
47. Cytosolic androgen receptor in regenerating rat levator ani muscle. Max S.R. Mufti S, Carlson B.M. J
Biochem 200 (1981) 77
48.
In vitro binding and metabolism of androgens in various organs: a comparative study. Kreig M., Voigt
K.D. J Steroid Biochem 7 (1976) 1005
49. Androgen concentrations in sexual and non-sexual skin as well as striated muscle in man. Deslypere J.P.,
Sayed A., Verdonck L., Vermeulen A. J Steroid Biochem 13 (1980) 1455-8
Synthetic AAS Chemistry
All anabolic/androgenic steroids are preparations containing one of the above
three natural steroid hormones, or chemically altered derivatives thereof. In
creating new synthetic compounds, one of the three natural hormones is selected
as a starting point, typically due to the possession of particular traits that may be
beneficial for the new compound. For instance, of the three natural steroids
above, dihydrotestosterone is the only steroid devoid of the possibility of
aromatization and 5-alpha reduction. It was likewise a very popular choice in the
creation of synthetics that lack estrogenic activity and/or exhibit a more balanced
androgenic to anabolic activity ratio. Nandrolone was typically used when even
lower androgenic action is desired, due to its weakening upon interaction with
the 5-alpha reductase enzyme. Nandrolone also aromatizes much more slowly
than testosterone. Testosterone is our most powerful muscle-building hormone,
and also exhibits strong androgenic activity due to its conversion to a more
potent steroid (dihydrotestosterone) via 5-alpha reductase.
Testosterone derivatives
Boldenone
Boldenone is testosterone with an added double-bond between carbon atoms one
and two. However, this bond changes the activity of the steroid considerably.
First, it dramatically slows aromatization, such that boldenone converts to
estradiol at about half the rate of testosterone. Secondly, this bond causes the
steroid to be a very poor substrate for the 5-alpha reductase enzyme. The more
active 5-alpha reduced metabolite 5alpha-dihydroboldenone is produced only in
very small amounts in humans. The hormone instead tends to convert via 5-beta
reductase to 5beta-dihydroboldenone (a virtually inactive androgen). This makes
it lean towards being an anabolic instead of an androgen, although both traits are
still notably apparent with this steroid. The c1-2 double bond also slows the
hepatic breakdown of the structure, increasing its resistance to 17-ketosteroid
deactivation and its functional half-life and oral bioavailability.
Methyltestosterone
This is the most basic derivative of testosterone, differing only by the added
17alpha methylation that makes the steroid orally active. Conversion to 17alpha
methylestradiol makes this steroid extremely estrogenic, despite the fact that this
alteration actually reduces interaction with the aromatase enzyme.
Methandrostenolone
In many regards, methandrostenolone is very similar to boldenone, as it too
exhibits reduced estrogenic and androgenic activity due to the c1-2 double-bond.
However, this steroid does have a reputation of being somewhat estrogenic,
owing to the fact that it converts to a highly active form of estrogen
(17alphamethylestradiol See: Methylated Compounds and Oral Dosing).
Methandrostenolone is also much more active milligram for milligram, as the
17alpha methyl group also gives it a longer half-life and allows it to exist in a
more free state than its cousin boldenone.
Fluoxymesterone
Fluoxymesterone is a c-17alpha alkylated oral derivative of testosterone. The 11-
beta group functions to inhibit aromatization, so there is no estrogen conversion
at all with this steroid. It also works to lower the affinity of this steroid toward
restrictive serum binding proteins, increasing its relative activity. Introduction of
fluorine at the 9-position also potentiates the action of this steroid.
Nandrolone derivatives
Norethandrolone
Norethandrolone is simply nandrolone with an added 17-alpha ethyl group. This
alteration is rarely used with anabolic/androgenic steroids, and is much more
commonly found with synthetic estrogens and progestins. Although 17-
ethylation inhibits 17-ketosteroid reduction just as well as 17-methylation, and
therefore allows this steroid to exhibit a similarly high level of oral activity, this
group also tends to increase progesterone receptor binding. Norethandrolone is
clearly a “troublesome” hormone in terms of water retention, fat gain, and
gynecomastia, which may in part be due to its heightened binding to this
receptor.
Ethylestrenol
Ethylestrenol is an oral derivative of nandrolone, very similar in structure to keto
group, which is vital to androgen receptor binding. As such, ethylestrenol is
possibly the weakest steroid milligram for milligram ever sold commercially.
Any activity this steroid does exhibit is likely from its conversion to
norethandrolone, which does seem to occur with some affinity (apparently the 3
oxygen group is metabolically added to this compound without much trouble).
This is probably the most interesting trait of ethylestrenol, which is an
undistinguished compound otherwise.
Trenbolone
Although a derivative of nandrolone, the two additional double-bonds present on
trenbolone make any similarities to its parent hormone extremely difficult to see.
First, the 9-10 bond inhibits aromatization. Nandrolone is very slowly
aromatized, however, some estrogen is still produced from this steroid. Not so
with trenbolone. The 11-12 bond additionally increases androgen receptor
binding. This steroid also does not undergo 5-alpha reduction like nandrolone,
and as such does not share the same dissociation between anabolic and
androgenic effects (trenbolone is much more androgenic in comparison).
Dihydrotestosterone derivatives
Mesterolone
Mesterolone is a potent orally active derivative of dihydrotestosterone. Similar
to methenolone, it possesses a non-toxic 1-methyl group, which increases its
resistance to hepatic breakdown. This alteration does not increase the stability of
the 3-keto group however, and as such, this steroid is a poor anabolic like its
parent.
Drostanolone
Drostanolone is simply dihydrotestosterone with an added 2-methyl group. This
addition greatly increases the stability of the 3-keto group, vital to androgen
binding. As such, the activity of this steroid in muscle tissue is greatly enhanced
(see: Anabolic/Androgenic Dissociation).
Oxymetholone
Oxymetholone is an orally active derivative of dihydrotestosterone. The 17-
methyl group is well understood at this point as we have discussed it with many
steroids, however, the 2-hydroxymethylene group is not seen on any other
commercial steroid. We do know that this group greatly enhances anabolic
potency by increasing the stability of the 3-keto group, and that the configuration
of this substituent also appears to allow this steroid to bind and activate the
estrogen receptor.
Stanozolol
Stanozolol is a potent anabolic steroid, owing to the fact that the 3-2 pyrazol
group creates a stable configuration off the A-ring that allows for androgen
receptor binding (this steroid is one of the few that does not possess an actual 3-
keto group). As such, it is highly active in muscle tissue, unlike
dihydrotestosterone.
Methenolone
Methenolone also is a potent anabolic steroid, due to the fact that the c1-2
double bond increases the stability of the 3-keto group. The 1-methyl group
works to increase its oral bioavailability, making methenolone (as methenolone
acetate) one of the few orally active non-17-alkylated orals. The c 1-2 bond may
also help increase hepatic resistance (slightly) to 17-ketosteroid deactivation as
well.
Oxandrolone
Oxandrolone is an orally active derivative of dihydrotestosterone, due to its 17-
methylation. It also differs from DHT by the substitution of its 2-carbon
molecule with oxygen. This is the only commercial steroid to carry this group,
and further, the only to have a modification to the base carbon structure of the
Steran nucleus. The 2-oxo group increases resistance of the 3-keto group to
metabolism considerably, making oxandrolone a potent anabolic.
Steroid Nomenclature
Perhaps not obvious at first glance, there is a naming convention in place that
was used to create identities for the various anabolic/androgenic steroid
hormones. This typically involves forming a root word to convey the structural
base of the steroid, and signifying other unique structural characteristics by
including appropriate prefixes or suffixes. Below, we will look at the common
roots, prefixes, and suffixes used in steroid nomenclature, and identify them, as
they are used in the various commercial compound names. As you will see, the
adoption of names like nandrolone, methandrostenolone, and ethylestrenol were
not as arbitrary as one might imagine. This section is also helpful if you wish to
understand the deeper chemical designations for the various substances that one
might find in the medical literature, which involve the exclusive use of this
terminology (such as is the representation of methandrostenolone as 17bhydroxy-17a-methylandrosta-1, 4-dien-3-one).
Common prefixes and suffixes used in steroid naming:
Common roots used in steroid naming:
Common Commercial Compound Names:
Clinical Applications
Anabolic/androgenic steroids are approved for sale by prescription in virtually
every pharmaceutical market around the world. Having been applied for many
decades to treat a variety of diseased states, today these drugs have a number of
well-established medical uses. They have been used to treat most patient
populations, including men and women of almost all ages, ranging from children
to the elderly. In many instances anabolic/androgenic steroids have proven to be
life saving medications, which is a fact easily overlooked with all of the
discussion about steroid abuse. This section details some of the most common
and accepted medical applications for anabolic/androgenic steroids.
Androgen Replacement Therapy/Hypogonadism
The most widely used medical application for anabolic/androgenic steroids in
the world is that of androgen replacement therapy. Also referred to as Hormone
Replacement Therapy (HRT) or Testosterone Replacement Therapy (TRT), this
therapy involves the supplementation of the primary male hormone testosterone
to alleviate symptoms of low hormone levels (clinically referred to as
hypogonadism). Patients may be adolescent males suffering from childhood
hypogonadism or a specific disorder that causes androgenic hormone disruption,
although most of the treated population consists of adult men over the age of 30.
In most cases hormone levels have declined in these men as a result of the
normal aging process.
The most common complaints associated with low testosterone in adult men
include reduced libido, erectile dysfunction, loss of energy, decreased strength
and/or endurance, reduced ability to play sports, mood fluctuations, reduced
height (bone loss), reduced work performance, memory loss, and muscle loss.
50
When associated with aging, these symptoms are collectively placed under the
label of “andropause”. In a clinical setting this disorder is referred to as lateonset hypogonadism. Blood testosterone levels below 350ng/dL are usually
regarded as clinically significant, although some physicians will use a level as
low as 200ng/dL as the threshold for normal. Hypogonadism is, unfortunately,
still widely under-diagnosed. Most physicians will also not recommend
treatment for low testosterone unless a patient is complaining about symptoms
(symptomatic androgen deficiency).
Androgen replacement therapy effectively alleviates most symptoms of low
testosterone levels. To begin with, raising testosterone levels above 350ng/dL
(the very low end of the normal range) will often restore normal sexual function
and libido in men with dysfunctions related to hormone insufficiency. With
regard to bone mineral density, hormone replacement therapy is also
documented to have a significant positive effect. For example, studies
administering 250 mg of testosterone enanthate every 21 days showed a 5%
increase in bone mineral density after six months.
51 Over time this may prevent
some loss of height and bone strength with aging, and may also reduce the risk
of fracture. Hormone replacement therapy also increases red blood cell
concentrations (oxygen carrying capacity), improving energy and sense of wellbeing.Therapy also supports the retention of lean body mass, and improves
muscle strength and endurance.
Unlike steroid abuse, hormone replacement therapy may have benefits with
regard to cardiovascular disease risk. For example, studies tend to show
hormone replacement as having a positive effect on serum lipids. This includes a
reduction in LDL and total cholesterol levels, combined with no significant
change in HDL (good) cholesterol levels.
52 53 Testosterone supplementation also
reduces midsection obesity, and improves insulin sensitivity and glycemic
control.
54 These are important factors in metabolic syndrome, which may also be
involved in the progression of atherosclerosis. Additionally, testosterone
replacement therapy has been shown to improve the profile of inflammatory
markers TNF·, IL-1‚ and IL-10.
55 The reduced inflammation may help protect
arterial walls from degeneration by plaque and scar tissue. The medical
consensus today appears to be that replacement therapy in otherwise healthy
men generally does not have a negative effect on cardiovascular disease risk, and
may actually decrease certain risk factors for the disease in some patients.
There are some concerns with initiating testosterone replacement therapy when
the individual is in poor health. One study examined the safety of HRT in men
aged 65 and older with limited mobility and various health conditions such as
obesity, hypertension, diabetes, or hyperlipidemia.
56 Each subject took a
transdermal testosterone gel (10g/100mg) or placebo gel daily for six months.
During the course of treatment, a total of 23 men in the testosterone group had
cardiovascular-related adverse events. This was compared to only 9 in the
placebo group. Another study with middle-aged hypogonadal men found that
testosterone replacement therapy (testosterone enanthate 250mg/2 weeks)
reduced vascular reactivity, an important factor in atherosclerosis.
57 These
studies suggest that care should be taken when considering HRT in men with
heart disease, strong contributing factors to heart disease, or other chronic health
conditions.
There are other areas of concern with elderly patients. To begin with,
testosterone administration may increase prostate volume and PSA values.
58 59
While this does not appear to be of clinical significance with normal healthy
patients, benign prostate hypertrophy and prostate cancer can be stimulated by
testosterone. Men with prostate cancer, high PSA values, or breast cancer are
generally not prescribed testosterone. Androgen supplementation has also been
linked to sleep apnea, which can interfere with the most restful (REM) phase of
sleep.
60 The studies have produced conflicting data, however, and the potential
relationship remains the subject of much debate.
61 Lastly, testosterone
replacement therapy has demonstrated negative, positive, and neutral effects on
cognitive functioning in elderly men.
62 63 64 Studies do suggest that the dose can
dictate the level of response, with the most positive effects noted when the
androgen level reaches the mid-to upper-range of normal, not
supraphysiological.
65 Elderly patients with preexisting deficits in cognitive
function should have their cognitive performance and blood hormone levels
monitored closely during hormone replacement therapy.
Common Treatment Protocols:
Transdermal: Transdermal application is the most commonly prescribed method
for supplementing testosterone in the United States and Canada, and is generally
the first course of therapy initiated with androgen replacement therapy patients.
This method of drug delivery offers a number of advantages to the patient when
compared to injection. Since the transdermal application is painless, patient
compliance and comfort is increased in comparison. Transdermal application
also provides stable day-to-day hormone levels, and does not produce the broad
fluctuations usually noticed with injectable testosterone esters. The most
common protocol among hormone replacement doctors is to prescribe a dosage
of 2.5-10 mg of testosterone per day (approximate absorbed dose). This is
applied as a rub-on gel or adhesive transdermal patch that is replaced daily. Note
that due to metabolism in the skin, transdermal application of testosterone tends
to increase serum dihydrotestosterone (DHT) levels more profoundly than
testosterone injection. This may exacerbate androgenic side effects during
therapy in some patients, causing some to seek out injectable forms of
testosterone as an alternative.
Injection: Testosterone enanthate and testosterone cypionate are the most widely
prescribed injectable testosterone drugs in the United States and Canada. In
many other markets the blended ester products Sustanon 100 and Sustanon 250
are also commonly prescribed. Injection of one of these testosterone ester
products will provide the patient supplemental androgen levels for
approximately 2 to 3 weeks after each application. The most common protocol
among hormone replacement doctors is to administer 200 mg of testosterone
enanthate or cypionate once every 2 to 3 weeks. It is important to remember that
testosterone esters will deliver varying levels of testosterone to the body on a
day-to-day basis throughout each application window. Levels will be highest the
first several days after injection, and will slowly decline to baseline over the
following weeks. Physicians are usually encouraged to monitor their patients
closely to ensure androgen supplementation is sustaining hormone levels within
the normal range (and alleviating symptoms of hypogonadism) throughout the
entire therapeutic period. The longer acting injectable testosterone preparation
Nebido (testosterone undecanoate) is undergoing review in the U.S., and has
already been approved in other markets. This drug requires only 4 to 5 injections
per year for most patients.
Oral: Testosterone undecanoate (Andriol) is the only prescription medication
that delivers testosterone via an oral capsule. This medication is not approved for
sale in the United States, but is a prescription drug in Canada and many other
markets around the world. Patient compliance and comfort are high with this
form of therapy, as there are no special routines or requirements aside from
taking a few capsules each day with meals. Oral testosterone undecanoate is
usually given at an initial dosage of 120 to 160 mg per day, which equates to
three to four 40 mg capsules. This dosage may be reduced in subsequent weeks
to 120 mg per day. The capsules are given in two divided doses per day, which
are usually taken with breakfast and dinner. While this form of therapy is highly
convenient, serum hormone levels can fluctuate greatly on a day-to-day basis.
The amount of fat consumption has a particularly strong impact on hormone
bioavailability, and meals providing at least 20 grams of fat are recommended
when taking the capsules for maximum absorption. Note that as with transdermal
testosterone, oral testosterone undecanoate tends to increase serum
dihydrotestosterone (DHT) levels more profoundly than testosterone injections.
Angioedema, Hereditary
Anabolic steroids are commonly prescribed for the treatment of hereditary
angioedema, a rare and potentially life-threatening disorder of the immune
system. Hereditary angioedema is caused by genetic mutations of blood clotting
factors, characterized by a decrease in the level or functioning of the protein C1
esterase inhibitor. This protein controls C1, which is a “complement system”
protein that plays an important role in the control of inflammation. Symptoms of
hereditary angioedema include an intermittent but rapid swelling of the hands,
arms, legs, lips, eyes, tongue, or throat. Swelling may also be noticed in the
digestive tract, resulting in abdominal cramping, nausea, or vomiting. In the
most serious cases, the patient may notice a swelling of the throat and a blockage
of the airway passages, resulting in asphyxiation and sudden death. Many attacks
occur without a specific trigger, although stress, trauma, surgery, and dental
work are commonly associated with angioedema attacks.
Oral c-17 alpha alkylated anabolic/androgenic steroids have been shown to be a
useful form of preventive therapy, stabilizing complement system protein levels
and reducing the frequency and severity of angioedema attacks.
66 They are
usually administered in a low dose, which is to be taken for long-term support of
this disorder. The anabolic steroids that have been most commonly used in the
United States for this purpose are stanozolol and danocrine, although historically
many other agents have also been prescribed including oxandrolone,
methyltestosterone, oxymetholone, fluoxymesterone, and methandrostenolone.
The amount of steroid needed can vary depending on the individual, and is
usually maintained at the lowest therapeutically effective dosage in an effort to
offset undesirable side effects. FDA approved prescribing guidelines for
stanozolol recommended an initial dosage of 2 mg three times daily (6 mg per
day). This would be slowly adjusted downward to a maintenance level after a
positive response was noted, usually to 2 mg given once every 1 to 2 days.
Anemia
As a class of drugs, anabolic/androgenic steroids stimulate the synthesis of
erythropoietin in the kidneys, a hormone that supports the manufacture of new
red blood cells. By doing this,the administration of steroids tends to increase the
red cell count and hematocrit level, making them of tangible therapeutic value
for treating certain forms of anemia (a disease characterized by insufficient red
blood cell production). Forms of anemia likely to respond to steroid therapy
include anemias caused by renal insufficiency, sickle cell anemia, refractory
anemias including aplastic anemia, myelofibrosis, myelosclerosis, agnogenic
myeloid metaplasia, and anemias caused by malignancy or myelotoxic drugs.
The level of response will vary depending on the patient, type of therapy, and
form of anemia, but in many cases the management of a normal hematocrit level
can be achieved.
In the United States, both oxymetholone (Anadrol 50) and nandrolone decanoate
(Deca-Durabolin) are approved by the FDA for the treatment of severe anemia.
The guidelines for using oxymetholone with both male and female anemic
patients (children and adults) recommend a dosage of 1-2 mg/kg/per day. This
would equate to a daily dosage of 75-150 mg for an individual weighing about
160 lbs. Doses as high as 5 mg/kg/day are sometimes necessary to achieve the
desired therapeutic response. The guidelines for nandrolone decanoate
recommend a dosage of 50-100 mg per week for women and 100-200 mg per
week for men. Children (2 to 13 years of age) are recommended a dosage of 25-
50 mg every 3 to 4 weeks.
In recent years, the advent of recombinant erythropoietin as a prescription drug
has changed the face of anemia treatment considerably. While
anabolic/androgenic steroids still offer therapeutic value here, and are still
marketed and sold to treat anemic patients, they are presently regarded as
adjunct or fallback medications for use only when therapy with an erythropoietin
alone has failed to achieve a desired response. The hematocrit increase from
anabolic/androgenic steroids is generally less predictable and positive than the
newer erythropoietins, and these drugs also tend to produce very noticeable side
effects when given in the levels necessary to stimulate erythropoiesis, especially
in women and children. In many instances the risks to therapy strongly outweigh
the benefits of anabolic/androgenic steroids, given that there are newer and
directly targeted medications available with much lower side effect potential.
Breast Cancer
Anabolic/androgenic steroids are sometimes prescribed to treat beast cancer in
postmenopausal women or premenopausal women who have had their ovaries
removed. These drugs are of value when the cancer is hormone responsive,
which means that its growth can be affected (positively or negatively) by
hormonal manipulation. Androgens and estrogens have opposing actions on
hormone-responsive tumors, with estrogens supporting the growth of breast
cancer tissue and androgens inhibiting it
67
. The supplementation of an
anabolic/androgenic steroid can shift the androgen to estrogen balance in a
direction that favors a reduction in tumor size, a therapy that has elicited a
successful response in a fair number of patients. The masculinizing side effects
of steroid therapy can be very pronounced in women, however, so therapy is
usually initiated with great caution. An oral androgen such as fluoxymesterone is
usually preferred to a slower acting injectable steroid such as nandrolone
decanoate as well, as it can be abruptly halted if undesirable side effects become
too apparent. Both primarily anabolic agents, however, have been widely
prescribed for this purpose.
In recent years the development of newer and more targeted anti-estrogenic
drugs such as selective estrogen receptor modulators (SERMs) and aromatase
inhibiting drugs have almost completely eliminated the use of
anabolic/androgenic steroids for breast cancer treatment. Medicative treatment
for breast cancer today usually consists of a SERM like Nolvadex (tamoxifen),
which may be used with a strong aromatase inhibitor such as Arimidex
(anastrozole) or Femara (exemestane). Anabolic/androgenic steroids are still
made available in the United States and many other nations for treating breast
cancer, and are sometimes still applied. They are very much regarded as adjunct
or fallback medications, however, for use only when therapy with anti-estrogenic
drugs alone has failed to achieve a desired response.
Decreased Fibrinolytic Activity
Anabolic steroids may be prescribed to treat conditions associated with
decreased fibrinolytic activity. Fibrinolysis is the process in which a blood clot is
broken down and metabolized by the body. It represents a counter to blood
coagulation, with the two systems working together to maintain the hemostatic
balance. Disorders of the fibrinolytic system are rare, although can be very
serious in nature when they do occur. Decreased fibrinolytic activity can result
in a shift in blood clotting factors that greatly favor coagulation
(hypercoagulability), increasing the risk of a serious cardiovascular event such
as thromboembolism, heart attack, or stroke. Oral C-17 alpha alkylated anabolic
steroids are recognized to increase fibrinolytic activity, and as a result have been
beneficial in many patients suffering from decreased fibrinolytic activity linked
to Antithrombin III deficiency or fibrinogen excess.
68 69 Stanozolol has been
most commonly used in the United States for this treatment, although similar
therapeutic benefits can be seen with many other anabolic steroids. The
maintenance dose is tailored to the individual, and is determined with close
monitoring of both side effects and changes to blood coagulation parameters.
Esterified injectables and oral non-alkylated steroids do not produce the same
fibrinolytic response.
70
Infertility (Male)
In a small percentage of cases, anabolic/androgenic steroids may be prescribed
for the treatment of male infertility. When the cause of infertility is low sperm
concentration due to Leydig-cell secretion deficiencies, an androgen might be
able to alleviate the condition. In such cases the steroid may increase the sperm
count, sperm quality and the fructose concentration,
71 72 which can increase the
chance of conception. The oral androgen mesterolone (Proviron) is most
commonly prescribed for this purpose, although has not been granted FDA
approval for sale in the United States. Note that anabolic/androgenic steroids
usually reduce male fertility, so the potential for these agents to successfully
treat male fertility is limited.
Growth Failure
Anabolic steroids may be prescribed to treat growth failure in children, both with
and without growth hormone deficiency. These agents have been shown to have
positive effects on both muscle and bone mass. When they are administered
before the ends of the long bones (epiphysis) have fused and further linear
growth has been halted, their anabolic effects on bone may support an increase
in height.
73 This can occur both through direct anabolic action of the steroid on
bone cells, and indirectly via the stimulation of growth hormone and IGF-1
release.
74 An anabolic steroid that is non-aromatizable and non-estrogenic is
typically used for this purpose, as estrogen is known to cause an acceleration of
growth arrest. Anabolic steroid therapy must always be used with caution in
pediatric patients, however. In addition to the possibility of common adverse
effects, even non-aromatizable steroids may accelerate the rate of epiphysis
closure.
75
In the United States, oxandrolone is the anabolic steroid most widely prescribed
for the treatment of growth failure. It is usually given as a supportive
medication, used to augment the anabolic effects of human growth hormone
therapy. The drug is typically taken for periods of 6-12 months at a time, in an
effort to accelerate the growth rate without substantially affecting the rate of
epiphysis fusion. A dosage of 2.5 mg per day is often used for this purpose,
although this may be adjusted upwards or downwards depending on the patient’s
sex, age, bodyweight, and sensitivity to adverse effects. When used under
optimal conditions, the result may be an enhancement of the growth rate and an
increase in total height compared to not initiating therapy. This benefit has been
difficult to achieve consistently in clinical studies, however. A number of trials
with oxandrolone have failed to produce a statistically significant effect on total
height, questioning its ultimate value.
76 The short-term benefits of anabolic
steroids on the growth rate, however, remain well supported.
Libido (Female)
The steroid methyltestosterone is approved for prescription sale in the United
States and many other markets to improve libido in female menopause patients.
Small doses of the drug are typically included in products that also supplement
estrogens, the combination aimed at treating the full spectrum of menopause
symptoms, including reduced female libido. The dosage used is low compared to
those of other clinical applications for methyltestosterone, and will usually
amount to no more than 2mg per day.
In the United States, however, the use of an anabolic steroid such as nandrolone
decanoate for the direct treatment of osteoporosis is presently viewed as
controversial. In spite of substantial clinical data and history supporting the use
of steroids for this purpose in the United States, many medical organizations
hold the opinion that the potential side effects of steroid therapy are too
substantial to justify their benefits with osteoporosis. No agent is presently FDA
approved for this purpose. Oxandrolone does remain FDA approved for
osteoporosis patients, but for the specific purpose of alleviating bone pain
associated with the disease, not for augmenting bone mineral density. Anabolic
steroids remain in use for osteoporosis in many other nations, however, and are
still prescribed to varying patient populations including men, women, and the
elderly.
Osteoporosis
Anabolic steroids increase bone mineral density, and may be prescribed for the
treatment of osteoporosis. Benefits of therapy include the stimulation of new
bone formation, inhibition of bone resorption (breakdown), and enhancement of
calcium absorption.
77 78 These drugs have additionally been shown to reduce
bone pain associated with osteoporosis
79
, a frequent complication with elderly
patients suffering from the condition. Osteoporosis is most common in
postmenopausal women, and is usually linked to the changes in hormonal
chemistry that are noted later in life. This disorder does occur to a high degree in
the elderly of both sexes, however. Osteoporosis can also be caused by the
prolonged administration of corticosteroids, which can directly stimulate bone
resorption and inhibit new bone growth. This is identified as steroid-or
glucocorticoid-induced osteoporosis.
Nandrolone decanoate is the anabolic steroid most commonly prescribed for the
treatment of osteoporosis. The drug tends to offer measurable benefits with
regard to bone density, and may reduce the likelihood of bone fracture in
patients.
80 81 The dosage used to treat postmenopausal women is usually 50 mg
once every 3 to 4 weeks. Adverse reactions are common with therapy, however,
including virilization symptoms (hoarseness and body/facial hair growth)
82 and
unfavorable alterations in serum cholesterol.
83 Therapy appears to be better
tolerated in patients above the age of 65, who as a group seem to notice lower
adverse effects. Male patients are given a nandrolone decanoate dosage of 50 mg
once every 1 to 2 weeks. Therapy for both sexes is usually conducted for at least
six months, and may last for one year or longer if necessary. The long
therapeutic window is usually required in order to give the drug enough time to
measurably effect bone strength.
Turner’s and Klinefelter's Syndrome
Anabolic/androgenic steroids may be used to treat certain genetic conditions,
most commonly Turner’s syndrome in females and Klinefelter’s syndrome in
males. Both are chromosomal disorders characterized by deviations from the
normal XX/XY pairing. They result in (among other health issues) abnormalities
in growth, sexual development, and ongoing sexual functioning. Males with
Klinefelter’s syndrome are sterile, and typically have a rounder (less muscular)
physique. They also develop small testicles (microorchidism), and may suffer
with gynecomastia. In these patients the supplementation of testosterone (in a
similar fashion to that used for androgen replacement therapy) is common, and
can help alleviate some of the issues with sexual functioning and body
composition. Females with Turner’s syndrome will be of short stature, and
develop other physical abnormalities including a broad chest, low hairline, lowset ears, and webbed neck. Low doses of a primarily anabolic steroid may be
used in adolescent patients as an adjunct to growth hormone therapy to support
the linear growth rate. Oxandrolone is the steroid most commonly used in the
United States for this purpose, and has been clinically successful at increasing
final height when used in dosage of .05-.1 mg/kg per day.
84
Weight Loss/Muscle Wasting
Anabolic steroids may be administered for the treatment of clinically significant
weight loss. Common causes include prolonged corticosteroid therapy, extensive
surgery, chronic infections or severe trauma. In a general sense, these agents can
be highly useful when a patient is subject to a long hospital stay or period of bed
rest, when normal daily muscle stimulation is not present and a significant loss
of muscle mass is noticed. Severe burn injuries may also call for the supportive
application of anabolic steroids, as this is a type of injury also associated with
secondary muscle loss. Anabolic steroids may additionally be prescribed to
individuals with weight loss not associated with any known cause. The failure to
maintain a healthy (normal) level of body weight for ones’ height, and an
inability of diet and exercise alone to correct weight loss, are usually the
determining factors in recommending such treatment.
The significant loss of lean body mass can present its own set of health issues.
Individuals that are chronically underweight may suffer from low energy and a
reduced sense of wellness, and are at greater risk of mortality.
85 Severe weight
loss during recovery from surgery or illness may also measurably delay or
complicate the recovery phase.
86
In the most severe cases, an ability of the
patient to maintain acceptable lean body mass can be the key determining factor
in recovery. The ability of anabolic steroids to increase protein synthesis makes
them among the most accepted agents for the treatment of clinically significant
weight loss, provided the patient does not have a health condition or is taking
any other medicine that would exclude them from using these drugs. They can
positively affect both muscle and bone as well, making them very versatile
anabolic agents.
In the United States, oxandrolone is the agent most frequently prescribed for
most kinds of clinically significant weight loss. The dosage used for this purpose
is typically 10 mg given twice per day (20 mg total), although lower doses may
be given in some female, elderly, or younger patients in an effort to avoid
undesirable androgenic side effects. The drug is commonly administered for a
period of 3 to 4 weeks during the early stages of recovery, although may be
given for a longer duration if necessary. Given that the support of constructive
protein metabolism is a trait shared by virtually all anabolic steroids, many
agents other then oxandrolone are clinically useful for this purpose. In many
other regions, agents with a high anabolic-to-androgenic activity ratio are
predominantly used for this purpose including stanozolol, nandrolone,
methenolone, and methandrostenolone.
Anabolic steroids may also be prescribed to treat more severe cases of muscle
wasting. This is a condition characterized by strong ongoing protein catabolism,
which means that muscle protein is being predominantly broken down (as
opposed to synthesized) in the body, and a progressive loss of weight, strength,
and energy is noticed. In a medical setting, severe muscle wasting is referred to
as cachexia. Cachexia is not associated with insufficient food intake (dietary
malnutrition), but has a metabolic cause than cannot be alleviated with changes
in diet. This cause is also usually identified when discussing the condition (ie,
cancer cachexia, HIV related cachexia). HIV related muscle wasting is the most
common form of cachexia treated with anabolic steroids. The use of these drugs
as supportive therapy for cancer cachexia has not been well established,
however, and currently the subject of ongoing investigation.
Nandrolone decanoate, oxandrolone, and oxymetholone have been the anabolic
steroids most commonly used in the U.S. to treat muscle wasting specifically
associated with HIV infection. Although no specific FDA recommendations
have been adopted, studies with nandrolone decanoate have shown a dosage of
150 mg every 14 days to have a similar anabolic benefit, and a significantly
lower incidence of side effects, as 6 mg (18 IU) of human growth hormone per
day.
87
In 2003, oxymetholone was the subject of successful Phase III clinical
trials for HIV wasting.
88 The dosage of this study (100-150 mg per day) mirrors
those that are most commonly prescribed by physicians. In recent years,
however, the discontinuance of nandrolone decanoate on the pharmaceutical
market and a perceived higher patient comfort profile in oxandrolone has made
oxandrolone the preferred agent for HIV cachexia. The dosage of oxandrolone
used may range from 20 mg to 80 mg per day. The most consistent clinical
benefits have been seen with a 40 mg and 80 mg daily dose.
89
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14.
Steroid Side Effects
While anabolic/androgenic steroids (AAS) are generally regarded as therapeutic
drugs with high safety, their use can also be associated with a number of adverse
cosmetic, physical, and psychological effects. Many of these side effects are
often apparent during therapeutic-use conditions, although their incidence tends
to increase profoundly as the dosages reach supratherapeutic ranges. Virtually
everyone that abuses anabolic/androgenic steroids for physique-or performanceenhancing purposes notices some form of adverse effects from their use.
According to one study, the exact frequency of tangible side effects in a group of
steroid abusers was 96.4%. This shows very clearly that it is far more rare to
abuse these drugs and not notice side effects than it is to endure them.
90
In
addition to the side effects that anabolic/androgenic steroids can have on various
internal systems, there are others which may not be immediately apparent to the
user. The following is a summary of the biological systems and reactions
effected by AAS use.
Cardiovascular System
The use of anabolic/androgenic steroids in supratherapeutic (and often
therapeutic) doses can have a number of adverse effects on the cardiovascular
system. This may be noticed in several areas including unfavorable alterations in
serum cholesterol, a thickening of ventricular walls, increased blood pressure,
and changes in vascular reactivity. In an acute sense these drugs are admittedly
very safe. The risk of an otherwise healthy person suffering a heart attack from
an isolated steroid cycle is extremely remote. The risk of stroke is also extremely
low. When these drugs are abused for long periods, however, their adverse
effects on the cardiovascular system are given time to accumulate. An increased
chance of early death due to heart attack or stroke is, likewise, a valid risk with
long-term steroid abuse. In order to better understand this risk, we must look
specifically at how anabolic/androgenic steroids affect the cardiovascular system
in several key ways.
Cholesterol/Lipids
Anabolic/androgenic steroids use can adversely affect both HDL (good) and
LDL (bad) cholesterol values. The ratio of HDL to LDL cholesterol fractions
provides a rough snapshot of the ongoing disposition of plaque in the arteries,
either favoring atherogenic or anti-atherogenic actions. The general pattern seen
during steroid use is a lowering of HDL concentrations, which is often combined
with stable or increased LDL levels. Triglyceride levels may also increase.The
shift can be unfavorable in all directions. Note that in some cases, the total
cholesterol count will not change significantly. The total cholesterol level can,
therefore, give a false representation of uncompromised lipid health. Almost
invariably the underlying HDL/LDL ratio will decrease. While this ratio should
return to normal following the cessation of steroid intake, plaque deposits in the
arteries are more permanent. If unfavorable shifts in lipids are exacerbated by
the long-term use of steroidal compounds, significant damage to the
cardiovascular system can result.
Over time, plaque deposits may begin to narrow and clog arteries.
Anabolic/androgenic steroids are most consistent in their lowering of HDL
levels. This adverse effect is mediated through the androgenic stimulation of
hepatic lipase, a liver enzyme responsible for the breakdown of HDL (good)
cholesterol.
91 With more hepatic lipase activity in the body, the favorable (anti-atherogenic)
HDL cholesterol particles are cleared from circulation more quickly, and their
levels drop. This is an effect that seems to be very pronounced at even modest
supratherapeutic dosage levels. For example, studies with testosterone cypionate
noted a 21% drop in HDL cholesterol with a dosage of 300 mg per week.
92
Increasing this dosage to 600 mg did not have any significant additional effect,
suggesting that the dosage threshold for strong HDL suppression is fairly low.
Oral steroids, especially c-17 alpha alkylated compounds, are particularly potent
at stimulating hepatic lipase and suppressing HDL levels. This is due to first pass
concentration and metabolism in the liver. A drug like stanozolol may, therefore,
be milder than testosterone with regard to androgenic side effects, but not when
it comes to cardiovascular strain. A study comparing the effects of a weekly
injection of 200 mg testosterone enanthate to only a 6 mg daily oral dose of
stanozolol demonstrates the strong difference between these two types of drugs
very well.
93 After only six weeks, 6 mg of stanozolol was shown to reduce HDL
and HDL-2 cholesterol levels by an average of 33 and 71% respectively. HDL
levels (mainly the HDL-3 subfraction) were reduced by only 9% in the
testosterone group. LDL cholesterol levels also rose 29% with stanozolol, while
they dropped 16% with testosterone. Esterified injectable steroids are generally
less stressful to the cardiovascular system than oral agents.
It is also important to note that estrogens can have a favorable impact on
cholesterol profiles. The aromatization of testosterone to estradiol may,
therefore, prevent a more dramatic change in serum cholesterol. A study
examined this effect by comparing the lipid changes caused by 280 mg of
testosterone enanthate per week, with and without the aromatase inhibitor
testolactone.
94 Methyltestosterone was also tested in a third group, at a dose of
20 mg daily, to judge the comparative effect of an oral alkylated steroid. The
group using only testosterone enanthate in this study showed a small but not
significant decrease in HDL cholesterol values over the course of the 12-week
investigation. After only four weeks, however, the group using testosterone plus
the aromatase inhibitor displayed an HDL reduction of an average of 25%. The
group taking methyltestosterone experienced the strongest HDL reduction in the
study, which dropped 35% after four weeks. This group also noticed an
unfavorable rise in LDL cholesterol levels.
The potential positive effect of estrogen on cholesterol values also makes the
issue of estrogen maintenance something to consider when it comes to health
risks. To begin with, one may want to consider whether or not estrogen
maintenance drugs are actually necessary in any given circumstance. Are side
effects apparent, or is their use a preventative step and perhaps unnecessary? The
maintenance drug of choice can also have a measurable impact on cholesterol
outcomes. For example, the estrogen receptor antagonist tamoxifen citrate does
not seem to exhibit anti-estrogenic effects on cholesterol values, and in fact
tends to increase HDL levels in some patients. Many individuals decide to use
tamoxifen to combat estrogenic side effects instead of an aromatase inhibitor for
this reason, particularly when they are using steroids for longer periods of time,
and are concerned about their cumulative cardiovascular side effects.
Enlarged Heart
The human heart is a muscle. It possesses functional androgen receptors, and is
growth-responsive to male steroid hormones. This fact partly accounts for men
having a larger heart mass on average than women.
95 Physical activity can also
have a strong effect on the growth of the heart. Resistance exercise (anaerobic)
tends to increase heart size by a thickening of the ventricular wall, usually
without an equal expansion of the internal cavity. This is known as concentric
remodeling. Endurance (aerobic) athletes, on the other hand, tend to increase
heart size via expansion of the internal cavity, without significant thickening of
the ventricles (eccentric remodeling). Even with concentric or eccentric
remodeling, diastolic function usually remains normal in the athletic heart. The
heart muscle is also dynamic. When regular training is removed from a
conditioned athlete, the wall thickening and cavity expansion tend to reduce.
Anabolic steroid abusers are at risk for thickening of the left and right
ventricular walls,
96 known as ventricular hypertrophy. Hypertrophy of the left
ventricle (the main pumping chamber) in particular is extensively documented in
anabolic/androgenic steroid abusers.
97 While left ventricular hypertrophy is,
again, also found in natural power athletes, substance-abusing athletes tend to
have a much more profound wall thickening. They also tend to develop
pathological issues related to this thickening, including impaired diastolic
function, and ultimately reduced heart efficiency.
98 The level of impairment is
closely associated with the dose and duration of steroid abuse. A left ventricle
wall exceeding 13mm in thickness is rare naturally, and may be indicative of
steroid-abuse or other causes.
99
It may further suggest that pathological left
ventricular hypertrophy has developed. Additional testing of such patients is
recommended.
Left ventricular hypertrophy (LVH) is an independent predictor of mortality in
overweight individuals with high blood pressure.
100
It has also been linked to
atrial fibrillation, ventricular arrhythmia, and sudden collapse and death.
101
While LVH in non-steroid-using athletes tends to be without clinical
significance, pathological increases in QT dispersion are noticed in steroid
abusers with LVH.
102 These changes tend to be similar to the increases in QT
dispersion noted in hypertensive patients with LVH.
103 Among other things, this
could leave a steroid abusing individual more susceptible to a serious adverse
event, including arrhythmia or heart attack. Isolated medical case studies of
longtime steroid abusers support an association between LVH and related
pathologies including ventricular tachycardia (arrhythmia originating in the left
ventricle), left ventricular hypokinesis (weakened contraction of the left
ventricle), and decreased ejection fraction (reduced pumping volume and
efficiency).
104
Heart mass can increase or decrease in relation to the current state of
anabolic/steroid use, the average dosage, and duration of intake. Likewise, the
heart usually begins to reduce in size once anabolic/androgenic steroids are no
longer being used. This effect is similar to the way the heart will reduce in size
once an athlete no longer follows a rigorous training schedule.
105 Even with this
effect, however, some changes in heart muscle size and function caused by the
drugs may persist. Studies examining the effects of steroid use and withdrawal
on left ventricular hypertrophy noted that athletic subjects who abstained from
steroid abuse for at least several years still had a slightly greater degree of
concentric left ventricular hypertrophy compared to non-steroid-using athletic
controls.
106 The disposition of pathological left ventricular hypertrophy
following long-term steroid abuse and then abstinence remains the subject of
investigation and debate.
Heart Muscle Damage
Anabolic/androgenic steroid abuse is suspected of producing direct damage to
the heart muscle in some cases. Studies exposing heart cell cultures to AAS have
reported reduced contractile activity, increased cell fragility, and reduced cellular
(mitochondrial) activity, providing some support for a possible direct toxic effect
to the heart muscle.
107 108 Furthermore, a number of case reports have found
such pathologies as myocardial fibrosis (scar tissue buildup in the heart),
myocardial inflammation (inflammation of heart tissue), cardiac steatosis
(accumulation of triglycerides inside heart cells), and myocardial necrosis (death
of heart tissue) in long-term steroid abusers.
109 110 111 112 A direct link between
drug abuse and cardiac pathologies is assumed in these cases, but cannot be
proven given the slow nature in which these cardiac pathologies develop, and the
influence many other factors (such as diet, exercise, lifestyle, and genetics) can
have on them. Individuals remain cautioned about the possibility of cardiac
muscle damage with long-term steroid abuse.
Blood Pressure
Anabolic/androgenic steroids may elevate blood pressure. Studies of
bodybuilders taking these drugs in supratherapeutic doses have demonstrated
increases in both systolic and diastolic blood pressure readings.
113 Another study
measured the average blood pressure reading in a group of steroid users to be
140/85, which was compared to 125/80 in weight lifting controls not taking
steroids.
114 Hypertension, or consistently high blood pressure at or above 140/90
for either systolic or diastolic measures, has been reported in steroid users,
115
although in most cases the elevations are more modest. Increased blood pressure
may be caused by a number of factors, including increased water retention,
increased vascular stiffness, and increased hematocrit. Aromatizing or highly
estrogenic steroids tend to cause the greatest influences over blood pressure,
although elevations cannot be excluded with non-estrogenic anabolic/androgenic
steroids. Blood pressure tends to normalize once anabolic/androgenic steroids
have been discontinued.
Hematological (Blood Clotting)
Anabolic/androgenic steroids can cause a number of changes in the
hematological system that affect blood clotting. This effect can be very variable,
however. The therapeutic use of these drugs is known to increase plasmin,
antithrombin III, and protein S levels, stimulate fibrinolysis (clot breakdown),
and suppress clotting factors II, V, VII, and X.
116 117 These changes all work to
reduce clotting ability. Prescribing guidelines for anabolic/androgenic steroids
warn of potential increases in prothrombin time, a measure of how long it takes
for a blood clot to form.
118
If prothrombin time increases too greatly, healing
may be impaired. The effects of anabolic/androgenic steroids on prothrombin
time are generally of no clinical significance to healthy individuals using these
drugs in therapeutic dosages. Patients taking anticoagulants (blood thinners),
however, could be adversely affected by their use.
Conversely, anabolic/androgenic steroid abuse has been linked to increases in
blood clotting ability. These drugs can elevate levels of thrombin
119 and Creactive protein,
120 as well as thromboxane A2 receptor density,
121 which can
support platelet aggregation and the formation of blood clots. Studies of steroid
users have demonstrated statistically significant increases in platelet aggregation
values in some subjects.
122 There are also a growing number of case reports
where (sometimes fatal) blood clots, embolisms, and stokes have occurred in
steroid abusers.
123 124 125 126 127 Although it has been difficult to conclusively
link these events directly to steroid abuse, the adverse effects of anabolic
steroids on components of the blood coagulation system are well understood.
These serious adverse effects are now regarded as recognized risks of steroid
abuse among many that study these drugs.
In therapeutic levels, the anti-thrombic effects of anabolic/androgenic steroids
seem to dominate physiology, and decreases in blood clotting ability may be
noted. At a certain supratherapeutic dosage point, however, the pro-thrombic
changes appear to overtake the anti-thrombic changes, and physiology begins to
favor fast and abnormally thick clot formation (hypercoagulability). The exact
dosage threshold or conditions required to increase blood clotting has not been
determined, and some studies with steroid users taking supraphysiological doses
fail to demonstrate increased coagulability.
128
Individuals remain warned of the
potential increases in thrombic risk with anabolic/androgenic steroid abuse.
Blood clotting tendency should return to the pretreated state after the
discontinuance of anabolic/androgenic steroids. point until the hematocrit issues
have been corrected. Minor elevations in hematocrit may be addressed with
phlebotomy. For this, 1 pint of blood may be removed periodically during
steroid intake, often every two months. Proper hydration is also important, as
dehydration can temporarily cause the hematocrit level to elevate, giving a false
positive for polycythemia. The daily intake of aspirin is also commonly advised
if the hematocrit is above normal, as this will reduce platelet aggregation, or the
tendency for platelets to stick together and form clots. Individuals remain
cautioned of the potential cardiovascular danger of high hematocrit levels
associated with anabolic/androgenic steroid use.
Hematological (Polycythemia)
Anabolic/androgenic steroids stimulate erythropoiesis (red blood cell
production). One potential adverse effect of this is polycythemia, or the
overproduction of red blood cells. Polycythemia can be reflected in the
hematocrit level, or the percentage of blood volume that is made up of red cells.
As the hematocrit rises, so too does the viscosity of the blood. If the blood
becomes too thick, its ability to circulate becomes impaired. This can greatly
increase the risk of serious thrombic event including embolism and stroke. A
high hematocrit level is also an independent risk factor for heart disease.
129 The
normal hematocrit level in men is 40.7 to 50.3%, and in women it is 36.1 to
44.3% (numbers may vary very slightly depending on the source). For the sake
of scale, while a hematocrit of 50% may be normal, a hematocrit of 60% or
above is considered critical (life threatening).
Anabolic/steroid administration tends to raise the hematocrit level by several
percentage points, sometimes more. As a result, many steroid-using
bodybuilders will have hematocrit levels that are above the normal range. For
example, one study measured the average hematocrit in a group of steroid
abusing competitive bodybuilders to be 55.7%.
130 This level is considered
clinically high, and would increase blood viscosity enough to raise the risk of
serious cardiovascular event. Although not likely to be an isolated cause, high
hematocrit is believed to have been a contributing factor in the deaths of a
number of steroid abusers, usually paired with high blood pressure,
homocysteine, and/or atherosclerosis. The average hematocrit level in
bodybuilders not taking anabolic/androgenic steroids was 45.6%, well within the
normal range for healthy adult men.
Many physicians that specialize in hormone replacement therapy consider a
hematocrit level of 55% to be an absolute cutoff point. At or above this point,
and anabolic/androgenic steroid therapy cannot be continued safely. Drug intake
would be ceased at this point until the hematocrit issues have been corrected.
Minor elevations in hematocrit may be addressed with phlebotomy. For this, 1
pint of blood may be removed periodically during steroid intake, often every two
months. Proper hydration is also important, as dehydration can temporarily cause
the hematocrit level to elevate, giving a false positive for polycythemia. The
daily intake of aspirin is also commonly advised if the hematocrit is above
normal, as this will reduce platelet aggregation, or the tendency for platelets to
stick together and form clots. Individuals remain cautioned of the potential
cardiovascular danger of high hematocrit levels associated with
anabolic/androgenic steroid use.
Homocysteine
Anabolic/androgenic steroids may elevate homocysteine levels. Homocysteine is
an intermediary amino acid produced as a byproduct of methionine metabolism.
High levels of homocysteine have been linked to elevations in the risk for
cardiovascular disease.
131
It is believed to play a direct role in the disease,
increasing oxidative stress, including the oxidation of LDL cholesterol, and
accelerating atherosclerosis.
132 Elevated levels of homocysteine may also induce
vascular cell damage, support platelet aggregation, and increase the likelihood of
thrombic event.
133 134 135 The normal range for homocysteine levls in men aged
30 to 59 years is 6.3-11.2umol/L. For women of the same age the average is 4.5-
7.9umol/L. Increased risk of heart attack, stroke, or other thrombic event are
noted with even modest elevations in homocysteine. According to one study, a
homocysteine level exceeding 15umol/L in patients with heart disease is
associated with a 24.7% increased likelihood of death within five years.
136
Androgens stimulate elevations in homocysteine,
137 and men have an
approximately 25% higher level on average than women.
138
Anabolic/androgenic steroid abuse has been associated with
hyperhomocysteinaemia, or consistent clinically high homocysteine levels.
139
One study found that the average homocysteine concentration in a group of 10
men that had been self-administering anabolic/androgenic steroids (in a cyclic
pattern) for 20 years was 13.2 umol/L.
140 Three of these men died of a heart
attack during the investigation, and had homocysteine levels between 15umol/L
and 18umol/L. The average homocysteine level in bodybuilders who had never
taken steroids was 8.7umol/L, while it was 10.4umol/L in previous steroid users
(3 months abstinence). One study did show that administering 200 mg of
testosterone enanthate (with and without an aromatase inhibitor) for three weeks
failed to produce a significant elevation in homocysteine.
141
It is unknown if the
moderate dosage, drug type (esterified injectable vs. c17-aa), or short duration of
intake were factors in the differing outcome from other studies. Individuals
remain warned of the potential for elevations in the homocysteine level with
steroid abuse.
Vascular Reactivity
The endothelium is a layer of cells that line the entire circulatory system. These
cells are found on the inside of all blood vessels, and help increase or decrease
blood flow and pressure by relaxing or constricting the vessels (referred to as
vasodilation and vasoconstriction, respectively). These cells also help regulate
the passage of materials in and out of blood vessels, and are involved in a
number of important vascular processes including blood clotting and new blood
vessel formation. Having a more flexible (reactive) endothelium is generally
considered desirable for health, and, likewise, the endothelium is often
compromised in individuals with cardiovascular disease. Patients with
endothelial dysfunction tend to notice greater vasoconstriction, restricted blood
flow, higher blood pressure, local inflammation, and reduced circulatory
capacity.
142 This may place them at greater risk for heart attack, stroke, or
thrombosis (blood clot).
Endothelial cells are androgen responsive, which may partly account for men
exhibiting less vascular reactivity than women.
143 Similarly,
anabolic/androgenic steroid use has been shown to impair endothelial activity
and vascular reactivity. Studies at the University of Innsbruck in Austria
compared the level of endothelial dilation in 20 steroid users to a group of
control athletes.
144 Those individuals using anabolic steroids noticed slight but
measurably impaired vascular dilation and endothelial function. Additional
studies at the University of Wales in Cardiff comparing vascular dilation in
active, previous, and non-steroid users, also demonstrated anabolic steroids to
cause a decline in endothelial-independent vasodilation.
145 These effects leave
the steroid user with more relative “stiffness” in the vascular system, which
could increase the chance of an adverse cardiovascular event. In both studies,
vascular reactivity improved after the discontinuance of anabolic/androgenic
steroids.
Proving an Association
Direct links between steroid abuse and individual cases of stroke and heart attack
have been difficult to prove. There are a number of things that have made this
difficult. For one, cardiovascular disease is very common in men. It also usually
takes decades to develop. This makes individual contributing factors (which
include many things such as diet, lifestyle, health status, and genetic variables)
extremely difficult to isolate. Data concerning the long-term use of steroids in
physique-or performance-enhancing doses is also very limited. It would be
unethical to conduct a controlled study where participants were given abusive
doses of steroids for many years, so the data that is referenced tends to be from
case studies. Individual case studies are important, but are usually considered too
week to meet the requirements of statistical proof. Still, it would be a mistake to
confuse this lack of proven association with proof of nonassociation. The
cardiovascular risks of steroid abuse remain well supported by both documented
acute changes in cardiovascular markers, and a growing body of case reports of
injury or death. There are few medical experts close to the study of these drugs
today that would actually deny their risks.
Anabolic/androgenic steroid abuse can produce changes in a number of
areas of cardiovascular health that can work together to increase the risk of
heart attack, stroke, or embolism.
Immune System
The human immune system is responsive to sex hormones. This results in
functional differences in immunity between the sexes.Women tend to have a
more active immune system compared to men, and are slightly more resistant to
bacterial infection and other types of infection.
146 The female immune system is
also more prone to developing autoimmune diseases, which may be linked to its
higher level of activity.
147 The day-to-day activity of the immune system can
also fluctuate throughout the menstrual cycle, further demonstrating the strong
influence of sex steroids.
148 The slightly weaker resistance to infection of men
appears to be caused by testosterone, which is an immunosuppressive
hormone.
149 Androgens may modulate the immune system directly, through
their conversion to estrogens,
150 or by modifying glucocorticoid activity.
151
Anabolic/androgenic steroids have displayed both immunostimulatory and
immunosuppressive actions in animal models.
152 Given that these drugs can
influence the immune system through a variety of pathways, and anabolic
steroids are a fairly diverse class of drugs, their effects on the immune system
may vary depending on the particular conditions. When used therapeutically,
changes in immune system functioning are usually minor, and have not
amounted to strong immunostimulation or immunosuppression.
Anabolic/androgenic steroids have also been used safely in many
immunocompromised patients, such as those with muscle wasting associated
with HIV infection, without any significant change in immune system or viral
markers.
153 154
The use of anabolic/androgenic steroids in supratherapeutic doses may slightly
impair immune system functioning, reducing an individual’s resistance to certain
types of infection. In one study, steroid abusers were shown to have lower serum
levels of IgG, IgM, and IgA immunoglobulins (antibodies) compared to
bodybuilding controls, consistent with immunosuppression.155 Although this
may logically increase the chance of contracting certain types of illness, a
significant increase in the history of illness could not be established in these
same steroid abusers. Given the very random nature of illness, however, it may
be difficult to establish such a link without extensive study. The effect of
hormone manipulation on immunity should also be temporary, and return to a
normal state once pre-treated hormonal chemistry is restored. Individuals remain
warned of the potential for minor immunosuppression and increased chance of
illness with steroid abuse.
Kidneys (Renal System)
Anabolic/androgenic steroids are generally well tolerated by the renal system.
These drugs are largely excreted from the body through the kidneys, although
there is no inherent strong toxicity in this process. In fact, there are many
instances in which these drugs may be used as supportive treatment in patients
with compromised kidney function. For example, anabolic steroids have been
prescribed to increase the production of red blood cells in patients with anemia
related to various forms of kidney disease.
156 157 They have even been used as
general anabolic (lean body mass) support, and to treat hypogonadism, in
patients undergoing dialysis.
158 159 While care must be taken with such patients,
therapy may often be conducted very safely. In otherwise healthy individuals,
clinical renal toxicity caused by the short-term administration of
anabolic/androgenic steroids is unlikely.
There have been isolated reports of severe kidney damage in steroid abusers. For
example, a handful of individuals have developed Wilms’ Tumor
(nephroblastoma),
160 161 which is a rare form of kidney cancer usually found in
children. Its appearance in adult steroid users is suspect, but not conclusive
evidence that drugs were the actual cause. There have also been isolated reports
of renal cell carcinoma in steroid abusers.
162 163 Since this is the most common
form of kidney cancer, however, conclusive links are again difficult to draw.
There have additionally been case reports of combined liver and renal failure
with steroid abuse.
164 165
In these cases kidney failure may have been subsequent
to steroid-induced liver toxicity, as cholestasis (bile duct obstruction) is known
to cause acute tubular necrosis and renal failure.
166
The use of anabolic/androgenic steroids in supratherapeutic doses may slightly
impair immune system functioning, reducing an individual’s resistance to certain
types of infection. In one study, steroid abusers were shown to have lower serum
levels of IgG, IgM, and IgA immunoglobulins (antibodies) compared to
bodybuilding controls, consistent with immunosuppression.
155 Although this
may logically increase the chance of contracting certain types of illness, Kidney
health should be a concern for long-term steroid-using bodybuilders and power
athletes. To begin with, excessive resistance training can produce some strain on
the renal system. A condition called rhabdomyolysis is caused by the extreme
damage of muscle tissue, which releases myoglobin and a number of
nephrotoxic compounds into the blood.
167
In high levels this can damage kidney
tissue and even cause renal failure. There have been rare case reports of severe
clinical rhabdomyolysis in bodybuilders, both with and without mention of
steroid abuse.
168 169 170 171 Steroid use may also cause hypertension, which can
lead to kidney damage.
172 While anabolic/androgenic steroids are generally not
regarded as direct kidney toxic drugs, they may be used to support a lifestyle and
long-term metabolic state characterized by extreme training, heightened daily
muscle protein turnover, and elevated blood pressure. Over time this may
compromise kidney health. Regular monitoring of kidney function is
recommended.
Liver (Hepatic System)
Many oral anabolic/androgenic steroids (or injectable forms of oral steroids) are
toxic to the liver (hepatotoxic). These compounds can cause serious and
sometimes life-threatening damage when abused, and occasionally even under
therapeutic conditions. Those agents commonly associated with clinical
hepatotoxicity include (but are not limited to) fluoxymesterone,
methandrostenolone, methylandrostenediol, methyltestosterone,
norethandrolone, oxymetholone, and stanozolol.
173 174 175 176 177 These steroids
all have either an ethyl or methyl group at carbon-17 (c-17alpha alkylation). All
c-17alpha alkylated anabolic/androgenic steroids possess some level of
hepatotoxicity. Liver strain, as assessed by elevated liver enzymes, has also been
reported with non-alkylated esterified injectable steroids including nandrolone
decanoate and testosterone enanthate in extremely rare instances.
178 179 These
steroids have never been associated with serious hepatic damage, however, and
are not regarded as liver toxic.
Alkylation of c-17alpha specifically protects the steroid molecule from
metabolism by the enzyme 17beta-hydroxysteroid dehydrogenase (17beta-HSD).
This enzyme normally oxidizes a steroid’s 17beta-hydroxyl (17beta-ol) group,
which must remain intact for the drug to impart any anabolic or androgenic
effect. Oxidation of 17-beta-ol is one of the primary pathways of hepatic steroid
deactivation. Without protection from this enzyme, very little active drug will
survive the first pass through the liver and reach circulation after oral dosing.
Alkylation of c-17alpha effectively protects the steroid from 17beta-HSD by
occupying a hydrogen bond necessary for the breakdown of 17beta-ol to 17-
keto. The compound must be metabolized through other pathways as a result,
and immediate hepatic deactivation is prevented. The process allows a very high
percentage of the steroid dose to pass into the bloodstream intact, but it also
places some strain on the liver in the process.
Te exact mechanism of hepatotoxicity induced by alkylated anabolic/androgenic
steroids remains unknown, but it is speculated to be due in large part to the
natural activity of androgens in the liver. This liver possesses a high
concentration of androgen receptors, and is responsive to these hormones.
180
With hysiological androgens such as testosterone and dihydrotestosterone,
however, only a moderate level of activity is permitted in this organ. This is
because the liver is normally very efficient at metabolizing steroids, which mutes
their local activity. But with the liver unable to easily deactivate alkylated
steroids, however, a far greater level of hepatic androgenic activity is allowed.
The concentration of steroid in the liver is also very high after oral
administration, as the digestive tract delivers the drug directly to this organ
before it can reach circulation. The fact that the most potent steroid ever given to
humans on a mg-for-mg basis is also the most liver toxic, also supports a close
association between androgenic potency and hepatotoxicity.
181 182
Early liver toxicity is usually visible in blood test results for hepatic function
before physical symptoms or dysfunction develop. This is most likely to include
elevations in amino-transferase enzymes AST and ALT, also called serum
glutamic-oxalocetic transaminase (SGOT) and serum glutamic pyruvic
transaminase (SGPT), respectively. The cholestatic enzymes alkaline
phosphatase (ALP) and gamma-glutamyltranspeptidase (GGT) may also be
elevated, along with other markers (see: Understanding Blood Tests). Screening
for abnormalities in hepatic markers is regarded as the most effective way of
preventing liver damage from steroid administration. Should asymptomatic
toxicity go unnoticed and without a change in drug intake, it is likely to progress
to more severe hepatic strain, injury, or hepatic dysfunction. Immediate
cessation of anabolic/androgenic steroid use and a full assessment of liver and
full-body health is advised should any signs of unacceptable liver toxicity
become apparent.
The most common form of actual liver dysfunction caused by the administration
of oral anabolic/androgenic steroids is cholestasis.
183 This describes a condition
where the flow of bile becomes decreased, usually because of obstruction of the
small bile ducts in the liver (intrahepatic). This causes bile salts and bilirubin to
accumulate in the liver and blood instead of being properly excreted thorough
the digestive tract. Inflammation (hepatitis) may also be present.
184 Symptoms of
cholestasis may include anorexia, malaise, nausea, vomiting, upper abdominal
pain, or pruritus (itching). The stool may also change to a clay color (alcholic
stool) due to the reduced excretion of bile, and the urine may become amber.
Cholestatic jaundice may develop, which is characterized by a yellowing of the
skin, eyes, and mucous membranes due to high levels of bilirubin in the blood
(hyperbilirubinemia). Intrahepatic cholestasis may also coincide with
hepatocellular necrotic lesions (death of liver tissue).
Intrahepatic cholestasis will usually resolve itself without serious injury or
medical intervention within several weeks of discontinuing all hepatotoxic
steroids. More serious cases may take several months before normal hepatic
enzyme levels and functioning are restored. Hepatic lesions are likely to heal
over time as well, at least partially. In some cases physicians have initiated
supportive treatment with ursodeoxycholic acid (ursodiol), which is a secondary
bile salt known to possess hepatoprotective and anti-cholestatic effects, in an
effort to hasten recovery.
185 The exact value of using this medication to treat
steroid-induced cholestatic jaundice remains unknown, however. The liver is
highly resilient, and intrahepatic cholestasis is unlikely to continue degrading
after drug discontinuance unless additional pathologies are present.
More serious hepatic complications are rare, but have included peliosis
hepatis
186
(blood-filled cysts on the liver), portal hypertension with variceal
bleeding
187
(bleeding caused by increased blood pressure in portal vein related
to obstructed blood flow), hepatocellular adenoma
188
(non-malignant liver
tumor), hepatocellular carcinoma
189
(malignant liver tumor), and hepatic
angiosarcoma
190
(aggressive malignant cancer of the lining of blood vessels
inside the liver). Some of these pathologies can be very insidious at times,
developing quickly and without clear early symptoms. Although many of these
potentially life-threatening side effects have often been attributed to very ill
patients receiving steroid medications, a growing number of case reports are now
involving otherwise healthy young bodybuilders abusing these drugs.
Additionally, there are at least two case reports of a previously healthy
bodybuilder developing liver cancer after taking high doses of oral
anabolic/androgenic steroids, and one confirmed death.
191 192
Physical
Acne
Androgens stimulate the sebaceous glands in the skin to secrete an oily
substance called sebum, which is made of fats and the remnants of dead fatproducing cells. Excess stimulation, as with steroid abuse, may also cause a
significant increase in the size of the sebaceous glands.
193 Sebaceous glands are
found at the base of the hair follicles in all hair-containing areas of the skin. If
the androgen level becomes too high and the sebaceous glands become
overactive, the hair follicles may begin to clog with sebum and dead skin cells,
resulting in acne. Acne vulgaris (common acne) is frequent in steroid users,
especially when the drugs are taken in supratherapeutic levels. This often
includes acne lesions on the face, back, shoulders, and/or chest.
A mild incidence of acne vulgaris is usually addressed with topical over-thecounter acne medications and a rigorous skin cleaning routine that removes
excess oil and dirt. More serious acne may develop in sensitive individuals,
including acne conglobata (severe acne with connected nodules under the skin)
or acne fulminans (highly destructive inflammatory acne). Such incidences may
require medical intervention, which usually involves treatment with isotretinoin.
Topical anti-androgen drugs are also under investigation for the treatment of
severe acne, and have shown a great deal of promise in early trials.
194 Acne is
typically resolved with the cessation of steroid use, although the overproduction
of sebum may persist until the sebaceous glands have had time to atrophy back
to original size. Serious forms of acne may produce lasting scars.
Acne on the chest caused by steroid use.
Hair Loss (Androgenetic Alopecia)
Anabolic/androgenic steroids may contribute to a form of hair loss on the scalp
known as androgenetic alopecia (AGA). This disorder is characterized by a
progressive miniaturization of hair follicles, and a shortening of the anagen
phase of hair growth, under androgen influence. The hair produced by affected
follicles will progressively thin, covering the scalp less and less effectively. In
men, the baldness produced is usually identified most simply as male pattern.
This will initially include a receding hairline (fronto-temporal thinning) and
thinning on the crown, areas where androgen receptor concentrations are high. In
women, the balding usually takes on a more diffuse pattern, with thinning
throughout the top of the head. Most women with androgenetic alopecia do not
have a receding hairline.
With male AGA, hair loss is most pronounced on the temples and crown.
Androgenetic alopecia is the most common form of hair loss in men and women
alike. It is especially common in males, and more than 50% of the population
will notice it by the age of 50.
195 As its name signifies, androgenetic alopecia involves the interplay of both
androgenic hormones and genetic factors. Individuals with this condition appear
to be more locally sensitive to androgens, and have higher levels of androgen
receptor protein and dihydrotestosterone in the scalp, in comparison to those
unaffected.
196 Although dihydrotestosterone is identified as the primary
hormone involved in the progress of androgenetic alopecia, it does not possess a
unique ability to influence this condition. All anabolic/androgenic steroids
stimulate the same cellular receptor, and as a result are capable of providing the
necessary androgenic stimulation. Baldness can result from steroid use, even in
the absence of steroids that convert to, or are derived from, dihydrotestosterone.
The genetics of androgenetic alopecia are not fully understood. At one time it
was believed this condition could be inherited solely from the maternal
grandfather. More recent evidence contradicts this notion, however, showing
strong support for father-to-son transmission in many cases.
197 A number of
genes have been identified as having a potential link to the disorder, including
certain variants (polymorphisms) of the androgen receptor gene.
198 199 No single
genetic variant alone has yet been able to explain all cases of androgenetic
alopecia, however. AGA is now believed to involve several genes
(polygenic).
200 The way these genes combine, and the level of androgens in the
scalp, may ultimately work together to control the onset and severity of
androgenetic alopecia. Estrogen is also known to lengthen the anagen
phase,
201and the pathogenesis of this condition may ultimately involve genes
that alter both androgen and estrogen activity.
Treatment for androgenetic alopecia in men usually involves topical minoxidil
and oral finasteride, a 5-alpha reductase enzyme inhibitor. Women are typically
prescribed anti-androgens and estrogen/progestin drugs. The focus in both cases
is on reducing relative androgenic action in the scalp, which may (at least
temporarily) stall the condition. With this in mind, many steroid users concerned
with hair loss will tailor their drug intake to minimize unnecessary androgenic
activity. This usually involves moderate dosing and the careful selection of drugs
with high anabolic-to-androgenic ratios, such as oxandrolone, methenolone, or
nandrolone. Alternatively, some may choose to use injectable testosterone esters
combined with finasteride to reduce scalp DHT conversion. These strategies are
met with varying degrees of success.
There has been no study on the role of genetics in baldness linked to steroid
abuse. Anecdotally, individuals with existing visible androgenetic alopecia
appear to be those most susceptible to the effects of anabolic/androgenic steroids
on the scalp. For many of these people, the loss of hair appears significantly
accelerated when taking these drugs. On the other hand, this side effect is
generally a much less significant issue with individuals that have not noticed
thinning beforehand. Many go on to abuse steroids for years without any visible
effect at all, making it clear that there is more to this disorder than local
androgen levels. It is well understood that androgens play a role in the
progression of androgenetic alopecia for those genetically prone. Steroid use
can, therefore, coincide with the first noticeable onset of this condition. It is
unknown, however, if anabolic/androgenic steroid abuse can cause baldness in
an individual that does not carry any genetic susceptibility.
Stunted Growth
Anabolic/androgenic steroids may inhibit linear growth when administered
before physical maturity. These hormones actually can have a dichotomous
influence on linear height. On one hand, their anabolic effects may increase the
retention of calcium in the bones, facilitating linear growth. A number of
anabolic steroid programs have been successful in helping children with short
stature achieve a faster rate of growth. At the same time, however,
anabolic/androgenic steroid use may cause premature closure of the growth
plates, which inhibits further linear growth. There have been a number of cases
of noticeably stunted growth (short stature) in juvenile athletes that have taken
these drugs.
202 The specific outcome of steroid therapy depends on the type and
dose of drug administered, the age in which it is administered, the length it is
taken, and the responsiveness of the patient.
While androgens, estrogens, and glucocorticoids all inherently participate in
bone maturity, estrogen is regarded as the primary inhibitor of linear growth in
both men and women.
203 Women are shorter on average than men, and also tend
to stop growing at a slightly earlier age, due to the effects of this hormone.
Anabolic/androgenic steroids that either convert to estrogen or are inherently
estrogenic are, likewise, more likely to inhibit linear growth than other agents.
Popular anabolic/androgenic steroids with estrogenic activity include (but are
not limited to) boldenone, testosterone, methyltestosterone, methandrostenolone,
nandrolone, and oxymetholone. These drugs must be used with additional
caution in young patients due to their stronger potential for inducing growth
arrest.
Estrogen acts directly on the epiphyseal growth plates to inhibit linear growth.
These plates are located at the end of growing bones, and contain a collection of
stem-like cells called chondrocytes. These cells proliferate and differentiate to
form new bone cells, slowly expanding the length of the bones and the height of
the individual. These cells have a finite life span, with programmed senescence
(cell death). This will cause the rate of chondrocyte proliferation to slow over
time, and eventually stop. The chondrocytes are replaced with blood and bone
cells at the point of physical maturity, “fusing” the bones and inhibiting further
linear growth. The stimulation of estrogen appears to accelerate bone age
advancement by exhausting the proliferative potential of chondrocytes at an
earlier time.
204
Age will also influence a patient’s sensitivity to epiphyseal fusion. As young
children are far from the point of bone maturity, the inhibitive effects of
hormone therapy take longer to manifest in growth cessation. As the juvenile
ages, they may become more sensitive to these effects. Studies treating teenage
boys (average age 14 years) for tall stature, for example, found that six months
of testosterone enanthate (500 mg every two weeks) was sufficient to reduce
final height by almost three inches compared to the predicted outcome.
205 This is
a moderately supratherapeutic dose, underlining the fact that steroid intake
during adolescence can have a very tangible impact on height. This issue may
not be as simple as avoiding estrogenic steroids either, as non-estrogenic steroids
have also induced skeletal maturation.
206
Individuals remain warned of the
potential for growth interruption when anabolic/androgenic steroids are used
before physical maturity.
Tendon Injury
Anabolic/androgenic steroid use is sometimes associated with an increased
incidence of tendon injury.
207 208 There are a few potential causes for this. One
of the most basic is the rapid growth of the muscles. Under the influence of
anabolic/androgenic steroids, the muscles are capable of becoming significantly
larger and stronger in a fairly short period of time. As the amount of weight
lifted by the steroid user increases, so too does the load placed on the tendons. If
the tendons are not given enough time to (or simply cannot) compensate for the
added strain, they may rupture during training or athletic performance. Thus,
anabolic steroids may indirectly lead to this type of injury in some users,
essentially by making them too strong for their own connective tissues.
There may also be more direct mechanisms contributing to this type of injury.
Similar to skeletal muscle tissue, the tendons are responsive to androgens.
Studies show that under the stimulation of anabolic steroids, the tendons become
more rigid.
209 As tissue flexibility is reduced, so is the relative strength and
forgiving nature of the tendons (essentially lowering the tearing point).
Furthermore, while anabolic steroids are known to aid the healing process in the
muscles, studies suggest that they may actually impair the healing of tendon
injuries.
210 While this is admittedly a post-injury event, one could speculate that
smaller areas of damage might not repair properly, weakening the tissues. These
factors, coupled with a rising workload due to expanded strength capacity, could
explain a greater potential for tendon injury during anabolic/androgenic steroid
use.
The data concerning the potential role of anabolic steroids in connective tissue
injury is equivocal. Some studies find no association between AAS use and
tendon injury.
211 Overall, these types of injuries are still fairly uncommon. This
could make proving an association with anabolic steroid use difficult. The level
of AAS use is also undoubtedly a strong contributing factor in this type of
injury. When we do see tendon ruptures, they tend to be reported in more
advanced bodybuilders and steroid abusers. On the other hand, tendon injury
(without a specific accident event) seems to be extremely uncommon in those
that use AAS moderately and keep their body mass within reasonable levels. The
potential for this type of injury is one reason many believe it is better to
accumulate mass slowly and steadily with AAS, instead of rushing to put on the
most bulk possible.
Water and Salt Retention
Anabolic/androgenic steroids may increase the amount of water and sodium
stored in the body. This may include increases in both the intracellular and
extracellular water compartments. Intracellular fluid refers to water that has been
drawn inside the cells. While this does not increase the protein content of the
muscles, it does expand the muscle cell, and is often calculated and viewed as a
part of total fat free body mass. Extracellular water is stored in the circulatory
system, as well as in various body tissues, in the spaces between cells
(interstitial). Increases in interstitial fluid can be noticeable and troubling
cosmetically. In strong cases this can bring about a very puffy appearance to the
body (peripheral or localized edema), with bloating of the hands, arms, body,
and face. This may reduce the visibility of muscle features throughout the
physique. Excess fluid retention can also be associated with elevated blood
pressure,
212 which can increase cardiovascular and renal strain.
Estrogen is a regulator of fluid retention in both men and women.
213 This effect
appears to be mediated in part by changes in hypothalamic arginine vasopressin
(AVP), the primary hormone involved in controlling water reabsorption in the
kidneys.
214
Increased levels of estrogen tend to increase AVP levels, which can
promote the increased storage of water. Estrogen also appears to act on the renal
tubes in the kidneys in an aldosterone-independent manner to increase the
reabsorption of sodium.
215 Sodium is the major electrolyte in the extracellular
environment, and helps to regulate the osmotic balance of cells. Higher levels
can significantly increase water in the extracellular compartment.
Anabolic/androgenic steroids that either convert to estrogen, or possess inherent
estrogenic activity, are, likewise, those steroids that are associated with
increased extracellular water retention.
216
Estrogenic anabolic/androgenic steroids are generally favored for mass gaining
(bulking) purposes. A steroid user may ignore water retention during this phase
of training, occasionally even finding the sheer increases in size to be a welcome
benefit. Estrogenic steroids such as testosterone and oxymetholone are also
regarded as the strongest mass-and strength-building agents, which may be
caused in part by anabolic benefits of elevated estrogenic activity. The excess
water stored in the muscles, joints, and connective tissues is also commonly
believed to increase an individual’s resistance to injury. With the use of many
strongly estrogenic anabolic/androgenic steroids, water retention can account for
a large portion (35% or more) of the initial body weight gain during steroid
treatment. This weight is quickly lost once the steroids are discontinued or
estrogenic activity is reduced.
Non-aromatizing steroids such as oxandrolone and stanozolol have also been
shown to promote increased water retention, so this effect is not entirely
exclusive to aromatizable or estrogenic substances.
217 218 Anabolic steroids with
low or no estrogenic action tend to produce modest increases in whole body
water and intracellular fluid retention, however, and not in the visible
extracellular compartment.
219 220 These steroids are considered to be more
cosmetically appealing, and are generally favored by bodybuilders and athletes
when looking to improve lean mass and muscle definition. Popular
anabolic/androgenic steroids that are associated with low visible water retention
include fluoxymesterone, methenolone, nandrolone, oxandrolone, stanozolol,
and trenbolone.
Excess water retention may be addressed with the use of ancillary medications
such as the anti-estrogen tamoxifen citrate, or an aromatase inhibitor such as
anastrozole. By minimizing the activity of estrogens, these drugs can effectively
reduce the level of stored water. In most cases where an aromatizable steroid is
used, aromatase inhibitors prove to be significantly more effective at achieving
this goal. A common practice among bodybuilders during competition is to also
use a diuretic, which can shed excess water by directly increasing renal water
excretion. This is regarded as the most effective method for rapidly improving
muscle definition, but it can also be one of the most acutely risky practices as
well. Water retention is not a persistent side effect of steroid use. Excess water is
quickly eliminated, and normal water balance returned, once
anabolic/androgenic steroid administration is halted.
Virilization
Physical (Male)
Dysphonia (Vocal Changes)
Although far less common than dysphonia in women, anabolic/androgenic
steroids may alter vocal physiology in men. This may include a deepening of the
voice. Dysphonia is most common when anabolic/androgenic steroids are
administered during adolescence, as the deeper adult voice has not yet been
established under the influence of androgens. The administration of
anabolic/androgenic steroids before maturity can, likewise, cause a progressive
lowering of the vocal pitch, and may trigger pubescent vocal changes in younger
patients. Androgens have much less (often minimal) effect on vocal physiology
in adulthood. Although a slight lowering of the voice may be noticed with
androgen use in some cases, reports of clinically significant changes in the vocal
quality of adult men are, likewise, very rare. There has also been an isolated
report of stridor (vibrating noise when breathing) and vocal hoarseness in
relation to anabolic/androgenic steroid abuse.
221 This instance also involved
smoking, however, making the direct influence of steroids more difficult to
discern. In general, vocal physiology is well established by adulthood. Aside
from very minor reductions in pitch, anabolic/androgenic steroids are not
expected to have strong audible effects on the voice.
Gynecomastia
Anabolic/androgenic steroids with significant estrogenic or progestational
activity may cause gynecomastia (female breast development in males). This
disorder is specifically characterized by the growth of excess glandular tissue in
men, due to an imbalance of male and female sex hormones in the breast.
Estrogen is the primary supporter of mammary gland growth, and acts upon
receptors in the breast to promote ductal epithelial hyperplasia, ductal
elongation/branching, and fibroblast proliferation.
222 Androgens, on the other
hand, inhibit glandular tissue growth.
223 High serum androgen levels and low
estrogen usually prevent this tissue development in men, but it is possible in both
sexes given the right hormonal environment. Gynecomastia is regarded as an
unsightly side effect of anabolic/androgenic abuse by most users. In extreme
cases the breast may take on a very female looking appearance, which is difficult
to hide even with loose clothing.
Gynecomastia tends to develop in a series of progressive stages. The severity of
this process will vary depending on the type and dose of drug(s) used, and
individual sensitivity to hormones. The first sign is typically pain in the nipple
area (gynecodynea). This may quickly coincide with minor swelling around the
nipple area (lipomastia). This is sometimes referred to as pseudo-gynecomastia,
as it primarily involves fat and not glandular tissue. At this stage, it may be
possible to address mild nipple swelling by reducing or eliminating the
offending steroidal compounds, and administering an appropriate anti-estrogenic
medication for several weeks. If left untreated, however, this may quickly
progress to clear gynecomastia, which involves significant fat, fibrous, and
glandular tissue growth. The hard tissue growth may be easily felt in the early
stages when pinching deeply around the nipple. Noticeable gynecomastia is
likely to require corrective cosmetic surgery (male breast reduction).
224
Although gynecomastia is a very common side effect of steroid abuse, given its
clear association with certain drugs or practices, it is also an easily avoidable
one. Careful steroid selection and reasonable dosing are usually regarded as the
most basic and reliable methods for preventing its onset. Many steroid users also
frequently take some form of estrogen maintenance medication, which may
effectively counter the effects of elevated estrogenicity. Common options
include the anti-estrogen tamoxifen citrate, or an aromatase inhibitor such as
anastrozole. The use of a post-cycle hormone recovery program at the
conclusion of steroid administration (which usually includes several weeks of
anti-estrogen use) is also commonly advised, as gynecomastia is sometimes
reported in the post-cycle hormone imbalance phase when steroids are not
actually being taken.
It is important to note that progesterone can also augment the stimulatory effect
of estrogen on mammary tissue growth.
225 As such, progestational drugs may be
able to trigger the onset of gynecomastia in sensitive individuals, even without
elevating levels of estrogen. Many anabolic steroids, particularly those derived
from nandrolone, are known to exhibit strong progestational activity. While
gynecomastia is not a common compliant with these drugs, they are occasionally
linked to this side effect in anecdotal reports. The anti-estrogen tamoxifen citrate
is usually taken in such instances, as it can offset the effects of estrogen at the
receptor, which are still necessary for progestins to impart their growthpromoting effects on the breast.
Early gynecomastia.
Physical (Female)
Birth Defects
Anabolic/androgenic steroid exposure to a woman during pregnancy can cause
developmental abnormalities in an unborn fetus. Virilization of a female fetus is
a particular concern, and may include clitoral hypertrophy or even the growth of
ambiguous genitalia (pseudohermaphroditism). Reconstructive surgery will be
required to correct these serious developmental abnormalities. Women who are
pregnant, or are attempting to become pregnant, should not use or directly
handle anabolic/androgenic steroid materials (raw powder, pills, crèmes,
patches). Although anabolic/androgenic steroids can reduce sperm count and
fertility in men, they are not linked to birth defects when taken by someone
fathering a child.
Dysphonia (Vocal Changes)
Anabolic/androgen steroids are commonly linked to a deepening of the voice in
females. This is caused by direct androgenic influence on the larynx and muscle
tissues involved in vocal physiology, which (in females) are not normally
exposed to high androgen levels. Early changes may include a light hoarsening
of the voice, with audible shifts in pitch at the high and low end of the vocal
spectrum (quiet speaking and voice projection).
226 There is typically a lower
general frequency during speech, a reduction of high frequency pitch, and voice
instability and cracking. In many cases the changes caused by AAS drugs may
resemble those of the pubescent male. If left to progress, these changes may go
on to develop into a raspy and recognizable male-characteristic voice.
Deepening of the voice is defined as an androgenic or masculinizing effect.
Anabolic/androgenic steroids with higher relative androgenicity such as
testosterone, fluoxymesterone, and methandrostenolone, likewise, have a high
tendency to produce voice changes when used in females.
227 228 229 230 All
anabolic/androgenic steroids are capable of altering the female voice given the
right level of stimulation, however. To this point, vocal changes have been
reported under therapeutic conditions with even mild anabolic substances such
as oxandrolone and nandrolone.
231 232 Care must be taken to monitor the voice
during all AAS intake, as changes are often easily generated. Immediately
discontinuing anabolic/androgenic steroids may reduce the severity of
symptoms, although some changes are likely to persist. Anabolic/androgenic
steroid use may, likewise, permanently alter vocal physiology in females.
Enlarged Clitoris (Clitoromegaly)
The male and female reproductive systems differentiate and develop under the
influence of estrogen and testosterone. Even as an adult, the female reproductive
system remains developmentally responsive to male sex hormones. An elevation
of the androgen level in women may stimulate the growth of the clitoris (clitoral
hypertrophy). If androgen levels are not abated quickly this may lead to
virilization of the external genitalia, characterized by clinically abnormal
enlargement of the clitoris (clitoromegaly). With clitoromegaly, the clitoris may
begin to resemble a small penis, and may even visibly enlarge during sexual
arousal (erection). In more serious cases its association to a male penis can be
very striking and clear. Clitoromegaly can be a very embarrassing condition,
usually prompting swift intervention when its onset is noticed.
Clitoromegaly is most commonly seen as a congenital disorder, although it may
be caused by anabolic/androgenic steroid administration or other pathology in
adulthood (acquired clitoromegaly). As a virilizing side effect, clitoromegaly
tends to occur in a dose-dependant (androgenicity-dependent) manner. As such,
higher doses and more androgenic substances (such as testosterone, trenbolone,
and methandrostenolone) are more likely to trigger its onset. Primarily anabolic
steroids such nandrolone, stanozolol, and oxandrolone are less androgenic and
virilizing, and favored for the treatment of women for this reason. Clitoromegaly
caused by steroid use is both avoidable and progressive. Mitigating excess
androgenic action early when it is noticed is the most fundamental part of
treatment. Reversal of significantly developed tissue, however, will require
reconstructive surgery (clitoroplasty).
233 Special care should be taken to preserve
the dorsal and ventral neurovascular bundles and normal tissue sensation.
234
A photograph of distinct clitoromegaly.Here, the clitoris begins to resemble
a penis-like structure under androgen influence. If left unabated, this may
progress to a more defined phallic abnormality. Source: Copcu et al.
Reproductive Health 2004 1:4 doi:10.1186/1742-4755-1-4.
Hair Growth (Hirsutism)
Anabolic/androgenic steroids may cause male-pattern hair growth in females.
Medically defined as hirsutism, this condition is characterized by the growth of
hair in androgen sensitive areas of the body. With hirsutism, dark coarse hair
(terminal hair) may develop on the face, chest, abdomen, and back, areas of the
body normally associated with hair growth in men, not women. Treatment for
hirsutism typically involves immediate abstinence from anabolic/androgenic
steroid intake, and initiation of a strategy to minimize androgen action at the hair
follicles. This may include the use of oral estrogens, anti-androgens
(spironolactone), or finasteride. Topical ketoconazole, an antifungal agent, has
also been used with some success. The response to medical treatments may be
slow, and the changes caused by anabolic/androgenic steroid use may persist for
a year or longer.
235 Regular hair removal of the affected areas may be necessary.
The severity of hirsutism will be related to the androgenicity of the drug(s)
taken, the dosage and duration of use, and sensitivity of the individual.
Menstrual Irregularities
Anabolic/androgenic steroids may alter the menstrual cycle in females, resulting
in infrequent or absent menses (amenorrhea). Fertility may also be interrupted.
Normal menstruation is expected to resume after anabolic/androgenic steroids
are discontinued, and the natural hormonal balance is restored. Complete
recovery of the female hormonal axis and fertility can take many months in
some cases, however, and long-term interruptions of fertility are possible,
though unlikely.
Reduced Breast Size
Anabolic/androgenic steroids can inhibit the growth-supporting effects of
estrogen on mammary tissues, and may cause a visible reduction in breast size
(breast atrophy). Androgen use in females has specifically been shown to cause a
reduction in glandular tissue size, and to promote an increase in fibrous
connective tissue.
236 These physiological changes are similar to those noted after
menopause, when female sex steroids are very low. Reductions in breast size
produced by AAS may be very persistent after the discontinuance of drug intake,
as there can be substantial local tissue remodeling under excess androgen
influence. Women are warned of the potential for substantial physical changes in
the breasts with anabolic/androgenic steroid abuse.
Psychological
The effects of anabolic/androgenic steroids on human psychology are complex,
controversial, and not fully understood. What is known for certain is that sex
steroids influence human psychology. They play a role in an individual’s general
mood, alertness, aggression, sense of well-being, and many other facets of our
psychological state. There are known psychological differences between men
and women because of differences in sex steroid levels, and, likewise, altering
hormone levels with the administration of exogenous steroids may influence
human psychology. The exact strength of this association, however, remains the
subject of much research and speculation. In reviewing some of the more
substantial data that has been presented thus far, we find a better (though
incomplete) understanding of the effects of AAS in several key areas of
psychological health.
Aggression
Men tend to be more aggressive than women, a characteristic that has been
partly attributed to higher androgen levels.
237 Physiologically, androgens are
known to act on the amygdala and hypothalamus, areas of the brain involved in
human aggression. They also affect the orbitofrontal cortex, an area involved
with impulse control.
238 Steroid abusers commonly report increases in
aggression (irritability and bad temper) when taking anabolic/androgenic
steroids. In fact, among the illicit steroid-using community, these drugs are often
differentiated from one another with regard to their aggression-promoting
properties. Many athletes in explosive strength sports even specifically favor
highly androgenic drugs such as testosterone, methyltestosterone, and
fluoxymesterone due to their perceived greater abilities to support aggression
and the competitive drive.
239 While some association between steroid use and
aggression is understood, the magnitude of this association remains the subject
of much debate.
The psychological effects of escalating dosages of testosterone esters have been
examined in a number of placebo-controlled studies. At therapeutic levels, no
adverse psychological effects are apparent. If anything, testosterone replacement
therapy tends to improve mood and sense of well-being. When used at a
contraceptive dosage (200 mg per week), again, no significant psychological
effects are seen.
240 241 As the dosage reaches a moderate supratherapeutic range
(300 mg per week), psychological side effects such as aggression began to
appear in some subjects, but these reports remain mild and infrequent.
242 At a
dosage of 500 to 600 mg per week (5 to 6 times the therapeutic level), mild
increases in aggression and irritability are frequently reported. Approximately
5% of subjects displayed manic or hypomanic behavior in reaction to this much
testosterone, although the vast majority of people still exhibited minor or no
psychological change.
243 244
One extensive placebo-controlled study furthers our understanding of the
psychological effects of steroid abuse, often characterized by extreme doses and
multi-drug combinations, through its examination of a group of 160 regular users
before and during the self-administration of a steroid cycle.
245 A placebo group
was also examined, which consisted of 80 people that were unknowingly taking
counterfeit medications. Extensive psychological evaluations were taken using
System Check List-90 (SCL-90) and the Hostility and Direction of Hostility
Questionnaire (HDHQ). Those using placebo steroids did not notice any
significant psychological changes. Steroid abuse, however, was associated with
higher levels of hostility in all HDHQ measures, with particular increases in
acting out, criticism of others, paranoid hostility, guilt, self-criticism, blaming of
others, blaming of self, and overall hostility. SCL-90 ratings were also high
during steroid abuse for obsessive compulsiveness, interpersonal sensitivity,
hostility, phobic anxiety, and paranoid ideation. Hostility measures tended to
increase significantly as the level of abuse escalated from light to heavy,
although no violent behavior was reported.
Criminality and Violence
Links between anabolic/androgenic steroid abuse and violence have been much
more difficult to establish. Most papers suggesting such an association either
used correlative data, or discussed individual case studies. These help broaden
the scope of research, but are not reliable for proving causality. For example, one
study questioned a group of 23 steroid abusing men, and reported that these men
were involved in a significantly greater number of verbal and even physical
fights with their girlfriends and wives during the times they were administering
AAS drugs.
246 With the known effects of anabolic/androgenic steroids on
aggression, this finding is compelling. It may very well be that some men are
more susceptible to this type of behavior when abusing AAS than others. A
paper like this is not sufficient, however, to substantiate a violent “roid rage”.
Further research is needed to determine if AAS can even trigger violent behavior
in an extremely small minority of users, and if so, what trait(s) makes these
individuals susceptible to this reaction when the vast majority of users are not.
Serious criminality has also been difficult to associate with steroid abuse. When
discussed, we again tend to see weak correlative data and case studies. For
example, one paper in Sweden reports an association between steroid abuse and
weapons and fraud crimes.
247
It is uncertain, however, if steroid abuse was
actually responsible for this criminality, or just associated with it. It is simply
possible these men were more exposed to, or more likely to use, illegal AAS for
some unidentified reason. Another paper discussed three individuals with no
prior criminal or psychiatric history that were arrested for murder or attempted
murder after abusing anabolic/androgenic steroids.
248 While stories like these are
interesting (and numerous), with millions of steroid users in the general
population they are far from compelling. To date, there is no conclusive medical
evidence that anabolic/androgenic steroid abuse can cause violent or serious
criminal behavior in a previously mentally stable individual.
Dependency/Addiction
Anabolic/androgenic steroids are considered to be drugs of abuse. Although
there is no universally accepted definition for this, abuse is commonly described
as the continued use of a substance in spite of adverse consequences. Given the
negative health consequences that are associated with supratherapeutic doses of
AAS drugs, this classification is a difficult one to dispute. Drugs of abuse are
very often also drugs of dependency, which in this context describes an impaired
ability to control the use of a substance. There has been a longstanding debate
over whether or not anabolic steroids also fit the definition of drugs of
dependency. Furthermore, among those that support the notion of an anabolic
steroid dependency, there is a split with regard to the nature of this dependency
(psychological or physical).
Physical dependency is usually regarded as the most serious form of drug
dependency, although both types can be very extreme and troubling depending
on the situation. Physical dependency is defined as the need to administer a
substance in order for the body to function normally. A physical dependency is
usually characterized by drug tolerance, and withdrawal symptoms if the drug is
discontinued abruptly. The most well known examples of drugs of physical
dependency are opiates such as morphine, hydrocodone, oxycodone, and heroin.
Opiates can be very difficult drugs for dependant individuals to quit using, since
stopping their use tends to produce extreme withdrawal symptoms including
physical pain, sweating, tremors, changes in heart rate and blood pressure, and
intense cravings for the drug. The physical symptoms may last for days to weeks
after the drug is discontinued, while the psychological symptoms can persist for
months longer.
Anabolic/androgenic steroid abuse could be associated with many of the DSMIV criteria necessary for a diagnosis of both psychological and physical drug
dependency. For instance, it is not uncommon for someone to take the drugs in
higher doses or for longer periods of time then they had initially planned (criteria
#1). Many abusers also have a desire to cut down on their use of these drugs, but
concerns over lost muscle size, strength, or performance may prevent this
decision (criteria #2). Individuals often continue to abuse steroids in spite of
negative health consequences (criteria #5). Steroid abuse is also associated with
a diminishing level of effect and escalating dosages (criteria #6). Lastly, steroid
discontinuance has been associated with withdrawal symptoms (criteria #7),
including reduced sex drive, fatigue, depression, insomnia, suicidal thoughts,
restlessness, lack of interest, dissatisfaction with body image, headaches,
anorexia, and a desire to take more steroids.
249
According to the American Psychiatric Association and its Diagnostic and
Statistical Manual of Mental Disorders (DSMIV), three or more of the following
criteria must be met for a diagnosis of psychoactive drug dependency.
1. Substance is taken in higher doses or for longer periods than intended.
2. Desire or unsuccessful efforts to cut down or control substance use.
3. Excessive time spent obtaining, using, or recovering from the substance.
4. Important activities are given up because of substance abuse.
5.Continued substance use despite negative psychological or physical
consequences.
6. Tolerance, or the need for higher amounts of the substance to achieve
desired effect.
7. Withdrawal symptoms.
A drug dependency that is isolated to criteria #1 to #5 would be described as
psychological. The meeting of criteria #6 or #7 indicates the dependency is also
a physical one.
The physical benefits of anabolic/androgenic steroids complicate the matter of
drug dependency a great deal. Unlike narcotics, the main motivator behind the
use of steroids is their positive effect on muscle and performance. With this in
mind, steroid addiction could actually be a misdiagnosis for muscle dysmorphia
in many cases. This is a psychological disorder characterized by persistent
feelings of physical inadequacy in spite of extreme muscular development.
Steroid abuse (often extreme) is highly common in muscle dysmorphics, along
with compulsive resistance training.
250 But steroid abuse is regarded as a
symptom of this disorder, not a cause. In a similar sense, the physique-, strength-
, and performance-improving qualities of anabolic/androgenic steroids could be
driving much or all of the abuse. An analogy would be the so-called addiction to
chocolate. Some individuals develop tangible psychological issues surrounding
the consumption of chocolate, with uncontrolled binging and negative social and
health consequences.
251 But we do not regard chocolate itself as a substance that
causes dependency.
There is some evidence that the reinforcing qualities of steroid use go beyond an
attraction to their physical benefits. Lab animals such as mice and hamsters will
repeatedly self-administer testosterone and other anabolic/androgenic steroids
for example, an effect that cannot be caused by a perception of physical
change.
252 Testosterone is also known to interact with the mesolimbic dopamine
system, which is common with other drugs of abuse.
253 254 Studies additionally
suggest that anabolic/androgenic steroids influence dopamine transporter density
and increase sensitivity of the brain reward system.
255 Steroids are known to
influence psychology, and abusers commonly report an increased sense of
wellness, vitality, and confidence when taking AAS drugs. Some speculate this
is due in part to an inherent psychoactive effect. Further research is needed to
determine if anabolic/androgenic steroids are actually mild psychoactive drugs.
Anabolic/androgenic steroids are not drugs of marked intoxication,
256 which
makes them very different from other drugs and abuse or dependency. This
makes diagnosing a drug dependency difficult. By definition, drug dependency
is related to the abuse of a psychoactive substance, and it is unknown if AAS
drugs can accurately be classified as psychoactive substances. At the present
time, most experts do not regard anabolic/androgenic steroids as drugs of true
physical dependency. It is difficult to correlate the post-cycle hormone
imbalance with traditional withdrawal symptoms,and tolerance is really a
function of metabolic limits on muscle growth, not necessarily a diminishing
biological effect. Individuals remain warned, however, that steroid abuse is
commonly associated with the signs of psychological dependency. Further
research is needed to evaluate the biological and psychological nature of steroid
abuse.
Depression/Suicide
Anabolic/androgenic steroids abuse may be associated with bouts of depression.
This is most common after the administration of AAS drugs has been
discontinued, especially following high doses or long cycles. During the time
that steroids are being administered, natural hormone production is diminished
because the body recognizes the excess hormone levels. When the steroid drugs
are abruptly discontinued, however, the body can enter a state of temporary
hypogonadism (low androgen levels). This may be associated with a number of
psychological symptoms including depression, insomnia, and loss of interest.
This condition is usually referred to as anabolic steroid withdrawal depression,
and can persist for weeks or even months as the body slowly resumes normal
hormone production.
257
The most common method of addressing anabolic steroid withdrawal depression
in men is preemptively, with the implementation of an aggressive post-cycle
hormone recovery program. These programs are typically based on the
combined use of HCG (human chorionic gonadotropin) and anti-estrogenic
drugs such as tamoxifen and clomiphene. They are used together in a way that
can stimulate and sensitize the hypothalamic pituitary testicular axis, allowing
natural hormone production to return more quickly. Alternately or concurrently,
fluoxetine (or other antidepressant medications) may help alleviate symptoms of
depression following steroid withdrawal, especially when this depression is
prolonged or severe.
258 These drugs must be used with caution, however, as they
also have been linked with increased thoughts of suicide in some patients.
259
Although less common, depression is sometimes reported during the active
administration of anabolic/androgenic steroids. This may be caused by an
imbalance of sex steroid levels, particularly with regard to relative androgenicity
or estrogenicity. In more cases than not, it will involve a situation where
sufficient androgenicity is not present, usually when primarily anabolic drugs are
being taken alone. Given the diverse nature in which sex steroids interact with
human psychology, however, it is difficult to clearly outline the parameters
necessary for this type of depression to develop. Further confusing the issue is
the fact that this depression can involve either elevated or suppressed levels of
certain sex steroids. The addition of testosterone to an anabolic steroid cycle
causing depression may alleviate the problem in many (but not all) instances, as
it can provide both supplemental androgenic and estrogenic action.
Suicide has been linked to anabolic/steroid abuse in rare instances.
260 Such
reports are usually case studies, involving individuals that were believed to be
psychologically stable before abusing AAS, and who committed suicide during
or after use of the drugs. It is known that depression is a common complaint
during anabolic steroid withdrawal. It is also known that a small percentage of
users are especially sensitive to the psychological effects of anabolic/androgenic
steroids, and notice dramatic mood swings, manic behavior, and/or severe
depression with their use. It is unknown why these individuals have such
extreme reactions, while the vast majority of users notice only mild or moderate
changes to their psychological state. Further research is needed to identify and
understand these individuals. Readers are cautioned that adverse psychological
effects, including severe depression and suicidal thoughts, have been associated
with steroid abuse in a small minority of users. Beyond this, there is no
compelling evidence suggesting that anabolic/androgenic steroid abuse will lead
to suicide in otherwise mentally stable users.
Insomnia
Anabolic/androgenic steroid use may be associated with insomnia. This adverse
reaction appears to be related to an imbalance of hormone levels, and has been
noticed during both excess and insufficient hormonal states. For example,
insomnia is a common complaint among men suffering from low androgen
levels (hypogonadism).
261
It is also frequently reported by steroid abusers during
the post-cycle refractory period, when endogenous androgen levels are also low
due to steroid-induced suppression.
262 At the same time, this side effect is also
seen during active AAS administration,
263 when androgen levels are very high.
The full etiology of steroid-related insomnia is not fully understood, although
increased cortisol or diminished estrogen is commonly blamed.
264 265 Given the
complex interactions between sex steroids and the human psyche, it is difficult
to predict how and when this adverse reaction will appear. While insomnia may
be frequently reported among steroid users, this side effect rarely reaches a
clinically significant level.
Reproductive (Male)
Infertility
Anabolic/androgenic steroid use may impair fertility. The human body strives to
maintain balance in its sex hormone levels (homeostasis). This balance is
regulated largely by the hypothalamic-pituitary-testicular axis (HPTA), which is
responsible for controlling the production of testosterone and sperm.The
administration of anabolic/androgenic steroids provides additional sex steroid(s)
to the body, which the hypothalamus can recognize as excess. It responds to this
excess by reducing signals that support the production of pituitary gonadotropins
luteinizing hormone (LH) and follicle-stimulating hormone (FSH). LH and FSH
normally stimulate the release of testosterone by the testes (gonads), and also
increase the quantity and quality of sperm. When LH and FSH levels drop,
testosterone levels, sperm concentrations, and sperm quality may all be reduced.
When given in supraphysiological levels, anabolic/androgenic steroids
commonly induce oligozoospermia. This is a form of reduced fertility
characterized by having less than 20 million spermatozoa per ml of ejaculate.
The quality of the sperm may also be impaired under the influence of AAS, as
noted by an increase in the number of abnormal or hypokinetic (noticing reduced
motion) sperm. Fertility is possible during oligozoospermia, however, as viable
sperm are still made by the body. The odds of conception are just significantly
lower than when sperm concentrations are normal. In many cases azoospermia is
reached during AAS administration, which is defined as having no measurable
sperm in the ejaculate. Conception is not possible with true steroid-induced
azoospermia. Note that in some cases, fertility has been temporarily restored
during active anabolic/androgenic steroid abuse with the use of human chorionic
gonadotropin (HCG).
266
Diminished fertility is considered a reversible side effect of anabolic/androgenic
steroid abuse. Sperm concentrations usually return to normal within several
months of discontinuing drug intake. A substantial post-cycle recovery program
based on the use of HCG, tamoxifen, and clomiphene may significantly shorten
the refractory period, and is highly recommended among those in the steroidusing community. In a small percentage of cases, particularly following long
periods of heavy steroid abuse, recovery of the HPTA can be very protracted,
taking up to a year or longer for full recovery.
267 268 Given the undesirable
psychological and physical symptoms that can be associated with a prolonged
state of low testosterone levels, such a long recovery window is rarely regarded
as acceptable. This will usually prompt an individual to seek medical
intervention or initiate an aggressive HPTA recovery program.
The ability of anabolic/androgenic steroids to suppress LH, FSH, and fertility
has initiated a great deal of research surrounding their use as male
contraceptives. Injectable testosterone has been extensively studied by the World
Heath Organization, for example, and was determined to be a safe and
moderately effective method of male birth control. In studies which administered
200 mg of testosterone enanthate per week to healthy men, azoospermia was
achieved in 65% of patients within six months.
269 Most of the remaining patients
were oligozoospermic. This diminished fertility was fully reversible, and
baseline sperm concentrations returned within seven months on average after
drug discontinuance. A state of full azoospermia is the desired endpoint of male
contraception, however, and this has not been reliably achieved with AAS drugs
alone, even in high doses.
270 Anabolic/androgenic steroids have, likewise, are
not approved for use as male contraceptives.
Libido/Sexual Dysfunction
Anabolic/androgenic steroids may alter sexual desire and functioning. The
nature of their effects, however, can vary depending on the drug(s) and dosage(s)
used, as well as the individual sensitivity of the user to hormonal manipulation.
One of the most common responses is a stimulatory one. Testosterone is the
primary male sex steroid. As such, it is responsible for increasing sexual desire
and supporting many male reproductive-system functions.
271 Since all
anabolic/androgenic steroids are derived from (and share similar action to)
testosterone, use of these drugs is often linked to increases in sexual desire, as
well as copulation and orgasm frequency.
272 A significant increase in the
frequency and duration of erections may also be noted. In most cases these side
effects are not troubling, and may even be regarded as positive by the individual
(some feel it improves their sex lives).
AAS use may also be associated with diminished libido and sexual functioning.
This could be due to several factors. One is insufficient androgenic activity. This
sometimes is noted with the use of primarily anabolic steroids such as
methenolone, nandrolone, or oxandrolone, which may not provide sufficient
androgenicity to compensate for suppressed endogenous testosterone.
273 Studies
also show that estrogen plays an important role in libido and sexual function in
men.
274 Therefore, the use of non-aromatizable steroids or aromatase-inhibiting
drugs sometimes also causes interference. The addition or substitution of
testosterone during a cycle is usually regarded as the most reliable way to correct
issues with male sexual functioning, as it supplements the full spectrum of sex
steroid activity. Note that sexual issues are also common after steroid
discontinuance, when endogenous steroid levels are low.
Priapism
In very rare instances, anabolic/androgenic steroids have been linked to
priapism.
275 276 277 This is a condition characterized by the development of an
erection that will not return to its flaccid state within four hours. Priapism is a
potentially very serious condition, which can require medical or surgical
intervention. If left untreated, priapism can lead to permanent penile damage,
erectile dysfunction, or even gangrene, which may necessitate removal of the
penis. When priapism is linked to steroid use, testosterone is usually responsible.
Furthermore, this condition appears to be more frequent in younger patients
undergoing treatment for hypogonadism. This may be due in part to a rapid
increase in androgenicity, in a male reproductive system that has not yet been
exposed to high levels of stimulation. Priapism is very unlikely to develop in
adult steroid abusers.
Prostate Cancer
Prostate cancer is dependent on androgens. This disease will not develop if
androgens are eliminated from the body at a young age (as with castration),
278
and abatement of androgenic activity in patients with active disease is regarded
as a standard path of treatment. A complete picture of the involvement of
androgens, however, remains unclear. Studies show there is no association
between the testosterone level and likelihood of developing prostate cancer.
279
On the same note, the administration of exogenous testosterone during androgen
replacement therapy seems to have no effect on the risk for developing this
disease.
280 A review of the available medical literature also does not support an
increased risk of prostate cancer in steroid abusers,
281 which typically endure
excessive levels of androgenic stimulation. The present model suggests that
while testosterone is a necessary component of prostate cancer, it does not
appear to be a direct trigger for its onset.
282
New diagnoses of prostate cancer are sometimes reported during testosterone
replacement therapy and steroid abuse.
283 284 Such reports may be the result of a
previously undiagnosed condition or unrelated development of this disease, with
androgen stimulation assisting the tumor growth rate. Many forms of prostate
cancer possess functional androgen receptors, and are highly androgen
responsive. As such, they can be stimulated to grow under the influence of
testosterone or other anabolic/androgenic steroids. Given this effect, AAS drugs
are usually contraindicated in patients with a history of prostate cancer.
285 While
steroid administration appears unlikely to cause prostate cancer, individuals
remain warned that the use of testosterone or other AAS drugs by someone with
previously undiagnosed (latent) malignant prostate cancer could result in the
more rapid advancement of this disease.
286
Prostate Enlargement
Anabolic/androgenic steroids may influence the size of the prostate. Androgens
are integral to the development of the prostate in early life, and are essential to
maintaining prostate structure and function throughout adulthood. Increases in
the androgen level often result in growth stimulation to this gland (prostate
hypertrophy). For example, increased prostate volume has been reported in some
patients receiving testosterone injections for the treatment of hypogonadism.
287
While extreme prostate hypertrophy is not common under therapeutic
conditions, prostate volume does tend to reach a size that is considered normal
for a given androgen level.
288 PSA (prostate-specific antigen) levels have also
been shown to increase under the influence of exogenous testosterone in some
patients,
289 which is a diagnostic marker of prostate health often correlated with
prostate volume.
290 291 Additionally, reducing stimulation of the prostate by
lowering the androgen level tends to reduce prostate volume.
292
Anabolic/androgenic steroid abuse may result in significant increases in prostate
volume. In more severe cases, this may lead to benign prostate hypertrophy
(BPH). BPH is a common condition in older men, characterized by reduced
urine flow, difficulty or discomfort urinating, and changes in urinary frequency.
Anecdotal reports of BPH among steroid-using bodybuilders are not common,
but do occur with enough frequency to warrant concern. Such reports are most
often linked to more androgenic drugs such as testosterone and trenbolone, or
the excessive dosing of AAS in general. One of the most extreme reports of
prostate hypertrophy came from Dr. John Ziegler, the U.S. Olympic physician
accredited with introducing Dianabol to sports.
293 Dr. Ziegler noted that during
the mid-1950s, many Russian weightlifters were abusing so much testosterone
that they needed catheterization to urinate. Dianabol was released soon after,
which is structurally a close derivative of testosterone with reduced
androgenicity.
Studies of anabolic/androgenic steroid abusers show a preferential stimulation of
the inner prostate under the influence of these drugs, in an area where benign
prostate hypertrophy is known to originate.
294
In contrast, prostate cancer
usually develops in peripheral areas of the gland. Some association between
BPH and prostate cancer is known to exist, however, although the exact nature
and strength of this association remains uncertain.
295 PSA values are often
(although not always) elevated in both disorders, and serve as a marker of
potential trouble. It is important for men to monitor prostate health regularly by
digital rectal examinations and blood testing for PSA levels.
Anabolic/androgenic steroid use is generally immediately discontinued if signs
of BPH or elevated PSA values become apparent.
In addition to androgens, estrogens are also known to be involved in prostate
growth and functioning.
296 While androgens are generally stimulatory towards
prostate growth, however, estrogen exerts both protective and adverse effects.
297
On the beneficial side, stimulation of estrogen receptor (ER-beta subtype) may
help protect the prostate from inflammation, cell hyperplasia, and
carcinogenesis. Conversely, stimulation of the alpha subtype of the estrogen
receptor is linked to abnormal cell proliferation, inflammation, and
carcinogenesis. How the aromatization of testosterone and AAS (which will
result in stimulation of both receptor subtypes) will effect prostate hypertrophy
remains unclear. Prostate growth and elevated PSA values have been noted
during steroid administration with both strongly and mildly estrogenic
steroids.
298 Furthermore, the administration of anastrozole (an inhibitor of
estrogen synthesis) during testosterone administration does not appear to block
stimulation of the prostate.
299 Presently, the most successful strategy to
minimizing prostate hypertrophy seems to be focused on reducing relative
androgenic, not estrogenic, action.
Testicular Atrophy
Anabolic/androgenic steroids may produce atrophy (shrinkage) of the testicles.
Testosterone is synthesized and secreted by the Leydig cells in the testes. Its
release is regulated by the hypothalamic-pituitary-testicular axis, a system that is
very sensitive to sex steroids. When anabolic steroids are administered, the
HPTA will recognize the elevated hormone levels, and respond by reducing the
synthesis of testosterone. If the testes are not given ample stimulation, over time
they will atrophy, a process that can involve both a loss of testicular volume and
shape. This atrophy may or may not be obvious to the individual. In some cases,
the testes will appear normal even though their functioning is insufficient. In
other cases, shrinkage is very apparent. Visible testicular atrophy is one of the
most common side effects of steroid abuse, appearing in more than 50% of all
anabolic/androgenic steroid abusers.
300 301
Although testicular atrophy is very common in frequency, it is also regarded as a
temporary reversible side effect.
302 The gonads, by their nature, will vary in size
under hormonal influence. Atrophy should not produce permanent damage.
Note, however, that it can be a somewhat persistent issue. It may take many
weeks or months of sufficient LH stimulation after steroid discontinuance for
original testicular volume to be restored. Likewise, testicular atrophy is usually
the root cause of prolonged post-cycle hypogonadism. In extreme cases, full
recovery can take more than 12 months, and may even require medical
intervention. A post-cycle recovery program inclusive of HCG (which mimics
luteinizing hormone activity) may be used to minimize this recovery phase.
303
This drug is also frequently effective for maintaining testicular mass when used
on a periodic basis during steroid administration.
304 HCG must be used with
caution, however, as overuse may cause desensitization of the testes to LH,
305
complicating HPTA recovery.
Some of the more potent anabolic/androgenic steroids, including testosterone,
nandrolone, trenbolone, and oxymetholone, appear to be more suppressive of
testosterone release than many other AAS drugs. This may be explained in part
by the additional estrogenic or progestational activity inherent in these steroids,
as estrogens and progestins both also provide negative feedback inhibition of
testosterone release.
306 307
It is important to note, however, that all
anabolic/androgenic steroids are capable of suppressing testosterone secretion.
This includes primarily anabolic compounds such as methenolone and
oxandrolone, which are normally regarded as milder in this regard. While these
compounds may be less inhibitive of testosterone synthesis under some
therapeutic conditions, when taken in the supratherapeutic doses necessary for
physique-or performance-enhancement, significant atrophy and suppression are
common, and distinctions less pronounced.
Other
Anaphylactoid Reactions
An anaphylactoid reaction is a serious and potentially life threatening allergic
response to the administration of a foreign substance. Symptoms of this disorder
include itching of the skin and eyes, swelling of the mucous membranes, hives,
lowered blood pressure, abdominal pain, vomiting, and dilated blood vessels.
The smooth muscles may also be stimulated to contract, thereby restricting
breathing. Anaphylactic shock may develop in severe cases, which is marked by
unconsciousness, coma, or death. The physical symptoms of this disorder are
medicated by the release of histamine, leukotriene C4, prostaglandin D2, and
tryptase. An anaphylactoid reaction has many of the same characteristics as
anaphylaxis, although is not immune system mediated. Anaphylactoid reactions
are highly uncommon with hormonal medications such as anabolic/androgenic
steroids. Warnings of this reaction remain standard on many (often) injectable
medications, however. Mild skin reactions may be effectively treated with an
antihistamine. More serious manifestations may require IV epinephrine and
other supportive care. Given the potential for rapid escalation of this condition,
immediate medical attention should be sought if an anaphylactoid reaction
develops.
Cancer, Brain
Anabolic/androgenic steroids are not associated with brain cancer.
Complications relating to a rare and usually fatal form of cancer called primary
central nervous system (brain) lymphoma caused the death of famous American
football player Lyle Alzado. This type of brain cancer most commonly appears
in immune-compromised patients, such as those suffering from Human
Immunodeficiency Virus (HIV), or organ transplant recipients taking
immunosuppressive drugs to prevent organ rejection.
308 309 Before his death,
Alzado had self-attributed his cancer to 14 years of anabolic/androgenic steroid
abuse.
310 While anabolic/androgenic steroids can be mildly immunosuppressive,
these drugs are not associated with extreme clinical immunosuppression that
could lead to brain lymphoma. Likewise, there is no clinical evidence or
understood mechanism that suggests AAS abuse is responsible for Alzado’s
death. Even though physicians say there is no proof of an association between
performance-enhancing drug abuse and Alzado’s cancer,
311
this story is
frequently recounted in the media to convey the dangers of steroid abuse.
Cancer, Breast
Although extremely rare, male breast cancer has been associated with the
administration of testosterone.
312
It is unknown, however, if the hormone
therapy was related to the onset of this disease, or if it was just incidental to its
progression and discovery. Androgens generally exhibit inhibitory effects on
hormone-responsive breast cancers, and have actually been used in their
treatment.
313 Estrogens, on the other hand, can support the growth of many
breast tumors. It is not uncommon for elevated estrogen levels to result from
testosterone therapy, and at least a supportive role is plausible. The exact
relationship between isolated cases of breast carcinoma and testosterone
administration in men remains unclear. Testosterone is presently contraindicated
in patients with breast cancer.
The data concerning the effects of anabolic/androgenic steroids on insulin
sensitivity is difficult to interpret. It does appear that when these drugs are used
initially, reductions in body fat are common, particularly visceral adipose tissue.
This may actually improve insulin sensitivity and the overall metabolic state, and
reduce certain specific risk factors for diabetes and cardiovascular disease.
Beyond this, the effects of AAS on glucose metabolism are not fully understood,
and difficult to predict. Studies using supratherapeutic doses of testosterone and
nandrolone have failed to produce any negative changes, suggesting that
moderate AAS abuse is probably not associated with impairments in insulin
sensitivity. At the same time, studies do suggest that there could be concerns
with heavy steroid abuse. Further research is needed is assess the impact of
steroid abuse on metabolic health.
Insulin Resistance
Anabolic/androgenic steroids may alter insulin sensitivity, an important measure
of metabolic health. The effect of these drugs may be variable, however. For
example, testosterone administration may improve insulin sensitivity in men
with hypogonadism.
314 Oxandrolone (20 mg per day) has also been shown to
improve insulin sensitivity in older men (60 to 87 years).
315 These beneficial
metabolic outcomes were correlated with reductions in visceral adipose tissue
(VAT). This is a deep layer of fat that surrounds the abdominal organs, and is
associated with insulin resistance.
316
Insulin resistance may also lead to other
health issues including hypertension, elevated triglycerides and cholesterol, and
increased risk of diabetes and cardiovascular disease. By reducing VAT levels,
testosterone and AAS may improve insulin sensitivity, and potentially metabolic
health.
Conversely, anabolic/androgenic steroid abuse has been associated with
impaired glucose metabolism.
317
In one study, powerlifters that had abused AAS
in high doses for up to seven years were shown to have diminished glucose
tolerance and increased insulin resistance.
318
In spite of a long history of
resistance exercise, these subjects secreted more insulin in response to measured
glucose ingestion than even obese sedentary control subjects. Additional studies
with methandrostenolone demonstrated significantly increased insulin secretion
and potential resistance.
319 A similar outcome is not found in all AAS studies,
however. For example, testosterone enanthate in doses as high as 600 mg per
week for 20 weeks failed to produce any changes in insulin sensitivity in healthy
young men.
320 Nandrolone decanoate (300 mg per week) also did not impair
glucose tolerance, and actually improved insulin independent glucose
disposal.
321 The data concerning the effects of anabolic/androgenic steroids on
insulin sensitivity is difficult to interpret. It does appear that when these drugs
are used initially, reductions in body fat are common, particularly visceral
adipose tissue. This may actually improve insulin sensitivity and the overall
metabolic state, and reduce certain specific risk factors for diabetes and
cardiovascular disease. Beyond this, the effects of AAS on glucose metabolism
are not fully understood, and difficult to predict. Studies using supratherapeutic
doses of testosterone and nandrolone have failed to produce any negative
changes, suggesting that moderate AAS abuse is probably not associated with
impairments in insulin sensitivity.At the same time, studies do suggest that there
could be concerns with heavy steroid abuse. Further research is needed is assess
the impact of steroid abuse on metabolic health.
Nosebleeds
Anabolic/androgenic steroid use may be associated with periodic nosebleeds.
According to one study, approximately 20% of illicit steroid users reported this
side effect, making it fairly common.
322 Nosebleeds are not a direct result of
androgenic action, but are secondary to steroid-induced increases in blood
pressure and/or reductions in blood clotting factors. Although they can be scary,
most nosebleeds are harmless, and will not require emergency medical attention.
When related to steroid use, however, they may reflect other more serious
underlying health issues, particularly hypertension. Nosebleeds that occur under
AAS influence usually stop reappearing shortly after drug discontinuance, as
blood pressure and/or clotting factors return to their normal pre-treated state.
Sleep Apnea
Obstructive sleep apnea (OSA) is a disorder characterized by brief pauses in
breathing during sleep, which occur when the soft tissues in the throat close and
block the air passages. Sleep apnea may interfere with normal gas exchange, and
can significantly reduce the productivity of sleep. It may also elevate the
hematocrit, thicken the blood, and increase the risk of other health issues
including hypertension and cardiovascular disease.
323 Sleep apnea can
sometimes go undiagnosed for years, as an individual may not be aware of the
obstructions during sleep. Symptoms of OSA include daytime sleepiness,
snoring, nocturnal awakenings, and morning headaches. Obstructive sleep apnea
seems to occur most commonly in overweight individuals, and is related to a
combination of hormonal, metabolic, and physical factors.
324 325
Anabolic/androgenic steroids may be associated with the development of
obstructive sleep apnea in a small percentage of individuals. The exact
relationship between AAS and OSA, however, remains unclear. This adverse
reaction seems to appear in some patients receiving testosterone drugs to treat
hypogonadism.
326 More detailed studies have shown that high does of
testosterone can disrupt sleep and breathing, as well as increase sleep-related
hypoxemia, effects that may precipitate obstructive sleep apnea.
327 While OSA
has not been clearly documented in steroid abusers, androgens have been shown
to alter the structure and function of the oropharynx in ways that can predispose
an individual to this disorder.
328 More research is needed to determine if steroid
abuse can trigger OSA in an otherwise healthy person. Individuals with a history
of obstructive sleep apnea should not use anabolic/androgenic steroids.
Physicians are advised to monitor their patients closely for signs of OSA during
AAS therapy.
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Acute Steroid Safety: Studies with Real-World Dosages
Few medicines have the type of stigma about them that anabolic/androgenic
steroids do. If you mention the decision to use these drugs to the average person,
you are likely to be lectured about the tremendous physical and psychological
risks you are about to undertake; how your hair might fall out, your testicles will
disappear, or the steroids will give you cancer. Or maybe you will just lose you
mind to uncontrolled fits of psychotic rage, or suffer a life-threatening heart
attack. Clearly, the public has been given a very strong message about steroids:
stay far away from them, they are deadly drugs. However, those actually taking
anabolic steroids usually see things very differently. They believe the dangers
are terribly exaggerated in the media, and the risks of serious injury or death
from an isolated steroid cycle are exceedingly low. Which position is correct?
The committed steroid user will usually point out the fact that a review of the
medical literature over the past 50 years will show that the overall safety profile
of these drugs has been quite favorable. Steroid opponents, on the other hand,
point out that an illicit user takes a much larger dose of steroids than those used
in medical situations, and are in much greater danger than the patients using
them. Who is right? Is the isolated steroid cycle really a serious health risk? One
thing that has always confounded this debate is the lack of pertinent medical
studies. Medical ethics make high-dosed studies with anabolic/androgenic
steroids (which may constitute abuse of the medication) very difficult to design
and gain approval for. Only a very small number of clinical studies actually
provide environments that could be viewed as relevant to those on both sides of
the argument.
In this section, we examine three medical studies that appear highly relevant for
examining real-word acute anabolic/androgenic steroid safety. They concern not
therapeutic doses, but a supratherapeutic level and duration of intake that any
illicit steroid user would recognize as sufficient for improving muscle mass,
strength, and performance. In fact, the dosages and administration periods used
in these studies reflect those taken by some of the more aggressive steroid-using
bodybuilders and strength athletes. A fairly comprehensive set of health markers
were assessed during these three investigations, including insulin sensitivity,
serum cholesterol and triglyceride, prostate specific antigen (PSA) levels, and
liver enzymes. Because of the protocols that were used, these studies give us a
fairly good basis to evaluate the negative health impact of anabolic/androgenic
steroids, at least as it relates to an isolated cycle.
600 mg/wk of Testosterone
The first is a testosterone dose-response study published in the American Journal
of Physiology Endocrinology and Metabolism in July of 2001, which looked at
the effects of various doses of testosterone enanthate on body composition,
muscle size, strength, power, sexual and cognitive functions, and various
markers of health.
329 61 normal men, ages 18-35, participated in this
investigation. They were divided into five groups, with each receiving weekly
injections of 25, 50, 125, 300, or 600 milligrams for a period of 20 weeks. This
treatment period was preceded by a control (no drug) period of 4 weeks, and
followed by a recovery period of 16 weeks. Markers of strength and lean body
mass gains were the greatest with larger doses of testosterone, with the 600 mg
group gaining slightly over 17 pounds of fat-free mass on average over the 20
weeks of steroid therapy. There were no significant changes in prostate-specific
antigen (PSA), liver enzymes (liver stress), sexual activity, or cognitive
functioning at any dose. The only negative trait noted was a slight HDL (good)
cholesterol reduction in all groups except those taking 25 mg. The worst
reduction of 9 points was noted in the 600 mg group, which still averaged 34
points after 20 weeks of treatment. All groups, except this one, remained in the
normal reference range for males (40-59 points).
600 mg/wk of Nandrolone
Next we look at a study conducted with HIV+ men, which charted the leanmass-building effects of nandrolone decanoate
330
. 30 people participated in this
investigation, with each given the same (high) weekly dose of this drug. Half
underwent resistance training so that two groups (trained and untrained) were
formed. The dosing schedule was quite formidable, beginning with 200 mg on
the first week, 400 mg on the second, and 600 mg for the remaining 10 weeks of
peak therapy. Doses were slowly reduced from weeks 13 to 16 to withdraw
patients slowly from the drug. Potential negative metabolic changes were looked
at closely, including cholesterol and lipid levels (including subfractions of HDL
and LDL), triglycerides, insulin sensitivity, and fasting glucose levels. Even with
the high dosages used here, no negative changes were noted in total or LDL
cholesterol, triglycerides, or insulin sensitivity. In fact, the group also
undergoing resistance exercise noticed significant improvements in LDL particle
size distribution, lipoprotein(a) levels, and triglyceride values, which all indicate
improved cardiovascular disease risk. Carbohydrate metabolism was also
significantly improved in this group. The only negative impact noted during this
study was a reduction in HDL (good) cholesterol values similar to that noted
with the testosterone study, with an 8-10 point reduction noted between both
groups.
100 mg/day of Anadrol
Lastly, we find a study looking at the potent oral steroid oxymetholone
(Anadrol).
331 This steroid is thought to be one of the most dangerous ones
around by bodybuilders, who as a group seem to treat it with both a lot of respect
and caution. It is not common to find them exceeding the doses and intake
durations of this investigation, making it a very good representation of realworld Anadrol usage. This study involves 31 elderly men, between the ages of
65 and 80. The men were divided into three groups, with each taking 50 mg, 100
mg, or placebo daily for a 12-week period. Changes in lean body mass and
strength were measured, as well as common markers of safety including total,
LDL and HDL cholesterol levels, serum triglycerides, PSA (prostate-specific
antigen), and liver enzymes. Muscle mass and strength gains were again relative
to the dosage taken, with the end results being similar to those noted with 20
weeks of testosterone enanthate therapy at 125 mg or 300 mg per week (about
6.4 and 12 lb of lean body mass gained for the 50 mg and 100 mg doses
respectively). There were no significant changes in PSA, total or LDL
cholesterol values, or fasting triglycerides; however, there was a significant
reduction in HDL cholesterol values (reduced 19 and 23 points for the 50 mg
and 100 mg groups respectively). Liver enzymes (transaminases AST and ALT)
increased only in the 100 mg group, but the changes were not dramatic, and were
not accompanied by hepatic enlargement or the development of any serious liver
condition.
Adding It All Up
One hundred and twenty-one men participated in these three studies, which
involved the use of moderate to high doses of steroids for periods of three to five
months. Although it may be shocking to most opponents of anabolic/androgenic
steroid use, an unbiased assessment of the metabolic changes and health risks
did not reveal any significant short-term dangers. The main negative impact of
steroid use in all three cases was a reduction in good (HDL) cholesterol values,
which is a legitimate concern when it comes to assessing one’s risk for
developing cardiovascular disease. It is uncertain, however, if a short-lived
increase in this particular risk factor relates to any tangible damage to one’s
health over the long-term. It is also unknown how much (if any) this may be
offset by the other positive metabolic changes that were seen to accompany
combined AAS use and exercise.
Logic would seem to suggest that the isolated use of steroids, under parameters
similar to those used in these three studies, should entail relatively minimal risks
to health. At the very least, it is extremely difficult to argue that an isolated cycle
with a moderate drug dose is tantamount to playing Russian roulette with your
body, as most media campaigns against the use of these drugs would seem to
suggest. But make no mistake. These same study results consistently
demonstrated pro-atherogenic changes in blood lipids with the doses necessary
for physique or performance enhancement, and underline how it is that longterm anabolic/androgenic steroid abuse can impair cardiovascular health.
329. Testosterone dose-response relationships in healthy young men. Shalender A, Woodhouse L et al. Am J
Physiol Endocrinol Metab 281: e1172-81 2001
330. Metabolic effects of nandrolone decanoate and resistance training in men with HIV. Sattler FR,
Schroeder ET, Dube MP, Jaque SV, Martinez C, Blanche PJ, Azen S, Krauss RM. Am J Physiol Endocrinol
Metab. 283(6) Dec (2002):E1214-22. Epub 2002 Aug 27.
331. Effects of an oral androgen on muscle and metabolism in older, community-dwelling men. Schroeder et
al. Am J Physiol Endocrinol Metab 284: E120-28
The Endocrinology of Muscle Growth
The road to anabolic insight must include a biological understanding of what
muscle growth actually entails. Often simplified by the term “protein synthesis”,
muscle growth is actually a highly complex process involving much more than
just building proteins from amino acids. Muscle hypertrophy, the correct
scientific term for the way we adult humans build skeletal muscle, actually
requires the fusion of new cells (called satellite cells) with existing muscle
fibers. Since this discovery of satellite cells in 1961, a great deal of research into
the mechanisms of muscle hypertrophy has been undertaken. Scientists have
come to understand that unlike normal muscle cells, these satellite cells can be
regenerated throughout adult life. Furthermore, they serve not as functional units
of their own, but provide some of the necessary components to repair and rebuild
damaged muscle cells. These satellite cells are normally dormant, and sit resting
in small indentations on the outer surface of the muscle fibers, waiting for
something to trigger them into activation.
Injury or trauma will provide the stimulus necessary to activate satellite cells.
Once activated, they will begin to divide, multiply, and form into myoblasts
(myoblasts are essentially donor cells that express myogenic genes). This stage
of hypertrophy is often referred to as satellite cell proliferation. The myoblasts
will then fuse with existing muscle fibers, donating their nuclei. This stage of the
process is usually called differentiation. Skeletal muscle cells are multinucleated,
which means they possess many nuclei. Increasing the number of nuclei allows
the cell to regulate more cytoplasm, which allows more actin and myosin, the
two dominant contractile proteins in skeletal muscle, to be produced. This
increases the overall cell size and protein content of the muscle cell. Incidentally,
the number of nuclei in relation to cross-sectional area also helps to determine
the fiber type of the cell,namely slow twitch (aerobic) or fast twitch
(anaerobic)
332 333
. It is important to note that we are not increasing muscle cell
number with muscle hypertrophy. We are only increasing cell size and protein
content, even though we are using satellite cells to help accomplish this. It is
possible for myoblasts to fuse together and actually form new muscle fibers.
This is called muscle hyperplasia, and equates to the legitimate growth of new
muscle tissue. This is, however, not the primary mechanism of muscle growth in
adult life.
The Anabolic Chain
Now that we know what muscle hypertrophy is really about, let's look at
anabolic stimulus and ongoing regulation. The following is a rundown of the
chain of hormones and growth factors that mediate muscle growth, from the
initiation of damage, to final recovery, repair, and growth. For the sake of
organization, I have presented them in what I consider to be three logical phases
of action. These are not scientifically accepted definitions. Additionally, we
could continue to go deeper and deeper into each of the various compounds,
messengers, binding proteins, and receptors involved in this intricate and
amazing biological activity. I believe the included text will demonstrate the
process of muscle anabolism in a very tangible way, however, without too much
unnecessary information. Each of the key areas of this section can be further
researched for more detail if you are interested. For one so inclined, the medical
references in the endnotes would be an excellent place to start.
Trigger
We all understand that weight training is fundamental to growing muscle tissue.
To date, no “sit on your ass and get huge and ripped”pill has been invented. The
reason is that a number of changes take place in your local muscle tissues during
intense training that are vital to the growth process. Without these early changes,
growth is difficult if not impossible to stimulate. So for our purposes, we will
start here. Training is the “trigger” in the anabolic process. More specifically, it
is the localized cellular damage that weight training produces that will first set us
down the road of anabolism. The body will respond by repairing this damage,
and in the process will try to adapt by making itself stronger. Muscle growth is
always a circular process, with a step back (damage) being necessary to take any
steps forward.
Phase I: Initial Response
The Initial Response phase covers those changes in muscle chemistry that begin
immediately, during training, which will lay the groundwork for later repair and
growth. In many regards, the Initial Response Phase will control the potential
magnitude of other signals to follow. In the anabolic process, this phase is
categorized by the release of arachidonic acid from muscle cells, and the
formation of active messengers including prostaglandins, cytokines,
leukotrienes, and prostacyclins. This begins with the breakdown of the outer
phospholipid layer of muscle cells, which is initiated by the cellular disruption of
damaging exercise.
334 Phospholipases are released inresponse to this trauma,
which causes some of the phospholipids stored in the outer layer of the muscle
cells to be released. The eccentric part of the exercise movement is of particular
importance here, which is the “negative” part of the lift, where the muscle is
stretched under resistance.
MUSCLE HYPERTROPHY AND THE 4 STAGES OF THE SATELLITE
CELL CYCLE
During the Activation stage, dormant satellite cells are stimulated to enter
the cell cycle. Proliferation marks the formation of new myoblasts (active
donor cells). These myoblasts will fuse with existing damaged muscle fibers
during the Differentiation phase. This allows for greater protein synthesis
and the expansion of cell size. Quiescence marks the return to a dormant
state, where the inactive satellite cells will again rest on the outer layer of
the fibers. Myostatin, a known inhibitor of muscle growth, is believed to be
a key regulator in this stage.
335 336
The amount of arachidonic acid, which is the central bioactive lipid in the
anabolic process, liberated will largely control what occurs during this phase.
Arachidonic acid is converted locally and immediately via enzymes to a number
of active anabolic end products, the most notable of which (in terms of muscle
growth) are prostaglandins, which are produced via interaction with
cyclooxygenase enzymes. These prostaglandins (PGE2 and PGF2alpha mainly)
will control much of the next phase, identified here as the Localized Tissue
Priming phase. Additionally, the prostaglandin PGE2 will work to increase local
nitric oxide levels, which is also an active molecule in the anabolic process. It
has such actions as dilating blood vessels (to increase the flow of nutrients and
hormones to the muscles) and increasing the production of HGF (hepatocyte
growth factor) for satellite cell activation. Arachidonic acid contributes to
inflammation and pain signaling as well, and its release plays an integral role in
the soreness that follows a productive bout of training.
Training intensity and the relative density of arachidonic acid in the
phospholipid layer (arachidonic acid availability is ultimately the rate-limiting
step in the formation of anabolic prostaglandins) will dictate how much of this
potent lipid can be liberated during exercise. The amount of arachidonic acid
stored in skeletal muscle tissue is also in a state of constant flux. A number of
factors are involved with its regulation, the most notable of which are dietary
intake and daily utilization. Regular resistance training depletes arachidonic acid
stores, replacing it with other, more abundant, fatty acids.
337 With less
arachidonic acid available, the responsiveness of the prostaglandin system to
regular exercise starts to diminish.
338 Have you ever wondered why you were so
sore when you first start training, or after you took a long break? Or why those
early workouts tended to be so much more productive than later ones, where you
struggle to notice even moderate soreness? Much of this is directly tied to your
arachidonic acid stores. The more arachidonic acid you have, the easier it is to
liberate during training, and vice versa. Thankfully, levels can be augmented
with dietary intervention (for more information, see the arachidonic acid profile).
Phase II: Localized Tissue Priming
Phase II is characterized by a localized increase in growth factor expression and
tissue sensitivity to anabolic hormones. Those who have always wondered why
anabolic drugs do not work without training will find a good explanation right
here. Simply put, your muscles need to be primed for the actions of these drugs
first. One way the body accomplishes this is to increase the density of certain
receptors in those specific muscles (fibers really) where it needs to initiate
repair. This includes, among others, androgen, IGF-1, MGF, and insulin
receptors. Stretch-induced muscle damage and the Phase I response are both
principle triggers here. Receptor density regulation is important because it
prevents anabolic hormones from stimulating tissue growth in areas of the body
that do not require it. Receptor density can, therefore, be as strong a regulating
force on the pharmacological activity of anabolic drugs as the serum levels of
the drugs themselves.
Note: Inhibition of the cyclooxygenase-2 enzyme with anti-inflammatory
drugs like ibuprofen, acetaminophen, or aspirin, prevents the formation of
active prostaglandins. The anabolic cascade is stalled without sufficient
prostaglandin formation (Am J Physiol Endocrinol Metab 282:E551-6),
interfering with the normal increase in protein synthesis rates after
exercise.It is often advised to use such drugs only when necessary if muscle
growth is a key focus.
To put it in perspective, we need to remember that there are two separate
components that interact before any message is sent to a muscle cell telling it to
increase growth. We have a hormone or growth factor on one hand, such as
testosterone, IGF-1, MGF, or insulin, and its corresponding receptor on the
other. Injecting exogenous anabolic drugs facilitates greater receptor binding and
anabolic signaling by providing more messenger hormones/growth factors
(obviously). The more hormones or growth factors you have around the cell, the
more binding and activation of receptor sites will take place. We cannot forget,
however, that having more receptor sites (instead of more hormones) can also
facilitate the process too. More receptors mean the existing hormones or growth
factors will find them faster. Faster binding means the anabolic message is sent
more quickly, and once completed that the anabolic messenger will be more
likely to find another receptor site (to send another message) before it is broken
down by enzymes. It is all about how much signal can be sent in a given time
period, and both sides of the equation are equally important in determining this.
While on one hand we have an increase in tissue sensitivity to anabolic
hormones and growth factors, also vital during the Localized Tissue Priming
phase is an increase in the localized expression of certain vital growth factors
themselves. This includes IGF-1, MGF, FGF, HGF, TNF, IL-1, and IL-6. These
compounds will be released, and will work together on the existing damaged
muscle fibers and satellite cells, in a sort of grand symphony of muscle
anabolism, with each playing its own vital role in the process. In many cases, the
actions of one compound will support the other, either by enhancing its levels,
suppressing restricting binding proteins, or supporting its signaling via
intertwined mechanisms. A detailed roadmap to all such interactions would go
well beyond the scope of this book, and in fact are as of yet not even fully
understood to science. A general overview of what is going on with each
compound itself, however, is provided in our review of Phase III.
Phase III: Repair
Your local muscle tissues are primed during Phases I and II. During Phase III,
the hormones and growth factors go to work to finish the job. We categorize this
phase as one of ongoing anabolic action, action mediated by the combined
effects of many anabolic hormones and growth factors including androgens,
insulin, IGF-1, IGF-2, MGF, FGF, HGF, TNF, IL-1, and IL-6. This is the time
when repair and hypertrophy are physically taking place in your muscles, and
each compound will play an intricate role in the process. We must not forget,
however, that everything leading up to this point (the actions in Phase I & II) has
still been determining how strong the growth response will be, via modifying
receptor densities and hormone/growth factor expression. We will follow the
individual actions of the anabolic components very closely here. During the third
phase, tissue repair and growth will be finalized with the help of the following
hormones and growth factors.
Hepatocyte Growth Factor (HGF):
HGF is a heparinbinding growth factor that resides on the outer surface of
uninjured cells. Upon injury, it migrates to satellite cells where it triggers their
activation and entry into the cell cycle.
339 HGF expression is regulated via nitric
oxide release,
340 which is stimulated upon injury to also aid in the flow of
nutrients and hormones to the area. PGE2 plays a pivotal role in nitric oxide
synthesis and HGF release.
341
Androgens:
Androgens (the hormones that anabolic/androgenic steroids mimic) are strong
supporters of protein synthesis rates in skeletal muscle tissue. They are also
known to stimulate local IGF-1 expression, so the effects of these hormones
extend to the satellite cell cycle (perhaps explaining why they are such strong
stimulators of muscle growth). It is also of note that arachidonic acid increases
androgen receptor density in skeletal muscle tissue. This helps to further piece
together the biochemical links between the Phase I and Phase II response.
Insulin-Like Growth Factor I (IGF-I):
IGF-I is an insulin-like hormone with marked anabolic effects. Owing to its
name, it also has some insulin-like effects as well. IGF-I increases protein
synthesis, and supports the proliferation and differentiation of satellite cells. The
prostaglandin PGF2alpha is known to strongly up-regulate local IGF-I receptor
expression.
342 343 PGE2 is also believed to play a role in increasing local IGF-1
synthesis.
344
Insulin-Like Growth Factor II (IGF-II):
IGF-II is a second insulin-like growth factor that plays a role in the proliferation
of satellite cells. Unlike IGF-I, IGF-II expression does not appear to drastically
increase in response to training.
345
Mechano-Growth Factor (MGF):
Mechano-Growth Factor is a recently discovered variant of Insulin-Like Growth
Factor I. This growth factor is produced during an alternate splicing sequence of
the IGF protein, and plays a strong role in the support of myoblast proliferation.
MGF expression, like many of the growth factors discussed here, is strongly upregulated in muscle tissue in response to stretch stimulus.
346
Fibroblast Growth Factor (FGF):
FGF is actually a family of growth factors, with nine different isoforms (FGF-1
through FGF-9). The full role that FGF plays in muscle hypertrophy in
adulthood is not fully understood, however, it is believed to be a strong
proliferator of satellite cells, serving to expand their population.
347 FGF's may
also play a role in cell differentiation. As with many growth factors, FGF
expression up-regulation is proportional to the degree of tissue damage.
348 FGF2 and FGF-4 seem to be the most prolific representatives of this family in mature
muscle tissue.
Insulin:
In addition to having some ability to increase protein synthesis and inhibit
protein breakdown, insulin is the body's chief nutrient transport hormone. The
actions of insulin allow cells to transport glucose and amino acids through the
plasma membrane. Insulin receptor expression is strongly up-regulated after
traumatic exercise, so as to provide more immediate nutrition to the affected
area. This up-regulation has been closely linked to the prostaglandin PGE2.
349
350
Cytokines (IL-1, IL-6, TNF):
Cytokines are a group of immunomodulatory compounds, though in the context
of this section we are loosely referring to them as growth factors. The IL
cytokines are called interleukins, and TNF is short for Tumor Necrosis Factor.
Among other things, cytokines are known to stimulate the migration of
lymphocytes, neutrophils, monocytes, and other healing cells to a site of tissue
damage, to aid in cell repair. They help in a number of other ways too, such as
aiding in the removal of damaged cells and regulating certain inflammatory
responses, including the production of some prostaglandins. Prostaglandins are
known to play important roles in the expression of all three of the cytokines
mentioned here,
351 352 however, they may not be the sole stimulus. Other
pathways of arachidonic acid metabolism may also be involved.
Prostaglandins:
Although these are the key initial reactionary chemicals, prostaglandins continue
to play a role throughout the muscle building process (including Phase III). This
includes their support of hormone receptor proliferation, the enhancement of
protein synthesis rates, and an intensification of the anabolic signaling of IGF-1
via a shared pathway (PI3K).
353
Estrogens:
Although not specifically highlighted in this outline, estrogens also play a minor
role in the anabolic process. This includes helping to increase androgen receptor
density in certain tissues (though perhaps not skeletal muscle), stimulating the
GH/IGF-1 axis, and enhancing glucose utilization for tissue growth and repair.
Bringing it All Together
So that, in a very loose nutshell, is what is going on inside your body from the
time you pick up a weight to the time your muscles are repaired, stronger, and
ready for more. If the above seems confusing to you, it should. The fact is, the
whole process of muscle growth has been confounding scientists for decades,
and undoubtedly will for decades more. We still have a great way to go before
being able to explain fully how it is that muscle hypertrophy occurs in humans.
But as you can see, we have traveled a great distance as well. During the mid1960s, scientists were only first learning that we grow muscle with the help of
satellite cells. More than forty years later we have identified, and are
experimenting with, dozens of growth factors that were unheard of back then. It
is a new world today, and despite not having all the answers, we know enough to
enhance human performance in many exciting new ways. But please don't
mistake the intention of this section. It is not here to give you a functional
roadmap of the entire anabolic process, or to guide you in the ultimate polydrug
program. It is here simply to open your mind to the true complexity of
anabolism. When we start to see muscle growth from its various angles and
intricacies, we begin to see our own potential opportunities for successful
exploitation. How many of these opportunities you act upon will depend on your
own goals and interests. But no matter how much or how little you actually
apply this information, I hope you feel better equipped by having it.
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332. Behind the Scenes: Hypertrophy. Gene. Mind and Muscle Magazine 5/2005
333. Regulation of skeletal muscle fiber size, shape and function. J Biomech. 24(suppl1):123-33 (1991)
334.
Initial events in exercise-induced muscular injury. Med Sci Sports Exerc 22(4):429-35 (1990)
335. Myostatin negatively regulates satellite cell activation and self-renewal. J Cell Biol. 162:1135-47
(2003)
336. Signaling satellite-cell activation in skeletal muscle: markers, models, stretch, and potential alternative
pathways. A Wozniak, J Kong et al. Muscle Nerve 31: 283-300 (2005)
337. Effects of physical exercise on phospholipid fatty acid composition in skeletal muscle. Agneta
Andersson et al. Am J Physiol. 274 (Endocrinol. Metab. 37): E432-8 (1998)
338. Effects of Exercise on parameters of blood coagulation, platelet function and the prostaglandin system.
H Sinzinger, I Virgolini. Sports Medicine 6:
238-45 (1988)
339. Mechanical stretch induces activation of skeletal muscle satellite cells in vitro. Tatsumi R, Sheehan SM
et al. Exp Cell Res 267(1) 107-14 (2001)
340. Release of hepatocyte growth factor from mechanically stretched skeletal muscle satellite cells and role
of pH and Nitric Oxide. Ryuichi Tatsumi et al. Mol Biol of the Cell 13 p 2909-18 (2002)
341. Hepatocyte growth factor as a key to modulate anti-ulcer action of prostaglandins in stomach. J Clin Inv
98:2604-11
342. The role of prostaglandins in bone formation. Harada SI, Balena R et al. Connect Tissue Res.
1995;31(4)279-82
343. Prostaglandin F2a stimulates proliferation of clonal osteoblastic MC3T3-E1 cells by up-regulation of
Insulin-like Growth Factor 1 receptors. Yoshiyuky Hakeda et al.J Biol Chem 266(31): 21044-50 (1991)
344. Prostaglandin E2 stimulates insulin-like growth factor I synthesis in osteoblast-enriched cultures from
fetal bone. McCarthy TL, Centrella M et al. Endocrinology 128(6):2895-900 (1991)
345. Sequence of IGF-I, IGF-II, and HGF expression in regenerating skeletal muscle. Hayashi S et al.
Histochem Cell Biol. 122(5):427-34 (2004)
346. Expression of insulin like growth factor-1 splice variants and structural genes in rabbit skeletal muscle
induced by stretch and stimulation. G McKoy, W Ashley et al. J Physiol 516(2) 583-92 (1999)
347. Expression of fibrolast growth factor family during postnatal skeletal muscle hypertrophy. P Mitchell, T
Steenstrup, K Hannon. J Applied Physiol
86:313-19 (1999)
348. Fibroblast growth factor is stored in fiber extracellular matrix and plays a role in regulating muscle
hypertrophy. Medicine and Science in Sports and Exercise 21(5) S173-80 (1989)
349. The insulin-like effect of muscle contraction. Ivy JL. Exerc Sport Sci Rev. 1987;15:29-51.
350. The role of prostaglandins as modulators of insulin-stimulated glucose metabolism in skeletal muscle.
Leighton B et al. Horm Metab Res Suppl.
22:89-95 (1990)
351. Differential effects of prostaglandins derived from n-6 and n-3 polyunsaturated fatty acids on COX-2
expression and IL-6 secretion. Dilprit Bagga et al. PNAS 100(4) 1751-56 (2003)
352. The role of arachidonic acid metabolism in the activities of Interleukin 1 and 2. W Farrar, J Humes. J of
Immunol 135(2) 1153-9 (1985)
353. Regulation of protein synthesis associated with skeletal muscle hypertrophy by insulin-, amino acid and
exercise-induced signaling. D Bolster, L Jefferson, S Kimball. Proc of the Nutrition Society 63: 351-56
(2004).
Part II
Practical Application
Steroid Cycles
Anabolic/androgenic steroids are not medically approved to promote excessive
muscle mass gains (bodybuilding) or improve athletic performance. Aside from
early experimentation on athletes by a handful of sports physicians, an extensive
effort to study the physique-and performance-enhancing properties of these
drugs, specifically with an eye on developing strategies for using them to
maximize benefits and minimize adverse effects, has not been undertaken by the
medical community. Because of this, illicit users have been left to develop their
own protocols for administering these drugs. The result has been a large variety
of different approaches to using these agents, some safer or more effective than
others. While it would not be possible to comprehensively evaluate all known
approaches, this section will discuss some of the most fundamental and timeproven methods for using AAS.
Steroid Selection
When first considering what steroid(s) to use, one will notice there are many
different medications that fall under the category of anabolic/androgenic
steroids. This has been the result of many years of development, where specific
patients and needs are addressed with drugs that have specific characteristics.
For example, some drugs are considered milder (less androgenic), and produce
fewer side effects in women and children. Others are more androgenic, which
makes them better at supporting sexual functioning in men. Some are injectable
medications, and others made for oral administration. There are limits to this
diversity, however. All AAS drugs activate the same cellular receptor, and as
such share similar protein anabolizing properties. In other words, while different
AAS drugs may have some differing properties, if your objective is to gain
muscle mass and strength, this could be accomplished with virtually any one of
the commercially available agents.
While all AAS drugs may be capable of improving muscle mass, strength, and
performance, it would not be correct to say there are no advantages to choosing
one agent over another for a particular purpose. Most fundamentally, the
quantity and quality of muscle gained may be different from one agent to
another. In a general sense, AAS that are also estrogenic tend to be more
effective at promoting increases in total muscle size. These steroids also tend to
produce visible water (and sometimes fat) retention, however, and are generally
favored when raw size is more important than muscle definition. Drugs with low
or no significant estrogenicity tend to produce less dramatic size gains in
comparison, but the quality is higher, with greater visible muscularity and
definition. In reviewing the most popular AAS drugs, we can separate them into
these two main categories as follows.
Mass (Bulking):
Methandrostenolone – Oral
Oxymetholone – Oral
Testosterone (cypionate, enanthate) – Injectable
Lean Mass:
Boldenone undecylenate – Injectable
Methenolone enanthate – Injectable
Nandrolone decanoate – Injectable
Oxandrolone – Oral
Stanozolol – Oral
The early stages of AAS use usually involve cycles with a single
anabolic/androgenic steroid. Building muscle mass is the most common goal,
and usually entails the use of one of the more androgenic substances such as
testosterone, methandrostenolone, or oxymetholone. Those looking for lean
mass often find favor in such anabolic staples as nandrolone decanoate,
oxandrolone, or stanozolol. First time users rarely welcome injecting
anabolic/androgenic steroids, and will usually choose an oral compound for the
sake of convenience. Methandrostenolone is the most common choice for mass
building, and is almost universally regarded as highly effective and only
moderately problematic (in terms of estrogenic or androgenic side effects).
Stanozolol is the oral anabolic steroid most often preferred for improving lean
mass or athletic performance.
The potential for adverse reactions should also be considered when choosing a
steroid to use, especially if AAS use is to be regularly repeated. For example, the
listed oral medications present greater strain on the cardiovascular system, and
are also liver toxic. For these reasons, the injectable medications listed are
actually preferred for safety (testosterone most of all). Potential cosmetic side
effects may also be taken into account. For example, men with a strong
sensitivity to gynecomastia sometimes prefer non-estrogenic drugs such as
methenolone, stanozolol, or oxandrolone. Individuals worried about hair loss, on
the other hand, may isolate their use to predominantly anabolic drugs, such as
nandrolone, methenolone, and oxandrolone. A detailed review of personal goals,
health status, and potential side effects of each drug is advised before
committing to any AAS regimen.
Dosage
The dosage used is important in determining the level of benefit received.
Anabolic/androgenic steroids tend to be most efficient at promoting muscle
gains when taken at a moderately supratherapeutic dosage level. Below this
(therapeutic), potential anabolic benefits are often counterbalanced, at least to
some extent, by the suppression of endogenous testosterone. At very high doses
(excessive supratherapeutic), smaller incremental gains are noticed (diminishing
returns). In the case of testosterone enanthate or cypionate, for example, a
dosage of 100 mg per week is considered therapeutic, and is generally
insufficient for noticing strong anabolic benefits. When the dosage is in the 200-
600 mg per week range, however, the drug is highly efficient at supporting
muscle growth (moderate supratherapeutic). Above this range, a greater level of
muscle gain may be noticed, but the amount will be small in comparison to the
dosage increase. Below are some commonly recommended dosages for the
steroids listed earlier.
- Boldenone undecylenate: 200-400 mg/wk
- Methandrostenolone: 10-30 mg/day
- Methenolone enanthate: 200-400 mg/wk
- Nandrolone decanoate: 200-400 mg/wk
- Oxandrolone: 10-30 mg/day
- Oxymetholone: 50-100 mg/day
- Stanozolol: 10-30 mg/day
- Stanozolol: 10-30 mg/day
- Testosterone (cypionate, enanthate): 200-600 mg/wk
There are additional considerations other than the cost effectiveness of a
particular dosage. To begin with, high doses of anabolic/androgenic steroids tend
to produce stronger negative cosmetic, psychological, and physical side effects.
In light of diminishing returns, the tradeoff between results and adverse reactions
becomes less and less favorable. Gains made on lower doses also tend to be
better retained after steroid discontinuance than those resulting from excessive
intake. It is generally not realistic to expect that rapid double-digit weight gains
induced by massive dosing will remain long after a cycle is over. Slower steadier
gains are advised. It is also very important to remember that higher doses aren’t
always what are needed to achieve greater gains. An individual more focused on
his or her training and diet will often make better gains on lower dosages of
AAS than a less dedicated individual taking higher doses. With this
understanding, AAS should only be considered when all other variables of
training and diet have been addressed, and always limited to the minimum
dosage necessary to achieve the next realistic training/performance goal.
Figure 1.Anabolic/androgenic steroids tend to be most effective in
moderately supratherapeutic doses.The anabolic benefits diminish in
relation to the amount of drug given at both the high and low ends of the
dosage range.
Duration (Cycling)
The administration of anabolic/androgenic steroids at a given dosage will
typically produce noticeable increases in muscle size and strength for
approximately 6-8 weeks. After this point, the rate of new muscle gain typically
slows significantly. A plateau may be reached soon after, where all forward
momentum has ceased. To continue making significant progress beyond this
point can entail escalating dosages, which is likely to coincide with a greater
incidence of adverse reactions and diminishing anabolic returns. Even without
dosage escalation, negative health changes are already likely to be apparent, and
should be corrected fairly quickly. The practice of extended or continuous
steroid administration is discouraged for these reasons. It is generally
recommended to use AAS drugs for no longer than 8 weeks at a time (10-12
weeks at the maximum), followed by an equal or longer period of abstinence
before another steroid regimen is initiated. This pattern of rotating between “on”
and “off” periods is referred to as cycling.
Off-Cycle (Recovery, Bridging, and Tapering)
The period immediately following steroid cession can involve a state of
hypogonadism (low androgen levels), and as a result protein catabolism. In an
effort to minimize muscle loss, the objective here is usually on restoring natural
testosterone production, maintaining an optimal level of muscle stimulation, and
remaining dedicated to proper nutrition. A hormonal recovery program is usually
initiated, which may involve the use of HCG, tamoxifen, and clomiphene (see
PCT: Post Cycle Therapy). A substantial off-cycle period is also advised,
involving abstinence from anabolic/androgenic steroids for at least 8-12 weeks.
Some AAS abusers have difficulties with complete drug abstinence, and will
initiate “bridging” routines between full-dose cycles. This may involve the
periodic low-dose administration of an injectable steroid, such as 200 mg of
testosterone enanthate or methenolone enanthate every 2-3 weeks. Such practice
is discouraged, however, as it can interfere with hormonal recovery, and prevent
a return to metabolic homeostasis.
When concluding a cycle, some steroid users also follow a practice of first
slowly reducing their dosages (tapering). This tapering may proceed for a 3-4
week period, and will involve an even stepping down of the dose each week
until the point of drug discontinuance. It is unknown, however, if such tapering
offers any tangible value. This practice has never been evaluated in a clinical
setting, and is not widely recommended with steroid medications as it is with
some other drugs such as thyroid hormones or antidepressants. Virtually every
high-dose AAS administration study can also be found to end at the maximum
dosage, with no time allotted to tapering. One flaw in the logic of using a
tapering program is that they are ostensibly designed to aid hormone recovery.
Recovery is not possible, however, while supraphysiological levels of androgens
are present, and such levels are usually found during all weeks of a normal
(nonmedical) steroid taper. Individuals remain cautioned that dosage tapering is
not a proven way to reduce post-cycle muscle catabolism.
Figure 2.Anabolic/androgenic steroids tend to be most effective at a given
dosage for approximately 6-8 weeks.After this point, the rate of new muscle
gain will slow, and soon after will usually hit a full plateau.
Stacking
As individuals become more experienced with anabolic/androgenic steroid use
they may begin experimenting with the use of more than one steroid at a time.
This practice is referred to as stacking. Stacking is most common with advanced
bodybuilders who find that at a certain level of physical development they begin
hitting plateaus that are difficult to break with a previous single-agent approach.
In many cases, however, it may simply be the greater cumulative steroid dosage
that is necessary for the resumed progress. Stacking usually involves the
combination of a more androgenic steroid with one or more primarily anabolic
agents. On the anabolic side, common steroids of choice include boldenone,
methenolone, nandrolone, oxandrolone, and stanozolol. Testosterone,
oxymetholone, or methandrostenolone will serves as the androgenic base of
most stacks.
The reasons for stacking androgenic and anabolic steroids together in this
manner are two fold. On the one hand, high doses of testosterone, oxymetholone,
or methandrostenolone are prone to producing strong androgenic and estrogenic
side effects. Stacking first became very popular during the 1960s, a time when
effective estrogen maintenance drugs were not widely available. An anabolicandrogen stack allowed the use of a higher total steroid dosage than would be
tolerable with a single androgen. Anabolic-androgen pairing also appears to
offer efficacy advantages over the use of primarily anabolic agents alone, even
when they are taken in higher doses. This conflicts with the original expectations
for “anabolic” steroids, which were specifically designed to emphasize musclebuilding properties, but is repeatedly noticed by users. The reason the basic
androgenic steroids are more anabolically productive is not fully understood, but
is believed to involve the interplay of estrogenic hormones, androgenic
stimulation in the central nervous system, and potentially other unidentified
synergisms necessary for optimal muscle growth.
Today, the availability of drugs that can reduce estrogenic activity makes the
continued use of single agent cycles based on a strong androgen like testosterone
enanthate or cypionate much more viable than it was decades ago. Side effects
like gynecomastia and water retention can now be effectively minimized with
anti-estrogens or aromatase inhibitors, even when taking higher doses.
Individuals should be aware that stacking is, likewise, not a necessary practice. It
is likely to remain commonly applicable in competitive bodybuilding circles,
however, or when an individual is sure they have progressed as far as they
possibly can with a single-agent approach. Otherwise, for many athletes and
recreational bodybuilders, the periodic use of a single steroid will be more than
sufficient to maintain optimal levels of muscle mass and performance, and it
may never be necessary to deviate from this approach.
Sample Steroid Cycles
The following cycles are presented as examples of common steroid
administration protocols. These programs have not been evaluated in a clinical
setting for safety and efficacy, and are provided for informational purposes only.
These are not recommendations for anabolic/androgenic steroid use. As with any
supplemental drug program, it is important to examine your own individual
health status, health risks, and performance goals before deciding to engage in
any anabolic/androgenic steroid use. For those who have made the decision, it is
important to emphasize again that the recommended approach to AAS use is to
limit drug intake to the lowest levels necessary to achieve the next rational goal.
More aggressive cycles should not be attempted unless one is sure they cannot
achieve the results needed on a more moderate program. Note that given the
difficulty in predicting androgenic threshold and dosages for female users, the
below cycles are examples of programs for men only.
Single Agent Cycles
Dianabol Cycle #1 (Mass)
Products: 100 tablets 5 mg Methandrostenolone
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4 g/day).
Estrogen Support: tamoxifen (10-20 mg/day).
Comments: This is a very common first cycle for building muscle mass, and
utilizes a single standard bottle of methandrostenolone. This cycle is likely to
produce very noticeable muscle growth in a first-time steroid user, often in
excess of 8-10lbs of weight gain. This is usually not accompanied by significant
visible side effects such as gynecomastia and water retention. Although this is
considered a beginner’s cycle, methandrostenolone is a c-17 alpha alkylated oral
steroid, and presents significant cardiovascular and liver toxicity. The repeated
use of such drugs should be limited.
Dianabol Cycle #2 (Mass)
Products: 200 tablets 5 mg Methandrostenolone
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day).
Comments: This is a common follow up to the first Dianabol cycle, utilizing a
slightly higher dose and longer duration of intake. The dosages used here are
more common for bodybuilding purposes. A slightly greater intensity of adverse
reactions is likely.
Testosterone Cycle #1 (Mass)
Products: 10 mL 200 mg/mL Testosterone (enanthate or cypionate)
All Weeks: Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4
g/day).
Estrogen Support: tamoxifen (20-40 mg/day) or anastrozole (.5 mg/day).
Comments: This mass building cycle is likely to yield similar quantitative
results as an early Dianabol cycle, but is favored over the oral for its lower
cardiovascular and hepatic strain. The doses used are expected to cause mild
shifts in the HDL/LDL cholesterol ratio, but not the substantial changes
normally seen with oral anabolic steroids. This sample cycle is likely to present
the least amount of health side effects of all listed in this section.
Testosterone Cycle #2 (Mass)
Products: 20 mL 200 mg/mL Testosterone (enanthate or cypionate)
All Weeks: Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day) or anastrozole (.5-1mg/day).
Comments: This cycle is a common follow up to the first testosterone only
cycle, with a higher dosage and 3 week longer duration of intake. The total
testosterone dosage given is double in comparison, and is likely to produce more
pronounced estrogenic and androgenic side effects. Cardiovascular strain may be
slightly higher than the first cycle, but should remain substantially lower than
cycles with oral AAS. Testosterone is arguably the safest, and at the same time
one of the most effective, muscle-building steroids available. The exclusive
repeated use of a cycle like this would be advised over more adventurous
cycling/stacking if possible.
Sustanon 250 Cycle (Mass)
Products: 15 mL 250 mg/mL Sustanon (testosterone blend)
All Weeks: Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day) or anastrozole (.5-1 mg/day).
Comments: This mass building program is similar to the other testosterone
cycles, but utilizes Sustanon 250, a form of blended testosterone more widely
used in Europe and other regions outside the U.S. The total steroid dosage of this
cycle is 3,750 mg, extremely close to the amount used in testosterone cycle #2.
A similar level of cardiovascular strain and visible side effects are expected.
Oxymetholone Cycle #1 (Mass)
Products: 50 tablets 50 mg oxymetholone
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day).
Comments: Oxymetholone is commonly regarded as the most potent mass
building steroid available. It is also prone to causing both strong estrogenic and
androgenic side effects. A steroid novice may gain 15-20 pounds or more on this
cycle, although a significant amount of this will be water retention, which will
subside soon after drug discontinuance. Oxymetholone is also known for
inducing strong cardiovascular and hepatic stress. While this drug may be more
convenient to use than an injectable testosterone, it is not regarded as a safe
alternative. Repeated use of c-17 alpha alkylated orals like this should be
limited.
Oxymetholone Cycle #2 (Mass)
Products: 100 tablets 50 mg oxymetholone
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day).
Comments: This is a more popular version of the oxymetholone only cycle. The
doses here are more common with experienced steroid users, and more than
sufficient to promote strong mass and strength increases. Side effects may be
more noticeable than the lower dose cycle, of course, which may necessitate a
higher dose of tamoxifen.
Stanozolol Cycle #1 (Lean Mass/Cutting)
Products: 200 tablets 2mg Stanozolol
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Comments: This is a common first-cycle for an athlete looking for performance
improvements or a bodybuilder looking for a lean mass or cutting steroid. This
cycle was more common when stanozolol was widely available in 2 mg tablets.
Such preparations are now uncommon except in Europe. The dosage used here is
low by bodybuilding standards, although similar cycles have been the backbone
programs for many athletic competitors, especially during the 1970s and 80’s.
Significant visible adverse reactions are unlikely at this dosage.
Stanozolol Cycle #2 (Lean Mass/Cutting)
Products: 200 tablets 5 mg oxymetholone
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Comments: This is a stronger version of a cutting/lean mass building cycle
utilizing stanozolol. The dosage used here is substantially higher than the first
stanozolol cycle, a fact that makes this cycle more properly suited for
bodybuilding purposes than Stanozolol Cycle #1. Cardiovascular and hepatic
strain will be more notable,and visible side effects more pronounced, than the
first cycle. There should be no need to addition an estrogen maintenance drug.
Stack Cycles
Deca/Dianabol Cycle #1 (Mass)
Products: 10 mL 200 mg/mL nandrolone decanoate
100 tablets 5 mg methandrostenolone
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day).
Comments: This is an extremely old and widely repeated steroid combination,
based on the predominantly anabolic steroid nandrolone decanoate.
Methandrostenolone serves as the androgenic component of this stack, and is
added during week 3, which is a time that side effects of reduced androgenicity
(with the exclusive use of nandrolone decanoate) are commonly noticed, such as
loss of libido and sexual dysfunction. The doses used in this cycle are not high
by most bodybuilding standards, but are sufficient to impart a noticeable
increase in muscle size and strength.
Deca/Dianabol Cycle #2 (Mass)
Products: 20 mL 200 mg/mL nandrolone decanoate
200 tablets 5 mg methandrostenolone
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day).
Comments: A more popular manifestation of the Deca/Dianabol Cycle, with
more commonly accepted dosages for a moderately experienced steroid user.
Incidences of side effects are expected to be higher at these dosages, although
overall this stack is likely to be less problematic than a combination of
testosterone and oxymetholone.
Testosterone/Anadrol Cycle (Mass)
Products: 20 mL 200 mg/mL testosterone (enanthate or cypionate)
100 tablets 50 mg oxymetholone
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day).
Comments: A combination of testosterone and oxymetholone is generally
regarded as the most potent 2-drug stack for gaining raw muscle mass. Both
drugs will present significant estrogenicity, and will be likely to induce
gynecomastia quickly unless an estrogen maintenance drug such as tamoxifen is
used. Inexperienced steroid users have been known to gain over 25-30 pounds
on a cycle such as this. Water retention will be very high with this stack,
however, and a rapid loss of water weight (possibly up to 10 pounds or more) is
expected soon after the cycle is discontinued.
Testosterone/Deca Cycle (Mass)
Products: 10 mL 200 mg/mL nandrolone decanoate
10 mL 200 mg/mL testosterone (enanthate or cypionate)
All Weeks: Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day) or anastrozole (.5-1mg/day).
Comments: Testosterone with nandrolone is considered to be one of the most
fundamental 2-drug combination stacks. Nandrolone compliments the
androgenic base of testosterone by supplementing additional anabolic activity
without strong estrogenicity. The resulting stack is almost as productive as a
cycle utilizing a higher dose of testosterone alone, but less problematic in terms
of estrogenic side effects such as water retention, gynecomastia, and fat buildup.
Estrogen conversion is still formidable enough to warrant the use of an estrogen
maintenance drug, however, and this stack remains in the realm of mass building
instead of lean mass or cutting.
Andriol/Anavar Cycle (Lean Mass)
Products: 360 capsules Andriol 40 mg
400 tablets oxandrolone 2.5 mg
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Comments: This is an effective but mild orals-only lean mass building cycle.
Andriol is used as the androgenic base, but in doses that do not greatly exceed
normal therapeutic levels. Oxandrolone is non-aromatizable, so significantly
elevated estrogenicity is unlikely. Tamoxifen 10-20 mg per day may be used
should the testosterone dosage turn out to be problematic. This stack is popular
among older men and those not wishing to use injections. The principle
drawback with this stack is that it uses a c-17 alpha alkylated oral, and therefore
has elevated cardiovascular and liver toxicity. This combination also tends to be
very expensive, and is far less cost effective than many stacks based on an
injectable testosterone.
Anabolic-Androgenic Bi-Phasic Stack (Lean Mass)
Products: 18 mL methenolone enanthate 100 mg/mL
50 mL boldenone undecylenate 50 mg/mL
20 mL testosterone (enanthate or cypionate) 200 mg/mL
All Weeks: Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20-40 mg/day) or anastrozole (.5-1mg/day).
Comments: This is a 3-month non-liver-toxic cycle that has 2 distinct phases,
mass and lean mass/cutting. The first 6 weeks of training and diet are focused on
mass building. Significant estrogenicity will be present in these weeks, and may
necessitate the use of tamoxifen or an aromatase inhibitor such as anastrozole to
prevent gynecomastia and excessive water retention. Estrogen maintenance
drugs may be reduced or possibly eliminated after the start of phase 2, which
focuses on increasing the androgen to estrogen ratio and solidifying the muscle
mass. A maintenance dosage of testosterone remains during this second phase, in
a effort to prevent sexual dysfunction or loss of libido, which often occurs with
the use of predominantly anabolic steroids alone.
Testosterone/Anadrol/Trenbolone Cycle (Mass)
Products: 30 mL 200 mg/mL testosterone (enanthate or cypionate)
20 mL 75 mg/mL trenbolone acetate
100 tablets 50 mg oxymetholone
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Estrogen Support: tamoxifen (20 mg/day) and anastrozole (.5-1mg/day).
Comments: One of the more extreme mass building cycles in common use
among bodybuilders. This stack will impart rapid gains in raw muscle size and
strength. This drug combination is highly prone to causing estrogenic and
androgenic side effects, including extremely significant levels of water retention.
Gynecomastia may also be an issue very early into the cycle. The use of an
aromatase inhibitor is likely to be necessary to cut down on the conversion of
testosterone to estrogen. Oxymetholone is highly estrogenic but does not
aromatize, however, which may necessitate the additional use of tamoxifen.
Although often highly problematic with regard to side effects, and therefore
rarely recommended to beginners, few steroid combinations can compare to
testosterone, oxymetholone, and trenbolone for building rapid muscle mass.
Masteron/Primobolan (Lean Mass/Cutting)
Products: 20 mL 100 mg/mL drostanolone propionate
20 mL 100 mg/mL methenolone enanthate
All Weeks: Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day)
Comments: This is an effective stack for hardening, cutting, and gaining lean
muscle mass. Neither agent is capable of converting to estrogen, so this cycle
should significantly elevate the androgen to estrogen ratio. This may assist in the
breakdown of fat tissue, enhancing muscle definition. This stack should not
present significant liver toxicity, although cholesterol ratios may be significantly
altered in light of reduced estrogenic activity.
Winstrol/Proviron/Trenbolone Cycle (Lean Mass/Cutting)
Products: 250 tablets stanozolol 5 mg
100 tablets mesterolone 25 mg
20 mL trenbolone acetate 75 mg/mL
All Weeks: Liver Support: Liver Stabil, Liv-52, or Essentiale Forte (label
recommended dosage).
Cholesterol Support: Lipid Stabil (3 caps/day) and Fish Oil (4g/day).
Comments: Stanozolol and trenbolone are popular steroids during cutting
phases of training, and impart strong anabolic and moderate androgenic effects
with no significant estrogenicity. This combination helps to impart a strong fat
loss/definition-enhancing effect. Two 25 mg tablets of mesterolone have been
added per day to supplement additional androgenic activity, which should help
maintain normal libido and sexual functioning. Additional anti-estrogenic drugs
should not be necessary. Some more aggressive competitive bodybuilders may
enhance this cycle by adding rHGH, clenbuterol, and/or thyroid hormones.
Higher doses of the individual steroids may also be used, but are expected to
impart stronger cardiovascular and hepatic strain, and are generally not advised.
PCT: PostCycle Therapy
PostCycle Therapy, or PCT for short, refers to the practice of using certain
medications to assistant in the discontinuance of anabolic steroids. While
steroids are not addictive drugs in a classical sense, they do suppress your own
hormone production, at least temporarily. This is an issue that should be
addressed at the conclusion of use. If the steroids are discontinued abruptly
without addressing internal hormone production, the result could be a prolonged
state of hypogonadism (low androgen levels) characterized by a substantial loss
of muscle mass, reduced energy levels, depression, and impaired libido/sexual
functioning. Steroid-using bodybuilders refer to this as the “post cycle crash”. In
this section, we will examine the natural control of hormone production as it
relates to this crash. We will also discuss certain medications that are commonly
used during the postcycle window to help stimulate natural testosterone
production and correct the hormonal imbalance.
The HPTA Axis
In the human body, the Hypothalamic-Pituitary-Testicular Axis (HPTA) controls
testosterone biosynthesis. The HPTA is a tightly regulated system of checks and
balances that works to assure the correct level of testosterone is maintained. We
can look at this regulating process as having three levels. At the top is the
hypothalamic region of the brain, which releases GnRH (GonadotropinReleasing Hormone) when it senses a need for more testosterone. GnRH sends a
signal to the second level of the axis, the pituitary, to produce Luteinizing
Hormone (LH). LH in turn sends a message to the Leydig’s cells in the testes
(level three) to secrete testosterone. Given this role, LH is regarded as the
primary direct messenger controlling testosterone synthesis. Testosterone and
other sex steroids that are produced as a result of this LH stimulation serve as a
counterbalance. They provide negative feedback to lower the secretion of LH
and testosterone, preventing overproduction. Synthetic anabolic steroids, of
course, send the same negative feedback. The serum level of testosterone is,
therefore, a reflection of both positive and negative stimulation fighting each
other for hormonal control.
The Hypothalamic-Pituitary-Testicular Axis: The hypothalamus releases
Gonadotropin Releasing Hormone (GnRH), which stimulates the pituitary
to release luteinizing hormone (LH) and follicle stimulating hormone (FSH).
This (primarily LH) promotes the release of testosterone from the testes.
Androgens, as well as estrogens and progestins, in turn cause negative
feedback inhibition at the hypothalamus and pituitary, lowering the output
of gonadotropins and testosterone when too much hormone is present.
Unaided HPTA Recovery
The suppression of natural testosterone synthesis by steroid use is typically a
temporary phenomenon. Even if you do nothing, your body’s normal androgen
synthesis will usually return a few to several months after the cycle is concluded.
The problem is, this can be a very long time when you are relying on
testosterone for so many things, including the maintenance of muscle tissue. In
fact, much of the muscle mass achieved during AAS administration can be lost
in the weeks and months to follow if low androgen levels are left unchecked.
PostCycle Therapy is widely used by bodybuilders and athletes to stimulate the
HPTA, so normal hormone production levels may come back more quickly. In
order to accomplish this effectively, however, we need to first understand what
HTPA recovery normally looks like without assistance. Only then can we
identify the levels of the HPTA that are most open to manipulation with support
medications.
Studies on the post-cessation aspect of anabolic steroid use, especially in AAS
abusers, are lacking. In most cases we must refer to single-agent studies, usually
of hormone replacement patients. One of the most detailed views of what a
postcycle crash probably looks like comes from an investigation into
testosterone enanthate.
354
It involves a group of men that were given weekly
injections (250 mg) for 21 weeks, a dose that admittedly does go beyond normal
HRT use. Various hormones were measured each week during the study, and for
more than 4 months after the medication was discontinued. A review of the data
shows that at the start of the study, LH levels were suppressed in direct relation
to the rise in testosterone (see Figure I). Once the steroid was withdrawn,
however, there was a delay between the return towards normal LH production
(which began to correct by the 3rd week) and testosterone (which took more
than 10 weeks before noticeable correction).
The above study suggests that one of the first things to happen after steroid
cessation is that the brain recognizes testosterone levels are low again. This will
cause GnRH and LH levels begin correcting fairly quickly. The substantial delay
between this and an increase in testosterone levels is caused largely by testicular
unresponsiveness to luteinizing hormone. After months of receiving extremely
weak stimulation, they will have lost a substantial amount of mass (atrophied).
This is a well-documented side effect of anabolic steroid use, even if a size
difference may not be immediately visible in all cases. When LH levels begin
surging back, the testes will initially be unable to handle the workload. This is
expected to correct itself in time, but it may take many weeks for the testes to
slowly restore to their original mass. With a good portion of the postcycle
recovery period actually being characterized by normal (even high) levels of LH,
we must address recovery broadly if we expect it to be effective.
Figure I. LH and Testosterone measurements starting 1 week after the last
injection of 250mg of testosterone enanthate (pretreated measures were 5
mU/ml and 4.5 ng/ml respectively).Note that between weeks 1 and 5, as
testosterone levels are declining due to the cessation of exogenous androgen
administration, LH levels are beginning to correct. From weeks 5 to 10,
testosterone levels remain at or very near baseline, although LH is
increasing by this point.No notable correction in testosterone occurs until
after the 10-week mark.
hCG in PCT
Human Chorionic Gonadotropin (hCG) is a fertility drug that mimics the actions
of luteinizing hormone. It is commonly used during the post-cycle period to
address testicular atrophy, which as we have seen is one of the fundamental
roadblocks to hormonal recovery. The hCG is typically taken at a substantial
dosage for a period of 2-3 weeks. Testicular atrophy is caused by a lack of LH
stimulation, and likewise recovery is function of increased LH. The objective
with hCG is to maximize stimulation of the testes so their original mass is
recovered more quickly than if we relied solely on physiological LH production.
It is important that hCG not be overused. Testicular sensitization to this hormone
is a delicately regulated mechanism. When hCG is taken for too long or at too
high a dosage, the LH receptor can become desensitized.
355 This can actually
interfere with recovery of hypothalamic-pituitary-testicular axis. A detailed
program utilizing hCG is outlined later in this section. For additional
information, please refer to the Human Chorionic Gonadotropin drug profile in
this book.
Anti-Estrogens in PCT
The anti-estrogenic drugs Clomid (clomiphene citrate) and Nolvadex (tamoxifen
citrate) are also commonly used during the post-cycle period. These drugs are
used to block the negative feedback inhibition of estrogen, which occurs
primarily at the hypothalamus.
356 This may foster the heightened release of
GnRH, and subsequently LH and testosterone. While estrogen levels are not
especially high in men, it is still a very strong inhibitor of testosterone release.
357
Since it is also formed from the aromatization of testosterone in peripheral
tissues, its role in the regulation of androgen biosynthesis is regarded as a fairly
direct one. The purpose of using anti-estrogens is to both trigger correction in
LH levels more quickly, and to augment total LH. They may also be necessary to
combat gynecomastia in some individuals, which can occur even with low
estrogen levels (it is partly a function of the androgen to estrogen balance in the
breast).
It is important to note that the use of anti-estrogens alone is generally not
regarded as an effectively strategy for addressing hormone recovery at the
conclusion of a steroid cycle. This is because these drugs only work by fostering
the heightened release of luteinizing hormone. We expect that the post-cycle
window is already partly characterized by normal/high LH levels. Thus, while
anti-estrogens may have an additive effect in this regard, they do not effectively
and directly address the main roadblock to hormonal recovery after steroid use,
namely testicular atrophy. Because of this, it is also generally advised to directly
target the testes with hCG. This usually means the initiation of a traditional PCT
program after every formidable period of AAS use, which utilizes all three of the
medications discussed in this section. There are some exceptions when an
abbreviated PCT program may be desirable, which we will discuss later on.
Traditional PCT Program
The following PCT program was developed by Dr. Michael Scally, one of the
most well known and accomplished individuals in the field of anabolic steroids
and male hormone replacement medicine. Scally has been a particularly strong
force lobbying the medical community and government to recognize the
hormonal imbalance that follows steroid use, something he has dubbed anabolic
steroid induced hypogonadism (ASIH). He has also treated and done blood work
on hundreds of patients, and while doing so developed the following PCT
program. A slightly modified form of this program was outlined in a clinical
report involving 19 healthy male subjects taking supraphysiological (highly
suppressive) doses of testosterone cypionate and nandrolone decanoate for 12
weeks. Scally’s “HPGA Normalization Protocol” focuses on the combined use
of hCG, Nolvadex, and Clomid, and is perhaps the most trusted and clinically
supported post-cycle therapy program presently available.
This PCT program begins with a substantial dose of hCG (2000 IU every other
day for 20 days). Anti-estrogens are also used during this period. This is
potentially important because hCG may up-regulate testicular aromatase
activity.
358 Thus, their use can minimize both estrogenic side effects and reduce
negative feedback inhibition of testosterone release. The anti-estrogens taken are
tamoxifen citrate (20 mg twice per day) and clomiphene citrate (50 mg twice per
day). Clomid is used for a shorter period of time, in a stepping down of the
program’s medications. While in the first couple of weeks the anti-estrogens
may not be highly effective, they should prove more critical towards the middle
and end of the program. In the published version of Scally’s program (which is
slightly modified from the above), normal hormonal function returned in all
subjects within 45 days. This is a definite success, far more favorable than the
protracted recovery window reported in the study with 250 mg/week of
testosterone enanthate.
Protocols: Human chorionic gonadotropin (hCG) is taken at 2000IU every
other day for 20 days. Clomiphene citrate 50 mg is taken twice per day for
30 days.Tamoxifen citrate is taken 20 mg twice per day for 45 days.
The timing for a Post-Cycle Therapy program can be as important as its
composition. If it is initiated too late, valuable days of normal hormone levels
(and also some muscle mass) may be lost. If you start the program too early, you
may miss the optimal window of effectiveness. The 20-day period of time in
which hCG is used is the most critical, and thus we time the PCT program
around this medication. In particular, we want to make sure that hCG is being
applied right around the time that exogenous steroids are dropping below the
threshold of physiological androgen stimulation. In the case of testosterone (the
easiest drug to understand and explain), this would be right before blood levels
drop below the normal level (350 ng/dL). There should be a small overlap with
the on-cycle period, so that hCG has a little time to work before AAS levels are
completely diminished.
The exact timing for PCT program is determined by the elimination half-life of
the drug(s) used. We will use testosterone cypionate/enanthate as an example.
We know each injection has an elimination half-life of approximately 8 days. A
dose of 200 mg/week should produce blood levels of around 2000-2400 ng/dL
after several weeks of use. It would take about 3 half lives (24 days) for
testosterone levels to drop to approximately 250-300 ng/dL at that dose. Thus,
the PCT program would be initiated a few days to one week after the last
testosterone injection. The program would be delayed with higher doses. For
example, at 500 mg per week of TC/TE it should take approximately 4 half lives
(32 days) for testosterone to drop below the normal range. In this case, PCT
would be initiated about two weeks after the last testosterone injection. With an
orals-only cycle (with no extended half-life due to an injection site reservoir),
PCT is initiated 7-10 days before the last steroid pills are taken.
354. Effect of long-term testosterone oenanthate administration on male reproductive function: Clinical
evaluation, serum FSH, LH, Testosterone and seminal fluid analysis in normal men.J. Mauss, G. Borsch et
al. Acta Endocrinol 78 (1975) 373-84
355. Desensitization to gonadotropins in cultured Leydig tumor cells involves loss of gonadotropin receptors
and decreased capacity for steroidogenesis. Freeman DA, Ascoli M Proc Natl Acad Sci U S A 1981
Oct;78(10):6309-13
356.
Inhibition of luteinizing hormone secretion by testosterone in men requires aromatization for its
pituitary but not its hypothalamic effects: evidence from the tandem study of normal and gonadotropinreleasing hormone-deficient men. Pitteloud N, Dwyer AA, DeCruz S, Lee H, Boepple PA, Crowley WF Jr,
Hayes FJ. J Clin Endocrinol Metab. 2008 Mar;93(3):784-91. Epub 2007 Dec 11.
357. The effect of aromatase inhibition on sex steroids, gonadotropins, and markers of bone turnover in older
men. Taxel P, Kennedy DG et al. J Clin Endocrinol Metab. 2001 Jun;86(6):2869-74.
358. Acute stimulation of aromatization in Leydig Cells by Human Chorionic Gonadotropin In-vitro. Proc
Natl Acad Sci USA 76:4460-3,1079
OCT: Off-Cycle Therapy
The objective of anabolic steroid therapy (when nonmedical applications are
involved) should be to elicit the desired benefits with the lowest cumulative
exposure and side effects. This normally includes diligence with optimizing all
aspects of training, rest, and diet, as well as adhering to a Post-Cycle Therapy
(PCT) program at the conclusion of each steroid cycle. One the one hand, we
want to make each cycle as productive as possible. On the other, we are striving
to retain the most gains so the starting point for the next cycle is that much
further along. When all aspects are in check, the result should be a need for
lower total doses, fewer cycles (longer durations of abstinence), and shorter
durations of use oncycle.
Given the importance of retaining our muscle and performance gains, however,
our efforts in this regard should not conclude with Post-Cycle Therapy. Indeed,
to receive the greatest long-term benefits from anabolic/androgenic steroid
therapy it is also advisable to initiate an Off-Cycle Therapy (OCT) program
when the PCT is over. The focus of OCT is typically to use all natural
substances (dietary supplements) that favor muscle retention, while
simultaneously allowing general physiology and hormonal balances to return.
While it is fair and even advisable to approach dietary supplements with a
healthy level of scepticism, the field has legitimately advanced enough that we
do have products with tangible value. We can find ways to make our programs
more effective in the absence of pharmaceuticals.
A well-organized OCT program lasts a minimum of six to eight weeks, and
consists of three distinct components. The first is “Testosterone Support,” which
seeks to extend an effective PCT program, but with a different and much more
basic approach. The second part is “Muscle Cell ReSensitization.” Heavy
training disrupts the muscle cell membranes, so that the muscles become less
responsive to exercise stimulation. We want to address this during OCT, and
prime the muscles for the next bout of intense training. Lastly, we want to
include one or more natural muscle-building substances in the program. This
part is called “Anabolic Supplementation”. If the right products are used, distinct
anabolic/anti-catabolic effects should be noticed, and more muscle mass will be
retained in the long run. All three OCT components are taken simultaneously,
sometimes for the full period between the end of PCT and the start of the next
AAS cycle.
Part I: Testosterone Support
The testosterone support aspect of our OCT program is substantially different
than what is used during traditional PCT. We are no longer looking to aid
endogenous testosterone production with anti-estrogenic drugs like tamoxifen or
clomiphene, nor to use pharmaceuticals that mimic endogenous luteinizing
hormones such as hCG. All pharmaceutical strategies have been concluded at
this point, and hopefully have elicited the necessary effects. During OCT, we
want to provide our bodies some of the natural components used in the synthesis
of testosterone. We want to augment our own natural processes, not artificially
shift them.
Vitamin D/Calcium/Zinc
The first thing to pay special attention to during OCT is our vitamin and mineral
status, particularly those components that are integral to testosterone
biosynthesis. This includes Vitamin D, Calcium, and Zinc. To begin with,
clinical studies have shown that higher levels of Vitamin D in the blood are
associated with increased testosterone output.
359 Thus, supplementing Vitamin D
may be advantageous during the long OCT period, when you will be relying
solely on your natural testosterone for the hormonal support of anabolism.
Calcium is another nutritive component involved in hormone function,
especially the level of bioavailable (free) testosterone.
360 A dose of 500-1,000
mg daily may be useful if dietary sources are insufficient. Lastly, a small dose of
zinc may also be taken if needed, as this mineral again is tied to androgen
biosynthesis.
361 Any deficiency in zinc will likely translate into suppressed (suboptimal) testosterone output.
D-aspartic Acid
D-aspartic acid (DAA) may also be useful during OCT. DAA is an amino acid
that is naturally found in the nervous and endocrine systems, and is believed to
play roles in such things as neurotransmission, spermatogenesis, and hormone
biosynthesis. Clinical studies that gave 3.2 g/day of D-aspartic acid per day (as
sodium salt) to healthy men resulted in a 42% increase in serum testosterone
levels in most subjects.
362 This same dose is recommended during OCT.
Part II: Cell Re-sensitization
Repeat high intensity exercise, especially resistance training, causes disruption
of the muscle cell membranes. This disruption is in many ways desirable, as it is
needed to initiate muscle growth and repair. Without damage, there is no
progress. There are some negatives to regular disruption of the muscle cells,
however. One of the most fundamental is that the outer membranes of the
muscle cells (which consist mainly of fatty acid compounds called
phospholipids) are rearranged. In particular, the concentration of arachidonic
acid (ARA) is lowered.
363 ARA supports the local anabolic process.
364
Likewise, its depletion is one of the common factors in training stagnation.
Arachidonic Acid
To help replenish membrane phospholipids and restore muscle cell
responsiveness to training, arachidonic acid should be supplemented during the
OCT period. A daily dose of 250 mg is recommended, which represents 50-
100% of the normal daily dietary intake of ARA. This amount should be
sufficient for phospholipid replenishment, and acceptable for long-term use.
Higher doses (500-1,000 mg per day) may provide a more distinct musclebuilding effect, but should be limited to six to seven weeks.
Fish Oil
It may also be useful to supplement with fish oil during the OCT period. The
main interests are docosahexaenoic acid (DHA) and eicosapentaenoic acid
(EPA), two Omega-3 essential fatty acids that are also important constituents of
muscle cell membrane phospholipids. Additionally, studies suggest that Omega3 essential fatty acids may enhance the membrane storage of arachidonic acid
under some conditions, and thus may indirectly support the pro-anabolic effects
of this EFA.
365 A daily dose of 2 grams of fish oil is typically recommended
during an Off-Cycle Therapy program.
Part III: Anabolic Supplementation
An optimal Off-Cycle Therapy program should also include natural products
with anabolic/anti-catabolic properties. Many AAS users are skeptical of
muscle-building supplements, and rightfully so. The market can be very
unreliable, with even the best products falling far short of AAS in terms of
efficacy and reliability. Still, the field has progressed a great deal over the years,
and there are many products of tangible value. And even a partial muscle sparing
effect during the OCT period is highly desirable, as it can significantly alter the
baseline muscle level by the start of the next steroid cycle (and thus may
influence the timing, dose, or duration of AAS required). It is recommended to
limit supplementation to only those ingredients with proven anabolic effects in
humans. For a more detailed analysis of natural anabolic supplements, please
reference William Llewellyn’s Sport Supplement Reference Guide.
366
Creatine Monohydrate
Creatine monohydrate is regarded as the “original” anabolic supplement, as it
was the first to offer substantial performance and body composition
improvements for most users. It is typically taken for 8-12 weeks or longer
(sometimes throughout the entire OCT period), at a dose of 5 grams per day.
Creatine augments muscle size and performance through several distinct
mechanisms. The two most prominent are cell volumization (water retention)
and cell energy enhancement (cellular ATP resynthesis), although the
supplement also has direct protein synthetic and anti-catabolic properties.
367
Beta Alanine
Beta Alanine is a non-essential amino acid that serves as a direct precursor for
carnosine synthesis. During exercise, hydrogen ions are produced in the muscle
cells, which cause the pH level to drop. This precipitates muscle fatigue.
Carnosine acts as an intramyocellular buffering agent, countering the build-up of
hydrogen ions. By serving as the rate-limiting step in the synthesis of muscle
carnosine, beta-alanine is a strong stabilizer of muscle pH.
368 A dose of 3-6
grams per day is typically used, which should allow the individual to perform
measurably longer during training. While this may not be a direct anabolic
effect, over time the increased training stimulation can lead to greater muscle
preservation/gains.
Branched-Chain Amino Acids
There are three essential Branched Chain Amino Acids (BCAA) – leucine,
isoleucine, and valine. These amino acids are very abundant in skeletal muscle
protein, accounting for 14-18% of the total content.
369 370 Supplementation with
BCAAs is desirable for a couple of reasons. The first is that they provide integral
building blocks for the synthesis of new muscle protein. From a nutritive
standpoint, BCAA supplements are very useful. Moreover, BCAA appear to
directly stimulate muscle cells to synthesize and retain protein.
371 They are, in
fact, among a small selection of clinically validated anabolic supplements in
humans. A dosage of 10 grams per day (post-training) is most often used.
Typical OCT Program (8-12 Weeks)
Testosterone Support:
Vitamin D 3000 IU/day
Calcium 500 mg/day
Zinc Sulphate 250 mg/day
D-Aspartic Acid 3.2 g/day
Muscle Cell Re-sensitization:
Arachidonic Acid 250 mg/day
Fish Oil 2 g/day
Anabolic Supplementation:
Creatine 5 g/day
Beta-Alanine 3-6 g/day
BCAA 10 g/day
359. Association of vitamin D status with serum androgen levels in men. Wehr E, Pilz S, Boehm BO, März
W, Obermayer-Pietsch B. Clin Endocrinol (Oxf ).
2009 Dec 29. [Epub ahead of print]
360. Testosterone levels in athletes at rest and exhaustion: effects of calcium supplementation. Cinar V,
Baltaci AK, Mogulkoc R, Kilic M. Biol Trace Elem Res. 2009 Summer;129(1-3):65-9. Epub 2008 Dec 20.
361.
Impact of oral zinc therapy on the level of sex hormones in male patients on hemodialysis. Jalali GR,
Roozbeh J, Mohammadzadeh A. et al. Ren Fail.
2010 May;32(4):417-9.
362. The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and
testosterone in humans and rats. Topo E, Soricelli A, D'Aniello A, Ronsini S, D'Aniello G. Reprod Biol
Endocrinol. 2009 Oct 27;7:120.
363. Fatty acid profile of skeletal muscle phospholipids in trained and untrained young men. Andersson, A.,
A. Sjodin, A. Hedman, R. Olsson, and B. Vessby. Am J Physiol Endocrinol Metab. 279:E744-751, 2000.
364. The COX-2 pathway regulates growth of atrophied muscle via multiple mechanisms. Bondesen BA,
Mills ST, Pavlath GK. Am J Physiol Cell Physiology 2006 Jun; 290(6): C1651-9. Epub 2006 Feb 8.
365. Eicosapentaenoic acid and arachidonic acid: collaboration and not antagonism is the key to biological
understanding. Horrobin DF, Jenkins K, Bennett CN, Christie WW. Prostaglandins Leukot Essent Fatty
Acids. 2002 Jan;66(1):83-90.
366. Sport Supplement Reference Guide. William Llewellyn © 2009-2010. Molecular Nutrition, USA.
367. Creatine in sports. Kreider RB. Essentials of Sport Nutrition & Supplements. Humana Press. Totowa,
NJ. 2007.
368.
Influence of beta-alanine supplementation on skeletal muscle carnosine concentrations and high
intensity cycling capacity. C.A. Hill et al. Amino Acids, 2007 Feb;32(2):225-33
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13C]phenylalanine. Riazi R, Wykes LJ, Ball RO, Pencharz PB. J Nutr. 2003 May;133(5):1383-9.
370. Dietary protein impact on glycemic control during weight loss. Layman DK, Baum JI. J Nutr. 2004
Apr;134(4):968S-73S.
371. Nutraceutical effects of branched-chain amino acids on skeletal muscle. Shimomura Y, Yamamoto Y,
Bajotto G, Sato J, Murakami T, Shimomura N, Kobayashi H, Mawatari K. J Nutr. 2006 Feb;136(2):529S532S.
Injection Protocols
Anabolic/androgenic steroid injections are always given deep in the muscle
(intramuscular). Some other performance-enhancing drugs such as human
growth hormone and insulin injections are given by injection in the fat layer
between the skin and muscle (subcutaneous). The protocols for both injection
types are provided. Improper injection technique can result in health
complications such as inflammation, bacterial abscess or other infection, scar
tissue development, septic shock, or other tissue or nerve injury. Furthermore,
the sharing of needles or vials may result in the transmission of blood-borne
pathogens including HIV and hepatitis. It is important to closely follow accepted
sterility and safety practices for every injection, including the proper disposal of
all equipment immediately after use.
General Preparation:
1. Make sure you have all the necessary supplies.
Intramuscular Injection:
(1) 3mL syringe
(1) 22-25g 1-1.5” needle for administering the injection
(1) 21g 1-1.5” needle for drawing solution (if using a multi-dose vial)
(2) Alcohol pads
(1) Dry cotton ball
(1) Plastic bandage
Syringe with needle attached. (intramuscular)
Subcutaneous Injection:
(1) Insulin syringe with needle attached (.5-1mL 27-30g)
(2) Alcohol pads
(1) Dry cotton ball
(1) Plastic bandage
Syringe with needle (insulin)
2. If applicable, keep the administration needle cold by leaving it in the freezer
for at least one hour before opening. This will help dull the pinch of penetration.
3. Select a well-lit room with a clean hard surface such as a tabletop or counter
to administer the injection.
4. Wash hands thoroughly with soap and warm water.
5. Assure that all injection equipment is sealed and unused. Never reuse needles.
Double check the expiration dates on all medications.
6. Clean top of vial thoroughly with an alcohol pad, if applicable. Let air dry for
15 seconds.
Precautions: Do not use injection equipment that is used or has been exposed to
air during storage. Never share needles or multi-dose vials. Discard unused
portions of the drug at the recommended time.
Drawing Solution into Syringe:
1. Remove syringe from packaging. Attach drawing needle, if applicable.
2. If using a multi-dose vial, fill syringe with air in the amount you are
withdrawing. This will help stabilize the pressure and make drawing easier.
3. If using an ampule, break open and place flat on a hard surface. The use of a
paper towel to cover the glass top may make breaking easier. Draw solution.
Skip below steps and go to Intramuscular or Subcutaneous Injection Procedure.
4. If using a vial, insert needle through the rubber stopper at a 90-degree angle.
Turn the vial upside down with needle attached. Inject air. Slowly withdraw
desired amount of solution. You may lightly tap the side of the needle to
dislodge air bubbles. Note that small air bubbles are not harmful.
5. Remove needle and syringe from vial, if applicable. Replace cap on the end of
needle.
Keep fingers away from needle when drawing.
6. Remove drawing needle and replace with new administration needle, if
applicable. This is highly advised with multi-dose vials, as passage through the
rubber stopper will have dulled the needle considerably. Remove any air in the
tip of the needle, and prepare for injection.
7. Place capped needle back inside wrapper and place on clean surface.
Precautions: Never touch the tip of the exposed syringe, the needle, or the top of
the vial stopper after it has been cleaned with alcohol. If you come into contact
with these surfaces you should consider the materials contaminated, and should
not use them for injection.
Intramuscular Injection Procedure:
Used for all anabolic/androgenic steroid injections.
1. Thoroughly clean the intended site of injection with second alcohol pad.
Preferred locations are the upper outer quadrant of the buttocks, or the outer side
of the thigh. Let air dry for 15 seconds.
2. Remove needle cap. With free hand, stretch the skin around the site of
injection with two fingers. Move the skin over the muscle to the side by 1-1.5”
(Z-Track method).
(Z-Track method).
3. In a swift motion, insert the needle into the target muscle at a 90-degree angle
with the dominant hand. Make sure the needle is deep within the muscle.
4. Pull back on the plunger (aspirate). If the syringe fills with blood you have hit
a blood vessel, and the injection should be aborted.
5. Inject the medication slowly into the muscle.
Upper/Outer buttocks is the preferred site for IM injection.
The outer side of the leg is also commonly used.
6. Withdraw the syringe. Release the skin with your other hand. The skin and
subcutaneous tissue will rebound, which helps close off the needle shaft and
prevent leaking.
7. Dry injection site with dry cotton ball. Cover with plastic bandage if
necessary.
Precautions: Never inject into skin that is discolored, broken, or irritated, or if
there are lumps, knots, or feelings of pain in the area. Do not inject more than
3mL at one time. Rotate the site of injection so that you do not inject in the same
muscle more than once every two weeks.
Subcutaneous Injection Procedure:
1. Thoroughly clean the intended site of injection with second alcohol pad. The
preferred location is the lower abdominal region. Let air dry for 15 seconds.
Shaded area denotes site for abdominal subcutaneous injection.
2. Remove needle cap. With free hand, pinch the skin around the site of injection
so it is lifted off the muscle.
3. In a swift motion, insert the needle into the target area at a 45-degree angle
with dominant hand. Make sure the needle rests within the subcutaneous tissues
between the skin and muscle.
4. Inject the medication slowly into the subcutaneous tissue. Do not aspirate.
5. Withdraw the syringe. Release the skin with your other hand.
The skin is pinched upwards to facilitate injection into the subcutaneous
tissues.
6. Dry injection site with dry cotton ball. Cover with plastic bandage if
necessary.
Precautions: Never inject into skin that is discolored, broken, or irritated, or if
there are lumps, knots, or feelings of pain in the area. Do not inject more than
1mL at one time. Rotate the site of injection each time so that you are at least 1”
away from the last site, and do not return to a previous site until all other
available sites have been used. This will help prevent overuse of the same
injection area.
Steroid Frequently Asked Questions
1) How much weight can someone expect to gain during the first cycle of
steroids?
Provided dosing is sufficient, a steroid user can expect to make the most
significant progress during their first cycle. Although this will vary from person
to person, it is not uncommon for someone to gain 20 pounds of weight or more
during a 6-8 week period of AAS use. Some of this may be water retention,
although a solid gain of more than 10-15 pounds of muscle mass is possible.
2) Are the gains from steroid use temporary?
Yes, and no. Steroids can help you do two basic things with regard to muscle
growth. First, they can allow you to more rapidly reach your genetic limits for
muscle growth. Provided you continue to train actively, eat properly, and use an
effective PCT program, you should be able to maintain at your genetic limit
indefinitely. So in this regard, the early gains do not have to be temporary.
Later, steroids can allow you to push well beyond your genetic limits. It is
important to emphasize this, as extreme physical development cannot be
maintained long-term without the repeat administration of anabolic substances.
The body will always revert back towards its normal metabolic limits once AAS
are removed. In this context, some of the gains will not be permanent.
Steroids do permanently alter the physiology of your muscles by adding more
cellular nuclei. With higher nuclei content, each muscle cell can manage its
volume more efficiently, which allows more rapid expansion. Even after a long
period of complete abstinence from training and AAS, the nuclei remain.
372 This
may provide a “muscle memory” effect, allowing you to reach your genetic limit
(perhaps a slightly extended limit) faster than if you had never used AAS in the
past. So in this regard, there are lasting benefits beyond the temporary increase
in muscle size itself.
3) Can steroids make me look like a professional bodybuilder?
If you have the underlying genetics to allow for this extreme muscle growth, this
may be possible with a lot of hard work and dedication. If you are like the vast
majority of people, however, steroids will not be able to make you look like a
professional bodybuilder. Genetics are a big factor in determining the ultimate
limits to your physique, even in an enhanced state. Many people use steroids and
look very big and impressive because of it, but very few users are able to make it
to the stage of a professional bodybuilding show.
4) How dangerous is an isolated cycle of steroids?
Anabolic/androgenic steroids are among the safest drugs available, at least in a
short-term sense. Fatal overdose is not reasonably possible, and the negative
health changes such as alterations in cholesterol, blood pressure, hematocrit, and
blood clotting (among other things) are very unlikely to manifest in serious
bodily harm or death after an isolated cycle. There are rare deaths from such
things as stroke and liver cancer in short-term abusers, but such occurrences are
statistically extremely rare in light of the millions of people that use these drugs.
If you had to comparatively rate the acute risks of AAS abuse, they would be
slightly higher than marijuana, but far less than virtually all other illicit
narcotics.
5) How dangerous is long-term steroid use?
The long-term use of steroids for nonmedical reasons can be a significantly
unhealthy practice. It has been difficult, however, to quantify the exact risk. The
main issue is the fact that AAS abuse can promote heart disease, the number one
killer of men. Heart disease is a slow progressive disease, which may build for
decades without symptoms. Steroid abuse may accelerate the silent process of
plaque deposition in the arteries, and also induce other changes in the
cardiovascular system that can increase susceptibility to stroke or heart attack. If
death finally occurs, however, it will be difficult for a medical examiner to
pinpoint AAS as the cause; too many variables play a role in the etiology of
cardiovascular disease. The vast majority of deaths where AAS have contributed
go unreported for this reason. The exact mortality rates of long-term steroid
abusers have, likewise, been difficult to calculate. According to one populationbased study, steroid abusers had a 4.6 times greater risk of early death from all
causes including suicide compared to non-users.
373
It is unknown, however, how
applicable this number is to the full steroid-using population. It is especially
important to closely monitor cardiovascular disease and other health risk factors
if long-term steroid use is a practice you will follow.
6) Can steroids be used to enhance an athletic career safely?
The nonmedical use of AAS by definition cannot be defined as a safe practice.
However, it can be argued that anabolic/androgenic steroids can be used with
high relative safety, even over a period of many years. The guidelines of steroid
harm reduction are important to minimizing the negative health effects of these
drugs. Provided an individual follows these guidelines and is careful with drug
selection, dosages, and durations of intake, follows a diet low in saturated fats,
cholesterol, sugar, and refined carbohydrates, actively trains with both resistance
and cardiovascular exercise, and uses cholesterol support supplements such as
fish oils and Lipid Stabil during all cycles, it may be difficult in many cases to
argue high tangible health risks. It takes a great deal of involvement and
planning to use AAS in this manner, which is always advised.
7) What are the safest steroids for men?
Testosterone, whatever the form, tends to be the safest steroid for men. When the
dose remains within the moderately supratherapeutic range (such as 200-400 mg
of an injectable testosterone ester per week), alterations in cardiovascular risks
factors are noticed, but not extreme. Some of this has to do with the beneficial
cardiovascular effects of estrogen in men. Also considered fairly safe are the
common injectable steroids boldenone, nandrolone, and methenolone. Isolating
your use to these drugs is recommended over using the full spectrum of oral and
injectable steroids.
8) What steroids will not cause hair loss?
For those with a genetic predisposition to hair loss, all anabolic/androgenic
steroids are capable of accelerating the process. Slowing the onset of this during
AAS use requires a focus on reducing relative androgenicity in the scalp. This
can be accomplished with the use of predominantly anabolic drugs such as
nandrolone, oxandrolone, or methenolone. Alternately, moderate doses of
testosterone can be used with finasteride, a drug that reduces DHT conversion
(and androgenic amplification) in the scalp. Still, those genetically prone to hair
loss can have problems with any steroid, and are always advised to limit dosing,
drug intake durations, and monitor effects on the hairline closely.
9) What are the safest steroids for women?
Women are generally most concerned with the virilizing (masculinizing) effects
of anabolic/androgenic steroids. The least virilizing agents are those with the
highest relative anabolic to androgenic effect, such as nandrolone, oxandrolone,
and methenolone. Care must always be taken, however, as all AAS are based on
male sex steroids, and as such can cause masculinizing effects in women.
10) Should I rotate my steroids every few weeks to prevent receptor
downregulation?
No, this is not necessary. Anabolic/androgenic steroids all work primarily by
attaching to and activating the same receptor. As such, you do not gain anything
by switching to a new compound that works via stimulating the same receptor. If
tolerance were induced by one AAS compound, it would be extended to all
compounds. The plateau effect that is noticed 6-8 weeks into most cycles is
poorly understood, but likely related to the new metabolic limits placed on
muscle cells under the influence of a certain AAS dosages, not insensitivity to
AAS. Classic downregulation does not occur with these drugs, and even if it did,
rotating steroids would not prevent it.
11) How likely am I to find real steroids on the black market? Does it
matter?
Although exact figures are difficult to calculate, real pharmaceutical
anabolic/androgenic steroids are estimated to represent half or less of the
products commonly circulated on the black market. In many regions this figure
may be below 25%. The majority of products sold presently are counterfeit
copies of real AAS, or products made and labeled by underground laboratories.
It does matter, because the quality of nonmedical AAS cannot be ensured. These
products are generally not advised for use. Given the potential issues with drug
safety, it is worthwhile to spend the extra time and money on steroid products
you can be assured came from legitimate pharmaceutical channels.
12) What do the anabolic and androgenic reference numbers under the
profile for each steroid mean?
These numbers come from early studies measuring the effect of each steroid on
certain muscle and sex organ tissues of animals, usually mice. These numbers
are useful for assessing the relative anabolic to androgenic balance of each drug
in humans. They are not as accurate at assessing the total muscle building
potential of each steroid, however, and should not be taken as absolute ratings of
potency.
372. Anabolic Steroids Withdrawal in Strength Trained Athletes: How Does It Affect Skeletal Muscles?,”
Anders Eriksson and Lars-Eric Thornell. American Physiological Society. The Integrative Biology of
Exercise V, Sep 24-27, 2008 Hilton Head, SC.
373.
Increased premature mortality of competitive powerlifters suspected to have used anabolic agents.
Pärssinen M, Kujala U, Vartiainen E, Sarna S, Seppälä T. Int J Sports Med. 2000 Apr;21(3):225-7.
Understanding Blood Tests
The abuse of anabolic/androgenic steroids can have a number of potential
negative health consequences, most commonly with regard to cardiovascular and
liver health. These issues, however, can almost always be identified in blood
work well before physical symptoms become apparent. Cardiovascular disease,
for example, is a disease that can take decades to progress. Cholesterol and
triglyceride testing can be used to identify and control early risk factors and
decisions that would support the disease over time. Liver damage is also
generally obvious in liver enzyme tests well before it becomes visibly noticeable
to the person. The same holds true for many areas of general health. If you are
using steroids, the regular assessment of health with blood work, and the
adjustment of therapy when the results call for it, is regarded as the most
effective strategy for reducing health risks.
Blood tests with regard to anabolic/androgenic steroids are usually conducted in
three separate phases. The first phase looks at your health before steroid use.
This is done to asses your current condition and risks before any therapy is
initiated, and to set baselines for later comparison. The next is on-cycle testing,
which is used to assess the direct impact of the anabolic/androgenic steroid use
(what the drugs are actually doing to your body while they are being taken). The
latter phase of testing is the follow-up, which is conducted to ensure your
original state of good health has been restored once the drugs are no longer in
the body. We generally refer to these three phases of testing as Baseline, OnCycle, and Post-Cycle, respectively.
Baseline (Pre-cycle):
Baseline (pre-cycle) testing is generally very broad. This is done to make sure
there are no underlying health conditions that may be worsened by anabolic
steroids, and to have a baseline for determining the on-cycle and post-cycle
impact. To begin with, a profile of steroid hormones (male users only) is done to
identify the current natural state. This can be especially important to know for
post-cycle follow up, as the range of what is considered normal for testosterone
on a standard blood test can be quite broad. If you started on the high end of
normal, for example, you might want to make sure you are not stuck on the low
end of normal following your cycles. A full liver panel is usually conducted as
well, especially if hepatotoxic oral or injectable steroids are planned. Since
cardiovascular disease is one of the most tangible risks with long-term steroid
use, lipid profiling is always important, and is usually conducted here and during
all other phases of testing. Additionally, other general markers of health are
generally examined here including blood, kidney, electrolytes, minerals, glucose,
and prostate.
Checklist (minimum):
Hormone (Steroid)
Lipids (Standard Full Set)
Full Liver Panel
Blood
Kidney
Electrolytes, Minerals, and Glucose
On-Cycle:
On-cycle testing is usually conducted 3 to 4 weeks after steroid therapy began.
The individual will generally look at those indicators of health most directly
affected by steroid use. A full lipid examination is conducted, and is often
regarded as the single most important set of health tests that can be initiated. It is
here that the cardiovascular impact of the steroids will begin to become
apparent. One should give special consideration to what these results may mean
for their health decades down the road if this type of steroid cycle is to be
repeated many times over many years. If hepatotoxic drugs are being used, a full
liver panel will be examined. It is also recommended to examine other general
health markers here such as blood, kidney, electrolytes, minerals, and glucose.
Checklist (Minimum):
Lipids (Standard Full Set)
Liver Panel, if taking hepatotoxic steroid(s)
Blood
Kidney
Electrolytes, Minerals, and Glucose
Post-Cycle
During the post-cycle testing phase it is common to once again look first at the
male steroid hormones. The hope here is to obtain values that closely mirror
your pretreatment levels. Note that there will always be some variation based on
the time of the day, and even in the day-to-day results. An exact match is
probably not feasible. It is also considered a good idea to look at pituitary LH
and FSH, because if testosterone levels come back low it will give you and your
physician a better understanding of the cause. High LH/FSH and low
testosterone (primary hypogonadism) may simply indicate that your testicles
have not yet fully restored their mass. Alternately, low LH/FSH can indicate
secondary hypogonadism, which is often cause to initiate corrective therapy with
an endocrinologist. A run of other general markers of health are also usually
conducted here including lipids, liver, blood, kidney, electrolytes, minerals,
glucose, and prostate.
Checklist (Minimum):
Hormone (Steroid, LH/FSH)
Lipids (Standard Full Set)
Liver Panel, if taking hepatotoxic steroid(s)
Blood
Electrolytes, Minerals, and Glucose
Blood Tests by Category
Hormone
Steroid (male)
Steroid:
This set of testing should look at both total and free testosterone. The former
measure is most commonly used by physicians to identify the androgen level and
determine if there is a need for therapy. The latter measure actually represents
the fraction of bioavailable (immediately active) testosterone in the body, and is
consequently regarded as more important for assessing the present state of
androgenicity. Estradiol is the principle active form of estrogen in the body, and
has roles both in potential side effects (gynecomastia, water/fat retention) and
hormone balance. This is the estrogen marker most often recommended during
hormone profiling.
LH/FSH Panel:
Luteinizing hormone (LH) and follicle stimulating hormone (FSH) are
responsible for stimulating testosterone production and spermatogenesis in the
testes. These measures are most relevant when evaluating the cause and potential
treatment options for hypogonadism, not the short-term health impact of
anabolic-steroid use. The short-term suppression of LH/FSH is expected with
anabolic/androgenic steroid administration.
Thyroid:
It is regarded as important to get a baseline measure of thyroid activity, usually
once per year. Follow up tests during and after steroid use may be an expense
some view as unnecessary. Anabolic/androgenic steroid use is unlikely to
permanently affect thyroid function, but may slightly elevate thyroid levels
during therapy. A misdiagnosis of hyperthyroidism (overactive thyroid) is
sometimes made in light of these elevated numbers. The effect of
anabolic/androgenic steroid use on thyroid levels should be taken into account
before treatment for hyperthyroid is ordered.
Lipids (Cardiovascular)
Anabolic/androgenic steroids can have strong adverse effects on lipids. The
abuse of anabolic/androgenic steroids (particularly long-term abuse) can,
likewise, increase the risk for developing cardiovascular disease as assessed by
these variables. Mitigating these risks with the careful examination of the lipid
profile is regarded as one of the most fundamental of all steroid-related blood
tests. While far from comprehensive with regard to assessing total heart disease
risk, a full panel examining the variables below (and comparing them to your
baseline values) can provide a good snapshot of the cardiovascular impact of
anabolic/androgenic steroid use. It is important to measure your blood lipids
only after 12 hours of fasting, as food intake can skew the outcome of some
measures (particularly triglycerides).
Standard Full Set:
This is a standard full lipid panel examination. Ideally, all values should be kept
within the normal ranges at all times during steroid therapy. Note that the
LDL/HDL ratio is regarded as the most important measure of the serum lipid
tests, as it reflects the ongoing balance between plaque deposition (LDL) and
removal (HDL) in the arteries. The LDL/HDL ratio is used to more closely
assess heart disease risk in individuals that have elevated LDL or total
cholesterol levels.
Additional Testing:
C-reactive protein and homocysteine are two additional markers that are
important to examining cardiovascular health. C-reactive protein is a key
indicator of inflammation in the body, and homocysteine is involved in blood
clotting and LDL cholesterol oxidation. It is also advisable to include these two
variables in your cardiovascular testing schedule.
Apo Ratio:
Apolipoprotein ratio testing is also recommended. Although not commonly used
in general medical practice, apolipoprotein testing is increasingly regarded as a
more accurate predictor of cardiovascular disease risk than cholesterol testing.
Apolipoprotein B (apoB) is found in all LDL particles, and is responsible for
attaching these lipoproteins to the artery walls. Apolipoprotein A-I (apoA-I) is
found mainly in HDL particles, and is responsible for initiating beneficial
reverse cholesterol transport. ApoA-I enables the HDL particles to pull
cholesterol from the artery walls and transport them back to the liver. The ratio
of apoB to apoA-I, therefore, appears to reflect a much truer measure of the
balance of potentially atherogenic and antiatherogenic particles in the blood. A
ratio above .9 is generally regarded as indicative of increased cardiovascular
disease risk. Lower ratios reflect reduced cardiovascular disease risk
assessments.
To Find A Testing Lab Near You, Visit:
www.HRT-Labs.com
Liver Function
A full liver panel is important to assessing hepatic strain. The two markers of
liver stress most commonly elevated in abusers of anabolic/androgenic steroids
are the enzymes alanine amino-transferase (ALT) and aspartate aminotransferase (AST). ALT and AST are necessary to amino acid metabolism in the
liver, and will leak into the bloodstream as the liver becomes inflamed or
damaged. These two enzymes are generally regarded as important indicators of
early steroid-induced liver toxicity. There have been cases in which substantial
liver damage has occurred without substantial elevations in ALT and AST,
however, so a more detailed examination of liver enzyme values is always
advised.
Alkaline phosphatase (ALP) and gamma-glutamyltranspeptidase (GGT) are
known as cholestatic liver enzymes, which mean they diminish or stop the flow
of bile (a greenish fluid that aids digestion and is produced in the liver). ALP and
GGT are important markers of liver health during steroid use, and should be
included in regular blood testing. Elevations in ALP and GGT can indicate bile
duct obstruction (intrahepatic cholestasis), which refers to a condition where the
liver can no longer properly transport and metabolize bile. Intrahepatic
cholestasis is a potentially very serious manifestation of steroid-induced liver
toxicity, so elevations in ALP and GGT should not be disregarded.
Mild elevations in ALT and AST may be caused by muscle damage (exercise)
and not steroid-induced liver toxicity. A comparison to baseline levels will be
important in determining the cause. If the only factor that has changed is the
addition of a hepatotoxic anabolic steroid (training is otherwise steady), the drug
is likely to blame. It is important to remember that ALP and GGT are not always
elevated with early liver strain. Therefore, the elevation of any hepatic markers
above the reference range (even if only ALT and AST) can indicate liver
toxicity, and should be cause to discontinue the offending steroids and reassess
risk.
Muscle Enzyme
The creatine kinase (CK) enzyme is used as a marker of muscle breakdown,
kidney damage, and heart damage. High levels usually indicate heart attack or
other organ trauma. This enzyme can also become elevated with exercise that
breaks down muscle tissue, especially intense endurance or resistance training.
Elevated CK levels caused by high intensity training are often mistaken for
organ damage. It is important to further examine other markers of kidney and
heart heath before such a determination is made. Note that creatine kinase levels
may also be useful in determining if liver strain or heavy training is the cause of
mild elevations in liver enzymes ALT and AST. Slight increases in ALT and
AST caused by muscle damage will usually coincide with elevated CK and
normal ALP and GGT levels.
Blood
A full blood count is one of the most commonly run blood tests, and can give
you a good snapshot of overall health in many regards. A full blood cell test will
give you a measure of white cell count (responsible for fighting infection),
platelet count (vital to blood clotting and healing), and red blood cell count
(responsible for carrying oxygen). Red and white cell counts will be further
subdivided into various individual measurements, often referred to as a
differential cell count. Hemoglobin is the specific carrier of gases in red cells,
and hematocrit is a measure of the percentage of red blood cells in the total
blood volume. Due to their effects on erythropoiesis, anabolic steroids tend to
increase red blood cell count, hematocrit, and hemoglobin concentrations. While
this may increase oxygen-carrying (aerobic) capacity, as the concentration of red
blood cells increases so does the thickness of the blood. Elevated hematocrit can
increase the risk of heart attack or stroke.
Kidney
This panel of tests looks at three primary waste products filtered and excreted
through the kidneys, urea, uric acid, and creatinine. Problems here can indicate
serious underlying problems with kidney function. Note that Blood Urea
Nitrogen (BUN) is often elevated with excess protein consumption, and is used
by many physicians as an indicator that too much protein is being consumed for
optimal metabolism. The high consumption of meat or creatine supplementation
can also elevate creatinine levels, diminishing the value of blood creatinine
testing as a marker of kidney health. Electrolyte, mineral, and fasting glucose
testing is important to further assessing kidney health, and is advised in addition
to the above kidney markers. A quick urine screen for pH, specific gravity, and
the presence of sugar, blood, and ketones is also available at most physicians’
offices, and is generally advised alongside blood work when possible.
Electrolytes, Minerals, and Glucose
Electrolyte levels are examined to help detect problems with the fluid and
electrolyte balance. Abnormal values may reflect something as small as sodium
or potassium deficiency, or a more serious condition such as kidney disease. A
variety of other health issues may also become apparent by looking at both
electrolyte and mineral levels, giving them somewhat broad prognostic value.
Fasting glucose is also examined to determine if the individual may be
hypoglycemic (low blood sugar) or hyperglycemic (high blood sugar). Problems
with fasting glucose may reflect potentially serious health conditions including
metabolic syndrome, diabetes, pancreatic disease, liver disease, kidney failure,
or acute stress.
Prostate
Prostate-specific antigen (PSA) is a protein produced by cells in the prostate
gland. Its levels can become elevated in cases of benign prostate hypertrophy or
prostate cancer. While it remains unknown if elevating the level of androgens in
the body with anabolic/androgenic steroids can increase the risk of prostate
cancer, it is known that this disease can be progressed by elevated hormone
(androgen and estrogen) levels. The PSA test is regarded as an important
diagnostic tool for screening individual prostate cancer risk. If PSA levels are
elevated, most will advise against using anabolic/androgenic steroids.
Individual Heath Markers Defined
Alanine amino-transferase (ALT): An enzyme produced primarily in the liver
but also in other tissues. ALT is involved in amino acid and protein metabolism.
Used as a primary marker of hepatic strain. Also called Serum Glutamic Pyruvic
Transaminase (SGPT).
Albumin: The main protein that circulates in the blood. Produced in the liver
and has antioxidant properties. Transports certain hormones, vitamins, and
minerals, and plays a role in water balance. Used as an indicator of liver health.
Higher levels are optimal.
Alkaline Phosphatase (ALP): A family of cholestatic enzymes produced
mainly in the liver, but also in the intestines, kidneys, and bone. Used as a
marker of hepatic strain, often relating to disease of the bile ducts.
Apolipoprotein A-I (apoA-I): A constituent of HDL (good) cholesterol, apoA-I
is responsible for initiating beneficial reverse cholesterol transport. This process
pulls cholesterol particles from the artery walls and transport them back to the
liver. Higher levels are optimal.
Apolipoprotein B (apoB): A constituent of LDL (bad) cholesterol, apoB is
responsible for attaching these lipoproteins to artery walls. ApoB is a promoter
of fatty plaque deposits in the arteries. Lower levels are optimal.
Aspartate amino-transferase (AST): An enzyme produced primarily in the
liver but also in muscle tissue. AST is involved in amino acid and protein
metabolism. Used as a marker of hepatic strain, although it is considered less
specific than ALT testing. Also called Serum Glutamic-Oxalocetic
Transaminase (SGOT).
Basophils: A type of white blood cell. Action not fully understood, but cells are
known to carry histamine, heparin, and serotonin. Levels are elevated with
allergic reaction and parasitic infection.
Bicarbonate: A measure of carbon dioxide content in the blood, and a common
marker of the acid-base balance.
Bilirubin: A waste product made from the breakdown of red blood cells.
Excreted into the bile. Regarded as an important indicator of liver health.
Elevated levels in the blood indicate liver toxicity.
Blood Urea Nitrogen (BUN): A waste product from the breakdown of proteins,
filtered and excreted through the kidneys. Elevated levels may indicate a number
of problems including excessive protein intake, kidney damage, dehydration,
heart failure, or reduced production of digestive enzymes. Low levels may be
indicative of many things including malnutrition or liver damage.
BUN/Creatinine Ratio: The ratio of Blood Urea Nitrogen to Creatinine, used as
a marker of kidney and liver health.
C-reactive Protein (CRP): A key marker of inflammation in the body. Elevated
levels may indicate increased risk of cardiovascular disease or stroke.
Carbon Dioxide (CO2): Byproduct of respiration, and a common marker of the
acid-base balance. See also Bicarbonate.
Calcium: Electrolyte involved in a myriad of body functions including bone
metabolism, protein utilization, muscle and nervous system functioning,
cardiovascular functioning, blood clotting, and nutrient transport.
Chloride: Electrolyte involved in the regulation of water balance. Elevated
levels may indicate a number of things including anemia, dehydration, excess
salt consumption, and hyperthyroid. Low levels may indicate heart or kidney
failure, severe vomiting, or a number of other health conditions.
Cholesterol, Total: A measerure of all fractions of cholesterol in the blood
(LDL, VLDL, and HDL). High total cholesterol is regarded as a risk factor for
cardiovascular disease.
Cholesterol, HDL: A measure of the beneficial high-density lipoprotein (HDL)
fraction of cholesterol, which helps remove plaque deposits from arteries. High
levels are optimal. Low levels may be found in cardiovascular disease.
Cholesterol, LDL: A measure of the low-density lipoprotein (LDL) fraction of
cholesterol. This is the primary atherogenic particle, meaning it tends to promote
the formation of plaque deposits in the arteries. Low levels are optimal.
Cholesterol, VLDL: A measure of the very low-density lipoprotein (LDL)
fraction of cholesterol. VLDL contains the highest amount of triglycerides.
Considered an atherogenic (“bad”) cholesterol particle. Lower levels are
optimal.
Cholesterol, LDL/HDL Ratio: A measure of the primary atherogenic particle
(LDL) in relation to the primary antiatherogenic particle (HDL). This ratio is
generally considered the most important cholesterol test value for assessing
cardiovascular disease risk. A low ratio is desirable.
Creatine Kinase: An enzyme found largely in the heart and muscle, and
responsible for converting creatine to phosphocreatine. Elevated levels may be
linked to a number of things including heart attack, kindey failure, or sever
muscle damange.
Creatinine: A waste product of muscle metabolism. Low levels may indicate
kidney disease, malnutrition, or liver disease. High levels may indicate a number
of things including reduced kidney function or muscle degeneration. Creatine
supplementation may also elevate creatinine levels.
Eosinophils: A type of white blood cell. Similar to basophils, eosinophils are
used by the body to protect against allergy and parasites. Levels are elevated
with infection, and are low with good health.
Estradiol: The principle active form of estrogen. High levels can be associated
with water retention, fat buildup, and gynecomastia (men). Also plays a role in
prostate hypertrophy. Low levels of estradiol may be associated with increased
heart disease risk.
Follicle Stimulating Hormone (FSH): A pituitary hormone involved in
reproduction. In men, FSH is mainly responsible for supporting
spermatogenesis. In women it supports ovulation.
Gamma-Glutamyl Transpeptidase (GGT): A cholestatic enzyme produced in
the bile ducts. GGT is involved in glutathione metabolism and the transport of
amino acids and peptides. Used as a marker of hepatic strain.
Globulin: A blood protein similar to albumin. Globulin is responsible for
transporting certain hormones, lipids, metals, and antibodies. Levels may be
elevated in many conditions including chronic infections, liver disease, arthritis,
cancer, or lupus. Lower levels may be found with a number of conditions
including suppressed immune system, malnutrition, malabsorption, and liver or
kidney disease.
Glucose (fasting): Glucose is the product of carbohydrate metabolism and the
primary source of energy for most cells in the body. Fasting glucose levels are
elevated in a number of conditions including diabetes, liver disease, metabolic
syndrome, pancreatitis, dieting, and stress. Low fasted glucose levels may
indicate liver disease, overproduction of insulin, hypothyroidism, or other
diseases.
Hematocrit: A measure of the percentage of red cells in the blood. Low levels
indicate an anemic condition. High levels may indicate a number of things
including dehydration, increased red cell breakdown in the spleen,
cardiovascular disease, or respiratory disease. Anabolic steroids may also
increase hematocrit.
Hemoglobin: A constituent of red blood cells, and the main carrier of oxygen
and carbon dioxide in the blood. Levels may be suppressed with a number of
conditions including malnutrition, malabsorption, and anemia. High levels may
indicate many things including dehydration, cardiovascular disease, or
respiratory disease. Anabolic steroids may also increase hemoglobin levels.
Homocysteine: A compound formed from the metabolism of the amino acid
methionine. Involved in blood clotting and LDL cholesterol oxidation. Elevated
levels of homocysteine indicate an increased risk of cardiovascular disease and
stroke.
Iron: Mineral necessary for many functions including the formation of
hemoglobin and certain proteins, and the transport of oxygen. Elevated levels
may be caused by many conditions including certain forms of anemia, liver
damage, hepatitis, iron poisoning, or vitamin B6 or B12 deficiency. Low levels
can indicate a number of things including gastrointestinal blood loss, heavy
menstrual bleeding, iron malabsorption, or dietary iron deficiency.
Lactic Acid Dehydrogenase (LDH): An intracellular enzyme found in many
tissues including the kidney, heart, skeletal muscle, brain, liver, and lungs. Used
as a marker of tissue damage. High levels are found in many conditions
including heart attack, anemia, low blood pressure, stroke, liver disease, muscle
injury, muscular dystrophy, and pancreatitis.
Luteinizing Hormone (LH): A pituitary hormone responsible for the
stimulation of testosterone production in the testes (men). LH primarily supports
ovulation in women.
Lymphocytes: A type of white blood cell. Primary role is to fight viral
infection. Levels are elevated with active infection. Low levels are associated
with suppressed immune system or active bacterial infection (noted by elevated
neutrophils).
Mean Corpuscular Volume (MCV): A measure of the size of red blood cells,
determined by measuring the volume of a single red blood cell. Useful in
determining the cause of anemia. Elevated levels may reflect a number of things
including a deficiency of vitamin B6 or folic acid. Low levels may reflect iron
deficiency, or other causes.
Mean Corpuscular Hemoglobin (MCH): A measure of the average weight of
the hemoglobin in red blood cells. Useful in determining the cause of anemia.
Mean Corpuscular Hemoglobin Concentration (MCHC): A measure of the
average concentration of hemoglobin in red blood cells. Useful in evaluating the
cause of, and therapy for, anemia. Low levels may indicate blood loss, B6 or
iron deficiency, or other causes.
Monocytes: A type of white blood cell. Primary role is to fight severe infection
not sufficiently countered by lymphocytes and neutrophils. Levels can be
elevated with a number of things including chronic infection and certain cancers.
Low levels indicate good health.
Neutrophils: A type of white blood cell, also known as granulocytes. The
primary white cell used by the body to fight bacterial infection. Levels are
elevated with infection. May be suppressed with compromised immune system
or bone marrow.
Phosphorous: An abundant electrolyte involved in a number of body functions
including the utilization of carbohydrates, fats, and proteins for cellular
maintenance, repair, and growth, the production ATP for the storage of cellular
energy, the transport of calcium, the maintenance of osmotic pressure, and the
maintenance of heartbeat regularity.
Platelet Count: A measure of the concentration of platelets (also known as
thrombocytes) in the blood. Platelets are involved in blood clotting, and protect
against excessive bleeding. Elevated levels may be linked with a number of
things including dehydration. Low levels are found in suppressed immune
system functioning, drug reactions, or deficiencies of vitamin B12 or folic acid,
or may have other causes.
Potassium: A key electrolyte necessary for nerve and muscle function, and the
transport of nutrients and waste products in and out of cells. Along with sodium
it helps maintain the acid-base balance and osmotic pressure. High levels may be
caused by a number of things including kidney failure, metabolic or respiratory
acidosis, and red blood cell destruction.
Prolactin: A reproductive hormone involved specifically in lactation. Prolactin
is sometimes (but not commonly) elevated in steroid abusers, and may be linked
to estrogen excess or hormone imbalance. Elevated prolactin may also indicate
other issues with the pituitary.
Prostate-specific antigen (PSA): A protein found in prostate cells. Used as a
screening for prostate cancer risk. Elevated levels reflect an increased risk of
developing prostate cancer. Low levels are desirable, although do not assure
against prostate cancer.
Red Blood Cell Count: A measure of the total concentration of red blood cells,
responsible for transporting oxygen and carbon dioxide in the body. High red
cell counts are seen with a number of conditions including heart disease,
dehydration, or pulmonary fibrosis. Low levels may be linked to many things
including anemia, bone marrow failure, red blood cell destruction, bleeding,
leukemia, and malnutrition.
Red Cell Distribution Width (RDW): A measure of the variation in size
between red blood cells. Useful in evaluating the cause of, and therapy for,
anemia. Increased values may indicate a number of things including vitamin
B12, folic acid, or iron deficiency.
Sodium: An abundant electrolyte necessary for many functions including the
maintenance of osmotic pressure, acid-base balance, and nerve impulse activity.
Disturbances in the sodium level may be caused by minor things including
excessive sweating, vomiting, diarrhea, water intake, or very serious conditions
including heart, kidney, or liver disease.
T3 Uptake: This test measures the level of unsaturated thyroxine binding
globulin (a carrier of thyroid hormones) in the blood. Increased levels may
indicate a number of things including hyperthyroidism (overactive thyroid), liver
disease, cancer, and decreased lung function. Low levels may be indicative of
hypothyroidism (under active thyroid), excess estrogen levels, pregnancy, or
other causes.
Testosterone, Total: The measure of both unbound (active) and bound
(inactive) portions of testosterone in the blood.
Testosterone, Free: The measure of free (unbound) testosterone in the blood.
This represents the total amount of testosterone immediately available to tissues.
Thyroid-Stimulating Hormone (TSH): A pituitary hormone responsible for
stimulating the release of thyroid hormones.
Thyroxine (T4): The more abundant of the two major thyroid hormones (T3 and
T4). T4 serves mainly as a reservoir for the more active thyroid hormone (T3),
which helps to stabilize and regulate thyroid supply. This is a key marker of the
state of thyroid health (low, normal, or overactive).
Thyroxine, Free Index: This measure is a calculation of the amount of unbound
(free) T4 in the blood. This is a key marker of the state of thyroid activity (low,
normal, or overactive).
Total Protein: A measure of the total serum protein concentration, mainly
albumin and globulin. Serum proteins are important to the function and supply
of enzymes, hormones, nutrients, and antibodies, and also play a role in
maintaining the water and pH balance. Low levels may indicate a number of
things including malnutrition, liver disease, malabsorption, diarrhea, or severe
burn injury. Elevated levels may indicate infection, liver damage, or other
disease.
Triglycerides: The main storage form of fatty acids in the body. May be
metabolized and used for energy. Elevated triglyceride levels may contribute to
hardening of the arteries (atherosclerosis), and increase the risk of heart disease
or stroke. Low levels are optimal.
Urea: (see Blood Urea Nitrogen)
Uric Acid: The waste product of purine metabolism, which is filtered and
excreted through the kidneys. Elevated levels may indicate a number of things
including gout, infection, kidney damage, and excessive protein intake. Low
levels may indicate kidney damage, malnutrition, liver damage, or other causes.
White Blood Cell Count: A measure of the total concentration of white blood
cells (also known as leukocytes), responsible for fighting infection and
protecting the body from pathogens. A differential measure of white blood cells
is usually also taken including neutrophils, eosinophils, basophils, lymphocytes,
and monocytes. Levels may be elevated with certain infections or allergic
conditions.
Harm Reduction / Safer Use Guidelines
Harm reduction is a concept among healthcare workers that seeks to reduce the
negative health consequences of drug abuse. The principles of harm reduction
call for an acceptance of the fact that, good or bad, illicit drugs exist in today’s
society. Instead of ignoring drug users, harm reduction practitioners actively
work with them to promote safer use strategies and decrease the health damage
of drug abuse. The effort of harm reduction is always helping, not judging, the
individual. Although previously focused exclusively on narcotic drugs of abuse,
harm reduction principles can (and should) also be developed for steroid users, a
group that rarely has the benefit of full physician oversight in its drug programs.
In an effort to further this goal, ANABOLICS has outlined the following
principles of steroid harm reduction. If followed, these principles should
measurably reduce the negative health impact of steroid use, making it a safer
(although not completely safe) practice.
Principles of Anabolic Steroid Harm Reduction
1. Avoid Counterfeit and Underground Steroids. Anabolic steroids produced
by illicit manufacturers are often of low quality, and may present additional
health risks to the user beyond what are presented by the steroids themselves.
Even if they contain actual steroids in properly labeled doses, underground drugs
may contain toxic heavy metals, use dirty raw materials, or even carry bacterial,
viral, and other forms of contamination. Pharmaceutical drug purity is assured to
the public only by an extremely costly, tedious, and methodical process of
quality assurance and government oversight. There is little financial and even
logistical incentive for most underground drug makers to produce their drugs at
such high levels of purity. Counterfeit and underground drugs are not considered
equal substitutes for real pharmaceutical products, and should be avoided.
2. Avoid Toxic Oral Steroids. Aside from Andriol, Primobolan, and Proviron,
every oral steroid discussed in this reference book is a c-17 alpha alkylated
compound and should be avoided whenever possible. While there may be a
number of clinical reasons to prescribe such a drug, when used in the higher
doses necessary for muscle growth these agents tend to have significant negative
impacts on certain health markers.Their most notable effect is to increase the
ratio of LDL (bad) to HDL (good) cholesterol in the body, which favors
increased plaque deposition in the arteries. Over time this may increase the risk
of heart disease. C-17 alpha alkylated steroids are also the drugs exclusively
associated with strong liver stress and (rarely) liver cancer. If injection can be
tolerated, and moderate physique or performance improvement is the goal, all of
the same results can be achieved without oral steroids. Note that injectable forms
of otherwise oral steroids (such as stanozolol and methandrostenolone) should
also be avoided, as they provide a similar level of hepatic and cardiovascular
strain regardless of the differing route of administration.
3. Think of Testosterone First. Of all the anabolic/androgenic steroids
produced, testosterone esters like cypionate, enanthate, and Sustanon tend to
have the lowest negative impact on health when taken in muscle building and
performance-enhancing doses. Testosterone drugs provide a hormone identical
to that already produced in the body, presenting the same spectrum of physical
and physiological effects. In addition to being one of the most efficient musclebuilders available, testosterone generally has a positive (not negative) effect on
libido, supports a positive mood, and supplements necessary estrogen so that
cholesterol levels are less negatively shifted. The exclusive use of testosterone
drugs for body or performance enhancement is advised if possible.
4. Limit Yourself to the “Safest” Drugs. If the exclusive use of an injectable
testosterone is not feasible, limiting use to the safest group of steroids is advised.
Of the injectable class, the following drugs have the lowest cardiovascular strain
and are recommended: Deca-Durabolin (nandrolone decanoate), Durabolin
(nandrolone phenylpropionate), Equipoise (boldenone undecylenate), and
Primobolan Depot (methenolone enanthate). If an oral steroid is desired, only
Andriol, Primobolan, or Proviron should be used. These drugs are not c-17 alpha
alkylated, and can all provide additional steroid activity without the same level
of cardiovascular and hepatic strain seen with other common oral steroids
including Anadrol (oxymetholone), Anavar (oxandrolone), Dianabol
(methandrostenolone), and Winstrol (stanozolol).
5. Use Health Support Supplements. Anabolic/androgenic steroid users can
help lower the negative health impact of steroid use with the consumption of
natural health support supplements. To begin with, the negative cardiovascular
effects of these drugs can be offset (at least to some degree) with cholesterol
supplements. Fish oil is recommended as a base, which should be stacked with a
number of other clinically studied cholesterol support ingredients including
green tea, garlic powder, resveratrol, phytosterols, niacin, and policosinol. The
blended product Lipid Stabil (Molecular Nutrition) includes these ingredients
and is recommended. Cholesterol support supplements should be taken at all
times during anabolic steroid therapy. Next, those taking oral steroids should be
reducing liver strain with a liver support supplement. Recommended products
include Liver Stabil (Molecular Nutrition), Liv-52 (Himalaya Drug Company),
and Essentiale Forte (Aventis). One of these products should be taken at all
times during therapy with hepatotoxic agents
6. Always Cycle Steroids. A steroid cycle usually consists of 6 to 12 weeks of
drug use followed by an equal period of time or more abstaining from all
anabolic/androgenic steroids. This practice is advised for a number of reasons.
For one, as you supplement male steroid hormones your body will reduce the
production of its own testosterone. Cycling helps reduce the risk of developing
long-term fertility and hormonal issues, which are sometimes caused by the
uninterrupted use of steroids for many months or years. Cycling also lets your
general markers of health (such as cholesterol levels, hematocrit, and blood
pressure) return to their normal state periodically, reducing the impact temporary
changes may have over time. Those individuals who use anabolic/androgenic
steroids for long periods of time without interruption run a greater risk that these
negative changes in health markers will result in long-term health issues.
7. Use Reasonable Dosages. High doses of steroids are not necessary to achieve
significant muscle growth, especially if moderate physique or performance
enhancement is desired. A dosage limit of 400 mg per week on injectables is
advised. In the case of testosterone cypionate, 400 mg per week equates to at
least 4 to 5 times the level of hormone naturally produced in a healthy male
body. This level of use will produce dramatic muscle gain if combined with
proper training and diet. In fact, during the 1970s and 80s the dosage range of
200-400 mg per week was considered “standard” for the bodybuilding use of
testosterone, nandrolone, boldenone, or methenolone. There is actually little real
need for extreme doses of 750-1,000 mg or more of steroid per week, or to
supplement an injectable base with additional orals. High doses may produce a
faster rate of gain, but are generally not cost effective for the extra muscle they
provide. Additionally, high doses of steroids greatly increase cardiovascular
strain and the incidence of other side effects.
8. Avoid Aromatase Inhibitors. Aromatase-inhibiting drugs counter estrogenic
side effects by preventing the production of estrogen in the body. While an
effective practice, they also deprive the body of a hormone that is important to
cardiovascular health. In particular, estrogen supports the production of good
(HDL) cholesterol, which means that aromatase inhibitors may inadvertently
increase the cardiovascular strain of a steroid cycle. If estrogenic side effects are
apparent and a reduction or elimination of the offending steroid(s) is not
considered an option, the SERM (Selective Estrogen Receptor Modulator) drug
Nolvadex could be used instead. This drug offers partial estrogenic action in the
liver, which may allow it to counter estrogenic side effects without the same
negative shift in cholesterol.
9. Get Regular Blood Tests. Comprehensive blood testing including an
examination of hormones, cholesterol, blood cell concentrations, and enzymes is
the most useful tool for assessing the negative health impact of steroid use.
Changes in cholesterol, for example, can help quantify for the user what effect a
particular drug regimen is having on their cardiovascular health. The individual
then has the opportunity to better assess long-term risk if this cycle is to be
repeated. At a minimum, blood testing should be conducted before a cycle is
initiated, 3 to 4 weeks into a cycle, and a couple of months after a cycle. This
allows for 1) a baseline for later comparison; 2) a snapshot of the on-cycle health
impact; and 3) an opportunity to assess if natural homeostasis has been restored
post-cycle.
10. Use Proper Injection Procedures. Careful attention to correct injection
procedures can help eliminate some of the complications associated with
nonmedical steroid use. Steroids are given via deep intramuscular injections. The
most common site of application is the upper outer quadrant of the gluteus
muscle, although the drugs are also commonly injected to the upper outer thigh
and shoulder. Site injections (in smaller muscle groups like the biceps, triceps, or
calf muscles) for cosmetic purposes are discouraged, as they are technically
more difficult to navigate and more prone to complications. Comfortable
injection volumes should also be used, generally no more than 3 mL per
application. Each injection site should be rotated so that the same muscle is not
injected more than once every two weeks. A general focus should be made on
cleanliness, including the use of alcohol pads on the vials and skin before
injection, and the proper disposal of all needles and empty vials/ampules after
use.
11. Sterilize. Though never advised, should the choice be made to use an
injectable steroid of underground origin, an effort should be made to sterilize the
solution before use. This will reduce the likelihood of illness or infection due to
microorganism.
12. Watch Your Diet. Anabolic/androgenic steroids can allow an individual
significantly more latitude with their diet than normal. The caloric demand
typically increases due to the effects of these drugs on muscle mass and
metabolism, allowing more calories to be consumed each day without adding fat
mass. It is important not to let this latitude affect your health in a negative way.
Remember, the use of steroids at physique-and performance-enhancing doses is
expected to cause an unfavorable shift in cholesterol levels and other
cardiovascular health markers, favoring a higher risk of cardiovascular disease.
Simultaneously feeding your body greater amounts of saturated fats, cholesterol,
and simple carbohydrates can make the impact of these drugs even worse. Diets
low in saturated fats, cholesterol, and simple sugars are recommended, and are
known to reduce cardiovascular disease risk. Note, however, that diet alone is
not effective at countering the negative cardiovascular effects of steroid use, but
dietary restrictions can reduce these risks.
13. Always Consider Reward AND Risk. It can be easy to ignore the potential
health impact of steroid use when the positive benefits are so rapid and the
negative consequences so remote. At the end of the day, however, it is very
important to remember that the use of steroids in doses sufficient to support
short term muscle gain are virtually always going to have some negative impact
on your body. Your cholesterol will shift in an unfavorable direction, your blood
pressure may go up a little bit, and you may ever so slightly thicken the
ventricles in your heart. Your hormones are out of balance when you take
steroids, which will invariably cause other things to go out of balance. Steroid
use is rarely dangerous over a short term period. These hormonal drugs are
acutely very safe. As use continues over the years, however, these short-term
periods accumulate, and total on-cycle time may become very long. Always
remember to consider the risks as well as the rewards of each cycle. Choosing
your drug program carefully and keeping the negative effects of steroid use in
check over the short term is the best way to reduce long term risks.
Sterilizing Injectable AAS
Anabolic steroid products made by licensed drug manufacturers have an
expectation of sterility. This is assured by the rigid government regulations
applied to these companies. Unfortunately, there is no such expectation for
counterfeit and underground steroid products. Most are assembled under
conditions that are not sterile. On many occasions, independent laboratory tests
have found bacterial contamination in products of illicit origin. There also
appears to be a slightly higher prevalence of abscess infection and other
injection-site complications with underground steroids, further underlying cause
for concern. Given this risk, it is often advisable to attempt sterilization before
using an injectable steroid of unknown quality.
Heat Sterilization
The simplest method to clear a steroid solution of microorganisms is to heat
sterilize it. The typical way to accomplish this is to place the steroid vial in an
oven for 30 minutes (bake at 120°C/250°F). You should leave a needle sticking
through the rubber top to equalize the pressure inside the vial, or it may break.
Note that a higher temperature and duration are typically used for complete dry
heat sterilization, but this is not practical for our purposes due to the potential
degradation of vial components, and possibly even the drug components. Still,
the recommended 30 minutes at 120°C/250°F should kill most bacteria, and can
be regarded as a viable harm reduction strategy.
Some people prefer to use the top of the stove for heat sterilization, and
submerge their anabolic steroid vials in a pot of boiling water (100°C/212°F).
The vial is kept in the boiling water for approximately 20-30 minutes. While this
temperature is sufficient for killing many forms of bacteria and other
microorganisms, it is generally not considered the best method of sterilization. A
higher temperature should be used. It can also be difficult to control the
temperature if the vial rests on the bottom of the pot, which is in direct contact
with the burner or heat source. Given these problems, it is preferred to attempt
heat sterilization in an oven, as discussed above.
Note that trenbolone appears to break down at fairly low heating
temperatures.
374
Its degradation increases with temperature and duration. Some
degradation may be notable even at 100°C/212°F. As such, trenbolone products
should be heat sterilized under slightly different conditions than those
recommended above. This typically involves baking the vial in an oven for two
hours at 80°C/175°F. Again, an unattached needle should be placed in the rubber
stopper to equalize pressure.
Syringe Filtration
Another way to attempt sterilization of a steroid solution is to use a filter. A filter
is a device that uses a membrane with tiny holes to prevent particles from
passing through. The smaller the holes are, the more effective the filter. For this
method a disposable syringe filter is used. These are usually found in .45-micron
and .22-micron micropour sizes. The .22-micron filter is preferred, as it allows
for the removal of almost all forms of bacteria. A .45-micron filter is also
acceptable, though more likely to pass certain strains of diminutive bacteria.
Syringe filters can be ordered through many mail-order suppliers, which can be
located through online search engines without much difficulty.
.22 micron Millipore syringe filter
The procedure for using a syringe filter is fairly simple. First, make sure you
have all of the necessary equipment: a syringe, two needles (minimum), a sterile
syringe filter, and a new sealed sterile vial. If you are attempting to sterilize a
standard 10 ml vial, it may be preferable to use a syringe large enough to draw
the full solution. This will reduce the exposure of your product to air. If drawing
more than 3 mL at a time, you will want an extra needle to use for equalizing the
pressure (you should leave it in the rubber while drawing from the vial). Be
careful not to touch critical surfaces (the exposed needle, rubber stopper) while
filtering.
Begin by drawing the steroid solution into the syringe. When you are done,
remove the needle and attach your newly unwrapped syringe filter. Attach a new
needle to the end of the filter, and inject the solution into the new sterile vial.
The sterile vial and new needle are very important, as using the original
components would only expose the product to bacteria again. Use enough
pressure to empty the syringe into the vial. Be careful, as too much pressure can
break the bindings or filter. The process is slow, especially with a larger syringe
or small .22-micron filter. Provided great care was taken not to contaminate the
steroid during the process, the resulting solution should be free of bacteria.
Also, these sterilization methods are applicable to oil-based steroids only. Heat
sterilization (as outlined here) tends to cause the rapid evaporation of
solvents/antimicrobial agents in water-based steroids. The suspended (instead of
dissolved) nature of the particles also makes them likely to jam a syringe filter.
Previous testing suggests there is a high prevalence of bacteria in counterfeit and
underground water-based steroids.
375 Given this, it is generally advised to only
use water-based steroids if they have been dispensed through legitimate supply
channels.
Syringe filtration of steroid solution. Use of new (sterile) vial reduces chance
of recontamination.
Limitations
It is important to emphasize that when applied in an uncontrolled environment
such as a house or apartment, there is always the possibility that you may
inadvertently contaminate your own product when attempting to filter it. You
should always use sterile gloves and clean hard surfaces with alcohol or bleach
before working on them. A mask is also a very good idea. Note also, these
sterilization techniques help only with contamination by microorganisms. They
do nothing to address other potential health concerns such as the presence of
heavy metals or unlisted chemicals/drugs.
Many forms of bacteria also produce endotoxins or pyrogens, which would
remain in solution even after filtration or heat sterilization. Thus, you can notice
fever or other adverse reaction even with no viable bacteria being left in the
solution. An additional issue (though very unlikely) is that certain
microorganisms (including some viruses and bacteria) are either small enough or
hardy enough to remain viable after these sterilization techniques. The safety
methods described here are highly effective, but not necessarily complete. For
the highest level of safety, it is always recommended to limit your use to
legitimate pharmaceutical products.
374. FDA Environmental Assessment Report, Finaplix R (trenbolone acetate). April 1987. Hoechst-Roussel
Agri-Vet Co.
375. Underground ANABOLICS. William Llewellyn, Ronny Tober. © 2010. Published by Molecular
Nutrition, Jupiter, FL 33458.
Counterfeit Steroids
As the name implies, counterfeit steroids are copies of real anabolic/androgenic
steroid products, which are made from illicit producers. These drugs are
intended for sale on the black market, ultimately to consumers who believe they
are buying a legitimate pharmaceutical item from the labeled company. There
are many important issues to consider with the potential use of counterfeit
steroids. For one, these products are made by criminal operations. The contents
of such products, by the very nature of these operations, cannot be verified. In
many cases, the counterfeiters will never even use any active steroid at all, and
will simply sell an expensive and essentially worthless bottle of inert carriers,
fillers, and binders. In other cases, they will substitute lower doses or cheaper
steroids to make their profit margins higher.
Even if a counterfeit does contain the active steroid in question, it may not be a
clean and safe product. Today, we take for granted the fact that our drug
products are made with sterile and pure ingredients. We also give little thought
to aseptic processing techniques, which manufacture our drug products free of
contamination by harmful bacteria, viruses, or microorganisms. This is
especially important with injectable medications, since many of the human
body's normal defenses against infection are bypassed when a drug is introduced
directly into the body. The theoretical risks of injecting a contaminated drug
product are innumerable, and range from simple injection-site infection, to life
threatening allergic reactions or illness. These risks are in addition to other
serious contamination risks that could be present in any drug product, injected or
otherwise. Counterfeiters very rarely produce their steroids with such
sophisticated and expensive materials and techniques.
As anyone that studies the illicit anabolic steroid trade knows, high demand and
huge profits offer strong incentive for the manufacture of counterfeit drugs. Over
the years, this segment of the illegal business has grown exponentially. What
was once a problem largely isolated to the United States can now be found in
literally every corner of the globe. Counterfeiting is a phenomenon not isolated
to anabolic steroids, of course, and is commonly seen when the significant sales
of anything valuable are diverted from legitimate to underground sources. Given
the nature of drug products, however, the counterfeit steroid phenomenon is an
especially important health concern for drug-using bodybuilders. As the number
of these products grows, so too does the number of reports of low or no product
efficacy, or worse, health consequences including abscess, infection,
anaphylaxis, and toxicity caused by heavy metal contamination.
Prevalence Study
By all estimates, counterfeit steroids are very common in all corners of the
global steroid black market. Given the illicit nature in which counterfeit steroid
products are traded, however, it is difficult to determine the exact prevalence of
these drugs. Analysis reports of law enforcement seizures offer an occasional
snapshot of the quality of steroid sales in a particular region. One such study was
conducted at the Center for Preventative Doping Research in Cologne, Germany,
and involved 70 different anabolic steroids and ancillary drug products. All of
the samples analyzed were obtained during police raids of three illegal dealers of
anabolic steroids. It is important to emphasize that while the amount seized is a
fairly large sample for this type of analysis, 70 drug products taken from three
dealers is not sufficient to prove any specific market trend, overall counterfeit
prevalence, or brand legitimacy.
Overall, more than one-third (34%) of the 50 anabolic steroids tested did not
have ingredients that matched their labels, and were clearly made from illicit
manufacturers. Of the failing products, nine were identified as copies of known
pharmaceutical brands, and would be considered classic counterfeits. These
made up 18% of the drug products in inventory by the arrested dealers. The
remaining eight (16%) that failed were underground steroid products, which are
discussed separately in this book. There were six additional products on the list
that passed testing that were made by underground manufacturers (British
Dragon, SB Labs, and International Pharmaceuticals). In total, legitimate drug
companies did not manufacture 46% of the steroid products that were being sold
by these dealers in Germany. The results are probably a good reflection of what
is happening on the European market in general. Given the tighter legal controls
on steroids in the United States, counterfeit and underground products are
expected to make up an even higher percentage of products illegally sold in this
market.
Visual Inspection
The researchers in Cologne Germany also made an important observation. Aside
from known underground products from labs such as British Dragon, SB Labs,
and International Pharmaceuticals, they noted it was not possible to ascertain
what product was real and what was a counterfeit upon visual inspection. While
this group may not have had the experience or reference materials necessary to
make an up-close product examination, and no product photos were provided in
the report to reference, it does underline a problem that the steroid using
community has been noticing for a long time, namely counterfeit manufacturing
operations are becoming increasingly sophisticated. Now more than ever it can
be difficult for someone shopping on the black market to determine product
legitimacy before making a purchase and actually consuming the product(s).
The “Best” Products
Of the confiscated German products, those that were manufactured in Western
Europe seemed to offer greater assurance of legitimacy than those of other
regions. Thailand also remains a common source country for legitimate products
not commonly manufactured in Western Europe including oxymetholone and
methandrostenolone. This is in great contradiction to the United States, where
regional products (U.S. and Canada) are those most likely to be the subject of
counterfeiting. Also, the study showed that the less costly testosterone products
were most likely to be legitimate, even if they originated outside of Europe. It
appears that, at least by way of these three dealers, a good deal of legitimate
Karachi Sustanon and Egyptian testosterone enanthate are being imported into
Germany. It is of note that the one failure of CID enanthate was due to the
inclusion of some testosterone cypionate in addition to the labeled enanthate. It
is unknown if this was an error that occurred at the manufacturing plant, or the
product was the subject of counterfeiting.
The “Worst” Products
Perhaps due to high recognition and demand, all of the Normal Hellas
nandrolone decanoate products tested during this analysis run were determined
to be counterfeit. These products were confiscated from each of the three dealers
independently. In all cases, these steroid products contained testosterone instead
of nandrolone decanoate. This is a common substitution with deviant nandrolone
products, as low doses of testosterone can provide a similar level of anabolic
effect as nandrolone for some users, with a similar low incidence of side effects.
Testosterone is also much less expensive to manufacture in comparison to
nandrolone decanoate. The hope is that many users will not be able to identify
testosterone as the content. Norma Hellas Deca, therefore, remains a product of
extremely high risk on the European and international markets. Great care
should be taken to examine any product closely for the required security features
shown in this book.
Other Bodybuilding “Ancillary” Drugs
A total of 20 non-steroid drugs were also tested. All products that would be
defined as common ancillary drugs including tamoxifen citrate (Nolvadex),
clomiphene citrate (Clomid), thyroid hormone, caffeine, and yohimbine hcl
turned out to be legitimate. This underlines the lower risk in these ancillary drug
items, no doubt due to the lower financial incentive for counterfeiters to
duplicate these cheap and easy to access pharmaceuticals. The only non-steroid
drugs where there was some substitution noted were in the male sexual
performance category, which constitute drugs such as Viagra and Cialis. In most
of the individual cases the drugs did test out as labeled. When they did fail
testing, however, it was usually for the substitution of active ingredients of the
same drug family. Male sexual performance products are known to be an active
area of counterfeiting, so care should be taken when purchasing these products
from illicit channels as well.
Steroid Analysis Results
Anadrol (oxymetholone):
1. Oxytone 50 mg (SB Labs, Thailand)
Result: PASS
2. Oxytone 50 mg (SB Labs, Thailand)
Result: PASS
3. Oxytone 50 mg (SB Labs, Thailand)
Result: PASS
Deca (nandrolone decanoate):
1. Norma Hellas (100 mg/mL)
Result:FAIL (testosterone)
2. Norma Hellas (100 mg/mL)
Result: FAIL (testosterone)
3.Norma Hellas (100 mg/mL)
Result: FAIL (testosterone)
4. Norma Hellas (100 mg/mL)
Result: FAIL (testosterone)
5. Decabol 250 (British Dragon, Underground)
Result:FAIL (testosterone)
Dianabol (methandrostenolone):
1. Anabol 5 mg (British Dispensary, Thailand)
Result: FAIL (methyltestosterone)
2. Anabol 5 mg (British Dispensary, Thailand)
Result: PASS
3. Anabol 5 mg (British Dispensary, Thailand)
Result: PASS
4. Danabol DS 10 mg (March, Thailand)
Result: PASS
5. Danabol DS 10 mg (March, Thailand)
Result: PASS
6. Naposim 5 mg (Terapia, Romania)
Result: FAIL (methyltestosterone)
Equipoise (boldenone undecylenate):
1. Boldabol 200 (British Dragon, Underground)
Result: PASS
Halotestin (fluoxymesterone):
1. Fluoxymesterone (IP, Underground)
Result: PASS
Primobolan (methenolone enanthate):
1. Primobol 100 (British Dragon, Underground)
Result: FAIL (nandrolone, testosterone)
Proviron (mesterolone):
1.Proviron 25 mg
Result: PASS
Sustanon 250 (testosterone mix):
1. Sustanon 250 (Karachi, Pakistan)
Result: PASS
2. Sustanon 250 (Nile, Egypt)
Result: FAIL (different testosterones)
3. Sustanon 250 (Nile, Egypt)
Result: FAIL (different testosterones)
4.Sustanon 250 (Karachi, Pakistan)
Result: PASS
5. Sustanon 250 (Karachi, Pakistan)
Result: PASS
6. Sustanon 250 (Karachi, Pakistan) Result: PASS
7. Sustanon 250 (Karachi, Pakistan)
Result: PASS
8. Sustanon 250 (Karachi, Pakistan)
Result: PASS
9. Sustanon 250 (Karachi, Pakistan)
Result: PASS
Testosterone Cypionate:
1. Testex Prolongatum 125 (Q Pharma, Spain)
Result: PASS
2. Testabol 200 (British Dragon, Underground)
Result: FAIL (different testosterones)
Testosterone Enanthate:
1. Testofort 250 mg/mL (Pliva, Pakistan)
Result: PASS
2. Testosterone Depot 250 (Eifelfango, Germany)
Result: PASS
3. Testosterone Depot 250 (Eifelfango, Germany)
Result: PASS
4. Testoviron Depot 250 (Medipharm, Pakistan)
Result: PASS
5. Testoviron Depot 250 (Medipharm, Pakistan)
Result: PASS
6. Cidoteston 250 (CID, Egypt)
Result: FAIL (includes T. cypionate)
7. Cidoteston 250 (CID, Egypt)
Result: PASS
Testosterone Propionate:
1. Testovis 100 mg/mL (SIT, Italy)
Result: PASS
2.Testovis 100 mg/mL (SIT, Italy)
Result: PASS
3. Testovis 100 mg/mL (SIT, Italy)
Result: PASS
4. Testovis 100 mg/mL (SIT, Italy)
Result: PASS
5. Testovis 100 mg/mL (SIT, Italy)
Result: PASS
6. Testabol (British Dragon, Underground)
Result: FAIL (different testosterones)
Trenbolone (various esters):
1. Trenabol 75 (British Dragon, Underground)
Result: FAIL (boldenone, testosterone)
2. Trenabol 100 (British Dragon, Underground)
Result: FAIL (boldenone, testosterone)
3. Tri-Trenabol 150 (British Dragon, Underground)
Result: FAIL (trenbolone, testosterone)
4. Trenabol 200 (British Dragon, Underground)
Result: FAIL (trenbolone, testosterone)
Winstrol (stanozolol):
1. Winstrol Depot 50 mg/mL (Zambon, Spain)
Result: PASS
2. Winstrol Depot 50 mg/mL (Zambon, Spain)
Result: PASS
3. Winstrol Depot 50 mg/mL (Zambon, Spain)
Result: PASS
4. Stanabol 50 (British Dragon, Underground)
Result: PASS
Counterfeit Steroid Identification
This section pertains to methods for differentiating between legitimate
pharmaceutical products and illegitimate copies (counterfeits). Before we begin,
I need to remind you that counterfeiting anabolic steroids is a very lucrative
business these days. Counterfeiters are investing a lot of money in printing and
packaging equipment so that you’ll have a hard time picking out their products.
Furthermore, there are now many large “commercial scale” counterfeiting
operations, with the capacity to manufacture all product formats including
ampules, logo imprinted pills, and push-through tablet strips. Given this high
level of sophistication, steroids purchased on the black market need to be
inspected with great care. The mistakes made by counterfeiters are often minor,
and noticed in the fine (not obvious) detail.
Step #1: Eliminate the Obvious
When counterfeit steroids first appeared decades ago, they were often very easy
to spot. The manufacturers operated on a small scale, and made small-scale
mistakes. For example, the printing might be sloppy, or the containers thin and
flimsy. They might have lacked the equipment to put the product in a box, or
even affix an expiration date and lot number to it. No legitimate pharmaceutical
would be sold like this. Much has changed over the years, however. Few
counterfeiters still make the basic mistakes that were once common. Don’t
expect identifying these products to be easy. Still, that is not to say that obvious
counterfeits aren’t available. Indeed, they can be found on the black market from
time to time. This first set of instructions, therefore, seeks to eliminate only the
most obvious fakes. For the rest, we will need a more detailed analysis.
1. Sloppy Printing. Drug manufacturing is not a small scale endeavor. Sizable
pharmaceutical companies control the global drug trade, and make products that
are typically very professional in appearance. You should not expect to see
things like runny inks, sloppy lines, or misaligned images on real drug
packaging. Sometimes counterfeiters still use cheap (small-scale) printing and
reproduction methods, which make labels and boxes that stand out as sloppy.
Don’t ever use a product if it just doesn't “look right” to you. You are probably
subconsciously picking up on minor deviations.
2. Cheap Packaging. Virtually all legitimate steroid products come in boxes.
Inside the box you should find a drug information sheet. Some counterfeiters
will skip these steps entirely. Real ampules, vials, and tablets are sometimes
smuggled loose, but let someone else take the risk. The box for a pharmaceutical
product should be structurally sound, closing tightly and evenly. Some
counterfeiters seal their own boxes by hand, and they may be uneven or poorly
glued. Real boxes should be printed (ink directly on cardboard). Some
counterfeiters cover plain white boxes with stickers. If the vial, ampule, or bottle
has a label, machines should have put it on straight. Counterfeiters often apply
labels by hand, so many will be crooked. Some counterfeiters use ampules, but
blank laboratory samples. These are filled by hand and sealed over a flame. They
are a bit larger than the average ampule, and somewhat unusual in appearance. A
good rule of thumb is to avoid any steroid that does not come in a professional
looking package.
The ampule is a laboratory blank, meant to be sealed by hand over a flame.
It is larger and more unusual in appearance than most traditional ampules.
3. Multi-dose Containers. In the United States, we are used to our injectable
medications coming in multi-dose vials (these have a rubber top to let needles
pass through more than once), and our pills loose in bottles. Most other
countries, however, do not allow this type of packaging for human medicines.
They consider it unsterile, and permit it only for animal drugs. Instead, they
require each dosage unit to be separate. This usually means break open glass
ampules for injectable medications, and push through blisters for pills and
capsules. Since you are unlikely to find real American products on the black
market, it may be best to avoid all multi-dose containers when it comes to
human pharmaceuticals. Most are going to be counterfeit. When you find
veterinary drugs in multi-dose containers, extra care should be taken to examine
them closely, since these products are more easily counterfeited.
The above is a crude copy of an American testosterone product, which uses
the same label on the box and vial. A counterfeit as simple as this is rare to
find today.
Another example of an obvious counterfeit. This box is crude in design and
uses a brand name that has been off the market since the 1980s.
The photographs below show what it looks like when the lot number and
expiration date are added after the initial box/label printing, as well as
counterfeit products without this feature. The characters on a real pharmaceutical
product should stand out from the rest of the printing, which will consist of tiny
dots blended together to create a solid image (see Step #3 for more information
on the ink). When the lot/expiration information is added with a mechanical
stamp, the ink will be much more solid under magnification (note that it may
appear blotchy under deep magnification). Depending on the equipment, it may
also have left a physical indent you can feel when rubbing your thumb over the
information. When the dates were added by computer, we usually see large dots
that are visible to the naked eye. Be careful to look at the characters closely.
Counterfeiters will try to make the information look like it was added by
machine or computer, even though it was printed. If you see that tiny dots make
up the characters under 200X magnification, it is not legitimate stamp or
computer printing.
Normal
20X
200X
Example #1. A real box of Proviron. Under magnification we can see that
the lot number and expiration date were stamped on mechanically.
Step #2: Examine Lot Number/Expiration
A more formal analysis should always begin with the lot number/expiration date.
Pharmaceutical companies have their boxes and labels manufactured in bulk,
Pharmaceutical companies have their boxes and labels manufactured in bulk,
usually at an offsite printing facility. They are not serialized; lot
numbers/expiration dates have not yet been applied to them. This information is
added with a mechanical stamping machine or computer/inkjet printer at the
time the drug is packaged. Counterfeiters often don’t wait, and simply print the
lot number/expiration date with the rest of the boxes and labels. This means less
work, less equipment, and less cost. Knowing this, examining the lot
number/expiration date information can be a good way to spot counterfeits. You
need to look at the lot/date information very closely, preferably with a handheld
microscope with 100-200X magnification.
20X
200X
Example #2. Another example of mechanical stamping of the lot number
and expiration date.
Normal
20X
200X
Example #3. Real testosterone cypionate from Watson (U.S.) The above
lot/expiration date were added by computer printer. Under magnification
we see the large dots are solid ink.
Normal
20X
200X
Example #4. Another real product (Proviron) with information applied
post-printing with a computer printer.
Normal
20X
200X
Example #5. (Counterfeit). At first glance the slight run on the ink appears
to be the result of mechanical stamping. Under magnification, however, we
see this is simulated.
Normal
20X
200X
Example #6. (Counterfeit). An example of simulated computer lettering.
You can see under magnification that the information was actually made by
normal process printing, along with the rest of the box.
Normal
20X
200X
Example #7. (Counterfeit). Again, the date was added with the rest of the
printing. This manufacturer simply made the text bold in an effort to hide
the printed nature of the information.
Step #3: Look at the Ink
One of the first things that the U.S. Secret Service does when it takes in a
counterfeit bank note is to examine the inks used by the counterfeiters. They
learned long ago that you can tell a great deal about a bill this way. You can tell
how and when it was printed, sometimes even where. Now we are not going to
analyze the inks on steroid boxes in the lab as the Secret Service does. We will,
however, look at the printing closely enough that it can help differentiate real
from fake in some cases. Once again, this will be done with a handheld
microscope, preferably at 200X magnification.
First, let’s go over some general information so you know what we are looking
at. For this examination we intend to find out how the printing was placed on the
box or label. Color printing is usually accomplished through two methods. The
first is called “process color,” and the second “spot color.” One method may be
used to print the product, or both methods may be combined on the same
packaging. Each method offers its own set of advantages. When we know how
and when these methods are typically applied, we can gain some insight into the
thoughts of the designer. More importantly, we might be able to tell if the
methods are appropriate for the product in question.
The process color method is most often used to reproduce photographs, or to
print multiple colors (three or more) on one piece. It is the more flexible and
visually deep method of coloring. Process color can give the appearance of
hundreds, thousands, even millions of colors at one time, although technically
hundreds, thousands, even millions of colors at one time, although technically
this is an illusion. Upon microscopic examination, you will see that the colors all
break down into a mix of only four separate inks: cyan, magenta, yellow, and
black (CMYK). The four CMYK colors are applied in tiny dots, which are
assembled in different patterns. They blend together to the naked eye, giving the
appearance of more colors.
The spot color method is used when a very specific color ink is required. Instead
of using a CMYK blend to reproduce a certain shade of green, for example, an
ink is mixed in to provide the exact green color that is needed. If you look at spot
color under 200X magnification, you will not see CMYK color dots. Small dots
are still used, but they are all the same color (they are placed closer or further
apart for shading). Note that it can be very hard to notice these dots in areas with
solid fill. The major advantage to spot color is consistency. A detailed color
matching system assures the desired color is exactly what is applied to the
printed packaging every time. You will usually find big companies using spot
color, especially with important corporate identifiers (logos, repeat images,
trademarks).
The main thing we are hoping to see under magnification is the use of some spot
color. While the lack of spot color does not necessarily mean that a product is
counterfeit, you should expect to see it on most real pharmaceutical packaging
samples. If the package has only two or three colors, they will probably use spot
color exclusively. If the packaging has more than three colors, they may use a
foundation of process color, but add spot color to certain key elements. Spot
color usually signifies some attention to detail, which sometimes the
counterfeiters miss.
Normal
20X
200X
Example #1. This box of Depo-Testosterone was printed entirely with spot
color. Large companies like Pfizer tend to prefer this method of
printing.Note the unified dots under 200X magnification, indicating spot
color.
Normal
20X
200X
Example #2. The above underground steroid product uses process color.
The small CMYK dots that blend the color can be seen well under 200X
magnification.
Step #4: Magnify Logos/Small Elements
Each counterfeiter is faced with the dilemma of duplicating an original steroid’s
packaging on their own equipment. The most common way to do this is to copy
the flattened box or label with a desktop scanner. The picture will be cleaned up
in a computer, and ultimately converted into plates for printing. In this process,
the drug packaging is duplicated in what amounts to a complicated form of
photocopying. Though a seemingly simple process, drug packaging made in this
manner can be surprisingly accurate in appearance. Some are done so well, in
fact, that you’d be hard pressed to pick out the legitimate box from the duplicate
without a little guidance first.
This type of counterfeiting does have its limitations though. Most notable is that
very fine detail is usually lost in the reproduced image. Much of this is due to the
scanned in image being pixilated, and thus not amenable to scaling and graphic
manipulation in the same way the original graphic would be. When examined
under magnification, the lines may appear choppy. Make sure you look at the
small graphic elements of the steroid package, not the text. Counterfeiters
usually rewrite the text so it is sharp. They cannot retype a company logo,
illustration, or image. If these graphic elements look “sloppy” under the
microscope, the product is probably a counterfeit.
Normal
20X
200X
Example #1. Real Cidoteston from CID Egypt.
Normal
20X
200X
Example #2 (Counterfeit) Cidoteston. Under magnification we notice that
the scan of the initial box was insufficient to reproduce the fine detail. The
inner ribbon around the logo is especially broken, and the letters “CID”
poorly defined.
Normal
20X
200X
Example #3. Real Sustanon from Egypt. Notice the fine detail on the snake.
Normal
20X
200X
Example #4 (Counterfeit) Sustanon. Notice how the finer details are lost on
the duplicate.
Normal
20X
200X
Example #5. Real Deca-Pronabol from P/B/L, India. Notice how the logo
remains smooth under magnification.
Normal
20X
200X
Example #6 (Counterfeit) Deca-Pronabol from P/B/L. Notice how the logo is
choppy under magnification, likely due to the image being scanned from an
original box.
Passing Inspection
It is important to once again emphasize that steroid counterfeiting is big
business. An efficient operation can net many millions of dollars per year for its
owners. With so much money at stake, sophistication is at an all time high. In
some cases, the counterfeiters will have very similar high-level capabilities to
the pharmaceutical companies they are copying. This means not only the ability
to reproduce complicated packaging such as break-open glass ampules and pushthrough tablet strips, but also fine details like lot number/expiration date
stamping, tablet ID markings, holographic security stickers, and even Braille
lettering. While the above counterfeit detection methods are among the most
detailed available, know that some counterfeits may still slip through undetected.
Therefore, care should always be taken to not only examine products very
closely, but also to try and maintain reliable sources for legitimate
pharmaceuticals.
Country Specifics
In most countries, a pharmaceutical company is required to meet a specific set of
regulations pertaining to the physical packaging of a pharmaceutical product. In
some cases these regulations can be used to help evaluate the legitimacy of black
market steroids, as all counterfeiters may not have the resources or forethought
to implement the required features. Here, we discuss a number of attributes to
examine, which should hold true for all of the drugs produced in the specified
country.
United States:
First, it is very important to stress the fact that steroids are a controlled substance
in the United States. Current controls are very effective at keeping American
products off of the black market. It is much easier for the illicit dealers to import
or manufacture their own products than it is to get any volume of legitimate
American pharmaceuticals to distribute. Be leery of American items you
encounter on the black market, as they are in all probability counterfeits. The
best rule is to avoid all American items unless you can personally trace them
back to a pharmacy.
The FDA provides us with a couple of strict requirements, which many
counterfeiters overlook. The most predominant is that all legitimate American
drugs cannot carry a label that will easily be removed from the vial/bottle. It
must be so saturated with glue that you can only remove it in small pieces. This
is done to protect the public from the possibility of drug mislabeling. With many
U.S. counterfeits, the label can be peeled off the bottle quickly, in one or a few
large pieces.
You should also moisten your thumb and rub the expiration date on the box and
label. Quite often the ink on the counterfeit will smear and rub off easily. The
stamping on a real U.S. pharmaceutical may streak slightly, but should remain
intact and legible. Again, this is a requirement to protect consumers.
Additionally, being a Schedule III controlled substance, all commercially
available human and veterinary anabolic/androgenic steroids are required to bear
the tag “CIII” (see sample picture). The only exceptions would be cattle implant
pellets, which are technically not controlled substances, or drugs from
compounding pharmacies, which do not have to adhere to the same production
guidelines. A small number of lazy counterfeiters continue to duplicate steroids
that were manufactured before 1991, when this tag was not present.
The FDA requires that all tablets and capsules are identifiable through unique
markings in case they are removed from the packaging. The manufacturer name,
or an abbreviation, is usually found on each pill, along with a specific code for
the product. Some steroid users have found the Poison Control Center to be a
very useful resource in verifying these markings. The Poison Control Center has
a full database of pill identification markings at their disposal, and should be
able to tell you the drug and dosage based on them. The offices are usually very
responsive if you explain it is not an emergency call. If your pill is not found in
their database, it should be considered a fake product.
Italy:
All drugs produced in Italy will bear the pictured drug identification sticker. The
sticker itself is white, with red and black print. The sticker rests on a laminated
surface, so that it can be peeled off and affixed to paperwork. You should never
purchase an Italian drug if this sticker is not present. Drugs from Italy will also
use abbreviations like Prep, Scad, and Del for the counterpart of lot #,
manufacture, and expiration dates. English writing here would indicate
counterfeiting.
Greece:
Greece also has a drug ID sticker that must be present on all drugs available for
sale. The sticker itself rests on a laminated surface, so that it can be peeled off of
the box and affixed to paperwork when a prescription is filled. Most importantly,
the sticker will show a hidden mark when placed under UV light. Some
counterfeiters have copied these stickers with excellent accuracy, right down to
the laminated surface. Copies of the sticker bearing a hidden UV watermark,
however, have not been located. Do not purchase any Greek drug without the
proper sticker attached.
Spain:
Spanish drugs do not bear a sticker, but instead have an area located on the box
that contains a bar code and some drug information. This area will sometimes
have indentations in the cardboard, so as to be removable if you tear the surface.
At other times, the barcode is simply printed on the box. Spanish drugs also use
the abbreviations Lote and Cad for lot number and expiration, respectively. date.
Many drug boxes also carry Braille lettering.
Printed Only
Removable Barcode
Braille Lettering
Portugal:
Drug boxes from Portugal contain a rectangular area which displays the bar code
and pricing information. This is sometimes found as a sticker, but most
commonly it is printed, not stamped, onto the surface. In many cases, the area is
indented, so that it can be removed from the box. Drugs from Portugal will also
use the abbreviations Lote: and Val. Ate: for lot number and expiration date
stampings.
Old one without
New area with price in Euros
France:
Drugs from France will bear a rectangular sticker somewhere on the surface of
the box. The text and format is often slightly different item to item. Also,
packaging always contains an area with a green and red box. In the sample
below, it is in the lower left side of the box.
Underground Steroids
An underground steroid is an anabolic/androgenic steroid product that was made
by an illegal (underground) laboratory. These drugs are specifically
manufactured for sale to athletes and bodybuilders on the black market, and are
not available through legitimate channels such as pharmacies and drug
distributors. These companies are unlicensed, unregulated, and operate in a
completely clandestine manner. At one time the term underground steroid was
considered synonymous with counterfeit steroid, but today many people view
these two categories as separate. The main point of distinction between an
underground steroid and a counterfeit steroid is that the latter is a copy of a
legitimate pharmaceutical product, which was made in an effort to deceive the
consumer. Underground steroid manufacturers, on the other hand, use distinct
brand names that are not to be confused with registered drug companies. They
often try to build recognition in the marketplace for their products, and
commonly use real steroid ingredients in substantial dosages.
Tighter government enforcement of steroid laws and legitimate distribution
channels has fueled an explosion of underground steroid manufacturing
operations over the past decade. The business model is now fairly common, and
may account for more than 50% of all anabolic/androgenic steroids illegally sold
in the United States. The manufacturing process typically involves the sourcing
of raw steroid materials from countries where strict regulations concerning the
manufacture and sale of drug ingredients are not in place. These ingredients are
then smuggled into an area of high regulation such as the United States or
Europe, where they are made into individual drug units (vials, ampules, pill
bottles, or blister cards) with the use of small-scale packaging machines. In some
cases these operations are so large they hire offshore drug manufacturing
facilities to assemble their products. Such operations are small in number
though, and account for a small portion of the total number of underground
laboratories.
Drug Purity
Drug manufacturing safety is a central focus in Western medicine.
Pharmaceuticals are intended to treat ill patients, not cause additional harm by
being improperly dosed or containing bacteria, heavy metal, or other forms of
contamination. Products made for human consumption are only made after
government approval by government-licensed companies. These companies are
highly regulated and routinely inspected. Their products must only contain
materials that come from other licensed suppliers, which also adhere to strict
pharmaceutical-grade purity standards (such as USP/BP). These companies must
also assemble their products in meticulously scrutinized “clean room” facilities
designed to prevent any contamination from air and personnel. Each material or
piece of equipment that comes into contact with the drug product must be sterile,
and the entire process must result in a preparation that contains exactly and only
what the label intends. In short, there is essentially zero margin for error when it
comes to pharmaceutical manufacturing.
The above description is in stark contract to the underground steroid
manufacturing business. By their very nature, these companies are not under
government license or oversight. A majority of underground steroid products
will, likewise, not be assembled in a sterile environment, or with the use of
expensive pharmaceutical grade materials and equipment. Instead, most are
manufactured in a dwelling home or small clandestine business with the use of
“food grade” raw materials and manually operated vial/bottle filling and sealing
tools. The opportunities for contamination in this type of process are great. By
Western medical standards, most underground steroids are, of course, not fit for
human consumption. Even so, many consumers still buy these products. They
may find attraction to cheaper prices, higher doses, greater selection, or easier
availability. Perhaps more simply, they may not be aware of the risks involved.
No analysis of product purity specific to underground steroids has previously
been published to help consumers weigh these risks.
ANABOLICS Underground Market Analysis
In an effort to help consumers assess the quality and potential health risks of
underground steroid products, ANABOLICS undertook a detailed joint drug
analysis project in April 2007. This project examined the quality of steroids
made from underground facilities, and exceeded the normal scope of testing by
examining a number of other variables often overlooked in dosage testing. A
total of 14 underground steroid samples were selected for laboratory testing,
which included products from Amplio Labs, British Dragon, Diamond Pharma,
Generic Anabolics, Generic Pharma, Lizard Laboratories, Medical Inc.,
Microbiological Labs, Nordic Supplements, Shark Laboratories, SWE
Supplements, and Troy Labs. Included in this list were drugs that were made
from small underground manufacturers, mid-level operations, and even
producers large enough to have their items assembled under contract by drug
manufacturing facilities. All 14 samples were analyzed at a registered and
licensed facility in the United States.
There were four specific areas of testing for the 2007 market analysis project.
The first test was to look for the presence of toxic heavy metals such as lead, tin,
mercury, and arsenic. These metals all pose specific threats to health if they
accumulate in the body. Those metals considered inert, such as iron and
aluminum, were not included. Next, we commissioned the standard steroid
quantification testing to see how these products were dosed, then checked for
unknown steroidal contaminants. Pharmaceutical grade steroids are highly pure.
Unprocessed intermediary chemicals or other contaminants should not appear
upon analysis. The presence of unknown steroidal substances would signify that
lower quality materials (not made to pharmaceutical standards) were used.
Finally, we examined the oil for the flavoring agen 2,4 decadienal. This material
is common to food products, and its presence would demonstrate that food-grade
oil (not pure pharmaceutical-grade oil for injection) was used during product
manufacture.
The specific results for each of the four testing sets are presented in the tables
below. Overall, the products examined in this study reflected poorly on the
quality of the underground steroid market. To begin with, more than 20% of the
products (1 in 5) contained heavy metal contamination. While pre-market testing
would have caught this, if such products were ever found on pharmacy shelves
in the United States it would trigger an immediate nationwide recall. Next, an
examination of basic drug dosing showed many deviations. Approximately 35%
of the products were actually significantly overdosed. While this was likely done
in an effort to produce a stronger user response and loyal customer base, this is
an unacceptable tactic which raises many potential safety issues. In the third set
of tests, more than 60% of the samples were shown to contain some type of
unidentified steroidal compound. This does not necessarily mean the products
were dangerous, as this may simply consist of inert steroid
precursors/intermediary compounds. It does, however, show that impure steroid
materials were used during the manufacturing process. Lastly, testing for 2,4-
decadienal confirmed that at least 14% of the steroids tested used food grade oil,
perhaps the type purchased in a grocery store.
Drug Analysis Results
Test #1: Heavy Metals Contamination
Test #2: Dosage vs. Label Claim (mg/mL)
Test #3: Steroidal Materials Purity
Test #4: Oil Purity
Conclusions
The scope of testing for this project was fairly limited, and fell well short of the
detailed analysis required to validate a real prescription drug product. Still, the
standards were rigid enough for a strong majority of the underground steroid
products to fail testing. These drugs did not achieve a passing result due to a
number of important purity concerns. The reasons being that 1) they contained
toxic heavy metals; 2) they were significantly under-or over-dosed; 3) they
contained impure (not pharmaceutical grade) raw steroid materials; and/or 4)
they were made with food-grade (not pharmaceutical grade) oil. It is important
to remember is that this analysis project only covered 14 products, which is a
very small number relative to the total number of underground steroid
manufacturing operations and products in existence. It is possible that a different
set of 14 samples would yield a considerably different set of results. Still, the
very high failure rate seen during this investigation appears to underline several
important purity concerns with underground steroid products.
Legitimate pharmaceutical products are manufactured under strict conditions for
a reason. It is very difficult to maintain an acceptable level of purity without
them. Even if pure USP/BP grade materials are being used, it can be very easy
for a microscopic biological pathogen or other contaminant to enter a solution
unless every single potential source of contamination is addressed. Underground
manufacturers have little financial incentive (or often logistical possibility) to
make their drugs according to these strict purity standards. Instead, a lower
quality (“food grade”) level of manufacturing may dominate the underground
market. There are likely few exceptions, involving only the largest and most
reputable underground operations. While the number of anecdotal reports of
injury from underground steroid products appears to be relatively low overall,
and admittedly a substantial dose of alcohol in solution will kill most biological
contaminants, consumers must be aware that there remains a high likelihood of
impurity with underground drugs. By the very nature of these products purity
cannot be assured, and results like those of the ANABOLICS Underground
Market Analysis only further highlight this. In general, underground steroids
should not be considered equal substitutes for licensed pharmaceuticals.
Designer Steroids
There is a fatal flaw in the steroid detection methods used by the various sports
agencies. That is, in order to test someone for anabolic steroids, you need to
know exactly what you are looking for. You can’t just look for “steroids” in the
urine, but are forced to test for each specific compound individually. To make
things even more complicated, you need to know more than just what these
steroids look like chemically before they are administered. You need to know
what they are going to look like by the time they appear in the urine, because the
original steroids themselves will largely be metabolized into other compounds.
For example, nandrolone use is most easily detected by looking for its major
metabolites 19-norandrosterone and 19-noretiocholanolone,
376 not nandrolone
itself. With this in mind, you need to investigate each potential steroid of
“misuse” very closely, and each plan of detection is going to be difficult, and
time-consuming, to develop. The past couple of decades have seen a lot of
progress in identifying the metabolites unique to most commercially available
synthetic steroids. As a result, they are almost all detectable in a urine sample
now. In reality, this may still only be a drop in the bucket.
You see, several hundred, if not a thousand or more, different steroids were
synthesized and investigated in various laboratories around the world during the
heyday of steroid research. In most cases, their anabolic and androgenic
potencies were measured, with the same methods that have been used on all of
the popular steroids we know today. Only a minute fraction of these research
compounds ultimately became commercially available drug products, leaving
many potentially excellent steroids by the wayside. This is to be expected in any
area of drug research though, as there would be no way for hundreds of similar
drugs to exist in the same market. But the early research is still out there, and
remains a very valuable source of information for the clever chemists of today.
Some of these old research steroids of the ‘50s and ‘60s still exist today, due to
the diligence of underground chemists and researchers. We refer to these drugs
collectively as “Designer Steroids”, and they are here only for the purpose of
defeating a drug screen. A true designer steroid is structurally unique next to the
known anabolic/androgenic steroids, sharing no common metabolites, so as to be
undetectable to even the most thorough steroid test. The thought of tracking
down metabolites for all possible steroids compounds, to eliminate the designer
steroids issue, seems like an impossible task to say the least. Even if somehow
this old research were to be exhausted, and metabolites identified for all known
steroids, there are still nearly limitless other ways to alter testosterone,
nandrolone, or dihydrotestosterone to make unique new steroids. The designer
steroid phenomena could obviously present an overwhelming problem to the
sports organizations given present drug testing methods. The athletes can easily
stay one or two steps ahead, and nobody on the sidelines is the wiser.
At this point in time, the fact that designer steroids exist is no secret to the sports
agencies. It became painfully obvious to the IOC (International Olympic
Committee) in March of 2002, when the UCLA Olympic Analytical Lab
detected norbolethone, a potent c-17 alpha alkylated nandrolone derivative
investigated back in the 1960s, in the urine samples from a female athlete
377
. It
turned out to be Tammy Thomas, a 32-year-old cyclist from Colorado Springs.
This was the second time she failed a drug test actually, which resulted in a
lifetime ban from competition. One of the samples in question was actually
flagged previously, with a group of others, because it had extremely low
endogenous steroid concentrations (suggesting suppression from exogenous
steroid administration). Don Catlin, who runs the UCLA Olympic Analytical
Laboratory, would connect it to the designer steroid norbolethone much later.
The fact that only one of these samples retroactively tested positive suggests that
other designer steroids were being used by competitors in addition to
norbolethone.
Catlin was able to obtain a sample of pure norbolethone from the drug company
Wyeth, and must have been greatly aided by the fact that metabolites of this
steroid had been identified in earlier studies.
378 The procedure for norbolethone
detection has now been made available to all testing agencies, and unfortunately
it is now unsafe for competition. Its value as a designer steroid has likewise
vanished overnight. Perhaps it was a bad idea to use a steroid that actual made it
all the way to the point of clinical trials in the U.S., as there is quite a bit of
information to be found on it (not having the urinary metabolites study would
have made things a lot harder on Catlin). Honestly, I can think of a number of
more effective and safer compounds to use than this hideously progestational
one (ooh, the water bloat). I don’t think the chemist was really thinking this one
through very thoroughly, and next time may want to get some help from
someone that really knows these agents.
The norbolethone story quietly fell from the public conscience not long after it
broke. The number of athletes that ultimately tested positive for the drug was
minimal, so it really never evolved into the big scandal that was initially
expected. The USADA thrives on negative media attention to steroids, because it
leads to more government funding, so no doubt this lack of public outrage was a
disappointment. I would suspect many involved were hoping for the global story
on par with what happened when Ben Johnson was stripped of his gold medal
during the 1988 summer Olympics. This would be of little matter by January
2004, however, because a much bigger doping scandal was about to hit. It
involved the use of the designer steroid tetrahydrogestrinone, and this time
would snare some of the biggest figures in amateur and professional sports. Not
just Olympic competitors, but professional football and baseball players were
being listed as potential violators. Many household names were being thrown
around, including Jason Giambi, Barry Bonds, and Gary Scheffield. Over 20
athletes ultimately tested positive for THG, or were specifically named for using
it in the evidence. The investigation continues today, so this number may rise.
Don Catlin was once again the scientist who helped identify this compound in
the first place, as well as a method of its detection in urine. This time around,
however, he had a lot more help then he did with norbolethone. THG was
actually handed over to the IOC testing laboratory in a syringe, by an
anonymous coach who did not approve of its use. With the help of an inside
informant, USADA got their Ben Johnson story, and then some. THG was at the
center of the biggest organized doping scandal in the history of competitive
sports, and would come to spark a more vigorous government fight against
steroid use than we had yet seen. The steroid-using community is only now
beginning to feel the backlash.
I include these stories not because they illustrate victories for the IOC. Quite the
contrary, I believe they underline the major failings in current steroid testing
methods. These two incidents logically do not represent the only two designer
steroids ever used in competitive sports. For one, we surely cannot expect a
100% success rate for the IOC when we know that THG use went completely
unnoticed for months, if not years. Nobody knew anything about this steroid
until a sample was handed over to the testing facility, which is the same facility
that had unwittingly been passing urine samples containing the same steroid just
days before. Were it not for the inside source, THG would probably still be in
use today. The norbolethone and THG stories spit in the face of those on the
sidelines, who insist that drug testing ensures their favorite athlete is drug free.
The fact is, many other potent designer steroids are probably out there, either in
the books, or in the gym bags, of many of the world’s top competitors. It may
take years for the next designer compound to be identified by the IOC labs, and
perhaps only a matter of weeks for a new one to be synthesized once it is. It is a
game the drug testers simply cannot win given the tools they have available to
them now. We may see repeats of these scandals in the future, but such events
will only exemplify the proficiency of those working against drug testing. They
show the public the unshakable will of the athletes who are going to use these
agents, not the testing agencies that police them.
376. Detection of nandrolone metabolites in urine after a football game in professional and amateur players:
a Bayesian comparison. Robinson N, Taroni F, Saugy M, Ayotte C, Mangin P, Dvorak J. Forensic Sci Int
2001 Nov 1;122(2-3):130-5
377. Detection of norbolethone, an anabolic steroid never marketed, in athletes’ urine. Catlin D, Ahrens B,
Kucherova Y. Rapid Commun. Mass Spectrom.
2002; 16: 1273-75
378. Schanzer W, Donike M. Anal Chim. Acta. 1993; 275: 23
Anabolic Steroids and the Law
United States law prohibits the possession of anabolic steroids without a legal
medical prescription, imparting severe penalties (including fine and/or
imprisonment) for those that choose to violate these laws. Under influence of
U.S. government officials, World Anti-Doping Agency (WADA) members, and
public criticism following numerous doping scandals, a growing number of
countries are following the U.S. by adopting their own laws against the
possession of anabolic steroids and other sports doping drugs. In many cases
similar severe criminal penalties have been enacted. The following section
discusses in more detail various national laws that concern the personal use of
anabolic steroids and other related drugs.
United States
Anabolic steroids have been classified as controlled substances in the United
States since 1991, with passage of the Anabolic Steroid Control Act of 1990
(Pub. L. No. 101-647, Sec. 1902, 104 Stat. 4851, 1990). This law makes it a
criminal offense to sell, distribute, manufacture, or possess anabolic steroids
without proper legal authorization. The outlined penalties for possession without
a legal prescription include a maximum of 1 year of imprisonment and/or a
minimum fine of $1,000. This may be increased to 2 years of imprisonment
and/or a $2,500 minimum fine for individuals with a prior drug conviction. Note
that this law was amended in 2005 following passage of the Anabolic Steroid
Control Act of 2004. The new law added 26 new steroid compounds to the list of
controlled substances, and also removed the legal requirement that a compound
be proven anabolic in humans before it can be added. This “promotes muscle
growth” clause was the key roadblock to removing many of the “legal steroids”
of the late 1990s and early 2000s.
State vs. Federal
Criminal laws against the possession of anabolic steroids exist at both the federal
and state level in the U.S. Depending on the circumstance, an individual may be
charged with a steroid related crime by either the federal government or the state
government where the crime took place. Unless the crossing of state lines was
involved, most criminal prosecutions for steroid-related crimes take place at the
state level in accordance with state laws. Most often the state laws mirror federal
statutes very closely although this is not always the case. There can also be a
great deal of variability in how punishments are determined between one state
and another. If you are not obtaining medications legally through a physician’s
prescription, it is advisable to study the steroid laws closely, particularly those of
your individual state. The book “Legal Muscle: Anabolics in America” by
lawyer Rick Collins [teamlegalmuscle.com] is an excellent review of the legal
situation concerning steroids in the U.S., including a detailed breakdown of all
state steroid laws.
The main body (drug listings) of the Anabolic Steroid Control Act has been
included for your review below.
`(A) The term `anabolic steroid' means any drug or hormonal substance,
chemically and pharmacologically related to testosterone (other than estrogens,
progestins, corticosteroids, and dehydroepiandrosterone), and includes--
`(i) androstanediol--
`(I) 3b,17b-dihydroxy-5a-androstane; and
`(II) 3a,17b-dihydroxy-5a-androstane;
`(ii) androstanedione (5a-androstan-3,17-dione);
`(iii) androstenediol--
`(I) 1-androstenediol (3b,17b-dihydroxy-5a-androst-1-ene);
`(II) 1-androstenediol (3a,17b-dihydroxy-5a-androst-1-ene);
`(III) 4-androstenediol (3b,17b-dihydroxy-androst-4-ene); and
`(IV) 5-androstenediol (3b,17b-dihydroxy-androst-5-ene);
`(iv) androstenedione--
`(I) 1-androstenedione ([5a]-androst-1-en-3,17-dione);
`(II) 4-androstenedione (androst-4-en-3,17-dione); and
`(III) 5-androstenedione (androst-5-en-3,17-dione);
`(v) bolasterone (7a,17a-dimethyl-17b-hydroxyandrost-4-en-3-one);
`(vi) boldenone (17b-hydroxyandrost-1,4,-diene-3-one);
`(vii) calusterone (7b,17a-dimethyl-17b-hydroxyandrost-4-en-3-one);
`(viii) clostebol (4-chloro-17b-hydroxyandrost-4-en-3-one);
`(ix) dehydrochloromethyltestosterone (4-chloro-17b-hydroxy-17a-methylandrost-1,4-dien-3-one);
`(x) *1-dihydrotestosterone (a.k.a. `1-testosterone') (17b-hydroxy-5a-androst-1-
en-3-one);
`(xi) 4-dihydrotestosterone (17b-hydroxy-androstan-3-one);
`(xii) drostanolone (17b-hydroxy-2a-methyl-5a-androstan-3-one);
`(xiii) ethylestrenol (17a-ethyl-17b-hydroxyestr-4-ene);
`(xiv) fluoxymesterone (9-fluoro-17a-methyl-11b,17b-dihydroxyandrost-4-en-3-
one);
`(xv) formebolone (2-formyl-17a-methyl-11a,17b-dihydroxyandrost-1,4-dien-3-
one);
`(xvi) furazabol (17a-methyl-17b-hydroxyandrostano[2,3-c]-furazan);
`(xvii) 13a-ethyl-17a-hydroxygon-4-en-3-one;
`(xviii) 4-hydroxytestosterone (4,17b-dihydroxy-androst-4-en-3-one);
`(xix) 4-hydroxy-19-nortestosterone (4,17b-dihydroxy-estr-4-en-3-one);
`(xx) mestanolone (17a-methyl-17b-hydroxy-5a-androstan-3-one);
`(xxi) mesterolone (1a-methyl-17b-hydroxy-[5a]-androstan-3-one);
`(xxii) methandienone (17a-methyl-17b-hydroxyandrost-1,4-dien-3-one);
`(xxiii) methandriol (17a-methyl-3b,17b-dihydroxyandrost-5-ene);
`(xxiv) methenolone (1-methyl-17b-hydroxy-5a-androst-1-en-3-one);
`(xxv) methyltestosterone (17a-methyl-17b-hydroxyandrost-4-en-3-one);
`(xxvi) mibolerone (7a,17a-dimethyl-17b-hydroxyestr-4-en-3-one);
`(xxvii) 17a-methyl-*1-dihydrotestosterone (17b-hydroxy-17a-methyl-5aandrost-1-en-3-one) (a.k.a. `17-a-methyl-1-testosterone');
`(xxviii) nandrolone (17b-hydroxyestr-4-en-3-one);
`(xxix) norandrostenediol--
`(I) 19-nor-4-androstenediol (3b, 17b-dihydroxyestr-4-ene);
`(II) 19-nor-4-androstenediol (3a, 17b-dihydroxyestr-4-ene);
`(III) 19-nor-5-androstenediol (3b, 17b-dihydroxyestr-5-ene); and
`(IV) 19-nor-5-androstenediol (3a, 17b-dihydroxyestr-5-ene);
`(xxx) norandrostenedione--
`(I) 19-nor-4-androstenedione (estr-4-en-3,17-dione); and
`(II) 19-nor-5-androstenedione (estr-5-en-3,17-dione;
`(xxxi) norbolethone (13b,17a-diethyl-17b-hydroxygon-4-en-3-one);
`(xxxii) norclostebol (4-chloro-17b-hydroxyestr-4-en-3-one);
`(xxxiii) norethandrolone (17a-ethyl-17b-hydroxyestr-4-en-3-one);
`(xxxiv) oxandrolone (17a-methyl-17b-hydroxy-2-oxa-[5a]-androstan-3-one);
`(xxxv) oxymesterone (17a-methyl-4,17b-dihydroxyandrost-4-en-3-one);
`(xxxvi) oxymetholone (17a-methyl-2-hydroxymethylene-17b-hydroxy-[5a]-
androstan-3-one);
`(xxxvii) stanozolol (17a-methyl-17b-hydroxy-[5a]-androst-2-eno[3,2-c]-
pyrazole);
`(xxxviii) stenbolone (17b-hydroxy-2-methyl-[5a]-androst-1-en-3-one);
`(xxxix) testolactone (13-hydroxy-3-oxo-13,17-secoandrosta-1,4-dien-17-oic
acid lactone);
`(xl) testosterone (17b-hydroxyandrost-4-en-3-one);
`(xli) tetrahydrogestrinone (13b,17a-diethyl-17b-hydroxygon-4,9,11-trien-3-
one);
`(xlii) trenbolone (17b-hydroxyestr-4,9,11-trien-3-one); and
`(xliii) any salt, ester, or ether of a drug or substance described in this
paragraph.';
Austria
The possession of anabolic steroids is not a criminal act according to Austrian
law. In 2008, Austrian government officials announced intent to place criminal
penalties on steroid possession.
Australia
It is a criminal act to import, supply, use, or possess anabolic steroids in
Australia without a prescription from a medical practitioner, dentist, or
veterinarian (Poisons and Drugs Act Amendment of 1994). The outlined
penalties for possession without a legal prescription include a maximum of 6
months of imprisonment and/or a fine of $5,000.
Canada
Anabolic steroids are included in the Canadian Controlled Drugs and Substances
Act as Schedule IV substances. It is illegal to sell, manufacture, or import
anabolic steroids into Canada without proper legal authorization. Possession of
anabolic steroids for personal use is not a criminal act.
Czech Republic
In 2008 it became a criminal act to manufacture, import, export, store, or
distribute anabolic steroids in the Czech Republic. The potential penalties
include a maximum of 3 years in prison. It is not a crime to possess steroids for
personal use.
Denmark
In Denmark it is a crime to manufacture, import, export, market, dispense,
distribute, or possess doping substances including anabolic steroids, human
growth hormone, and erythropoietin without proper medical or scientific reason
(The Act on Prohibition of Certain Doping Substances No. 232 of 21 April
1999). The potential penalties for possession include a maximum of 2 years in
prison.
France
In 2008 it became a criminal offense to manufacture, transport, acquire, or
possess doping substances including anabolic steroids, human growth hormone,
and erythropoietin in France. The potential penalties for possession include a
maximum of 5 years imprisonment and/or a 75,000 Euro fine.
Greece
The possession of anabolic steroids is not a criminal act according to Greek law.
In 2008, government officials announced intent to place criminal penalties on
steroid possession in Greece.
Sweden
In Sweden it is a crime to import, manufacture, transport, sell, possess, or use
doping substances such as anabolic steroids and growth hormone without proper
legal authorization (The Swedish Act prohibiting certain doping substances
(1991,1969). The potential penalties include a maximum of 2 years in prison.
Possession for personal use is usually regarded as a petty offense and given a
maximum penalty of 6 months imprisonment.
United Kingdom
The importation, possession, and use of anabolic steroids are not criminal acts
according to UK law. There has been a great deal of pressure in recent years
from the U.S. and World Anti-Doping Agency to place criminal penalties on the
possession of anabolic steroids without a prescription.
Acquiring AAS (Best Practices)
This section assumes that the decision has already been made to use anabolic
steroids. It places no judgment on the decision itself, and concentrates only on
reducing risks relating to the drug supply. How one goes about obtaining these
substances is an extremely important consideration. Much more than money is at
stake with this decision. The illicit market for anabolic steroids can be a highly
volatile place, with significant quantities of low quality counterfeit and
underground drugs in circulation. In this section we will review the four general
sources for anabolic steroids. When possible, we examine tips that should
increase, at least to some small extent, relative safety for the buyer. The main
objective in all cases is to obtain legitimate pharmaceutical grade products so
that no additional risks due to contamination, drug substitution, or inaccurate
dosing are presented to the user.
By Prescription
Provided you are in some way in valid need of therapy, it is always preferable to
obtain anabolic steroids through a physician's prescription. In addition to
offering the potential benefit of having some medical oversight to your use, most
pharmaceutical markets (in Western nations especially) are very secure. It is
unlikely that you will come across counterfeit drugs when your medications are
dispensed from a real pharmacy. In the United States, in fact, the risk is so low
that it is not even worth considering. Furthermore, if you reside in a country
where there are criminal penalties for the unapproved possession of steroids, a
prescription is the only way to legally own and use these substances. The
criminal and civil penalties can be very serious in many cases, even when the
drugs are for personal use.
Most readers are probably under the incorrect assumption that it is nearly
impossible to get a prescription for anabolic steroids in the United States. While
this may have been true following the doping scandals of the late 1980s, the
market has changed considerably since then. The legal sale of these drugs is
again on the rise. The shift began in the mid-1990s, when drug companies
started to put forth a strong effort to educate physicians and the public on the use
of steroids (specifically testosterone) to treat age-related hormone deficiency in
men. It is a fact that men deal with hormonal decline just like women do, and
suffer ill health effects from it. Treating hormonal deficiency with drugs to
restore youthful testosterone levels has become a widely accepted part of
medicine. By the time men hit their thirties, a high percentage are legitimate
candidates for hormone replacement treatment.
If you feel that you are a candidate for a prescription, you may need to take an
active role in finding a physician. Unfortunately, many doctors are still unsure
about these drugs.They might not prescribe testosterone at all, or may be too
conservative in their treatment if they do. You may have to interview several
before you find the one that is right for you. Don’t worry about “doctor
shopping”. This illegal practice involves seeing multiple doctors, or withholding
information, to gain prescriptions you don’t need. You should never lie to your
doctor, or try and gain prescriptions from more than one at a time. Otherwise, it
is perfectly legal to take the time to find one you feel comfortable with.
Medical necessity is usually supported with a blood test, ordered by the treating
physician. Testosterone levels tend to be highest in the morning and lowest at the
end of the day. The blood test should be planned accordingly. Before reviewing
the results, understand that there are no specific established protocols for treating
men with hormone deficiency. The medical community does not even agree on
the point in which therapy should be initiated. For example, the “normal” level
of testosterone in an adult man is 250-1,200 ng/dL. Some physicians will not
prescribe anything to you unless you are symptomatic and your levels fall below
250 ng/dL. Others are comfortable prescribing even if your levels read 500
ng/dL, the objective being to maintain hormonal levels at the high end of normal
(“optimal”). Note that some people choose to pre-test themselves to determine
how they might quality before approaching a physician. You can request such
testing at www.HRT-Labs.com.
How testosterone medication is prescribed also varies a great deal depending on
not only the needs of the patient, but also the comfort level of the physician. For
example, more rigid physicians will often only prescribe testosterone gels or
patches. This is because these forms allow the very controlled daily release of
testosterone, and are harder for the patient to abuse. Other doctors are
comfortable working with testosterone injections that are taken home and selfadministered by the patient. Even when testosterone injections are prescribed,
some doctors refuse to give more than 100 mg per week. Others routinely give a
200 mg per week dose, assuring that low levels are not endured at any point
during treatment. You will not need to find a crooked doctor. You just want to
find a progressive physician that understands the value of optimizing your
hormone levels.
You have a few options open to you when first seeking treatment. You can
approach your family doctor, a hormone specialist (endocrinologist), or an
antiaging physician. In my experience, antiaging medicine is where you find the
most progressive physicians and treatments. These are the doctors that are
working with both steroids and off-label medications like anti-estrogens and
growth hormone, and forcing the establishment to rethink hormonal medicine.
Doctors in this field are often certified by private physician groups such as the
American Academy of AntiAging Medicine (A4M), which lobby the FDA and
help establish effective protocols for HRT/antiaging doctors. Don’t expect any
antiaging physician to support drug abuse. Like all doctors, they take an oath to
protect their patients. It is not unreasonable, however, to find a good antiaging
physician that will work closely with you to keep you healthy, physically fit, and
hormonally optimized.
One benefit to being a writer and educator on anabolic substances is that I am
regularly meeting progressive physicians and hormone clinic owners. I've had
the pleasure of getting to know a great many over the years. It has given me
confidence that this field of medicine is here to stay, if not continuing to grow
rapidly. It occurred to me that my list of contacts puts me in a unique position to
help potential HRT/antiaging patients. Male testosterone deficiency is grossly
under-treated in this country. I’d like to do my part to help change this. If you
are interested in consulting with a doctor in your area, please visit my free
website below. I will use it as a portal to put visitors in contact with
HRT/antiaging physicians. If you think HRT may be an option for you, I
strongly encourage you to explore it further, regardless of how you go about
seeking treatment. Supporting the physicians that offer this type of treatment is
the best way to help legitimize and advance this area of medicine.
For hormone replacement therapy & antiaging doctor referrals, visit the website
www.HRT-Rx.com to find a physician in your area.
Ordering Steroids in the Mail
Unlike most traditional drugs that are under strict legal controls (such as
narcotics), the sale of anabolic steroids seem to be openly advertised on the
Internet and in the back pages of bodybuilding magazines. Much of this
probably has to due with the strong variance in laws between countries. In
particular, many countries without close ties to the United States find little need
to criminalize these drugs. Steroid prohibition is largely a western concept. As
such, a situation exists where many markets have weak regulatory controls on
these drugs. This helps to maintain an active global supply. As such, much
international commerce still takes place with anabolic steroids. While it might
not be a simple task to take out your credit card and order other illegal drugs
over the Internet, it is still fairly easy to shop for anabolic steroids this way.
The first major difference between obtaining anabolic steroids via prescription
and ordering them through the mail (illegally) is that you may not receive
genuine pharmaceutical products. The potential health risks of counterfeit drugs
are significant, and detailed in other sections of this book. Counterfeiting is
serious and widespread. The World Health Organization recently warned that
more than half of all drugs ordered over the Internet from unlicensed pharmacies
are illegitimate. The rampant problem of counterfeiting is likely no better
exemplified than it is with anabolic steroids. With the large lucrative markets
and steadily increasing demand, steroids have been highly attractive targets of
counterfeiters for decades now. The cited WHO statistics undoubtedly
underestimate the problem as it relates to the counterfeiting of steroids.
Below are several rules to follow when ordering steroids through the mail. These
rules can help increase the chances that your order will contain pharmaceutical
grade drug products.
1. Order from a country with legal access to steroid medications. If it is easy for
your source to get legitimate products, it is likely what is sent to you will be
legitimate. Avoid ordering from countries with strict prohibitive laws such as the
United States, Canada, Western Europe, or Australia. Consistent supply in these
areas invariably involves the sourcing of clandestinely manufactured products.
2. Buy local brand drugs from the chosen source country. If you are ordering
from a pharmacy in Thailand, buy Thai drugs. The chances of running into
counterfeits will increase significantly when the drugs you buy are not domestic
to the supplier’s country.
3. Immediately avoid any foreign pharmacy that says it carries American steroid
products. These will be counterfeit over 99% of the time, which means the
pharmacy probably deals in counterfeit drugs.
4. Buy from a place that shows pictures of its products. Scrutinize the offerings
closely. Are there any known fakes? Many suppliers work hard to keep their
company clear from counterfeit drugs. You want to deal with one of these.
The purpose of this book is to reduce harm, not encourage or support criminal
activity. Thus the previous rules address only the validity of the drugs, not
smuggling them. If you reside in an area where steroids are illegal to import
without a prescription such as the United States, Canada, Scandinavia, or
Australia, you need to be aware that there can be serious legal consequences to
ordering these drugs through the mail. If authorities intercept your package, you
may be charged with a variety of crimes including drug possession and illegal
importation. You may even be charged with trafficking if the quantity is large
enough. While in the United States many individuals receive only a seizure
notice when their steroids are discovered, the police visit and arrest many others.
Being forced into the legal justice system is not the outcome you want. Please
consider this carefully before you order steroids through the mail.
Purchasing Steroids on Vacation
Another common option is to travel to a country where anabolic steroids are
widely available, and purchase the drugs directly from a pharmacy. Many
popular vacation spots are common sources, including Mexico, Thailand, and
Turkey. So it is not uncommon to see dual-purpose trips (vacation/sourcing),
with the individual bringing back only a small personal use supply. As with all
illicit sourcing options, there are some benefits and drawbacks to this practice.
The principle benefit, provided the individual chooses the right country and
shops intelligently, should be more consistent access to real pharmaceutical
grade compounds, and the chance for inspection before purchase. The main
drawback, of course, is that you will be required to clear Customs upon your
return. If you are found to be in possession of the drugs while attempting to enter
a country with steroid prohibition laws, you could face serious criminal charges.
In an effort to help readers avoid the added risks of counterfeit drug products,
the following points of advice are provided. All readers are cautioned that
smuggling is illegal and can be a very risky practice. Again, since this book is
about harm reduction we will not be discussing means of smuggling.
1. Loose regulations on the steroid supply typically also mean loose oversight of
pharmacies. In some countries, pharmacies in tourist areas will commonly stock
counterfeits. You should become well-versed with the products of a particular
region before traveling.
2. Always buy local. You want to get the drugs that are readily available to
pharmacies through normal legal channels, not exotic drugs that may or may not
have been legally imported by the pharmacy. For example, never buy European
or American drugs in a Mexican pharmacy.
3. If possible, avoid the obvious tourist pharmacies. Travel to an area more
known to the locals. The smaller a percentage of business the pharmacy makes
on tourists, the less likely they are to be stocking counterfeits.
4. Ask for products by name. Most tourists stumble in and ask for "steroids,
anabolicas, testosterona." If instead you ask for something very specific, such as
"Bayer Primoteston," you are probably going to be taken more seriously.
The Local Black Market
Where steroids are difficult to obtain through legitimate channels, robust trade
usually continues on a black market. The United States in particular has the
largest and most lucrative steroid black market in the world. If you plan to obtain
anabolic steroids this way, you should be aware of its unique drawbacks and
advantages. To begin with, unlike ordering over the Internet, purchasing in
person from a local black market dealer should allow you an opportunity to
inspect products before purchasing. You also do not have to deal with the
uncertainty and wait of ordering through the mail. On the other hand, however,
strict criminal laws may seriously limit the diversion of real steroid drugs to the
black market. The United States has some of the most pronounced issues with
drug contamination, adulteration, and mislabeling because of this. You should
know that of all the options available to you, purchasing on the black market
could be the most risky, especially if you do not have experience differentiating
real from counterfeit drugs.
Again, our focus in this section is only on increasing the likelihood of obtaining
real pharmaceutical products. Towards that objective, the following points of
advice should be followed when shopping on the local black market.
1. Consider the country of origin for each drug. Only buy drugs that make sense.
For example, Mexican steroids are common in the United States due to their
open supply and close proximity. You would expect to see them. On the other
hand, you are very unlikely to find legitimate drugs from Australia in the United
States, which is very far away and also seriously restricts its own steroid supply.
2. Try to stick with a group of fellow steroid users. Sharing experiences and
knowledge can help keep the group better supplied with legitimate medications.
3. Try to buy from other steroid users. Individuals who sell steroids but don’t use
them are probably less concerned with product quality.
4. If you are trying to purchase legitimate pharmaceutical products, don’t buy
multi-dose vials or bottles with loose pills unless you are absolutely sure of the
company and source. These forms of medication are rarely used outside of the
U.S. and Canada. Single use ampules and push through pill blisters are much
more common in other countries, and may be slightly more secure due to the
difficulty involved in making them.
Part III
Drug Profiles
Agovirin Depot (testosterone isobutyrate)
Description:
Testosterone isobutyrate is an injectable steroid preparation that contains the
isobutyrate ester of testosterone in a water base. Among bodybuilders,
testosterone isobutyrate is often considered analogous to testosterone suspension
(no ester). Although both are usually found as water-based suspensions, the
pharmacokinetics of the two products are admittedly very different. While
testosterone (free) suspension is very fast-acting, requiring injections to be given
every few days, testosterone isobutyrate is much slower to release, and is usually
administered once every two weeks in a clinical setting. As an injectable
testosterone, testosterone isobutyrate is favored for its ability to promote rapid
gains in muscle mass and strength.
History:
Injectable testosterone isobutyrate microcrystal suspension was first described in
1952.
379 This agent was developed in an effort to create an injectable (depot)
form of testosterone that would be slower acting that regular (free) testosterone
suspension or testosterone propionate, the most widely prescribed forms of
testosterone at the time. This is accomplished by providing a microcrystalline
depot with very low water solubility, delaying the release of free steroid into the
bloodstream. Although effective for this purpose, testosterone isobutyrate was
developed at a time when many new esters of testosterone were being introduced
to the market. By the mid-1950’s, testosterone enanthate would emerge as the
dominant slow-acting injectable testosterone, and the isobutyrate ester would
ultimately see little commercial success.
The only modern steroid product to use testosterone isobutyrate is Agovirin
Depot, developed by Biotika in Czechoslovakia. It is primarily prescribed to
treat males with insufficient androgen levels and adolescents with delayed
puberty, although it is indicated for a variety of other purposes including the
treatment of Klinefelter syndrome (a disease where an extra chromosome results
in an imbalance of androgenicity and estrogenicity), aplastic anemia, Cushing’s
syndrome (as an anabolic agent to preserve lean tissue), postmenopausal
osteoporosis, advanced breast cancer, mastodynia (breast pain), and cachexia
(wasting of the body due to severe illness). Agovirin Depot is still produced by
Biotika (currently in the Slovak Republic), and remains a popular export to
European black markets.
How Supplied:
Testosterone isobutyrate suspension is available on the human drug market in
the Slovak Republic as Agovirin Depot (Biotika). It contains 25 mg/ml of steroid
mixed in a water-based solution; packaged in a 2 mL ampule (5 ampules per
box). Testosterone isobutyrate has low water solubility; the steroid will
noticeably separate from the water-based solution when an ampule is left to sit.
A quick shake will temporarily place the drug back into suspension, so that the
withdrawn dosage should always be consistent.
Structural Characteristics:
Testosterone isobutyrate is a modified form of testosterone, where a carboxylic
acid ester (2-methyl propionic acid) has been attached to the 17-beta hydroxyl
group. Esterified forms of testosterone are less polar than free testosterone, and
are absorbed more slowly from the area of injection. Once in the bloodstream,
the ester is removed to yield free (active) testosterone. Esterified forms of
testosterone are designed to prolong the window of therapeutic effect following
administration, allowing for a less frequent injection schedule compared to
injections of free (unesterified) steroid. Testosterone isobutyrate microcrystalline
suspension is designed to provide physiological androgen concentrations for
approximately 2 weeks following injection.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone more likely to require the
concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention
and loss of muscle definition are common with higher doses of testosterone, this
drug is usually considered a poor choice for dieting or cutting phases of training.
Its moderate estrogenicity makes it more ideal for bulking phases, where the
added water retention will support raw strength and muscle size, and help foster
a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
380
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely effect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
381 Studies using 300 mg of testosterone ester
(enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated
only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached
21%.
382 The negative impact of aromatase inhibition should be taken into
consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less of testosterone per week, the
impact on lipid profile tends to be noticeable but not dramatic, making an antiestrogen (for cardioprotective purposes) perhaps unnecessary. Doses of 600 mg
or less per week have also failed to produce statistically significant changes in
LDL/VLDL cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive
protein, and insulin sensitivity, all indicating a relatively weak impact on
cardiovascular risk factors.
383 When used in moderate doses, injectable
testosterone esters are usually considered to be the safest of all
anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
The design of testosterone isobutyrate (as Agovirin Depot) is slightly different
than that of most testosterone esters, which are usually made as oily solutions.
Agovirin Depot instead contains a microcrystalline aqueous suspension.The
crystals form a repository in the muscle following injection, where they slowly
dissolve over time. Injections of testosterone isobutyrate may require a large
needle (21 gauge), and may result in local irritation, pain, and redness.
Administration (Men):
To treat androgen insufficiency, testosterone isobutyrate suspension is usually
administered in a dose of 50-100 mg every 14 days. When used for musclebuilding purposes, testosterone isobutyrate suspension is often administered at a
dose of 200-400 mg (4-8ml) per week. Although active for longer periods of
time, weekly injections would be preferred due to the low dosage and tendency
for pain at the site of injection (large injection volumes would not be advised).
To reduce injection volume, the weekly dosage may be further subdivided into
smaller injections, which are taken every 2nd or 3rd day. Cycles are generally
between 6 and 12 weeks in length. This level is sufficient to provide noticeable
gains in muscle size and strength. Testosterone drugs are ultimately very
versatile, and can be combined with many other anabolic/androgenic steroids
depending on the desired effect.
Administration (Women):
Testosterone isobutyrate suspension is not commonly used with women in
clinical medicine. When applied, it is usually given in a dose of 25-50 mg every
14 days. Testosterone isobutyrate suspension is not recommended for women for
physique-or performance-enhancing purposes due to its strong androgenic
nature, tendency to produce virilizing side effects, and slow acting
characteristics (making blood levels difficult to control).
Availability:
Pharmaceutical preparations containing testosterone isobutyrate are rare. The
only known product at this time is Agovirin Depot, produced in the Slovak
Republic by Biotika. It contains 50 mg per 2 mL ampule; 5 packaged per box.
Anadrol®- 50 (oxymetholone)
Description:
Oxymetholone is a potent oral anabolic steroid derived from
dihydrotestosterone. More specifically, it is a close cousin of
methyldihydrotestosterone (mestanolone), differing only by the addition of a 2-
hydroxymethylene group. This creates a steroid with considerably different
activity than mestanolone, however, such that it is very difficult to draw
comparisons between the two. For starters, oxymetholone is a very potent
anabolic hormone. Dihydrotestosterone and mestanolone are both very weak in
this regard, owing to the fact that these molecules are not very stable in the high
enzyme (3-alpha hydroxysteroid dehydrogenase) environment of muscle tissue.
Oxymetholone remains highly active here instead, as is reported in standard
animal assay tests demonstrating a significantly higher anabolic activity than
testosterone or methyltestosterone. Such assays suggest the androgenicity of
oxymetholone is also very low (1/4th to 1/7th its anabolic activity), although real
world results in humans suggest it is decidedly higher than that.
Oxymetholone is considered by many to be the most powerful steroid
commercially available. A steroid novice experimenting with this agent is likely
to gain 20 to 30 pounds of massive bulk, and it can often be accomplished within
6 weeks of use. This steroid produces a lot of water retention, so a good portion
of this gain is going to be water weight. This is often of little consequence to the
user, who may be feeling very big and strong while taking oxymetholone.
Although the smooth look that results from water retention is often not
attractive, it can aid quite a bit to the level of size and strength gained. The
muscle is fuller, will contract better, and is provided a level of protection in the
form of extra water held into and around connective tissues. This will allow for
more elasticity, and will hopefully decrease the chance for injury when lifting
heavy. It should be noted, however, that a very rapid gain in mass might also
place too much stress on your connective tissues. The tearing of pectoral and
biceps tissue is commonly associated with heavy lifting while massing up on
steroids, and oxymetholone is a common offender. There can be such a thing as
gaining too fast.
History:
Oxymetholone was first described in 1959.
384 The agent was released in the
United States as a prescription drug during the early 1960’s, sold under the brand
names Anadrol-50 (Syntex) and Androyd (Parke Davis & Co.). Syntex
developed the agent, and would hold patent rights to it until their expiration
many years later. The drug was originally approved for use in conditions where
anabolic action was necessary. Indicated uses included geriatric debilitation,
chronic underweight states, pre-and postoperative preservation of lean mass,
convalescence from infection, gastrointestinal disease, osteoporosis, and general
catabolic conditions. The recommended dose for such uses was usually 2.5 mg
three times per day. The drug was originally supplied in a 2.5 mg, 5 mg, or 10
mg tablet.
In spite of the many potential therapeutic uses or a strong anabolic activity of
this drug, the FDA soon strictly narrowed the indicated uses of oxymetholone.
By the mid-1970’s, the drug was FDA approved only for the indicated treatment
of anemia characterized by deficient red blood cell (RBC) production.
Admittedly the stimulation of erythropoiesis is an affect that is characteristic of
nearly all anabolic steroids, which as a group tend to increase RBC
concentrations. Oxymetholone, however, seemed fairly reliable in this regard;
demonstrating an increase in erythropoietin levels as much as 5 fold.
385 This has
led to its adoption for this relatively new medical use, as well as the institution of
a higher (50 mg) dosage with the updated Anadrol-50 product, necessary for a
stronger effect on RBC count. The Parke Davis item would not be brought up to
the higher dosage, however, and was discontinued.
Recent years have brought fourth a number of new treatments for anemia, most
notably Epogen (recombinant erythropoietin) and related erythropoietic peptides.
These drugs directly mimic the body’s natural red blood cell producing
hormone, and as such provide a much more focused form of therapy, with less of
the unrelated side effects one would have to endure with the use of a strong
androgen. Although Anadrol was once viewed as an effective drug for this
purpose, sales were now dropping. Financial disinterest finally prompted Syntex
to halt production of the U.S. Anadrol 50 in 1993, which was around the same
time they decided to drop this item in a number of foreign countries. Plenastril
from Switzerland and Austria were dropped; following soon was Oxitosona from
Spain. During the mid-1990’s, many Athletes feared oxymetholone was on the
way out for good.
In July 1997, Syntex sold all rights to Anadrol-50 in the U.S., Canada, and
Mexico to Unimed Pharmaceuticals. Unimed reintroduced Anadrol-50 to the
U.S. market in 1998, this time targeting HIV/AIDS patients. Patients with HIV
are commonly anemic, often caused by the disease itself, opportunistic
infections, or the antiretroviral drugs used to treat the disease. The anemia in
HIV patients is typically categorized by impaired red blood cell production in
bone marrow, the FDA approved indication for oxymetholone use. Adding to
this, oxymetholone was showing great promise in studies combating HIV
associated wasting. Unimed soon initiated Phase II/III trials with Anadrol for
HIV wasting syndrome, and continued to research its use for treating such things
as chronic obstructive pulmonary disease and lipodystrophy (a disorder
characterized by a selective loss of body fat, insulin resistance, diabetes, high
triglycerides levels, and a fatty liver).
In April 2006, Solvay Pharmaceuticals (parent company of Unimed) sold the
rights to Anadrol-50 to Alaven Pharmaceutical, LLC. Alaven continues to
market the drug in the United States, although given the transition it is uncertain
what additional uses the company plans to pursue with oxymetholone. At the
present time the only FDA approved indication remains that of treating red blood
cell deficient anemia. Syntex seems to have removed itself from the
oxymetholone market globally, discontinuing product or transferring license to
other companies whenever possible. Oxymetholone remains available outside of
the United States, although it is mostly still sold in smaller and less tightly
regulated markets.
How Supplied:
Oxymetholone is available in select human drug markets. Composition and
dosage may vary by country and manufacturer. Most brands contain 50 mg of
steroid per tablet.
Structural Characteristics:
Oxymetholone is a modified form of dihydrotestosterone. It differs by 1) the
addition of a methyl group at carbon 17alpha, which helps protect the hormone
during oral administration, and 2) the introduction of a 2-hydroxymethylene
group, which inhibits its metabolism by the 3-hsd enzyme and greatly enhances
the anabolic and relative biological activity of methyldihydrotestosterone.
Side Effects (Estrogenic):
Oxymetholone is a highly estrogenic steroid. Gynecomastia is often a concern
during treatment, and may present itself quite early into a cycle (particularly
when higher doses are used). At the same time water retention can become a
problem, causing a notable loss of muscle definition as both subcutaneous water
retention and fat levels build. To avoid strong estrogenic side effects, it may be
necessary to use an anti-estrogen such as Nolvadex® or Clomid®.
It is important to note that oxymetholone does not directly convert to estrogen in
the body. This steroid is a derivative of dihydrotestosterone, and as such cannot
be aromatized. Anti-aromatase compounds such as Cytadren and Arimidex®
will, likewise, not effect the relative estrogenicity of this steroid. Some have
suggested that the high level of estrogenic activity in oxymetholone is actually
due to the drug acting as a progestin, similar to nandrolone. The side effects of
both estrogens and progestins can be very similar, which might have made this
explanation a plausible one. There was a medical study examining the
progestational activity of oxymetholone, however, and it determined that there
was no such activity present.
386 With such findings, it seems most plausible that
oxymetholone can activate the estrogen receptor, similar to, but more profoundly
than, the estrogenic androgen methandriol.
Side Effects (Androgenic):
Although oxymetholone is classified as an anabolic steroid, androgenic side
effects are still possible with this substance. These may include bouts of oily
skin, acne, and body/facial hair growth. Higher doses are more likely to cause
such side effects. Anabolic/androgenic steroids may also aggravate male pattern
hair loss. Women are additionally warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement. While Anadrol is classified as an anabolic steroid, it does retain a
notable androgenic component.
It is interesting to note that oxymetholone does exhibit some tendency to convert
to dihydrotestosterone in the body, although this does not occur via the 5-alpha
reductase enzyme. Oxymetholone is already a dihydrotestosterone-based steroid,
so no such alteration can take place. Aside from the added c-17 alpha alkylation
(discussed below), oxymetholone differs from DHT only by the addition of a 2-
hydroxymethylene group. This grouping can be removed metabolically, reducing
oxymetholone to the potent androgen 17alpha-methyl dihydrotestosterone
(mestanolone).
387 There is little doubt that this biotransformation contributes at
least on some level to the androgenic nature of this steroid. Note that since 5-
alpha reductase is not involved, the relative androgenicity of oxymetholone is
not affected by the concurrent use of finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Oxymetholone is a c17-alpha alkylated compound. This alteration protects the
drug from deactivation by the liver, allowing a very high percentage of the drug
entry into the bloodstream following oral administration. C17-alpha alkylated
anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure
may result in liver damage. In rare instances life-threatening dysfunction may
develop. It is advisable to visit a physician periodically during each cycle to
monitor liver function and overall health. Intake of c17-alpha alkylated steroids
is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain.
Oxymetholone has a saturated A-ring, which slightly reduces its relative
hepatotoxicity.
388 Still, this agent, particularly at the doses commonly used, can
present substantial hepatotoxicity to the user. Studies administering 50 mg or
100 mg daily to 31 elderly men for 12 weeks produced significant increases in
liver enzymes (transaminases AST and ALT) only in patients taking 100 mg. A
second study administering 50 mg daily to 30 patients for up to and exceeding
one year (in some patients) has demonstrated elevations in y-glutamyltransferase
(GGT) in 17% of patients, significant increases in bilirubin in 10%, and serum
albumin increases in 20%.
389 One patient developed a liver tumor that could
have been peliosis hepatitis, a life-threatening adverse event characterized by
blood filled cysts in the liver. A small number of other cases of peliosis hepatitis
have been linked to oxymetholone, suggesting the potential for hepatotoxicity
should still be carefully considered before use.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Oxymetholone has a strong effect on the hepatic management of cholesterol due
to its structural resistance to liver breakdown and route of administration.
Studies administering 50 mg or 100 mg daily to a group of elderly men for 12
weeks have demonstrated insignificant increases in LDL cholesterol,
accompanied by very significant (dramatic) suppressions of HDL cholesterol
(reduced 19 and 23 points in the 50 mg and 100 mg groups, respectively).
390 The
use of oxymetholone should be undertaken only after careful consideration in
people with high cholesterol or a familial history of heart disease.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
Note that when discontinuing oxymetholone, the crash can be as equally
powerful as the on-cycle results. To begin with, the level of water retention will
quickly diminish, dropping the user’s body weight dramatically. This should be
expected, and not of much concern. What is usually of most concern is restoring
endogenous testosterone production with a proper PCT program (see: Post Cycle
Therapy in this book). Before going off, some alternately choose to first switch
over to a milder injectable like Deca-Durabolin® for several weeks. This is in an
effort to “harden up the new mass,”and can prove to be an effective practice, at
least from a mental standpoint. A drop of weight is likely when making the
switch, although the end result is still often viewed as allowing the retention of
more (quality) muscle mass. It is sort of stepping down, first off the water
retention, and weeks later finally off the hormones. Remember ancillaries
though, as testosterone production will not be rebounding during Deca therapy.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
408 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, this steroid should be taken on an empty stomach.
Administration (Men):
Early prescribing guidelines for oxymetholone recommended a dosage of 2.5 mg
three times per day to reverse the wasting process and provide lean body mass
gain. Doses as high as 30 mg were employed in some cases. Current prescribing
guidelines recommend a dosage of 1-5 mg per kilogram of bodyweight per day
for treating anemia, although indicate that a dose of 1-2 mg/kg is typically
sufficient. A 175-pound person would take approximately 150 mg per day at the
2 mg/kg dosage level. In some other countries, it is recommended to limit the
dosing of oxymetholone to 100 mg per day. Therapy is usually given for a
minimum of three to six months. When used for physique-or performanceenhancing purposes, an effective oral daily dosage would fall in the range of 25-
150 mg, taken in cycles lasting no more than 6-8 weeks to minimize
hepatotoxicity. This level is sufficient for dramatic increases in muscle mass and
strength. Higher doses are rarely administered due to the strong estrogenic nature
of the drug, as well as the high potential for hepatotoxicity. When used for
physique-or performance-enhancing purposes, an effective oral daily dosage
would fall in the range of 25-150 mg, taken in cycles lasting no more than 6-8
weeks to minimize hepatotoxicity. This level is sufficient for dramatic increases
in muscle mass and strength. Higher doses are rarely administered due to the
strong estrogenic nature of the drug, as well as the high potential for
hepatotoxicity.
Administration (Women):
Prescribing information for oxymetholone in the U.S. makes no distinction with
the dose for females. Oxymetholone is generally not recommended for women
for physique-or performance-enhancing purposes due to its very strong nature
and tendency to produce virilizing side effects.
Availability:
Pharmaceutical preparations containing oxymetholone are fairly limited. The
legitimate supply seems to be scattered into isolated markets of Europe, Asia,
and the Americas. Most of the supply for this drug comes in the form of
underground and export-only products. In reviewing some of the remaining
products and changes in the legitimate global pharmaceutical market, we have
made the following observations.
Anapolon (Turkey) was recently updated to reflect a new logo for the
manufacturer Abdi Ibrahim. The product is still packaged in boxes of 20 tablets
each.
Oxymetholone-Alhavi (Iran) was recently updated. It is now packaged in foil
and plastic strips of 10 tablets each, 10 strips per box.
Oxymetholone IH (Iran Hormone) was also updated recently. The presentation
remains similar (strips of 10 tablets, 10 per box), though the box looks more
modern with gradient coloring.
Oxyanabolic from Asia Pharma (Malaysia) is now registered for sale in
Thailand.The product comes in strips of 10 tablets, each with an embedded AP
and 50. The product should also carry a unique product ID number that can be
verified on the company website.
Androlic from British Dispensay (Thailand) is also still in production. The
product comes in bottles of 100 tablets each. The tablets are green, scored on one
side, and stamped with the BD snake emblem logo on the other. The product
carries a holographic sticker to deter counterfeiting, though even this sticker has
been duplicated with high accuracy.
Balkan Pharmaceuticals (Moldova) makes the product Anapolon. It is prepared
in 50 mg tablets, with 20 tablets contained in each foil and plastic strip.
Oxybolone from Genepharm Greece is again in production. It contains 50 mg of
steroid per tablet, with 10 packaged in each foil and plastic blister. Two strips
are packed in each box. This product is widely distributed through export.
Oxitoland is manufactured in Paraguay by Laboratorio Farmaceutico/Landerlan.
Each box holds 2 strips foil and plastic blisters of 10 tablets each.
Anadur® (nandrolone hexyloxyphenylpropionate)
Description:
Nandrolone hexyloxyphenylpropionate is a slow-acting injectable form of the
anabolic steroid nandrolone. Hexyloxyphenylpropionate, also called
parahexyloxyphenylpropionate, is a fairly unusual nandrolone ester in a
structural sense. It is essentially nandrolone phenylpropionate, which has been
extended with a tail of one additional oxygen atom and 6 more carbons. It is the
largest, and likely the slowest acting, ester of nandrolone to ever be introduced
into clinical medicine. It is considerably slower acting than the popular DecaDurabolin (nandrolone decanoate), and generally would be administered once
every three to four weeks in a medical setting. Nandrolone
hexyloxyphenylpropionate is no longer manufactured, but when available was
favored by athletes and bodybuilders for its ability to promote slow steady gains
in lean mass with low estrogenic and androgenic side effects.
History:
Nandrolone hexyloxyphenylpropionate was first described in 1960.
391
It was
developed into a medicine shortly after, and was sold mainly under the Anadur
brand name in such markets as Austria, Sweden, Switzerland, Belgium,
Netherlands, and Germany. Anadur persisted through the early 1990’s, and,
following some mergers and acquisitions, was sold mainly by Kabi Pharmacia.
Kabi would also sell the drug in France, but under the brand name Anador.
Indicated uses for the drug included osteoporosis, chronic renal and intestinal
disorders, and radiation and chemotherapy induced suppression of red blood
cells (anemia). It was also used as a general lean-tissue-building anabolic, with
certain diseased states, injury, or convalescence.
Nandrolone hexyloxyphenylpropionate was not widely distributed outside of
Europe, and in spite of a long history of relative safety,would not last as a
medicinal product. The 1995 merger of Kabi with Upjohn formed the company
Pharmacia & Upjohn, and would soon spell the commercial end to Anadur.
Pharmacia & Upjohn did continue to market the drug in Austria, but only
briefly, and soon refined its offerings to eliminate all forms of nandrolone
hexyloxyphenylpropionate in all countries. It is of note that this ester of
nandrolone was also sold by Leo in Spain (Anadur), Lundbeck in Denmark
(Anadur), Eczacibasi in Turkey (Anadur), and by Xponei in Greece (Anadurin),
much under direct license with Kabi. All such preparations have since been
discontinued as well, however, and nandrolone hexyloxyphenylpropionate is no
longer available as a commercial medicine.
How Supplied:
Nandrolone hexyloxyphenylpropionate is no longer available as a prescription
drug product. When supplied, it usually contained 25 mg/mL or 50 mg/mL of
steroid dissolved in oil in a 1 mL or 2 mL ampule.
Structural Characteristics:
Nandrolone hexyloxyphenylpropionate is a modified form of nandrolone, where
a carboxylic acid ester (parahexyloxyphenylpropionic acid) has been attached to
the 17-beta hydroxyl group. Esterified steroids are less polar than free steroids,
and are absorbed more slowly from the area of injection. Once in the
bloodstream, the ester is removed to yield free (active) nandrolone. Esterified
steroids are designed to prolong the window of therapeutic effect following
administration, allowing for a less frequent injection schedule compared to
injections of free (unesterified) steroid. Nandrolone hexyloxyphenylpropionate is
designed to provide a slow release of nandrolone for up to four weeks following
injection.
Side Effects (Estrogenic):
Nandrolone has a low tendency for estrogen conversion, estimated to be only
about 20% of that seen with testosterone.
392 This is because while the liver can
convert nandrolone to estradiol, in other more active sites of steroid
aromatization such as adipose tissue nandrolone is far less open to this
process.
393 Consequently, estrogen related side effects are a much lower concern
with this drug than with testosterone. Elevated estrogen levels may still be
noticed with higher dosing, however, and may cause side effects such as
increased water retention, body fat gain, and gynecomastia. An anti-estrogen
such as clomiphene citrate or tamoxifen citrate may be necessary to prevent
estrogenic side effects if they occur. One may alternately use an aromatase
inhibitor like Arimidex® (anastrozole), which more efficiently controls estrogen
by preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
It is of note that nandrolone has some activity as a progestin in the body.
394
Although progesterone is a c-19 steroid, removal of this group as in 19-
norprogesterone creates a hormone with greater binding affinity for its
corresponding receptor. Sharing this trait, many 19-nor anabolic steroids are
shown to have some affinity for the progesterone receptor as well.
395 The side
effects associated with progesterone are similar to those of estrogen, including
negative feedback inhibition of testosterone production and enhanced rate of fat
storage. Progestins also augment the stimulatory effect of estrogens on
mammary tissue growth. There appears to be a strong synergy between these
two hormones here, such that gynecomastia might even occur with the help of
progestins, without excessive estrogen levels. The use of an anti-estrogen, which
inhibits the estrogenic component of this disorder, is often sufficient to mitigate
gynecomastia caused by nandrolone.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance, especially with higher doses. This may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are warned of the
potential virilizing effects of anabolic/androgenic steroids. These may include a
deepening of the voice, menstrual irregularities, changes in skin texture, facial
hair growth, and clitoral enlargement. Nandrolone is a steroid with relatively low
androgenic activity relative to its tissue-building actions, making the threshold
for strong androgenic side effects comparably higher than with more androgenic
agents such as testosterone, methandrostenolone, or fluoxymesterone. It is also
important to point out that due to its mild androgenic nature and ability to
suppress endogenous testosterone, nandrolone is prone to interfering with libido
in males when used without another androgen.
Note that in androgen-responsive target tissues such as the skin, scalp, and
prostate, the relative androgenicity of nandrolone is reduced by its reduction to
dihydronandrolone (DHN).
396 397 The 5-alpha reductase enzyme is responsible
for this metabolism of nandrolone. The concurrent use of a 5-alpha reductase
inhibitor such as finasteride or dutasteride will interfere with site-specific
reduction of nandrolone action, considerably increasing the tendency of
nandrolone to produce androgenic side effects. Reductase inhibitors should be
avoided with nandrolone if low androgenicity is desired.
Side Effects (Hepatotoxicity):
Nandrolone is not c-17 alpha alkylated, and not known to have hepatotoxic
effects. Liver toxicity is unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Studies
administering 600 mg of nandrolone decanoate per week for 10 weeks
demonstrated a 26% reduction in HDL cholesterol levels.
398 This suppression is
slightly greater than that reported with an equal dose of testosterone enanthate,
and is in agreement with earlier studies showing a slightly stronger negative
impact on HDL/LDL ratio with nandrolone decanoate as compared to
testosterone cypionate.
399 Nandrolone injectables, however, should still have a
significantly weaker impact on serum lipids than c-17 alpha alkylated agents.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production. For
sake of comparison, studies administering 100 mg per week of nandrolone
decanoate for 6 weeks have demonstrated an approximate 57% reduction in
serum testosterone levels during therapy. At a dosage of 300 mg per week, this
reduction reached 70%.
400
It is believed that the progestational activity of
nandrolone notably contributes to the suppression of testosterone synthesis
during therapy, which can be marked in spite of a low tendency for estrogen
conversion.
401 Without the intervention of testosterone stimulating substances,
testosterone levels should return to normal within 2-6 months of drug secession.
Note that prolonged hypogonadotrophic hypogonadism can develop secondary
to steroid abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
When used for physique-or performance-enhancing purposes, a dose of 200-400
mg given every week to 10 days was most common, taken in cycles eight to
twelve weeks in length. This level is sufficient for most users to notice
measurable gains in lean muscle mass and strength, which should be
accompanied by a low level of estrogenic and androgenic activity.
Administration (Women):
When used for physique-or performance-enhancing purposes, a dosage of 50 mg
per week, or 100 mg every 10-14 days, was most common. Although only
slightly androgenic, women are occasionally confronted with virilization
symptoms when taking this compound. Should virilizing side effects become a
concern, the drug should be discontinued immediately to help prevent their
permanent appearance. After a sufficient period of withdrawal, the shorter acting
nandrolone Durabolin® might be considered a safer (more controllable) option.
This drug stays active for only several days, greatly reducing the withdrawal
time if indicated.
Availability:
Nandrolone hexyloxyphenylpropionate is no longer available as a prescription
drug product.
Anavar (oxandrolone)
Description:
Oxandrolone is an oral anabolic steroid derived from dihydrotestosterone. It was
designed to have a very strong separation of anabolic and androgenic effect, and
no significant estrogenic or progestational activity. Oxandrolone is noted for
being quite mild as far as oral steroids are concerned, well tailored for the
promotion of strength and quality muscle tissue gains without significant side
effects. Milligram for milligram it displays as much as six times the anabolic
activity of testosterone in assays, with significantly less androgenicity.
402 This
drug is a favorite of dieting bodybuilders and competitive athletes in
speed/anaerobic performance sports, where its tendency for pure tissue gain
(without fat or water retention) fits well with the desired goals.
History:
Oxandrolone was first described in 1962.
403
It was developed into a medicine
several years later by pharmaceutical giant G.D. Searle & Co. (now Pfizer),
which sold it in the United States and the Netherlands under the Anavar trade
name. Searle also sold/licensed the drug under different trade names including
Lonavar (Argentina, Australia), Lipidex (Brazil), Antitriol (Spain), Anatrophill
(France), and Protivar. Oxandrolone was designed to be an extremely mild oral
anabolic, one that could even be used safely by women and children. In this
regard Searle seems to have succeeded, as Anavar has shown a high degree of
therapeutic success and tolerability in men, women, and children alike. During
its early years, Anavar had been offered for a number of therapeutic applications,
including the promotion of lean tissue growth during catabolic illness, the
promotion of lean tissue growth following surgery, trauma, infection, or
prolonged corticosteroid administration, or the support of bone density in
patients with osteoporosis.
By the 1980’s, the FDA had slightly refined the approved applications of
oxandrolone to include the promotion of weight gain following surgery, chronic
infection, trauma, or weight loss without definite pathophysiologic reason. In
spite of its ongoing track record of safety, Searle decided to voluntarily
discontinue the sale of Anavar on July 1, 1989. Lagging sales and growing
public concern about the athletic use of anabolic steroids appeared to be at the
root of this decision. With the Anavar brand off the market, oxandrolone had
completely vanished from U.S. pharmacies. Soon after, oxandrolone products in
international markets (often sold by or under license from Searle) began to
disappear as well, as the leading global manufacturer of the drug continued its
withdrawal from the anabolic steroid business. For several years during the early
1990’s, it looked as if Anavar might be on its way out of commerce for good.
It would be approximately six years before oxandrolone tablets would be back
on the U.S. market. The product returned to pharmacy shelves in December
1995, this time under the Oxandrin name by Bio-Technology General Corp.
(BTG). BTG would continue selling it for the FDA approved uses involving lean
mass preservation, but had also been granted orphan-drug status for the
treatment of AIDS wasting, alcoholic hepatitis, Turner's syndrome in girls, and
constitutional delay of growth and puberty in boys. Orphan drug status gave
BTG a 7-year monopoly on the drug for these new uses, allowing them to
protect a very high selling price. Many patients were outraged to learn that the
drug would cost them (at wholesale price) between $3.75 and $30 per day,
which was many times more costly than Anavar had been just several years
back. The release of a 10 mg tablet from BTG several years later did little to
reduce the relative cost of the drug.
Oxandrin® continues to be sold in the U.S., but is now under the Savient label
(formerly known as BTG). It is currently approved by the FDA for “adjunctive
therapy to promote weight gain after weight loss following extensive surgery,
chronic infections, or severe trauma and in some patients who without definite
pathophysiologic reasons fail to gain or to maintain normal weight, to offset the
protein catabolism associated with prolonged administration of corticosteroids,
and for the relief of the bone pain frequently accompanying osteoporosis.”
Generic versions of the drug are now available in the U.S., which has reduced
the price of oxandrolone therapy. Outside of the U.S., oxandrolone remains
available, although not widely.
How Supplied:
Oxandrolone is available in select human drug markets. Composition and dosage
may vary by country and manufacturer. The original Anavar brand contained 2.5
mg of steroid per tablet. Oxandrin contains 2.5 mg or 10 mg per tablet. Other
modern brands commonly contain 2.5 mg, 5 mg, or 10 mg of steroid per tablet.
Structural Characteristics:
Oxandrolone is a modified form of dihydrotestosterone. It differs by: 1) the
addition of a methyl group at carbon 17-alpha to protect the hormone during oral
administration and 2) the substitution of carbon-2 in the A-ring with an oxygen
atom. Oxandrolone is the only commercially available steroid with such a
substitution to its basic ring structure, an alteration that considerably increases
the anabolic strength of the steroid (partly by making it resistant to metabolism
by 3-hydroxysteroid dehydrogenase in skeletal muscle tissue).
Side Effects (Estrogenic):
Oxandrolone is not aromatized by the body, and is not measurably estrogenic.
Oxandrolone also offers no related progestational activity.
404 An anti-estrogen is
not necessary when using this steroid, as gynecomastia should not be a concern
even among sensitive individuals. Since estrogen is the usual culprit with water
retention, oxandrolone instead produces a lean, quality look to the physique with
no fear of excess subcutaneous fluid retention. This makes it a favorable steroid
to use during cutting cycles, when water and fat retention are major concerns.
Oxandrolone is also very popular among athletes in strength/speed sports such as
sprinting, swimming, and gymnastics. In such disciplines one usually does not
want to carry around excess water weight, and may find the raw muscle-growth
brought about by oxandrolone to be quite favorable over the lower quality mass
gains of aromatizable agents.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance. This may include bouts of oily skin, acne, and
body/facial hair growth. Anabolic/androgenic steroids may also aggravate male
pattern hair loss. Women are warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement. Oxandrolone is a steroid with low androgenic activity relative to its
tissue-building actions, making the threshold for strong androgenic side effects
comparably higher than with more androgenic agents such as testosterone,
methandrostenolone, or fluoxymesterone.
The low androgenic activity of oxandrolone is due in part to it being a derivative
of dihydrotestosterone. This creates a less androgenic steroid because the agent
lacks the capacity to interact with the 5-alpha reductase enzyme and convert to a
more potent “dihydro”form. This is unlike testosterone, which is several times
more active in androgen responsive target tissues such as the scalp, skin, and
prostate (where 5-alpha reductase is present in high amounts) due to its
conversion to DHT. In essence, oxandrolone has a more balanced level of
potency between muscle and androgenic target tissues. This is a similar situation
as is noted with Primobolan and Winstrol, which are also derived from
dihydrotestosterone and not known to be very androgenic substances.
Side Effects (Hepatotoxicity):
Oxandrolone is a c17-alpha alkylated compound. This alteration protects the
drug from deactivation by the liver, allowing a very high percentage of the drug
entry into the bloodstream following oral administration. C17-alpha alkylated
anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure
may result in liver damage. In rare instances life-threatening dysfunction may
develop. It is advisable to visit a physician periodically during each cycle to
monitor liver function and overall health. Intake of c17-alpha alkylated steroids
is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain.
Oxandrolone appears to offer less hepatic stress than other c-17 alpha alkylated
steroids. The manufacturer identifies oxandrolone as a steroid that is not
extensively metabolized by the liver like other 17-alpha alkylated orals, which
may be a factor in its reduced hepatotoxicity. This is evidenced by the fact that
more than a third of the compound is still intact when excreted in the urine.
405
Another study comparing the effects of oxandrolone to other alkylated agents
including methyltestosterone, norethandrolone, fluoxymesterone, and
methandriol demonstrated that oxandrolone causes the lowest
sulfobromophthalein (BSP; a marker of liver stress) retention of the agents
tested.
406 20 mg of oxandrolone produced 72% less BSP retention than an equal
dosage of fluoxymesterone,which is a considerable difference being that they are
both 17-alpha alkylated.
A more recent study looked at escalating doses (20 mg, 40 mg, and 80 mg) of
oxandrolone in 262 HIV+ men.The drug was administered for a period of 12
weeks. The group taking 20 mg of oxandrolone per day showed no statistically
significant trends of hepatotoxicity in liver enzyme (AST/ALT; aminotransferase and alanine amino-transferase) values. Those men taking 40 mg
noticed a mean increase of approximately 30-50% in liver enzyme values, while
the group of men taking 80 mg noticed an approximate 50-100% increase.
Approximately 10-11% of the patients in the 40 mg group noticed World Health
Organization grade III and IV toxicity according to AST and ALT values. This
figure jumped to 15% in the 80 mg group. While serious hepatotoxicity cannot
be excluded with oxandrolone, these studies do suggest that it is measurably
safer than other alkylated agents.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Oxandrolone has a
strong effect on the hepatic management of cholesterol due to its structural
resistance to liver breakdown, non-aromatizable nature, and route of
administration. In the previously cited study in HIV+ males, 20 mg of
oxandrolone daily for 12 weeks caused a mean serum HDL reduction of 30%.
HDL values were suppressed 33% in the 40 mg group, and 50% in the 80 mg
group. This was accompanied by a statistically significant increase in LDL
values (approximately 30-33%) in the 40 mg and 80 mg groups, further
increasing atherogenic risk. Anabolic/androgenic steroids may also adversely
effect blood pressure and triglycerides, reduce endothelial relaxation, and
support left ventricular hypertrophy, all potentially increasing the risk of
cardiovascular disease and myocardial infarction.
At one time oxandrolone was looked at as a possible drug for those suffering
from disorders of high cholesterol or triglycerides. Early studies showed it to be
capable of lowering total cholesterol and triglyceride values in certain types of
hyperlipidemic patients, which was thought to signify potential for this drug as a
lipid-lowering agent.
407 With further investigation it was found, however, that
any lowering of total cholesterol values was accompanied by a redistribution in
the ratio of good (HDL) to bad (LDL) cholesterol that favored greater
atherogenic risk.
408 409 This negates any positive effect this drug might have on
triglycerides or total cholesterol, and actually makes it a potential danger in
terms of cardiac risk, especially when taken for prolonged periods of time.
Today we understand that as a group, anabolic/androgenic steroids tend to
produce unfavorable changes in lipid profiles, and are really not useful in
disorders of lipid metabolism. As an oral c17 alpha alkylated steroid,
oxandrolone is even more risky to use in this regard than an esterified injectable
such as a testosterone or nandrolone.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Oxandrolone is no exception. In the above-cited study on HIV+ males, twelve
weeks of 20 mg or 40 mg per day caused an approximate 45% reduction in
serum testosterone levels. The group taking 80 mg noticed a 66% decrease in
testosterone. Similar trends of decrease were noticed in LH production, with the
20 mg and 40 mg doses causing a 25-30% reduction, and the 80 mg group
noticing a decline of more than 50%. Additionally, studies on boys with
constitutionally delayed puberty have demonstrated significant suppression of
endogenous LH and testosterone with as little as 2.5 mg per day.
410 Without the
intervention of testosterone stimulating substances, testosterone levels should
return to normal within 1-4 months of drug secession. Note that prolonged
hypogonadotrophic hypogonadism can develop secondary to steroid abuse,
necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
411 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, this steroid should be taken on an empty stomach.
Administration (Men):
The original prescribing guidelines for Anavar called for a daily dosage of
between 2.5 mg and 20 mg per day (5-10 mg being most common). This was
usually recommended for a period of two to four weeks, but occasionally it was
taken for as long as three months. The dosing guidelines recommended with the
current U.S. production form of the drug (Oxandrin, Savient Pharmaceuticals)
also call for between 2.5 and 20 mg of drug per day, taken in intermittent cycles
of 2 to 4 weeks. The usual dosage for physique-or performance-enhancing
purposes is in the range of 15-25 mg per day, taken for 6 to 8 weeks. These
protocols are not far removed from those of normal therapeutic situations.
Oxandrolone is often combined with other steroids for a more dramatic result.
For example, while bulking one might opt to add in 200-400 mg of a
testosterone ester (cypionate, enanthate, or propionate) per week. The result
should be a considerable gain in new muscle mass, with a more comfortable
level of water and fat retention than if taking a higher dose of testosterone alone.
For dieting phases, one might alternately combine oxandrolone with a nonaromatizing steroid such as 150 mg per week of a trenbolone ester or 200-300
mg of Primobolan® (methenolone enanthate). Such stacks are highly favored for
increasing definition and muscularity. An in-between (lean mass gain) might be
to add in 200-400 mg of a low estrogenic compound like Deca-Durabolin®
(nandrolone decanoate) or Equipoise® (boldenone undecylenate).
Administration (Women):
The original prescribing guidelines for Anavar did not offer separate dosing
recommendations for women, although it was indicated that women who were
pregnant, or may become pregnant, should not use the drug. The current
guidelines for Oxandrin also do not make special dosing recommendations for
women. Women who fear the masculinizing effects of many steroids would be
quite comfortable using this drug, as these properties are very rarely seen with
low doses. For physique-or performance-enhancing purposes, a daily dosage of
5-10 mg should illicit considerable growth without the noticeable androgenic
side effects of other drugs. This would be taken for no longer than 4-6 weeks.
Eager females may wish to add another mild anabolic such as Winstrol®,
Primobolan® or Durabolin®. When combined with such anabolics, the user
should notice faster, more pronounced muscle-building effects, but it may also
increase the likelihood of seeing androgenic side effects (or hepatotoxicity in the
case of Winstrol).
Availability:
Pharmaceutical preparations containing oxandrolone are fairly limited. The drug
is unavailable in Europe, and with a handful of exceptions in the west, its
production is increasingly being shifted to less regulated markets in Asia. In
reviewing some of the remaining products and changes on the global
pharmaceutical market, we have made the following observations.
Various forms of generic oxandrolone are now available in the U.S. in both 2.5
mg and 10 mg dosages, from manufacturers such as Par Pharm, Sandoz, Upsher
Smith, and Watson.
Brand name Oxandrin is still available in the U.S. under the Savient brand name.
It comes in bottles of 60 (10 mg) tablets or 100 (2.5 mg) tablets each.
The generic Italian product Oxandrolone (SPA) is no longer available. It was
previously being made for export sales only. There are no remaining
oxandrolone products available on the Italian market.
Atlantis (Mexico) produces an oxandrolone product called Xtendrol. It carries
2.5 mg of steroid per tablet, and comes in a box of 30 tablets each.
Asia Pharma makes the product Oxanabolic in Malaysia. It comes in strips of 10
tablets each, 10 strips per box. Each product should carry a unique product ID
code that can be verified with the company for authenticity. This product is
presently export only, but the manufacturer claims to be in the process of
seeking Thai FDA approval.
Balkan Pharmaceuticals (Moldova) makes the product Oxandrolon. It is
prepared in 10 mg tablets, with 20 tablets contained in each foil and plastic strip.
Andractim® (dihydrotestosterone)
Description:
Andractim is a prescription steroid preparation that contains the potent
androgenic steroid dihydrotestosterone. This product comes in the form of a
transdermal gel, typically containing 2.5% dihydrotestosterone by weight in an
80gram tube. As with Androgel, roughly 10% of the active steroid will make it
into circulation with each application.This would equate to 80 doses of 25 mg,
with each dose delivering approximately 2.5 mg of steroid to the body.
Dihydrotestosterone itself is the most active androgen in the human body,
displaying an ability to bind and activate the androgen receptor at least three or
four times greater than that of its parent steroid testosterone. This trait, however,
is not accompanied by equally powerful anabolic tendencies. In the case of
dihydrotestosterone, we have a steroid that is almost purely androgenic, with
only minimal muscle-building (anabolic) action.
Dihydrotestosterone is a weak muscle builder because it is extremely open to
alteration by the 3-alpha-hydroxysteroid-dehydrogenase enzyme, responsible for
breaking down active steroids like DHT into their inactive metabolites. 3a-HSD
is present in high quantities in muscle tissue, running interference between the
outer cell membrane and the androgen receptors that all steroid hormones are
trying to reach. In humans, little DHT ends up actually reaching this receptor.
Testosterone is very resistant to this enzyme, however, which allows it to be a
much more effective muscle-building agent. 3a-HSD steroid deactivation in
muscle tissue causes the same problem with Proviron (1-methyldihydrotestosterone). DHT and Proviron both have very effective uses in areas
such as fat loss, hardening, increasing CNS activity, and pure strength gains, but
they do not perform well as anabolic agents.
History:
Dihydrotestosterone was first synthesized in 1935.
412 This strong androgen was
put into consistent medical use during the late 1950’s, after a series of
experiments demonstrating that it had measurable anabolic effects. Prior to this it
was largely believed that DHT was exclusively an androgenic substance, and
was of little value clinically. Dihydrotestosterone gels were developed more
recently, and have been investigated for a number of medical purposes. At
present, these preparations are primarily indicated for the treatment of androgen
deficiency, gynecomastia, and insufficient genital growth. Transdermal DHT has
been successful as an androgen replacement medication in older men at risk for
developing prostate hypertrophy largely because of its non-aromatizable
nature,
413 414 as this disorder is fueled partly by estrogens. The latter two
indications are considered local applications of the drug, and the DHT gel is
applied directly to the tissues requiring treatment.
The primary manufacturer of dihydrotestosterone gel globally is Besins
International, based in France. Besins produces the drug under the Andractim
name, selling it in France and scarcely in other parts of Europe.
Dihydrotestosterone gels are found much less commonly outside of Europe, and
presently no such preparation is commercially available in the United States. In
1995, U.S. manufacturer Unimed Pharmaceuticals purchased the rights to
Andractim from Besins in the U.S., Mexico, and Canada. The firm announced an
interest in the drug for several uses, including androgen replacement in men over
age sixty, treating benign prostate hypertrophy, and combating HIV-associated
wasting. Its use as an anabolic may be desirable with HIV because it had been
determined that many patients lack an ability to properly convert testosterone to
DHT, and therefore lack sufficient levels of this important androgen. It appears
that Unimed has since sold its interests in the anabolic steroid market, however,
leaving the potential reemergence of dihydrotestosterone in the U.S. in question.
How Supplied:
Hydroalcoholic transdermal dihydrotestosterone gels are available in select
human drug markets. Composition and dosage may vary by country and
manufacturer, but usually contain 2.5% dihydrotestosterone by weight.
Structural Characteristics:
Andractim® is a hydroalcoholic gel containing 2.5% of dihydrotestosterone
(free) by weight. It is designed to provide a continuous transdermal delivery of
dihydrotestosterone for 24 hours following application to the skin.
Approximately 10% of the applied dose is absorbed across the skin during each
24-hour period.
Side Effects (Estrogenic):
Dihydrotestosterone is not aromatized by the body, and is not measurably
estrogenic. An anti-estrogen is not necessary when using this steroid, as
gynecomastia and water retention should not be concerns even among sensitive
individuals. DHT also has inherent anti-estrogenic properties, competing with
other substrates for binding to the aromatase enzyme. Percutaneous
dihydrotestosterone may be an effective option for the treatment of
gynecomastia. Studies have reported a good level of success when treating
certain forms of this disorder with Andractim, the drug affecting the ratio of
androgenic to estrogenic action in the breast area enough that a notable
regression of mammary tissue has been achieved in many cases.
415 416
Side Effects (Androgenic):
Dihydrotestosterone is the strongest natural male androgen. Higher than normal
therapeutic doses are likely to produce androgenic side effects including oily
skin, acne, and body/facial hair growth. Men with a genetic predisposition for
hair loss (androgenetic alopecia) may notice accelerated male pattern balding.
Women are warned of the potential virilizing effects of anabolic/androgenic
steroids, especially with a strong androgen such as dihydrotestosterone.These
may include deepening of the voice, menstrual irregularities, changes in skin
texture, facial hair growth, and clitoral enlargement. Note that the 5-alpha
reductase enzyme does not metabolize dihydrotestosterone, so its relative
androgenicity is not affected by finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Dihydrotestosterone does not have hepatotoxic effects; liver toxicity is unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction. Therapeutic doses of dihydrotestosterone used to correct
insufficient androgen production in otherwise healthy aging men are unlikely to
increase atherogenic risk. Higher doses are likely to increase atherogenic risk,
but less dramatically than equivalent doses of synthetic oral anabolic/androgenic
steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
To treat androgen insufficiency, hydroalcoholic transdermal dihydrotestosterone
gels have been used in doses ranging from 16 to 64mg per day (1.6-6.4mg of
hormone delivered). For physique-or performance-enhancing purposes, higher
doses would be necessary to achieve strong supraphysiological levels of
dihydrotestosterone. Logical effective doses begin in the range of 50-100 mg per
day, or 5-10 mg of hormone delivered systemically. Dihydrotestosterone is of
little value for building muscle, and is most commonly applied for cutting or
pure-strength-promoting purposes.
Administration (Women):
Hydroalcoholic transdermal dihydrotestosterone gel is not recommended for
women for physique-or performance-enhancing purposes due to its strong
androgenic nature and tendency to produce virilizing side effects.
Availability:
Pharmaceutical preparations containing transdermal dihydrotestosterone gel
remain scarce. The legitimate supply seems to be scattered into isolated markets
of Europe, Asia, and South America. In reviewing some of the remaining
products and changes in the global pharmaceutical market, we have made the
following observations.
One of the most notable preparations is Andractim from Besins-Iscovesco in
France. It contains 25 mg/mL of hormone in a 100 gram tube.
Andractim is produced in Belgium by Piette. It contains 25 mg/mL of hormone
in an 80 gram tube.
Andractim is produced in India by Chemec. It contains 25 mg/mL of hormone in
a 100 gram tube.
Andriol® (testosterone undecanoate)
Description:
Andriol® is an oral testosterone preparation that contains 40 mg of testosterone
undecanoate (in an oil base) in a soft gelatin capsule. This drug is very different
than most oral anabolic steroids, which are usually c-17 alpha alkylated to
survive first pass metabolism through the liver. Instead, esterification and
suspension in oil allows the testosterone undecanoate in Andriol® to be partially
absorbed through the lymphatic system along with dietary fat. This bypasses the
destructive first-pass through liver, providing sustained physiological levels of
testosterone to the body. The actual oral bioavailability of Andriol is estimated
to be approximately 7%. In design, this steroid is essentially a non-toxic and
orally active testosterone, intended to provide a unique alternative to testosterone
injections and other hepatotoxic oral anabolic/androgenic steroids.
History:
Oral testosterone undecanoate capsules were developed by international drug
giant Organon (now Merck/MSD), and first introduced into clinical trials during
the early 1980’s. The drug was soon approved for use as a prescription agent in a
number of countries around the globe, generally under the Andriol brand name,
although Organon has also marketed it as Androxon, Panteston, Restandol,
Undestor, and Virigen in certain markets. This drug preparation is indicated for
testosterone replacement therapy in males with conditions associated with
insufficient endogenous androgen production. Although there is a large market
for androgen replacement drugs in the United States, the drug is not approved for
sale on the U.S. market. It has been approved as a prescription agent in the
bordering markets of Mexico and Canada, however.
In 2003, Organon began replacing its Andriol products with Andriol®
Testocaps®. The new formulation improves on the storage limitations of the
original Andriol preparations, which needed to be kept under refrigeration at the
pharmacy. The drug was stored at room temperature once dispensed, as the
product needed to be consumed at room temperature. Outside of refrigeration,
however, the drug functionally had only a 3-month shelf life. The new Andriol
Testocaps are designed to always be stored at room temperature, and have a
shelf life of 3 years. The new formulation is considered to be bioequivalent to
the older version, and can be substituted in patients without any change in
dosage.
417 Given the handling advantages and bioequivalency, it is likely that
the new Testocaps will slowly come to replace all of the older Andriol
preparations.
In spite of its wide availability, Andriol has never been a popular item among
athletes. This is likely due to the high relative cost of the drug, and its low
potency compared to other pharmaceutical preparations, particularly injectable
testosterone compounds and the more potent synthetic oral anabolic steroids.
Still, Andriol remains a product of choice among those athletes not interested in
using injectable medications and preferring to avoid the greater risks of
hepatotoxicity and lipid alterations inherent in c-17 alpha alkylated orals. Today,
decades after its initial release, Merck/MSD remains the sole global producer of
prescription oral testosterone undecanoate. Andriol itself has maintained a
prominent share of the global hormone replacement market since the 1990’s.
How Supplied:
Oral testosterone undecanoate preparations are available in various human drug
markets. The older formulations supply 40 mg of testosterone undecanoate in
oleic acid, contained in small soft gelatin capsules. Andriol Testocaps supplies
40 mg of testosterone undecanoate in castor oil and propylene glycol
monolaurate, contained in small soft gelatin capsules. Packaging is commonly as
bottles of 30 or 60 capsules, or foil/plastic strips of 10 capsules. Subtracting the
ester weight, each 40 mg Andriol capsule contains 25.3mg of (base) testosterone.
Structural Characteristics:
Andriol® contains testosterone that has been modified with the addition of
carboxylic acid ester (undecanoic acid) at the 17-beta hydroxyl group. The
esterified hormone is more fat soluble than base (free) testosterone, and has been
dissolved in oil and encapsulated for oral administration. Significant absorption
of oral testosterone undecanoate takes place through the lymphatic route,
bypassing the first pass through the liver. Andriol® is designed to provide a peak
in testosterone levels several hours after administration, and with repeated
dosing maintain physiological concentrations for 24 hours.
Figure 1. Median response pharmacokinetics after oral administration of 80
mg of testosterone undecanoate in fasted and fed states. Testosterone
absorption is impaired when taken without meals. Source: Andriol
Testocaps online information, Organon. Citation Bachus et al, 2001.
Andriol.com.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. Exceeding therapeutic doses will increase the
likelihood of estrogenic side effects. In such cases, an anti-estrogen such as
clomiphene citrate or tamoxifen citrate is commonly applied to prevent
estrogenic side effects. One may alternately use an aromatase inhibitor like
Arimidex® (anastrozole), which more efficiently controls estrogen by
preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Taking oral testosterone undecanoate in
doses exceeding normal therapeutic levels is likely to produce androgenic side
effects including oily skin, acne, and body/facial hair growth. Men with a
genetic predisposition for hair loss (androgenetic alopecia) may notice
accelerated male pattern balding. Women are warned of the potential virilizing
effects of anabolic/androgenic steroids, especially with a strong androgen such
as testosterone. These may include deepening of the voice, menstrual
irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of oral
testosterone by administering 400 mg of the hormone per day (2,800 mg per
week) to a group of male subjects. The hormone was given daily for 20 days,
and produced no significant changes in liver enzyme values including serum
albumin, bilirubin, alanine-amino-transferase, and alkaline phosphatases.
418 No
study in which liver enzymes were examined has demonstrated an adverse
hepatotoxic effect from Andriol, including an examination of patients on
continuous therapy for 10 years.
419
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely effect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction. Therapeutic doses of oral testosterone undecanoate used
to correct insufficient androgen production in otherwise healthy aging men are
unlikely to increase atherogenic risk, and may actually improve lipid profiles and
cardiovascular risk factors.
420
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Andriol should always be taken with meals, preferably containing a moderate fat
content (20 grams) to maximize lymphatic absorption. Very low bioavailability
has been reported when taken in the fasted state. The total daily dosage should
be divided into a minimum of two applications, taken in the morning and
evening, to maintain more consistent elevations of serum testosterone.
Administration (Men):
For the treatment of low androgen levels, prescribing guidelines for Andriol
recommend an initial dosage of 120-160 mg daily for 2-3 weeks. Based on the
level of effect, a daily maintenance dosage of 40-120 mg is usually continued at
this point. For bodybuilding purposes, higher doses would be required to reach
strong supraphysiological levels of testosterone. This would generally call for a
minimum dosage of 240-280 mg per day (6-8 capsules), taken in cycles of 6-8
weeks. A more common effective dosage, however, would fall in the range of
400-480 mg (10 to 12 capsules) per day. These doses can be quite costly given
the relative price of Andriol preparations, making injectable testosterones much
more cost effective and popular. Given the relative low potency of Andriol,
when taken by athletes it is most commonly used in combination with other
agents. Testosterone drugs are ultimately very versatile, and can be stacked with
many other anabolic/androgenic steroids depending on the desired effect.
Administration (Women):
Andriol is not prescribed to women in clinical medicine. This drug is not
recommended for women for physique or performance-enhancing purposes due
to its strong androgenic nature and tendency to produce virilizing side effects.
Availability:
Oral testosterone undecanoate remains widely available. It is produced almost
exclusive by or under license from Organon (now Merck/MSD). In reviewing
some of the more popular products and changes on the global pharmaceutical
market, we have made the following observations.
In November 2009, Organon (a subsidiary of ScheringPlough since 2007)
became part of Merck/MSD. All Organon products are expected to transition
over to this label. It is unknown what (if any) changes to expect in the global
distribution of Andriol products.
The softgel design of the Andriol products is extremely difficult to duplicate.
Andriol® is prepared as a brown/red colored capsule that contains oil inside. It is
completely sealed. The Testocaps® are also soft oval glossy capsules, but these
are made out of a transparent orange gelatin mixture. Inside there is a yellow
oily liquid. DV3 and ORG are printed on the surface of both types of capsules.
Legitimate Organon oral testosterone undecanoate has been sold under the brand
names Andriol®, Andriol® Testocaps®, Androxon, Panteston, Restandol,
Undestor, and Virigen. Andriol is regarded as an older version of this
preparation, and remains available only in a limited number of markets
worldwide.
Androderm® (testosterone)
Description:
Androderm® is a testosterone delivery system that utilizes an adhesive “patch”
to deliver the hormone transdermally. The testosterone itself is dissolved in an
alcoholic gel similar to AndroGel®, except here the gel is contained in a
protected external drug reservoir. This design provides approximately double the
hormone bioavailability of AndroGel®, and also severely limits the transfer of
testosterone to other people during rigorous skin-to-skin contact. The patches
come in two strengths, 2.5 mg and 5 mg, indicating the amount of testosterone
each is to supply systemically over a 24-hour period (they contain 12.2 and
24.3mg of testosterone respectively). Androderm® was designed to mimic the
natural circadian rhythm of testosterone release in healthy young men, higher
during the first 12 hours and lower during the next 12 hours of each day. The
clinical significance of this, if any, is not known.
History:
Androderm® was developed in the United States by TheraTech (Salt Lake City).
It was approved for sale as a prescription agent by the Food and Drug
Administration in September 1995, and is indicated for testosterone replacement
therapy in men with a deficiency or absence of endogenous testosterone. This
includes cases of primary hypogonadism, which may be caused by
cryptorchidism, bilateral torsion, orchitis, vanishing testis syndrome,
orchiectomy, Klinefelter’s syndrome, chemotherapy, or alcohol/heavy metal
toxicity. It is also prescribed to treat hypogonadotrophic hypogonadism,
including patients with luteinizing hormone or luteinizing hormone-releasing
hormone (LHRH) deficiency caused by tumors, injury, or radiation. Primary
hypogonadism is usually characterized by low testosterone and high
gonadotropin (LH/FSH) levels, while hypogonadotrophic hypogonadism is
usually associated with low testosterone and low to normal gonadotropin levels.
Watson currently sells this product in the United States under the Androderm®
brand name. In Europe, the ATMOS® brand from Astra is most commonly
found.
How Supplied:
TheraTech’s transdermal testosterone system is available in select human drug
markets, where it is commonly sold as Androderm® or ATMOS®. It is
produced in two strengths, one containing 12.2mg of testosterone, and one
containing 24.3mg of testosterone. These are intended to deliver approximately
2.5 mg and 5 mg of testosterone systemically to the patient over a 24-hour
period.
Structural Characteristics:
Androderm® is a transdermal drug delivery system that contains an alcoholic gel
of testosterone (free) enclosed in an adhesive patch with a protected drug
reservoir. It is designed to provide steady but varying levels of testosterone
transdermally during each 24-hour period of application.
Figure 1. Mean serum testosterone concentrations (ng/dL) measured during
single-dose applications of two Androderm 2.5 mg systems applied at night
to the back. The figures reflect the greatest response in a study comparing
four different sites of application (abdomen, back, thigh and upper arm) in
34 hypogonadal men. Source: Androderm® prescribing information.
Watson Pharma, Inc.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. Exceeding therapeutic doses will increase the
likelihood of estrogenic side effects. In such cases, an anti-estrogen such as
clomiphene citrate or tamoxifen citrate is commonly applied to prevent
estrogenic side effects. One may alternately use an aromatase inhibitor like
Arimidex® (anastrozole), which more efficiently controls estrogen by
preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Exceeding therapeutic doses is likely to
produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
421
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction. Therapeutic doses of testosterone used to correct
insufficient androgen production in otherwise healthy aging men are unlikely to
increase atherogenic risk, and may actually reduce the risk of cardiovascular
mortality.
422
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Androderm® is applied daily (before bed) to intact, clean, dry skin of the back,
upper arms, thighs, and/or abdomen. The site(s) of application should be rotated
so that no patch is reapplied to the same area in less than 7 days. Lower
bioavailability may be noticed in some areas of the body, such as the chest and
calves. Androderm should not be applied to the scrotum. It should also not be
applied over a bony area of the body, or any part of the body that could be
subject to prolonged pressure during sleep or sitting. Application to these sites
has been associated with burn-like blister reactions. Skin irritation causes
approximately 1 in 20 patients to discontinue treatment. Irritation may be
ameliorated by treatment of the affected area with over-the-counter topical
hydrocortisone cream applied after the patch is removed. A small amount of
prescription 0.1% triamcinolone acetonide cream may also be applied to the
center of each patch before application, which should reduce irritation and not
significantly alter the transdermal absorption of testosterone. Many OTC
ointments will significantly reduce the penetration of testosterone when applied
to the skin before use, and should be avoided.
Administration (Men):
To treat androgen insufficiency, the prescribing guidelines for Androderm®
recommend two 2.5 mg patches or one 5 mg patch per day. Morning serum
testosterone levels are later measured, at which point the physician may adjust
upwards or downwards if necessary. For physique-or performance-enhancing
purposes, higher doses would be necessary to achieve supraphysiological levels
of testosterone. This would require at least three or four 5 mg or eight 2.5 mg
patches per day, delivering approximately 15-20 mg of testosterone. This level is
sufficient for most users to notice gains in muscle size and strength, although
this is not a very realistic idea in a practical sense. Lower doses may be used, but
typically when accompanied by other anabolic/androgenic steroids. Testosterone
is ultimately very versatile, and can be combined with many other
anabolic/androgenic steroids to tailor the desired effect.
Administration (Women):
Androderm® is not FDA approved for use in women. Testosterone is not
recommended for women for physique-or performance-enhancing purposes due
to its strong androgenic nature and tendency to produce virilizing side effects.
Availability:
Transdermal testosterone patches are manufactured in many countries
worldwide, and remain widely available. Common trade names include
Androderm® and ATMOS®. Given the high sophistication and low black
market value, counterfeits have not yet been reported.
AndroGel® (testosterone)
AndroGel® is a transdermal hydroalcoholic testosterone gel that contains a 1%
concentration of testosterone by weight. It was originally released in 2.5 gram
and 5-gram sachets, equating to a total per-application testosterone dose of 25
mg and 50 mg respectively. The AndroGel® prescribing information states that
the product has a transdermal bioavailability of approximately 10%. This means
that each 2.5 or 5 gram dose will deliver approximately 2.5 mg or 5 mg of
hormone systemically. With this mode of administration, testosterone levels
begin to elevate approximately 30 minutes after the gel is applied to the body,
and substantial elevations in serum androgen levels are achieved within 4 hours.
Testosterone levels will remain elevated for approximately 24 hours after
administration, so that that the drug is applied once per day. Regular dosing will
provide a steady hormone balance over each 24-hour period.
History:
AndroGel® was developed in the United States by Unimed Pharmaceuticals, a
division of Solvay. It was approved by the FDA for sale as a prescription drug in
February of 2000. It is indicated for use in adult males with conditions
associated with a deficiency or absence of endogenous testosterone. This
includes cases of primary hypogonadism, which may be caused by
cryptorchidism, bilateral torsion, orchitis, vanishing testis syndrome,
orchiectomy, Klinefelter’s syndrome, chemotherapy, or alcohol/heavy metal
toxicity. It is also prescribed to treat hypogonadotrophic hypogonadism,
including patients with luteinizing hormone or luteinizing hormone-releasing
hormone (LHRH) deficiency caused by tumors, injury, or radiation. Primary
hypogonadism is usually characterized by low testosterone and high
gonadotropin (LH/FSH) levels, while hypogonadotrophic hypogonadism is
usually associated with low testosterone and low to normal gonadotropin levels.
AndroGel® is said to have a clinical success rate of 87%, perhaps owing to the
greater patient comfort and compliance this form of testosterone offers in
comparison with hormone injections.
Other transdermal testosterone hydroalcoholic gels have been released in the
U.S. and abroad since the introduction of AndroGel®. Testim® by Auxilium
Pharmaceuticals is perhaps the most well-known competing brand, sold widely
in the U.S. and Europe. This product also comes in the form of a 1% testosterone
gel claiming a 10% level of bioavailability. Studies have demonstrated that
Testim® delivers as much as 38% more free testosterone for a given dose
compared to AndroGel®, however.
423 Testim® is noted to use a thicker and
stickier gel compared to AndroGel®, which may explain the greater transfer of
hormone. In January 2006, the FDA approved the first generic testosterone gel in
the U.S., made by Watson Pharmaceuticals. Testosterone gels are one of the
most popular methods of testosterone delivery in clinical medicine at the present
time, and are likely to be soon found in every market globally that supports an
active hormone replacement therapy industry.
How Supplied:
Hydroalcoholic transdermal testosterone gels are available in many human drug
markets. Composition and dosage may vary by country and manufacturer, but
usually contain 1% testosterone by weight; packaged in volume tubes or singledose packets containing 2.5 grams or 5 grams of gel. AndroGel® (U.S.) is also
produced in a pump dispenser containing 75 grams of gel, which delivers 60
metered applications of 1.25 grams each.
Structural Characteristics:
AndroGel® is a hydroalcoholic gel containing 1% of testosterone (free) by
weight. It is designed to provide a continuous transdermal delivery of
testosterone for 24 hours following application to the skin. Approximately 10%
of the applied dose is absorbed across the skin during each 24-hour period.
Figure 1. Steady-state testosterone concentrations in blood, measured 30
days after beginning therapy with AndroGel (10g application). Drug was
applied to the body once daily.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. Exceeding therapeutic doses will increase the
likelihood of estrogenic side effects. In such cases, an anti-estrogen such as
clomiphene citrate or tamoxifen citrate is commonly applied to prevent
estrogenic side effects. One may alternately use an aromatase inhibitor like
Arimidex® (anastrozole), which more efficiently controls estrogen by
preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Exceeding normal therapeutic doses is
likely to produce androgenic side effects including oily skin, acne, and
body/facial hair growth. Men with a genetic predisposition for hair loss
(androgenetic alopecia) may notice accelerated male pattern balding. Women are
warned of the potential virilizing effects of anabolic/androgenic steroids,
especially with a strong androgen such as testosterone. These may include
deepening of the voice, menstrual irregularities, changes in skin texture, facial
hair growth, and clitoral enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
424
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely effect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction. Therapeutic doses of testosterone used to correct
insufficient androgen production in otherwise healthy aging men are unlikely to
increase atherogenic risk, and may actually reduce the risk of cardiovascular
mortality.
425
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production.Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Testosterone hydroalcoholic gel is applied daily (preferably in the morning) to
intact, clean, dry skin of the shoulders, upper arms, and/or abdomen. Patients
should be careful about transferring testosterone to their female partner(s). The
prescribing information for AndroGel® suggests that patients wash their hands
immediately with soap and water after application, and also recommends
covering the application site(s) with clothing after the gel has dried. Studies with
AndroGel® have demonstrated that female partners of male patients noticed as
much as a doubling of serum testosterone levels following 15 minutes of
rigorous skin-on-skin contact. This contact was initiated between 2 and 12 hours
after drug administration. Testosterone transfer was completely avoided when
the male subjects wore a shirt.
Administration (Men):
To treat androgen insufficiency, the prescribing guidelines for AndroGel®
recommend initiating therapy with a 5g daily dose (delivering 5 mg of
testosterone systemically). Serum testosterone levels are measured after 14 days,
at which point the physician may adjust upwards to 7.5g or 10g if necessary. For
physique-or performance-enhancing purposes, higher doses would be necessary
to achieve supraphysiological levels of testosterone. The most common dose
here is 20 grams per day, which delivers approximately 20 mg of testosterone.
This level is sufficient for most users to notice significant gains in muscle size
and strength. Lower doses are also regularly used by some athletes, but typically
when accompanied by other anabolic/androgenic steroids. Testosterone is
ultimately very versatile, and can be combined with many other
anabolic/androgenic steroids to tailor the desired effect.
Administration (Women):
Hydroalcoholic transdermal testosterone gels are not FDA approved for use in
women. Testosterone is not recommended for women for physique-or
performance-enhancing purposes due to its strong androgenic nature and
tendency to produce virilizing side effects.
Availability:
Hydroalcoholic transdermal testosterone gels are manufactured in many
countries worldwide, and remain widely available. Common trade names include
Androgel®, Testim®, and Testogel®. Given the high sophistication and low
black market value, counterfeits have not yet been widely reported.
Andronaq (testosterone suspension)
Description:
Testosterone suspension is an injectable preparation containing testosterone (no
ester), usually in a water base. Among bodybuilders, “suspension” is known to
be an extremely potent mass agent. It is often said to be the most powerful
injectable steroid available, producing very rapid gains in muscle mass and
strength. This is largely due to the very fast action of the drug. When using a
slow-acting oil-based steroid like Sustanon® 250, it can take weeks before a
peak testosterone level is reached. With suspension, it is just a matter of hours.
This will usually result in the athlete starting to notice size and strength gains by
the end of the first week. By the time the athlete is 30 days into a cycle of
suspension, the length it will usually take for Sustanon® 250 to really begin
working consistently, the mass gains are already (generally) very extreme.
History:
Testosterone suspension is one of the oldest anabolic/androgenic steroids, dating
all the way back to the 1930’s. Used generically to describe any injectable form
of free testosterone, testosterone suspension predates the development of slowacting (depot) injections of esterified testosterone by several years. Even after
the development of esterified derivates, testosterone suspension remained on the
U.S. and other select drug markets. For example, testosterone propionate and
testosterone enanthate were both commercially available by the 1950’s, yet
testosterone suspension remained a regularly produced item in the U.S. for
decades more. Previous American trade names for the drug have include
Sterotate (Ulmer), Andronaq (Central), Aquaspension Testosterone (PitmanMoore), Injectable Aqueous Testosterone (Arlington-Funk), Virosterone (Endo),
and Testosterone Aqueous (National Drug). A full accounting of the former
generic manufacturers and brand names for this drug would be too numerous to
list.
Testosterone suspension shares a clinical application history similar to that of
other testosterone products. Early prescribing guidelines called for its use to
ameliorate a loss of sex drive, impotence, and general loss of vitality in aging
males with declining hormone levels. Testosterone was/is also used to treat
pubertal adolescents with undescended testicles. With women, the drug was
commonly prescribed for the treatment of excessive or painful lactation
following childbirth, as well as inoperable mammary cancer. By the 1990’s,
however, the FDA had refined the approved uses for testosterone suspension
slightly, which began to focus more tightly on the treatment of male androgen
insufficiency. The drug may, however, still be used as a secondary therapy in
inoperable breast cancer, although its high tendency to produce virilization
makes it an uncommon choice.
Although the number of products containing testosterone suspension steadily
dwindled over the years, the drug enjoyed uninterrupted availability on the U.S.
prescription drug market all the way up to 1998. That year, the FDA had taken
action against Steris Laboratories (a subsidiary of Henry Schein), which at the
time was the principal U.S. supplier for testosterone products (manufacturing
them for their label and several other brands). The firm was also the last
remaining producer of testosterone suspension. The dispute arose over Steris’
inventory reports for their Class III drugs. The FDA forced the company to
suspend production of all C-III pharmaceuticals until certain “discrepancies”
could be addressed. Years later, Steris was able to resume producing testosterone
drugs again, but by this time had made the decision not to resume making
testosterone suspension. Currently, testosterone suspension is still available in
the U.S., but only through private compounding pharmacies, which may produce
the drug on special order from a licensed doctor.
How Supplied:
Testosterone suspension is available in select human and veterinary drug
markets. Composition and dosage may vary by country and manufacturer, but
usually contain 50 mg/ml or 100 mg/ml of steroid mixed in a water-based
solution. Testosterone has low water solubility, so the steroid will noticeably
separate from a water-based solution when a vial or ampule is left to sit. A quick
shake will temporarily place the drug back into suspension, so that the
withdrawn dosage should always be consistent.
Structural Characteristics:
Testosterone suspension contains (free) testosterone in a water-based
suspension, although oils are sometime also used as carriers. Without
esterification, testosterone has a short half-life in the body. Testosterone
suspension may require a minimum of 2-3 injections per week to maintain
consistent hormone elevations. When calculating dose, especially when moving
from one testosterone preparation to another, it is also important to remember
that testosterone suspension contains more active testosterone per milligram than
its esterified derivatives. For example, when the weight of the ester is taken into
account, 100 mg of testosterone enanthate actually only provides 72 mg of raw
testosterone.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone more likely to require the
concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention
and loss of muscle definition are common with higher doses of testosterone, this
drug is usually considered a poor choice for dieting or cutting phases of training.
Its moderate estrogenicity makes it more ideal for bulking phases, where the
added water retention will support raw strength and muscle size, and help foster
a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
426
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
427 Studies using 300 mg of testosterone ester
(enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated
only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached
21%.
428 The negative impact of aromatase inhibition should be taken into
consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less of testosterone per week, the
impact on lipid profile tends to be noticeable but not dramatic, making an antiestrogen (for cardioprotective purposes) perhaps unnecessary. Doses of 600 mg
or less per week have also failed to produce statistically significant changes in
LDL/VLDL cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive
protein, and insulin sensitivity, all indicating a relatively weak impact on
cardiovascular risk factors.
429 When used in moderate doses, injectable
testosterone esters are usually considered to be the safest of all
anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Testosterone suspension contains undissolved testosterone particles, which form
a short-acting repository in the muscle following injection. Depending on the
size of the particles and other agents present, injections of testosterone
suspension may result in local irritation, pain, and redness. Veterinary
testosterone suspensions may use large particles that require a needle as large as
21 gauge for injection, for example, and can be very uncomfortable to use.
Modern testosterone suspension preparations made for human use often contain
microcrystalline steroid particles. These crystals are highly refined, and are too
small to see with the naked eye. This design provides significantly more patient
comfort than less refined products, and is generally well tolerated.
Administration (Men):
To treat androgen insufficiency, the prescribing guidelines for testosterone
suspension recommend a dose of 25-50 mg, which is given 2-3 times per week.
When used for muscle-building purposes, testosterone suspension is often
administered at a dose of 100-200 mg per injection, which is given every 2nd or
3rd day. Athletes looking to achieve an extremely rapid bulk gain will inject as
much as 100 mg daily. In most cases this higher dose can be amazing, the user
seeming to just inflate with bloated muscle mass in a very short period of time.
Back when they were being manufactured, the U.S. 30 mL vials (100 mg/mL)
were always the most sought after for this procedure, as each would run the
cycle for about a month. Although this drug does require a frequent injection
schedule, a well-refined suspension should pass through a needle as fine as 27
gauge (insulin). This allows the user more available injection sites, hitting the
smaller muscle groups such as the deltoid, triceps, and calves.
Those looking for only a potent mass agent are often extremely happy with the
results provided by testosterone suspension; this product certainly has a strong
reputation for performing. But those athletes who want not just quantity but
quality are likely to be disappointed, as the muscle mass gain is not going to be a
hard, dense one. In fact, the user will often have to contend with excessive fat
and water-weight gains when building their physique with this drug, and will
often seek the benefit of cutting agents soon afterwards to clean up the look of
muscularity. Alternately, one could make use of a smaller dosage of testosterone
suspension, which would allow for less estrogen buildup. In such a scenario, one
could stack it with any of a variety of other less or non-aromatizable steroids,
depending on the desired goals.
Administration (Women):
Testosterone suspension is rarely used with women in clinical medicine. When
applied, it is most often used as a secondary treatment for inoperable breast
cancer. Doses given for this application may reach 100 mg three times per week,
a level well into the threshold likely to cause strong virilizing side effects.
Testosterone suspension is not recommended for women for physique-or
performance-enhancing purposes due to its strong androgenic nature and
tendency to produce virilizing side effects.
Availability:
Pharmaceutical preparations containing testosterone in an aqueous suspension
remain scarce. The bulk of the supply presently comes from underground and
export steroid manufacturers. In reviewing some of the remaining products and
changes in the global pharmaceutical market, we have made the following
observations.
Testosterone suspension has been unavailable in the United States for many
years now. No old products should still be in circulation. Because the FDA never
officially withdrew this drug from, it can be specially ordered through a small
number of compounding pharmacies. Anything else bearing a U.S. manufacturer
name is counterfeit.
Testosterone suspension is still produced in India under the Aquaviron brand
name, now by Piramal HC. It comes in the strength of 25 mg/mL, and is
packaged in 1 mL ampules.
Cheque Drops® (mibolerone)
Description:
Mibolerone is an oral anabolic steroid, structurally derived dimethylated
nandrolone. This agent is specifically 7,17-dimethylated nandrolone,
significantly more potent as an anabolic and androgenic agent than its nonmethylated parent. Over the years, mibolerone has earned a reputation among
bodybuilders as being one of the strongest steroids ever made. This is correct in
a technical sense, as it is one of only a select few commercial steroid products
effective in microgram, not milligram, amounts. During standard animal assays,
mibolerone was determined to have 41 times the anabolic activity of
methyltestosterone when given orally. In contrast, it had only 18 times the
androgenic activity. Although both properties are strongly pronounced with this
agent, it retains a primarily anabolic character (in a relative sense). Estrogenic
and progestational properties are also very pronounced with this drug, however.
Among athletes it is most commonly applied during bulking phases of training,
or to stimulate aggression before a workout or competition.
History:
Mibolerone was first described in 1963.
430
It was developed into a veterinary
medicine during the 1960’s by Upjohn, which sold the drug under the brand
name Cheque Drops. The preparation contained 100 mcg/ml of steroid in a 55
mL bottle, for a total steroid content of 5.5 milligrams (illustrating the high
relative potency of mibolerone). Pharmacia & Upjohn later also sold a
preparation called Cheque Medicated Dog Food, of obvious composition. The
drug was administered orally, and had been used to interrupt the estrous cycle of
female dogs, preventing them from going into heat. It is approved for use in an
animal for no longer than 24 months. Use of the drug is considered carefully by
most veterinarians, mainly because longer-term administration can produce side
effects such as clitoral enlargement, aggression, urinary difficulties, and liver
damage.
Among athletes, mibolerone has always been seen with a high level of mystique,
perhaps partly due to its limited availability. Those actually familiar with the
Upjohn (then Pharmacia & Upjohn) product were likely disappointed during the
early 2000’s, when the Cheque products were officially discontinued by the
manufacturer. The company, now Pfizer Animal Health, presently lists no
mibolerone-containing products on its inventory, despite retaining the rights to
market the drug. Mibolerone is still available in the U.S., but only in generic
form from a private compounding pharmacy, obtained under special order by a
licensed veterinarian. The removal of the Pharmacia & Upjohn products from
the U.S. market marked the commercial end of mibolerone. No prescription
preparation, human or veterinary, is currently known to contain mibolerone
worldwide.
How Supplied:
Mibolerone is no longer available as a prescription drug product. When
produced it most commonly came in the form of an oral solution based in
propylene glycol, carrying 100mcg of steroid per milliliter in a 55 mL bottle.
Structural Characteristics:
Mibolerone is a modified form of nandrolone. It differs by 1) the addition of a
methyl group at carbon 17-alpha to protect the hormone during oral
administration and 2) the introduction of a methyl group at carbon 7 (alpha),
which inhibits 5-alpha reduction and increases relative androgenicity. 7,17-
dimethylated steroids also tend to be very resistant to metabolism and serumbinding proteins, greatly enhancing their relative biological activity.
Side Effects (Estrogenic):
Mibolerone is aromatized by the body, and is considered a highly estrogenic
steroid due to its conversion to 7,17-dimethylestradiol (an estrogen with high
biological activity). Gynecomastia may be a concern during treatment, especially
when higher than normal therapeutic doses are used. At the same time water
retention can become a problem, causing a notable loss of muscle definition as
both subcutaneous water retention and fat levels build. To avoid strong
estrogenic side effects, it may be necessary to use an anti-estrogen such as
Nolvadex®. One may alternately use an aromatase inhibitor like Arimidex®
(anastrozole), which is a more effective remedy for estrogen control. Aromatase
inhibitors, however, can be quite expensive in comparison to standard estrogen
maintenance therapies, and may also have negative effects on blood lipids.
It is of note that mibolerone also displays strong activity as a progestin in the
body. The side effects associated with progesterone are similar to those of
estrogen, including negative feedback inhibition of testosterone production and
enhanced rate of fat storage. Progestins also augment the stimulatory effect of
estrogens on mammary tissue growth. There appears to be a strong synergy
between these two hormones here, such that gynecomastia might even occur
with the help of progestins without excessive estrogen levels being present. The
use of an anti-estrogen, which inhibits the estrogenic component of this disorder,
is often sufficient to mitigate gynecomastia caused by mibolerone.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
common with this substance. This may include bouts of oily skin, acne, and
body/facial hair growth. Anabolic/androgenic steroids may also aggravate male
pattern hair loss. Individuals sensitive to the androgenic effects of this steroid
may find a milder anabolic such as Deca-Durabolin® to be more comfortable.
Women are additionally warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement. Note that 7-methylation inhibits steroid 5-alpha reduction.
431 The
relative androgenicity of mibolerone is not affected by the concurrent use of
finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Mibolerone is a c17-alpha alkylated compound. This alteration protects the drug
from deactivation by the liver, allowing a very high percentage of the drug entry
into the bloodstream following oral administration. C17-alpha alkylated
anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure
may result in liver damage. In rare instances life-threatening dysfunction may
develop. It is advisable to visit a physician periodically during each cycle to
monitor liver function and overall health. Intake of c17-alpha alkylated steroids
is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain.
Severe liver complications are rare given the periodic nature in which most
people use oral anabolic/androgenic steroids, although cannot be excluded with
this steroid, especially with high doses and/or prolonged administration periods.
Note that U.S. prescribing information for Cheque Drops mentions only one
human study being conducted on mibolerone, and that the study was terminated
early due to high hepatotoxicity.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Mibolerone has a
strong effect on the hepatic management of cholesterol due to its structural
resistance to liver breakdown and route of administration. Anabolic/androgenic
steroids may also adversely affect blood pressure and triglycerides, reduce
endothelial relaxation, and support left ventricular hypertrophy, all potentially
increasing the risk of cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
432 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, this steroid should be taken on an empty stomach.
Administration (Men):
Mibolerone was never approved for use in humans. Prescribing guidelines are
unavailable. In the athletic arena, the drug is used intermittently due to its high
level of hepatotoxicity, with cycles usually lasting no more than 6 weeks
followed by 6-8 weeks off. A daily dosage of 200 to 500mcg is most common
for bodybuilding purposes. This level is typically sufficient for gains in strength
and muscle mass (bulk). The high progestational and estrogenic activity of
mibolerone makes it of little value in speed and endurance sports, causing an
unwanted retention of water weight.
Administration (Women):
Mibolerone was never approved for use in humans. Prescribing guidelines are
unavailable. Mibolerone is generally not recommended for women for physiqueor performance-enhancing purposes due to its very strong nature and tendency to
produce virilizing side effects.
Availability:
Mibolerone is sold in the U.S. as a compounded veterinary medicine only. No
commercial preparations containing this drug are known to exist worldwide.
Mibolerone remains available on the black market in underground preparations
only.
Deca-Durabolin® (nandrolone decanoate)
Description:
Nandrolone decanoate is an injectable form of the anabolic steroid nandrolone.
The decanoate ester provides a slow release of nandrolone from the site of
injection, lasting for up to three weeks. Nandrolone is very similar to
testosterone in structure, although it lacks a carbon atom at the 19th position
(hence its other name, 19-nortestosterone). Like testosterone, nandrolone
exhibits relatively strong anabolic properties. Unlike testosterone, however, its
tissue-building activity is accompanied by weak androgenic properties. Much of
this has to do with the reduction of nandrolone to a weaker steroid,
dihydronandrolone, in the same androgen-responsive target tissues that potentate
the action of testosterone (by converting it to DHT). The mild properties of
nandrolone decanoate have made it one of the most popular injectable steroids
worldwide, highly favored by athletes for its ability to promote significant
strength and lean muscle mass gains without strong androgenic or estrogenic
side effects.
History:
Nandrolone decanoate was first described in 1960,
433 and became a prescription
medication in 1962. It was developed by the international pharmaceuticals giant
Organon, and sold under the brand name Deca-Durabolin. The name DecaDurabolin denotes that the product contains a variant of Organon’s previously
popular nandrolone injectable Durabolin (nandrolone phenylpropionate) using
an ester of 10 carbon atoms. Organon expanded the market for nandrolone
decanoate very rapidly following its release. Probably owing to a combination of
its favorable properties and the large market presence of Organon, DecaDurabolin soon became one of the most widely distributed anabolic steroids in
the world.
When first introduced to the United States, nandrolone decanoate (like
Durabolin) was prescribed for a variety of ailments. Listed indications included
pre-and postoperative use for building lean mass, osteoporosis, advanced breast
cancer, weight loss due to convalescence or disease, geriatric states (general
weakness and frailty), burns, severe trauma, ulcers, adjunct therapy with certain
forms of anemia, and selective cases of growth and development retardation in
children. The drug was initially sold in a dosage of only 50 mg/ml, owing to the
very low recommended doses (usually 50-100 mg every 3-4 weeks). The drug
was soon updated to include a 100 mg/ml version, reflecting the need for higher
doses in some situations, particularly those with refractory anemia and advanced
breast cancer. Later, a 200 mg/ml product was released by Organon as well.
Although the drug had been applied favorably for a great many medical uses for
approximately a decade, by the mid-1970’s the indicated uses for nandrolone
decanoate were being refined, both in the U.S. and abroad. FDA approved
prescribing information from 1975 lists nandrolone decanoate as “probably
effective” as adjunct therapy in senile and postmenopausal osteoporosis, as well
as for treating pituitary-deficient dwarfism until growth hormone is more
available. It was also deemed “possibly effective” in aiding the retention of lean
mass, controlling advanced breast cancer, and as adjunctive therapy for certain
types of anemia. More time was given to investigate the potential “less than
effective” uses of the drug.
Modern (approved) medical applications for the drug are even more refined than
they were in the mid-1970’s. In the United States, the drug is now only FDA
approved for treating anemia, although it is often also used “off label” to
preserve lean mass in HIV positive patients and others suffering from wasting
diseases. Outside of the U.S., Organon seems to support the use of this drug
mainly with patients suffering from severe anemia, osteoporosis, and advanced
breast cancer. The Organon Deca-Durabolin brand of nandrolone decanoate
remains widely available today, now distributed by new parent company
Merck/MSD. In addition, nandrolone decanoate is produced as a generic drug in
many countries, and is also manufactured under numerous other distinctive
brand names, both for human and veterinary use.
How Supplied:
Nandrolone decanoate is widely available in human and veterinary drug markets.
Composition and dosage may vary by country and manufacturer, but usually
contain 25 mg/ml, 50 mg/ml, 100 mg/ml, or 200 mg/ml of steroid dissolved in
oil.
Structural Characteristics:
Nandrolone decanoate is a modified form of nandrolone, where a carboxylic acid
ester (decanoic acid) has been attached to the 17-beta hydroxyl group. Esterified
steroids are less polar than free steroids, and are absorbed more slowly from the
area of injection. Once in the bloodstream, the ester is removed to yield free
(active) nandrolone. Esterified steroids are designed to prolong the window of
therapeutic effect following administration, allowing for a less frequent injection
schedule compared to injections of free (unesterified) steroid. Nandrolone
decanoate provides a sharp spike in nandrolone release 24-48 hours following
deep intramuscular injection, which steadily declines to near baseline levels
approximately two weeks later. The half-life of nandrolone decanoate is 7-12
days.
Figure 1. Pharmacokinetics of 200 mg Nandrolone Decanoate injection.
Source: Pharmacokinetic parameters of nandrolone (19-nortestosterone)
after intramuscular administration of nandrolone decanoate (DecaDurabolin®) to healthy volunteers. Wijnand H, Bosch A, Donker C. Acta
Endocrinol 1985 supp 271 19-30.
Side Effects (Estrogenic):
Nandrolone has a low tendency for estrogen conversion, estimated to be only
about 20% of that seen with testosterone.
434 This is because while the liver can
convert nandrolone to estradiol, in other more active sites of steroid
aromatization such as adipose tissue nandrolone is far less open to this
process.
435 Consequently, estrogen-related side effects are a much lower concern
with this drug than with testosterone. Elevated estrogen levels may still be
noticed with higher dosing, however, and may cause side effects such as
increased water retention, body fat gain, and gynecomastia. An anti-estrogen
such as clomiphene citrate or tamoxifen citrate may be necessary to prevent
estrogenic side effects if they occur. One may alternately use an aromatase
inhibitor like Arimidex® (anastrozole), which more efficiently controls estrogen
by preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
It is of note that nandrolone has some activity as a progestin in the body.
436
Although progesterone is a c-19 steroid, removal of this group as in 19-
norprogesterone creates a hormone with greater binding affinity for its
corresponding receptor. Sharing this trait, many 19-nor anabolic steroids are
shown to have some affinity for the progesterone receptor as well.
437 The side
effects associated with progesterone are similar to those of estrogen, including
negative feedback inhibition of testosterone production and enhanced rate of fat
storage. Progestins also augment the stimulatory effect of estrogens on
mammary tissue growth. There appears to be a strong synergy between these
two hormones here, such that gynecomastia might even occur with the help of
progestins, without excessive estrogen levels. The use of an anti-estrogen, which
inhibits the estrogenic component of this disorder, is often sufficient to mitigate
gynecomastia caused by nandrolone.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance, especially with higher doses. This may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are warned of the
potential virilizing effects of anabolic/androgenic steroids. These may include a
deepening of the voice, menstrual irregularities, changes in skin texture, facial
hair growth, and clitoral enlargement. Nandrolone is a steroid with relatively low
androgenic activity relative to its tissue-building actions, making the threshold
for strong androgenic side effects comparably higher than with more androgenic
agents such as testosterone, methandrostenolone, or fluoxymesterone. It is also
important to point out that due to its mild androgenic nature and ability to
suppress endogenous testosterone, nandrolone is prone to interfering with libido
in males when used without another androgen.
Note that in androgen-responsive target tissues such as the skin, scalp, and
prostate, the relative androgenicity of nandrolone is reduced by its reduction to
dihydronandrolone (DHN).
438 439 The 5-alpha reductase enzyme is responsible
for this metabolism of nandrolone. The concurrent use of a 5-alpha reductase
inhibitor such as finasteride or dutasteride will interfere with site-specific
reduction of nandrolone action, considerably increasing the tendency of
nandrolone to produce androgenic side effects. Reductase inhibitors should be
avoided with nandrolone if low androgenicity is desired.
Side Effects (Hepatotoxicity):
Nandrolone is not c-17 alpha alkylated, and not known to have hepatotoxic
effects in healthy subjects. Liver toxicity is unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Studies
administering 600 mg of nandrolone decanoate per week for 10 weeks
demonstrated a 26% reduction in HDL cholesterol levels.
440 This suppression is
slightly greater than that reported with an equal dose of testosterone enanthate,
and is in agreement with earlier studies showing a slightly stronger negative
impact on HDL/LDL ratio with nandrolone decanoate as compared to
testosterone cypionate.
441 Nandrolone decanoate should still have a significantly
weaker impact on serum lipids than c-17 alpha alkylated agents.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Studies administering 100 mg per week of nandrolone decanoate for 6 weeks
have demonstrated an approximate 57% reduction in serum testosterone levels
during therapy. At a dosage of 300 mg per week, this reduction reached 70%.
442
It is believed that the progestational activity of nandrolone notably contributes to
the suppression of testosterone synthesis during therapy, which can be marked in
spite of a low tendency for estrogen conversion.
443 Without the intervention of
testosterone-stimulating substances, testosterone levels should return to normal
within 2-6 months of drug secession. Note that prolonged hypogonadotrophic
hypogonadism can develop secondary to steroid abuse, necessitating medical
intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
For general anabolic effects, early prescribing guidelines recommend a dosage
of 50-100 mg every 3-4 weeks for 12 weeks. To treat renal anemia, the
prescribing guidelines for nandrolone decanoate recommend a dosage of 100-
200 mg per week. The usual dosage for physique-or performance-enhancing
purposes is the range of 200-600 mg per week, taken in cycles 8 to 12 weeks in
length. This level is sufficient for most users to notice measurable gains in lean
muscle mass and strength.It is often stated that nandrolone decanoate will exhibit
its optimal effect (best gain/side effect ratio) at 2 mg per pound of
bodyweight/weekly, although individual differences in response will likely
dictate varying ideal doses for different users. Deca is not known as a very “fast”
builder. The muscle-building effect of this drug is quite noticeable, but not
dramatic. In general, one can expect to gain muscle weight at about half the rate
of that with an equal amount of testosterone.
Nandrolone decanoate is often combined with other steroids for an enhanced
effect. A combination of 200-400 mg/week of nandrolone decanoate and 10-20
mg daily of Winstrol®, for example, is noted to greatly enhance the look of
muscularity and definition when dieting/cutting. A strong non-aromatizing
androgen like Halotestin® or trenbolone could also be used, again providing an
enhanced level of hardness and density to the muscles. Being a moderately
strong muscle builder, nandrolone can also be incorporated into bulk cycles with
acceptable results. The classic “Deca and D-bol” stack (usually 200-400 mg of
nandrolone decanoate per week and 15-25 mg of Dianabol per day) has been a
bodybuilding basic for decades, and always seems to provide excellent muscle
growth. A stronger androgen such as Anadrol 50® or testosterone could also be
substituted, producing greater results, but with more water retention.
Administration (Women):
For general anabolic effects, early prescribing guidelines recommend a dosage
of 50-100 mg every 3-4 weeks for 12 weeks. To treat renal anemia, the
prescribing guidelines for nandrolone decanoate recommend a dosage of 50-100
mg per week. When used for physique-or performance-enhancing purposes, a
dosage of 50 mg per week is most common, taken for 4-6 weeks. Although only
slightly androgenic, women are occasionally confronted with virilization
symptoms when taking this compound. Studies have demonstrated high
tolerability (minor but statistically insignificant incidence of virilizing side
effects) with a dose of 100 mg every other week for 12 weeks,
444 while longterm studies (+12 months of use) have demonstrated virilizing side effects on a
dose as low as 50 mg every 2-3 weeks.
445 Should virilizing side effects become
a concern, nandrolone decanoate should be discontinued immediately to help
prevent their permanent appearance. After a sufficient period of withdrawal, the
shorter-acting nandrolone Durabolin® might be considered a safer option. This
drug stays active for only several days, greatly reducing the withdrawal time if
indicated.
Availability:
Nandrolone decanoate continues to decline in prominence as a pharmaceutical
product due to its limited use in clinical medicine. The drug is presently
unavailable in the United States. Many Western nations continue to market the
drug, though its production is increasingly being shifted to less regulated
markets in Asia. Legitimate pharmaceutical forms are highly sought after on the
black market, and thus subject to a great deal of counterfeiting. In reviewing
some of the more popular products and changes on the global pharmaceutical
market, we have made the following observations.
In November 2009, Organon (a subsidiary of ScheringPlough since 2007)
became part of Merck/MSD. All Organon products are expected to transition
over to this label. It is unknown what (if any) changes to expect in the global
distribution of Deca-Durabolin products.
Brand name Deca-Durabolin is not available in the United States. All products
bearing this label are counterfeit. Watson Labs and Schein Pharmaceuticals
generics have also been discontinued. This drug is presently unavailable in the
U.S.
Norma Hellas Deca (100 mg/mL nandrolone decanoate in 2 mL vials) from
Greece is available, but also widely counterfeited. The firm uses a patented
photochromic label to deter counterfeiting, which carries a metallic/holographic
watermark of the Norma Hellas logo.
Greek Deca-Durabolin (formerly from Organon) has been another widely
counterfeited product. It is one of only a handful of European nandrolone
injectables to be found in multi-dosed vials, making it an easy target for
counterfeiters that lack the capacity to produce glass ampules. This product
should be considered fake unless it comes in a box with the proper Greek drug
ID sticker. As with all Greek drugs, the sticker should show a hidden mark under
UV light.
Greek Extraboline may be in circulation. It is also a common target of
counterfeiting. As with all Greek drugs, this product should contain a peel-off
pharmacy sticker that reveals a hidden watermark under UV lighting. All
Extraboline in circulation will also carry a holographic image directly on the vial
label.
Deca-Pronabol from P&B Labs India is no longer in production. The company
currently markets only a 25 mg/mL version of this drug in 1 mL ampules. Many
counterfeits of the former 100 mg/mL product are still in circulation.
Decabolic from Asia Pharma (Malaysia) is now approved for sale through
pharmacies in Thailand, and is fairly popular on the black market. Each box
should carry a scratch-off security sticker, which will display a code that can be
validated on the company website.
Balkan Pharmaceuticals (Moldova) makes the product Nandrolona D. It is
prepared in both 1 mL ampules and multi-dose vials.
Delatestryl® (testosterone enanthate)
Description:
Testosterone enanthate is a slow-acting injectable form of the androgen
testosterone. Following deep intramuscular injection, the drug is designed to
provide a sustained release of testosterone into the bloodstream for
approximately 2 to 3 weeks. In order to maintain normal physiological levels of
testosterone during androgen replacement therapies, injections of testosterone
enanthate are usually required at least every two weeks, although more
meticulous physicians will administer the drug weekly. As with all testosterone
injectables, testosterone enanthate is highly favored by athletes for its ability to
promote strong increases in muscle mass and strength.
History:
Testosterone enanthate first appeared on Western drug markets during the early
1950’s. It was the first slow-acting oil-based injectable ester of testosterone to be
widely adopted in Western medicine, and effectively replaced testosterone
propionate and testosterone suspension for most therapeutic uses. The first brand
of this drug to be sold in the U.S. was Delatestryl® by Squibb. Over the years
the Delatestryl® brand has changed hands several times, most notably to Mead
Johnson, BTG, Savient, and in December 2005, Indevus. The most prominent
brand of testosterone enanthate outside of the United States is Testoviron®, a
drug that has seen uninterrupted production by the same manufacturer (Schering
AG, Germany) for more than 50 years. Globally, the Testoviron® brand from
Schering is the single most widely used injectable testosterone preparation.
Testosterone enanthate is most often used clinically to replace normal levels of
testosterone in adult males suffering diminished androgen levels. This may
manifest itself with a loss of libido, lean muscle mass, and normal energy and
vigor. Testosterone enanthate is also used to treat undescended testicles and
delayed puberty in adolescent males, and occasionally as a secondary medication
during inoperable breast cancer in women. This form of testosterone has also
been studied with great success as a male birth control option.
446 Weekly
injections of 200 mg were shown to efficiently lower sperm production for most
men within three months of treatment, a state of suppression that remained until
after the drug was discontinued. With the current stigma surrounding
anabolic/androgenic steroids, however, it is unlikely that such therapy will
become adopted in Western medical practice. Today, in spite of the growing
number of alternative therapies, testosterone enanthate remains the most widely
prescribed form of testosterone in the world.
How Supplied:
Testosterone enanthate is widely available in human and veterinary drug
markets. Composition and dosage may vary by country and manufacturer, but
usually contain 50 mg/ml, 100 mg/ml, 200 mg/ml, or 250 mg/ml of steroid
dissolved in oil.
Structural Characteristics:
Testosterone enanthate is a modified form of testosterone, where a carboxylic
acid ester (enanthoic acid) has been attached to the 17-beta hydroxyl group.
Esterified forms of testosterone are less polar than free testosterone, and are
absorbed more slowly from the area of injection. Once in the bloodstream, the
ester is removed to yield free (active) testosterone. Esterified forms of
testosterone are designed to prolong the window of therapeutic effect following
administration, allowing for a less frequent injection schedule compared to
injections of free (unesterified) steroid. The half-life of testosterone enanthate is
approximately eight days after injection.
Figure 1. Pharmacokinetics of 194mg testosterone enanthate injection.
Source: Comparison of testosterone, dihydrotestosterone, luteinizing
hormone, and follicle-stimulating hormone in serum after injection of
testosterone enanthate or testosterone cypionate. Schulte-Beerbuhl M,
Nieschlag E. Fertility and Sterility 33 (1980):201-3. Side Effects
(Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone more likely to require the
concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention
and loss of muscle definition are common with higher doses of testosterone, this
drug is usually considered a poor choice for dieting or cutting phases of training.
Its moderate estrogenicity makes it more ideal for bulking phases, where the
added water retention will support raw strength and muscle size, and help foster
a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
447
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely effect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
448 Studies using 300 mg of testosterone ester
(enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated
only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached
21%.
449 The negative impact of aromatase inhibition should be taken into
consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less per week, the impact on lipid
profile tends to be noticeable but not dramatic, making an anti-estrogen (for
cardioprotective purposes) perhaps unnecessary. Doses of 600 mg or less per
week have also failed to produce statistically significant changes in LDL/VLDL
cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive protein, and insulin
sensitivity, all indicating a relatively weak impact on cardiovascular risk
factors.
450 When used in moderate doses, injectable testosterone esters are
usually considered to be the safest of all anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
As with all anabolic/androgenic steroids, it is unlikely that one will retain every
pound of new bodyweight after a cycle is concluded. This is especially true
when withdrawing from a strong (aromatizing) androgen like testosterone, as
much of the new weight gain is likely to be in the form of water retention;
quickly eliminated after drug discontinuance. An imbalance of anabolic and
catabolic hormones during the post-cycle recovery period may further create an
environment that is unfavorable for the retention of muscle tissue. Proper
ancillary drug therapy is usually recommended to help restore hormonal balance
more quickly, ultimately helping the user retain more muscle tissue.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
To treat androgen insufficiency, the prescribing guidelines for testosterone
enanthate call for a dosage of 50-400 mg every 2 to 4 weeks. Although active in
the body for a longer time, testosterone enanthate is usually injected on a weekly
basis for muscle-building purposes. The usual dosage for physique-or
performance-enhancing purposes is in the range of 200-600 mg per week, taken
in cycles 6 to 12 weeks in length. This level is sufficient for most users to notice
exceptional gains in muscle size and strength.
Testosterone is usually incorporated into bulking phases of training, when added
water retention will be of little consequence, the user more concerned with raw
mass than definition. Some do incorporate the drug into cutting cycles as well,
but typically in lower doses (100-200 mg per week) and/or when accompanied
by an aromatase inhibitor to keep estrogen levels under control. Testosterone
enanthate is a very effective anabolic drug, and is often used alone with great
benefit. Some, however, find a need to stack it with other anabolic/androgenic
steroids for a stronger effect, in which case an additional 200-400 mg per week
of boldenone undecylenate, methenolone enanthate, or nandrolone decanoate
should provide substantial results with no significant hepatotoxicity.
Testosterone is ultimately very versatile, and can be combined with many other
anabolic/androgenic steroids to tailor the desired effect.
Administration (Women):
Testosterone enanthate is rarely used with women in clinical medicine. When
applied, it is most often used as a secondary medication during inoperable breast
cancer, when other therapies have failed to produce a desirable effect and
suppression of ovarian function is necessary. Testosterone enanthate is not
recommended for women for physique-or performance-enhancing purposes due
to its strong androgenic nature, tendency to produce virilizing side effects, and
slow-acting characteristics (making blood levels difficult to control).
Availability:
Testosterone enanthate remains the most widely manufactured form of injectable
testosterone worldwide. It is produced in many generic and brand name forms.
In reviewing some of the products and changes in the global pharmaceutical
market, we have made the following observations.
In 2006, Savient sold the rights for Delatestryl to Indevus (United States).
Indevus subsequently became a subsidiary of Endo Pharmaceuticals in March of
2009. Brand name Delatestryl remains available in the United States under the
new company (at 200 mg/mL strength).
Generic versions are also available in the United States (also at a dosage of 200
mg/mL) by Watson, Paddock, and Synerex.
Norma Hellas (Greece), makers of Norma Hellas Nandrolone, recently added a
generic 250 mg/mL testosterone enanthate injectable to their product offerings.
It comes in a single dark amber 1 mL glass ampule,and is packaged 1 ampule per
box. Be sure to look at the Greek Pharmacy sticker under UV light to assure you
have a legitimate product.
Bayer took control of Schering AG in December 2006. Following this
acquisition, the Schering Primoteston and Testoviron Depot products were
transitioned over to the Bayer brand and logo (the products now bear the full
company name Bayer Schering Pharma). Note that many counterfeiters have not
yet made this change in their own products, and thus are still duplicating the old
Schering labels and boxes.
Cidoteston is produced in Egypt by CID (Chemical Industries Development). It
comes in 1 mL ampules, containing 250 mg/mL of steroid. This product has
been counterfeited, though the current most popular copy can be quickly
identified by close examination of the fine details (logo, graphics) on the box.
The French version Testosterone Heptylate is still in production. It is now sold
under the S.E.R.P. label, and available in the familiar 250 mg/mL strength and 1
mL ampule. This drug is frequently exported to developing markets with close
trade relations to France, such as Lebanon.
Androtardyl is also produced in France, and occasionally circulates on the black
market. Again, be sure to look for the proper box before buying.
Testo-Enant is another brand in Europe, this one being made by Geymonat in
Italy. These ampules contain 250 mg of steroid, either in 1 mL or 2 mL of oil.
Currently fakes are not a problem; however, this steroid is not found on the
black market in high volumes.
Galenika makes Testosteron Depo in Serbia. These 1 mL ampules contain 250
mg/mL of steroid, and are extremely cheap at the retail level in their country of
origin.
Jelfa produces Testosteronum Prolongatum in Poland. It is made at a dosage of
100 mg/mL. Each box contains five 1 mL ampules, which are themselves made
of clear glass and carry a paper label.The packaging of this product was recently
updated to reflect a more modern color-gradient design.
Testoviron Depot from German Remedies in India remains in production. The
product comes is made in foil and plastic blister packs.
The Indian export firm Alpha-Pharma also makes a testosterone enanthate,
called Testobolin. It comes in 1 mL glass ampules.
Testofort Inj from Albert Davis Pakistan is commonly found on the international
market. It contains 250 mg/ml of steroid in 1 mL ampules. Three ampules come
packaged to each cardboard box.
Geofman Pharmaceuticals also makes a generic in Pakistan.The product contains
250 mg of steroid in each 1 mL ampule. Like Testofort, three ampules are
contained in each box. Note that the lot number and expiration date are
electronically printed on the bottom inside flap of the box, in addition to the
proper placement on the outside.
Aburaihan makes a generic enanthate in Iran, which is becoming increasingly
popular on the black market. Note that the packaging of this product was
recently updated. Counterfeits of this product have historically been a problem.
Balkan Pharmaceuticals (Moldova) makes the product Testosterona E. It is
prepared in both 1 mL ampules and multi-dose vials.
Depo®-Testosterone (testosterone cypionate)
Description:
Testosterone cypionate is a slow-acting injectable ester of the primary male
androgen testosterone. Testosterone is also the principle anabolic hormone in
men, and is the basis of comparison by which all other anabolic/androgenic
steroids are judged. As with all testosterone injectables, testosterone cypionate is
highly favored by athletes for its ability to promote strong increases in muscle
mass and strength. It is interesting to note that while a large number of other
steroidal compounds have been made available since testosterone injectables,
they are still considered to be the dominant bulking agents among bodybuilders.
There is little argument that these are among the most powerful mass drugs
available, testosterone cypionate included.
History:
Testosterone cypionate first appeared on the U.S. drug market during the mid1950’s under the brand name of Depo-Testosterone cyclopentylpropionate (soon
abridged to simply Depo-Testosterone). It was developed by the pharmaceutical
giant Upjohn, and is still sold to this day by the same company under the same
trade name (although now they are called Pharmacia & Upjohn). This is a drug
with limited global availability, and has historically been (largely) identified as
an American item. It is not surprising that American athletes have long favored
this form of testosterone over testosterone enanthate, the dominant slow-acting
ester of testosterone on the global market. This preference, however, is likely
rooted in history and availability, not actual therapeutic advantages.
Testosterone cypionate and testosterone enanthate provide extremely
comparable patterns of testosterone release. Not only are physical advantages
not possible in one over the other, but actual differences in pharmacokinetic
patterns are hard to notice (these two drugs are for all intents and purposes
functionally interchangeable). The only key difference between the two seems to
be in the area of patient comfort. Cypionic acid is less irritating at the site of
injection than enanthoic acid (enanthate) for a small percentage of patients. This
makes testosterone cypionate a more favorable choice for those with recurring
issues of injection-site pain with testosterone enanthate. This difference likely
had something to do with the early development of this testosterone ester as a
commercial drug product.
The main use of testosterone cypionate in clinical medicine has historically been
the treatment of low androgen levels in males, although many other applications
have existed for this drug as well. During the 1960’s, for example, the drug’s
prescribing recommendations called for such uses as supporting bone structure
maturity, treating menorrhagia (heavy menstrual bleeding) and excessive
lactation in females, and increasing muscle mass and combating osteoporosis in
the elderly. It was also being recommended for increasing male fertility,
whereby induced testosterone/spermatogenesis suppression (caused by
administering 200 mg of testosterone cypionate per week for 6 to 10 weeks) was
potentially followed by a period of rebound spermatogenesis (due to temporarily
higher than normal gonadotropin levels).
By the 1970’s, the FDA had been granted much stronger control over the
prescription drug market, and the broad uses in which testosterone cypionate was
first indicated were now being refined. For example, “testosterone rebound
therapy” as a way to increase male fertility was proving to be unreliable,
especially in the face of newer more effective medications, and was soon
eliminated from prescribing guidelines. So too was the recommendation for its
use to treat things like excessive menstrual bleeding and lactation. In general,
testosterone therapy was being pulled back to focus mainly on male androgen
deficiency, and less on other applications, especially when involving populations
more susceptible to androgenic side effects, such as women and the elderly.
Today, testosterone cypionate remains readily available on the U.S. prescription
drug market, where it is FDA-approved for hormone replacement therapy in men
with conditions associated with a deficiency of endogenous testosterone, and as
a secondary treatment for inoperable metastatic breast cancer in women
(although it is not widely used for this purpose anymore). Testosterone cypionate
is currently available outside of the United States, but not widely. Known
international sources for the drug include Canada, Australia, Spain, Brazil, and
South Africa.
How Supplied:
Testosterone cypionate is available in select human and veterinary drug markets.
Composition and dosage may vary by country and manufacturer, but usually
contain 50 mg/ml, 100 mg/ml, 125 mg/ml, or 200 mg/ml of steroid dissolved in
oil.
Structural Characteristics:
Testosterone cypionate is a modified form of testosterone, where a carboxylic
acid ester (cyclopentylpropionic acid) has been attached to the 17-beta hydroxyl
group. Esterified forms of testosterone are less polar than free testosterone, and
are absorbed more slowly from the area of injection. Once in the bloodstream,
the ester is removed to yield free (active) testosterone. Esterified forms of
testosterone are designed to prolong the window of therapeutic effect following
administration, allowing for a less frequent injection schedule compared to
injections of free (unesterified) steroid. The half-life of testosterone cypionate is
approximately 8 days after injection.
Figure 1. Pharmacokinetics of 200 mg testosterone cypionate injection.
Source: Comparison of testosterone, dihydrotestosterone, luteinizing
hormone, and follicle-stimulating hormone in serum after injection of
testosterone enanthate or testosterone cypionate. Schulte-Beerbuhl M,
Nieschlag E. Fertility and Sterility 33 (1980):201-3. Side Effects
(Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone cypionate more likely to
require the concurrent use of an anti-estrogen or aromatase inhibitor. Since water
retention and loss of muscle definition are common with higher doses of
testosterone cypionate, this drug is usually considered a poor choice for dieting
or cutting phases of training. Its moderate estrogenicity makes it more ideal for
bulking phases, where the added water retention will support raw strength and
muscle size, and help foster a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
451
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
452 Studies using 300 mg of testosterone ester
(enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated
only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached
21%.
453 The negative impact of aromatase inhibition should be taken into
consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less per week, the impact on lipid
profile tends to be noticeable but not dramatic, making an anti-estrogen (for
cardioprotective purposes) perhaps unnecessary. Doses of 600 mg or less per
week have also failed to produce statistically significant changes in LDL/VLDL
cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive protein, and insulin
sensitivity, all indicating a relatively weak impact on cardiovascular risk
factors.
454 When used in moderate doses, injectable testosterone esters are
usually considered to be the safest of all anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
As with all anabolic/androgenic steroids, it is unlikely that one will retain every
pound of new bodyweight after a cycle is concluded. This is especially true
when withdrawing from a strong (aromatizing) androgen like testosterone
cypionate, as much of the new weight gain is likely to be in the form of water
retention, quickly eliminated after drug discontinuance. An imbalance of
anabolic and catabolic hormones during the post-cycle recovery period may
further create an environment that is unfavorable for the retention of muscle
tissue. Proper ancillary drug therapy is usually recommended to help restore
hormonal balance more quickly, ultimately helping the user retain more muscle
tissue.
Another way to lessen the post-cycle “crash” is to first replace testosterone
cypionate with a milder anabolic such as nandrolone decanoate or methenolone
enanthate. The new steroid would be administered alone for one to two more
months, at a dosage of 200-400 mg per week. In this “stepping down” procedure
the user is attempting to eliminate the watery bulk of a testosterone-based drug
while simultaneously preserving the solid muscularity underneath. This practice
can prove to be effective, even if mainly for psychological reasons (some may
view it as simply dividing the crash into water and hormonal stages).
Testosterone-stimulating drugs are still typically used at the conclusion of
therapy, as endogenous testosterone production will not rebound during the
administration of nandrolone decanoate or methenolone enanthate.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
To treat androgen insufficiency, the prescribing guidelines for testosterone
cypionate call for a dosage of 50-400 mg every two to four weeks. Although
active in the body for a longer time, testosterone cypionate is usually injected on
a weekly basis for physique-or performance-enhancing purposes. The usual
dosage is in the range of 200-600 mg per week, taken in cycles 6 to 12 weeks in
length. This level is sufficient for most users to notice exceptional gains in
muscle size and strength.
Testosterone is usually incorporated into bulking phases of training, when added
water retention will be of little consequence, the user more concerned with raw
mass than definition. Some do incorporate the drug into cutting cycles as well,
but typically in lower doses (100-200 mg per week) and/or when accompanied
by an aromatase inhibitor to keep estrogen levels under control. Testosterone
cypionate is a very effective anabolic drug, and is often used alone with great
benefit. Some, however, find a need to stack it with other anabolic/androgenic
steroids for a stronger effect, in which case an additional 200-400 mg per week
of boldenone undecylenate, methenolone enanthate, or nandrolone decanoate
should provide substantial results with no significant hepatotoxicity.
Testosterone is ultimately very versatile, and can be combined with many other
anabolic/androgenic steroids to tailor the desired effect.
While large doses are generally not advised, some bodybuilders have been
known to use excessively high dosages of this drug (1,000 mg per week or
more). This was much more common before the 1990’s, when cypionate vials
were usually very cheap and easy to find. A “more is better” attitude is easy to
justify when paying only $20 for a 10cc vial (today the typical price for a single
injection). At dosages of 800-1000 mg per week or more, water retention will
likely account for more of the additional weight gain than new muscle tissue.
The practice of “megadosing” is inefficient (not to mention potentially
dangerous), especially when we take into account the typical high cost of
steroids today.
Administration (Women):
Testosterone cypionate is rarely used with women in clinical medicine. When
applied, it is most often used as a secondary medication during inoperable breast
cancer, when other therapies have failed to produce a desirable effect and
suppression of ovarian function is necessary. Testosterone cypionate is not
recommended for women for physique-or performance-enhancing purposes due
to its strong androgenic nature, tendency to produce virilizing side effects, and
slow-acting characteristics (making blood levels difficult to control).
Availability:
Testosterone cypionate remains widely available as a prescription drug product.
Its production is largely associated with American companies, although recently
has been expanding into loosely regulated Asian markets that still cater to
demand by bodybuilders and athletes. In reviewing some of the products and
changes in the global pharmaceutical market, we have made the following
observations.
Brand name testosterone cypionate (Depot-Testosterone) remains available in
the United Stated from Prizer. This is a high-profile target of counterfeiters. All
legitimate boxes will carry a “Jh” symbol hidden on one of the top inside flaps.
It will appear when placed under UV light.
Many generic forms of the drug are also produced in the U.S. market by
manufacturers such as Watson, Sandoz, Paddock, Synerx, and Bedford. All
come packaged in multiple-dose vials. Due to strict controls these products are
rarely diverted for illicit sale. There are also several pharmacies customcompounding testosterone cypionate for doctors that specialize in androgen
replacement therapy.
Cypionax is available in Thailand by T.P. Drug Laboratories. It comes in 2 mL
ampules containing 100 mg/mL of steroid.
Cypiobolic from Asia Pharma (Malaysia) is now approved for sale through
pharmacies in Thailand. Each box should carry a scratch-off security sticker,
which will display a code that can be validated on the company website.
Testex Prolongatum remains available in Spain. This steroid is produced by
Laboratorios Q Pharma. It is packaged in 2 mL dark glass ampules with grey
silkscreen lettering. It comes in two doses, containing a total of 100 mg or 250
mg of steroid. Testex has always been a high-profile item for counterfeiters.
Found in Chile is a high-dose cypionate product called ciclo-6. The product is
manufactured by the firm Drag Pharma, and contains 300 mg/ml of steroid in a 2
mL ampule (600 mg of cypionate in total).
Balkan Pharmaceuticals (Moldova) makes the product Testosterona C. It is
prepared in both 1 mL ampules and multi-dose vials.
Deposterona (testosterone blend)
Description:
Deposterona is an injectable veterinary steroid preparation that contains a blend
of three different testosterone esters. Each milliliter contains 12mg of
testosterone acetate, 12mg of testosterone valerate, and 36mg of testosterone
undecanoate, for a total steroid concentration of 60 mg/mL. This is currently the
only commercial steroid product available that contains testosterone valerate,
which is a short to medium acting ester with a half-life approximately double
that of testosterone propionate.
455 With its blend of slow-and fast-acting esters,
Deposterona is essentially a low-dosed alternative to Sustanon, although given
the use of testosterone undecanoate it will be longer acting with more
unbalanced pharmacokinetics.
History:
Deposterona was developed by Syntex Animal Health Company several decades
ago, and has been sold on the Mexican veterinary drug market since. It is used
primarily to treat impotence, weakness, fatigue, and hypogonadism in male
breeding animals (cows, pigs, canines, and sheep), and also as a general proteinsparing anabolic. Deposterona is now sold under the Fort Dodge Animal Health
label, which acquired Syntex Animal Health in the mid-1990’s.
How Supplied:
Deposterona is available on the Mexican veterinary drug market.It contains
12mg of testosterone acetate, 12mg of testosterone valerate, and 36mg of
testosterone undecanoate per milliliter of oil; packaged in a 10 mL multi-dose
vial.Twelve vials are packed in each box.
Structural Characteristics:
Deposterona contains a mixture of three testosterone compounds, which where
modified with the addition of carboxylic acid esters (acetic, valeric, and
undecanoic acids) at the 17-beta hydroxyl group. Esterified forms of testosterone
are less polar than free testosterone, and are absorbed more slowly from the area
of injection. Once in the bloodstream, the ester is removed to yield free (active)
testosterone. Esterified forms of testosterone are designed to prolong the window
of therapeutic effect following administration, allowing for a less frequent
injection schedule compared to injections of free (unesterified) steroid.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone more likely to require the
concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention
and loss of muscle definition are common with higher doses of testosterone, this
drug is usually considered a poor choice for dieting or cutting phases of training.
Its moderate estrogenicity makes it more ideal for bulking phases, where the
added water retention will support raw strength and muscle size, and help foster
a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
456
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
457 Studies using 300 mg of testosterone ester
(enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated
only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached
21%.
458 The negative impact of aromatase inhibition should be taken into
consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less per week, the impact on lipid
profile tends to be noticeable but not dramatic, making an anti-estrogen (for
cardioprotective purposes) perhaps unnecessary. Doses of 600 mg or less per
week have also failed to produce statistically significant changes in LDL/VLDL
cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive protein, and insulin
sensitivity, all indicating a relatively weak impact on cardiovascular risk
factors.
459 When used in moderate doses, injectable testosterone esters are
usually considered to be the safest of all anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
For bodybuilding purposes, Deposterona is usually injected on at least a weekly
basis, in a dosage of 120-360 mg (2-6 ml). Dividing the weekly dosage into two
or more smaller applications can reduce injection volume. Cycles are generally
between 6 and 12 weeks in length. This level is sufficient to provide noticeable
gains in muscle size and strength. Testosterone drugs are ultimately very
versatile, and can be combined with many other anabolic/androgenic steroids
depending on the desired effect.
Administration (Women):
Deposterona is not recommended for women for performance-enhancing
purposes due to its strong androgenic nature, tendency to produce virilizing side
effects, and slow-acting characteristics (making blood levels difficult to control).
Availability:
Deposterona is only known to be manufactured in Mexico. Because it contains
such a low concentration of steroid,this product is not in high demand, and not
readily diverted for illicit sale.
Dianabol® (methandrostenolone, methandienone)
Description:
Dianabol is the most recognized trade name for the drug methandrostenolone,
also referred to as methandienone in many countries. Methandrostenolone is a
derivative of testosterone, modified so that the hormone’s androgenic
(masculinizing) properties are reduced and its anabolic (tissue building)
properties preserved. Having a lower level of relative androgenicity than
testosterone, methandrostenolone is classified as an “anabolic” steroid, although
quite a distinct androgenic side is still present. This drug was designed, and is
principally sold, as an oral medication, although it can also be found in a number
of injectable veterinary solutions. Dianabol is today, and has historically been,
the most commonly used oral anabolic/androgenic steroid for physique and
performance-enhancing purposes.
History:
Methandrostenolone was first described in 1955.
460
It was released to the U.S.
prescription drug market in 1958, under the brand name Dianabol by Ciba
Pharmaceuticals. Ciba developed methandrostenolone into a medicine with the
help of Dr. John Ziegler, who was the team physician for a number of U.S.
Olympic teams, including weightlifting. Ziegler makes note in Bob Goldman’s
Death in the Locker Room that he was first exposed to steroids at the 1956
World Games, seeing that the Russians were heavily abusing testosterone on
their strength athletes. According to Ziegler, the hormone was having noticeable
side effects, and one athlete had such profound prostate enlargement that he was
forced to urinate with the aid of a catheter. While working with Ciba, the
company tested a steroid (synthesized earlier) that had reduced androgenicity
compared to testosterone, but with retained tissue-building (anabolic) properties.
This had been accomplished by altering the basic chemical structure of
testosterone in a way that altered its metabolism and disposition in the body.
With the help of Dr. Ziegler, Ciba brought to market one of the most effective
oral “anabolic” steroid medicines ever known, methandrostenolone. The success
of the drug was rapid and far-reaching.
Dr. Ziegler’s athletes were quickly making great advancements in their
competitive careers with the help of the drug. According to reports, Ziegler too
seemed to be very impressed, at least for a while.
461 But by the early 1960’s, it
was starting to look like Dianabol had sparked a great wave of steroid abuse in
competitive sports. Dr. Ziegler’s early recommendations, which depending on
the source called for as little as 5 mg per day or as much as 15 mg per day, were
being largely ignored, as athletes developed their own more aggressive (and
potentially dangerous) dosing strategies. Dr. Ziegler soon became disgusted with
the misuse of the drug, and would eventually become a voice of opposition to
sports doping. By 1967, approximately 10 years after first introducing Dianabol
to his athletes, he had categorically condemned the use of anabolic steroids in
sports.
462
As early as 1965, Dianabol was already starting to fall under scrutiny of the U.S.
Food and Drug Administration. That year the FDA requested Ciba clarify
Dianabol’s medical uses,which were then stated to include helping patients in
debilitated states and those with weakened bones. In 1970, the FDA accepted
that Dianabol was “Probably Effective” in treating post-menopausal osteoporosis
and pituitary-deficient dwarfism. These changes were reflected in the drug’s
prescribing recommendations during the 1970’s, and Ciba was allowed to
continue selling and studying the agent. Ciba eventually lost patent protection,
however, and companies like Parr, Barr, Bolar, and Rugby were soon cutting
deeply into their market with their own generic version of the drug.
By the early-80’s the FDA had withdrawn its “Probably Effective” position on
the pituitary-deficient dwarfism, and continued to press Ciba for more data.
Sufficient clarification never came, and in 1983 Ciba officially withdrew
Dianabol from the U.S. market.
463 Perhaps financial disinterest had a hand in
their abandoned push to keep the drug approved. The FDA pulled all generic
forms of methandrostenolone from the U.S. market in 1985, a time when most
Western nations were also eliminating the drug, finding its existence to be
justified mainly by sports doping. Methandrostenolone is still produced today,
but typically in nations with loose prescription drug regulations, and by
companies that still prefer to cater to an underground athletic market.
How Supplied:
Methandrostenolone is widely available in both human and veterinary drug
markets. Composition and dosage may vary by country and manufacturer.
Methandrostenolone was designed as an oral anabolic steroid containing 2.5 mg
or 5 mg of steroid per tablet (Dianabol). Modern brands usually contain 5 mg or
10 mg per tablet. Methandrostenolone can also be found in injectable veterinary
preparations. These are typically oilbased solutions that carry 25 mg/ml of
steroid.
Structural Characteristics:
Methandrostenolone is a modified form of testosterone. It differs by: 1) the
addition of a methyl group at carbon 17alpha to protect the hormone during oral
administration and 2) the introduction of a double bond between carbons 1 and
2, which reduces its relative androgenicity. The resulting steroid also has a much
weaker relative binding affinity for the androgen receptor than testosterone, but
at the same time displays a much longer half-life and lower affinity for serumbinding proteins in comparison. These features (among others) allow
methandrostenolone to be a very potent anabolic steroid in spite of a weaker
affinity for receptor binding. Recent studies have additionally confirmed that its
primary mode of action involves interaction with the cellular androgen
receptor.
464
Side Effects (Estrogenic):
Methandrostenolone is aromatized by the body, and is a moderately estrogenic
steroid.
465 Gynecomastia is often a concern during treatment, and may present
itself quite early into a cycle (particularly when higher doses are used). At the
same time water retention can become a problem, causing a notable loss of
muscle definition as both subcutaneous water retention and fat levels build.
Sensitive individuals may therefore want to keep the estrogen under control with
the addition of an anti-estrogen such as Nolvadex® and/or Proviron®. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which is a
more effective remedy for estrogen control. Aromatase inhibitors, however, can
be quite expensive in comparison to standard estrogen maintenance therapies,
and may also have negative effects on blood lipids.
It is interesting to note that methandrostenolone is structurally identical to
boldenone, except that it contains the added c17-alpha-methyl group. This fact
makes clear the impact of altering a steroid in such a way, as these two
compounds appear to act very differently in the body. A key dissimilarity seems
to lie in the tendency for estrogenic side effects. Equipoise® (boldenone
undecylenate) is known to be quite mild in this regard, and users commonly take
this drug without the need to add an anti-estrogen. Methandrostenolone is much
more estrogenic, often necessitating anti-estrogen use. But this difference is not
caused by methandrostenolone being more easily aromatized. In fact, the
17alpha methyl group and c1-2 double bond both slow the process of
aromatization considerably. The issue actually is caused by methandrostenolone
converting to 17alpha-methylestradiol, a more biologically active form of
estrogen than estradiol.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
common with this substance. This may include bouts of oily skin, acne, and
body/facial hair growth. Anabolic/androgenic steroids may also aggravate male
pattern hair loss. Individuals sensitive to the androgenic effects of
methandrostenolone may find a milder anabolic such as Deca-Durabolin® to be
more comfortable. Women are additionally warned of the potential virilizing
effects of anabolic/androgenic steroids. These may include a deepening of the
voice, menstrual irregularities, changes in skin texture, facial hair growth, and
clitoral enlargement.
While methandrostenolone does convert to a more potent steroid via interaction
with the 5-alpha reductase enzyme (the same enzyme responsible for converting
testosterone to dihydrotestosterone), it has an extremely low affinity to do so.
466
The androgenic metabolite 5-alpha dihydromethandrostenolone is produced only
in trace amounts, so the relative androgenicity of methandrostenolone is not
significantly affected by finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Methandrostenolone is a c17-alpha alkylated compound. This alteration protects
the drug from deactivation by the liver, allowing a very high percentage of the
drug entry into the bloodstream following oral administration. C17-alpha
alkylated anabolic/androgenic steroids can be hepatotoxic. Prolonged or high
exposure may result in liver damage. In rare instances life-threatening
dysfunction may develop. It is advisable to visit a physician periodically during
each cycle to monitor liver function and overall health. Intake of c17-alpha
alkylated steroids is commonly limited to 6-8 weeks, in an effort to avoid
escalating liver strain.
Studies have shown that several weeks of methandrostenolone administration
offers minimal hepatic stress so long as it is given at a dosage of 10 mg per day
or below. At a dose of 15 mg per day, a majority of patients will begin to
demonstrate disturbed liver function as measured by clinically elevated
bromosulphalein retention (a marker of hepatic stress).
467 Even at 2.5 and 5 mg
per day, elevations in BSP retention have been reported in patients. Severe liver
complications are rare given the periodic nature in which most people use oral
anabolic/androgenic steroids, although cannot be excluded with
methandrostenolone, especially with high doses and/or prolonged administration
periods.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Methandrostenolone has a strong effect on the hepatic management of
cholesterol due to its structural resistance to liver breakdown and route of
administration. Anabolic/androgenic steroids may also adversely affect blood
pressure and triglycerides, reduce endothelial relaxation, and support left
ventricular hypertrophy, all potentially increasing the risk of cardiovascular
disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Methandrostenolone is no exception, and is noted for its strong influence on the
hypothalamic-pituitary-testicular axis. Clinical studies giving 15 mg per day to
resistance-training males for 8 weeks caused the mean plasma testosterone level
to fall by 69%.
468 Without the intervention of testosterone-stimulating
substances, testosterone levels should return to normal within 1-4 months of
drug secession. Note that prolonged hypogonadotrophic hypogonadism can
develop secondary to steroid abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
469 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, this steroid should be taken on an empty stomach.
Administration (Men):
The original prescribing guidelines for Dianabol called for a daily dosage of 5
mg. This was to be administered on an intermittent basis, with the drug taken for
no more than 6 consecutive weeks. Thereafter, a break of 2 to 4 weeks was
advised before therapy was resumed. For physique-or performance-enhancing
purposes, the drug is also used intermittently, with cycles usually lasting
between 6 and 8 weeks in length followed by 6-8 weeks off. Although a low
dose of 5 mg daily may be effective for improving performance, athletes
typically take much higher amounts. A daily dosage of three to six 5 mg tablets
(15-30 mg) is most common, and typically produces very dramatic results. Some
venture even higher in dosage, but this practice usually leads to a more profound
incidence of side effects, and is generally discouraged.
Dianabol stacks well with a variety of other steroids. It is noted to mix
particularly well with the mild anabolic Deca-Durabolin®, for example.
Together one can expect exceptional muscle and strength gains, with side effects
not much worse than one would expect from Dianabol alone. For sheer mass, a
long-acting testosterone ester like enanthate or cypionate can be used. With the
high estrogenic/androgenic properties of this androgen, however, side effects
should be more pronounced. Gains would be pronounced as well, which usually
makes such an endeavor worthwhile to the user. As discussed earlier, ancillary
drugs can be added to reduce the side effects associated with this kind of cycle.
The half-life of Dianabol is only about 3 to 5 hours. A single daily dosage
schedule will produce a varying blood level, with ups and downs throughout the
day. The user, likewise, has a choice, to either split up the tablets during the day
or to take them all at one time. The usual recommendation has been to divide
them and try to regulate the concentration in your blood. This, however, will
produce a lower peak blood level than if the tablets were taken all at once, so
there may be a trade-off with this option. Both options work fine, but anecdotal
evidence seems to support single daily doses as being better for overall results.
With such a schedule, it seems logical that taking the pills earlier in the day
would be optimal. This would allow a considerable number of daytime hours for
an androgen-rich metabolism to heighten the uptake of nutrients, especially the
critical hours following training.
Administration (Women):
Being moderately androgenic, Dianabol is really only a popular steroid with
men. When used by women, strong virilization symptoms are possible. Some do
experiment with it, however, and often find low doses (2.5-5 mg) of this steroid
quite effective for new muscle growth. Studies have demonstrated that a
majority of women will notice acne, which is indicative of androgenicity, at a
dosage of only 10 mg per day. Children are likely to notice virilizing effects with
as little as 2.5 mg per day.
Availability:
Methandrostenolone remains readily available as a pharmaceutical product,
though its supply is largely isolated to less regulated markets in Asia and Eastern
Europe. In reviewing some of the more popular products and changes on the
global pharmaceutical market, we have made the following observations.
British Dispensary produces Anabol tablets in Thailand. This product comes in
three strengths, 5 mg, 10 mg, and 15 mg. All products come in bottles (100, 200,
500, and/or 1000 depending on the dose). All tablets themselves are imprinted
with the company’s snake emblem, and will vary in color. The pink tablets are 5
mg, the yellow 10 mg, and blue 15 mg. The company also uses a holographic
sticker on all products to deter counterfeiting, though this feature has been
copied with high accuracy.
March Pharmaceuticals in Thailand manufacturers Danabol DS. These small
blue heart-shaped tablets come in bottles of 500. The company recently
instituted a small circular holographic sticker to deter counterfeiting. The logo is
also embedded into the label in a metal foil.
Dronabol DS is remains available in Thailand by Bangkok Lab & Cosmetic.
This product comes in a 10 mg tablet strength, and is prepared in bottles of 500
and 1,000 tablets each.
Methandon is also found in Thailand, made by Acdhon. This product comes as a
5 mg tablet, and is packaged in plastic tubs of 1,000 tablets each.
Generic “Russian D-Bol” (METAHAPOCTEHOROH) is no longer in
production. All products bearing this label should be considered counterfeit.
Naposim (Romania) is still in production, now under the joint Teraphia Ranbaxy
label. It is sold in boxes of 20 tablets, which are separated into two foil/plastic
blisters of 10 each. The tablets carry a triangle stamp on one side. This product
has been the subject of widespread counterfeiting in the past.
Metanabol from Jelfa (Poland) is still in production, though its appearance has
changed. The new packaging reflects a more modern red gradient look. The
enclosed foil and plastic strip is also much wider than it was previously.
The generic from Formula Magistral (Argentina) is also commonly located on
the international market, especially throughout North and South America. The
product comes loose in bottles, although now also carries a holographic sticker
to deter counterfeiting.
Landerlan in Paraguay makes a generic methandrostenolone. It comes in a 10
mg tablet dosage. The product is packaged in bottles of 100 tablets each.
Balkan Pharmaceuticals (Moldova) makes the product Danabol. It is prepared in
both 10 mg and 50 mg tablets, with 20 tablets contained in each foil and plastic
strip.
Drive® (boldenone/methylandrostenediol blend)
Description:
Drive is an Australian injectable veterinary steroid preparation that contains a
blend of methandriol dipropionate and boldenone undecylenate. The two steroids
are present in a dose of 25 mg/mL and 30 mg/mL respectively, for a total steroid
concentration of 55 mg/mL. Boldenone undecylenate is a highly common steroid
most notably identified with the preparation Equipoise®. Methandriol
dipropionate, however, is very rarely seen on the U.S. black market. Its character
is that of a moderately strong anabolic steroid, which is accompanied by a
notable androgenic component. When combined with boldenone, the result is a
moderately androgenic/anabolic blend inclined to produce notable muscle mass
and strength gains, usually without excessive water retention.
History:
Drive is a product of RWR Veterinary Products (formerly a subsidiary of Nature
Vet), sold only on the Australian veterinary drug market. It is designed for use in
horses, typically as a general anabolic or health tonic drug for when an animal is
weak from vigorous performance. It is supposed to aid the growth of muscle
tissue, help avoid dehydration, and improve the digestion of dietary proteins.
The dosage used for an adult 1,100lb horse is 5 mL (110 mg) every two weeks.
Australia is a country with a robust veterinary drug market, known to carry a
variety of unusual steroids and odd multi-component steroid blends. Drive is
perhaps the most well-known of these products. Being that it is neither the most
concentrated preparation nor the most effective, however, much of its popularity
is likely due to its well-coined trade name and early sales history. Drive remains
on the Australina market today, although tight controls and its relatively low permilliliter steroid concentration make diversion for athletic use much less
common than it was many years ago.
How Supplied:
Drive is available on the Australian veterinary drug market. It contains 55
mg/mL of steroid in oil in a 10 mL vial.
Structural Characteristics:
For a more comprehensive discussion of the individual steroids boldenone
undecylenate and methandriol dipropionate, refer to their respective profiles.
Side Effects (Estrogenic):
Methylandrostendiol is not directly aromatized by the body, although one of its
known metabolites is methyltestosterone, which can aromatize.
Methlyandrostenediol is also believed to have some inherent estrogenic
activity.
470 Combined with boldenone, which also aromatizes, Drive is
considered a moderately estrogenic steroid. Gynecomastia is possible during
treatment, but generally only when higher doses are used. Water and fat
retention can also become issues, again depending on dose. Sensitive individuals
may need to add an anti-estrogen such as Nolvadex® to minimize related side
effects.
Side Effects (Androgenic):
Although classified as an anabolic steroid preparation, androgenic side effects
are still common with this substance. This may include bouts of oily skin, acne,
and body/facial hair growth. Anabolic/androgenic steroids may also aggravate
male pattern hair loss. Women are warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth,and clitoral
enlargement.
Side Effects (Hepatotoxicity):
Methylandrostenediol is a c17-alpha alkylated compound. This alteration
protects the drug from deactivation by the liver, allowing a very high percentage
of the drug entry into the bloodstream following oral administration. C17-alpha
alkylated anabolic/androgenic steroids can be hepatotoxic. Prolonged or high
exposure may result in liver damage. In rare instances life-threatening
dysfunction may develop. It is advisable to visit a physician periodically during
each cycle to monitor liver function and overall health. Intake of c17-alpha
alkylated steroids is commonly limited to 6-8 weeks, in an effort to avoid
escalating liver strain. Injectable forms of the drug may present slightly less
strain on the liver by avoiding the first pass metabolism of oral dosing, although
may still present substantial hepatotoxicity.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Methylandrostenediol has a strong effect on the hepatic management of
cholesterol due to its structural resistance to liver breakdown and (with the oral)
route of administration. Anabolic/androgenic steroids may also adversely affect
blood pressure and triglycerides, reduce endothelial relaxation, and support left
ventricular hypertrophy, all potentially increasing the risk of cardiovascular
disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
Drive has not been approved for use in humans. Prescribing guidelines are
unavailable. Typical dosing schedule for physique-or performance-enhancing
purposes would be in the range of 220 mg (4mL) to 440 mg (8mL) per week, a
level that should provide quality lean mass gain without strong bloating or body
fat retention. Due to the high injection volume and fastacting nature of
methandriol dipropionate, the total weekly dosage is commonly divided into 2-3
smaller applications.
Administration (Women):
Drive has not been approved for use in humans. Prescribing guidelines are
unavailable. Drugs containing methylandrostenediol are generally not
recommended for women for physique-or performance-enhancing purposes due
to its androgenic nature and tendency to produce virilizing side effects.
Availability:
Drive remains in production, though legitimate products are now rarely diverted
to the black market given the heightened controls over anabolic steroids in
Australia.
Durabolin® (nandrolone phenylpropionate)
Description:
Nandrolone phenylpropionate is an injectable form of the anabolic steroid
nandrolone. The properties of this drug are strikingly similar to those of DecaDurabolin®, which uses the slower acting drug nandrolone decanoate. The
primary difference between these two preparations is the speed in which
nandrolone is released into the blood. While nandrolone decanoate provides a
release of nandrolone from the area of injection lasting approximately 3 weeks,
nandrolone phenylpropionate is active for only about a week. In clinical
situations, Deca-Durabolin can thus be injected once every 2 or 3 weeks, while
Durabolin® is usually administered every several days to once weekly.
Otherwise, the two drugs are virtually interchangeable. Like Deca-Durabolin,
Durabolin is valued by athletes and bodybuilders for its abilities to promote
strength and lean muscle mass gains without significant estrogenic or androgenic
side effects.
History:
Nandrolone phenylpropionate was first described in 1957.
471
It became a
prescription medication shortly after, sold by the international pharmaceuticals
giant Organon (now Merck/MSD) under the brand name Durabolin. When first
introduced to the United States, indicated uses of nandrolone phenylpropionate
included pre-and postoperative lean mass retention, osteoporosis, advanced
breast cancer, weight loss due to convalescence or disease, geriatric states
(general weakness and frailty), burns, severe trauma, ulcers, adjunct therapy with
certain forms of anemia, and selective cases of growth and development
retardation in children. During the 1970’s, the FDA began revising the indicated
uses of this drug, however, and they were soon significantly narrowed. Moving
forward, the drug was mainly being indicated for the treatment of advanced
metastatic breast cancer, and as adjunct therapy for the treatment of senile and
post-menopausal osteoporosis.
Durabolin was a key focus of Organon’s marketing efforts only for well less
than a decade following its release. Once Deca-Durabolin was introduced during
the 1960’s, this shorter-acting counterpart, although still available, started to take
a back seat. Durabolin was not completely abandoned by Organon at the time,
however, partly due to the fact that it was given a slightly different set of
therapeutic uses in certain countries, and therefore continued to hold onto a
niche market for some time. As the size of the anabolic steroid market continued
to grow throughout the 1970’s and ’80’s, it was nandrolone decanoate that was
attracting the most attention of other drug manufacturers. Numerous drug
companies had produced their own versions of nandrolone phenylpropionate
over the years, however. Today, the drug remains scarcely available. It is
unknown if the present owner of Organon (Merck/MSD) will market Durabolin,
or if its production (as a brand name product) has ended.
How Supplied:
Nandrolone phenylpropionate is available in select human drug markets.
Composition and dosage may vary by country and manufacturer, but usually
contain 25 mg/mL or 50 mg/mL of steroid dissolved in oil.
Structural Characteristics:
Nandrolone phenylpropionate is a modified form of nandrolone, where a
carboxylic acid ester (propionic phenyl ester) has been attached to the 17-beta
hydroxyl group. Esterified steroids are less polar than free steroids, and are
absorbed more slowly from the area of injection. Once in the bloodstream, the
ester is removed to yield free (active) nandrolone. Esterified steroids are
designed to prolong the window of therapeutic effect following administration,
allowing for a less frequent injection schedule compared to injections of free
(unesterified) steroid. Nandrolone phenylpropionate provides a sharp spike in
nandrolone release 24-48 hours following deep intramuscular injection, and
declines to near baseline levels within a week.
Side Effects (Estrogenic):
Nandrolone has a low tendency for estrogen conversion, estimated to be only
about 20% of that seen with testosterone.
472 This is because while the liver can
convert nandrolone to estradiol, in other more active sites of steroid
aromatization such as adipose tissue nandrolone is far less open to this
process.
473 Consequently, estrogen-related side effects are a much lower concern
with this drug than with testosterone. Elevated estrogen levels may still be
noticed with higher dosing, however, and may cause side effects such as
increased water retention, body fat gain, and gynecomastia. An anti-estrogen
such as clomiphene citrate or tamoxifen citrate may be necessary to prevent
estrogenic side effects if they occur. One may alternately use an aromatase
inhibitor like Arimidex® (anastrozole), which more efficiently controls estrogen
by preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
It is of note that nandrolone has some activity as a progestin in the body.
474
Although progesterone is a c-19 steroid, removal of this group as in 19-
norprogesterone creates a hormone with greater binding affinity for its
corresponding receptor. Sharing this trait, many 19-nor anabolic steroids are
shown to have some affinity for the progesterone receptor as well.
475 The side
effects associated with progesterone are similar to those of estrogen, including
negative feedback inhibition of testosterone production and enhanced rate of fat
storage. Progestins also augment the stimulatory effect of estrogens on
mammary tissue growth. There appears to be a strong synergy between these
two hormones here, such that gynecomastia might even occur with the help of
progestins, without excessive estrogen levels. The use of an anti-estrogen, which
inhibits the estrogenic component of this disorder, is often sufficient to mitigate
gynecomastia caused by nandrolone.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance, especially with higher doses. This may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are warned of the
potential virilizing effects of anabolic/androgenic steroids. These may include a
deepening of the voice, menstrual irregularities, changes in skin texture, facial
hair growth, and clitoral enlargement. Nandrolone is a steroid with relatively low
androgenic activity relative to its tissue-building actions, making the threshold
for strong androgenic side effects comparably higher than with more androgenic
agents such as testosterone, methandrostenolone, or fluoxymesterone. It is also
important to point out that due to its mild androgenic nature and ability to
suppress endogenous testosterone, nandrolone is prone to interfering with libido
in males when used without another androgen.
Note that in androgen-responsive target tissues such as the skin, scalp, and
prostate, the relative androgenicity of nandrolone is reduced by its reduction to
dihydronandrolone (DHN).
476 477
The 5-alpha reductase enzyme is responsible for this metabolism of nandrolone.
The concurrent use of a 5-alpha reductase inhibitor such as finasteride or
dutasteride will interfere with site-specific reduction of nandrolone action,
considerably increasing the tendency of nandrolone to produce androgenic side
effects. Reductase inhibitors should be avoided with nandrolone if low
androgenicity is desired.
Side Effects (Hepatotoxicity):
Nandrolone is not c-17 alpha alkylated, and not known to have hepatotoxic
effects. Liver toxicity is unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Studies
administering 600 mg of nandrolone decanoate per week for 10 weeks
demonstrated a 26% reduction in HDL cholesterol levels.
478 This suppression is
slightly greater than that reported with an equal dose of testosterone enanthate,
and is in agreement with earlier studies showing a slightly stronger negative
impact on HDL/LDL ratio with nandrolone decanoate as compared to
testosterone cypionate.
479 Nandrolone should still have a significantly weaker
impact on serum lipids than c-17 alpha alkylated agents. Anabolic/androgenic
steroids may also adversely effect blood pressure and triglycerides, reduce
endothelial relaxation, and support left ventricular hypertrophy, all potentially
increasing the risk of cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Studies administering 100 mg injection of nandrolone phenylpropionate
demonstrated a rapid suppression of serum testosterone following a single
injection. Testosterone levels declined to approximately 30% of initial level by
day 3 after drug administration, and stayed suppressed for approximately 13
days. Regular use is expected to significantly lengthen the endogenous hormone
recovery window. It is believed that the progestational activity of nandrolone
notably contributes to the suppression of testosterone synthesis during therapy,
which can be marked in spite of a low tendency for estrogen conversion.
480
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 2-6 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
For general anabolic effects, early prescribing guidelines recommend a dosage
of 25-50 mg per week for 12 weeks. The usual dosage for physique-or
performance-enhancing purposes is in the range of 200-400 mg per week, taken
in cycles 8 to 12 weeks in length. This level is sufficient for most users to notice
measurable gains in lean muscle mass and strength. Note that due to the
fastacting nature of the phenylpropionate ester, the weekly dosage is usually
subdivided into 2 separate applications spaced evenly apart.
Administration (Women):
For general anabolic effects, early prescribing guidelines recommend a dosage
of 25-50 mg per week for 12 weeks. When used for physique-or performanceenhancing purposes, a dosage of 50 mg per week (given in a single weekly
injection) is most common, taken for cycle lasting 4 to 6 weeks. Higher doses or
longer durations of use are discouraged due to potential for androgenic side
effects. Although only slightly androgenic, women are occasionally confronted
with virilization symptoms when taking this compound. Should virilizing side
effects become a concern, nandrolone phenylpropionate should be discontinued
immediately to help prevent a permanent appearance.
Availability:
Nandrolone phenylpropionate has declined extensively as a pharmaceutical
product. Given its short action, and the limited use of its longer-acting cousin
nandrolone decanoate in clinical medicine, there are very few (if any) unique
applications remaining for this drug. Thus, there is little justification for its
continued production.
Brand name Durabolin appears to be unavailable in all markets worldwide.
A small number of generic and brand name products remain in less regulated
markets (mainly in Asia), due to continued demand by athletes and
bodybuilders.
Superanabolon from Spofa in the Czech Republic is also still in manufacture. It
contains only 25 mg of steroid per 1 mL ampule, which makes it in relatively
low demand among athletes.
Iran Hormone (Iran) makes a 25 mg/mL generic nandrolone phenylpropionate in
1 mL ampules. Counterfeits are not known to be a problem.
Dynabol® (nandrolone cypionate)
Description:
Nandrolone cypionate is an injectable form of the anabolic steroid nandrolone.
This ester provides a pattern of hormone release virtually identical to that of
testosterone cypionate, with peak levels of drug being noted approximately 24-
48 hours after administration, and a substantial hormone release sustained for
about weeks. In this case the active hormone is nandrolone, which is a
moderately strong anabolic steroid that carries mild estrogenic and androgenic
properties. This product is essentially identical in overall effect to DecaDurabolin® (nandrolone decanoate), producing measurable gains in strength and
lean muscle mass, which tend to be accompanied by a low level of side
effects.The one point of difference is that nandrolone cypionate may appear to
be a faster-acting compound to some users. Otherwise, there is no discernable
difference between the two compounds, and nandrolone cypionate could replace
nandrolone decanoate in virtually all cycles.
History:
Nandrolone cypionate was first developed during the 1960’s. It was sold for a
brief time as a human-use pharmaceutical, under such brand names as Anabo,
Depo-Nortestonate, Nortestrionate, and Sterocrinolo. Such preparations did not
last, however, and in recent years the drug has been available only as a product
of veterinary medicine. The most notable appearance has come from Jurox in
Australia, which marketed a 50 mg/mL version of the drug called Dynabol 50.
Jurox also included nandrolone cypionate as part of an anabolic steroid blend
called Nandrabolin. Both products, however, were discontinued in 2001, when
Jurox scaled back its steroid line.This was likely done in response to media
criticisms of heavy Australian veterinary exports to Mexico, which largely fuel
the American black market.
The discontinued Jurox products were quickly transferred to SYD Group in
Australia, assuring they would not be completely eliminated from commerce.
They were subsequently reintroduced to market in 2002, under the names
Anabolic DN and Anabolic NA, respectively. The new names made loose
reference to the former Jurox trademarks, likely in an effort to retain some of the
original market for the products. SYD Group had also introduced a high-dose
version of Anabolic DN directly to the Mexican veterinary drug market, but the
product has since been withdrawn. This time the product was discontinued
following U.S. DEA charges against the firm, alleging that they were conspiring
to illegally export Mexican steroids to the U.S. Today, the Anabolic DN and
Anabolic NA products remain available on the Australian veterinary drug
market, although tight controls limit diversion for off-label use.
How Supplied:
Nandrolone cypionate is available on the Australian veterinary drug markets. It
is supplied as 50 mg/mL of steroid dissolved in oil, in a 10 mL vial.
Structural Characteristics:
Nandrolone cypionate is a modified form of nandrolone, where a carboxylic acid
ester (cyclopentylpropionic acid) has been attached to the 17-beta hydroxyl
group. Esterified steroids are less polar than free steroids, and are absorbed more
slowly from the area of injection. Once in the bloodstream, the ester is removed
to yield free (active) nandrolone. Esterified steroids are designed to prolong the
window of therapeutic effect following administration, allowing for a lessfrequent injection schedule compared to injections of free (unesterified) steroid.
Nandrolone cypionate provides a sharp spike in nandrolone release 24-48 hours
following deep intramuscular injection, and sustains a substantial release of
hormone for approximately 2 weeks.
Side Effects (Estrogenic):
Nandrolone has a low tendency for estrogen conversion, estimated to be only
about 20% of that seen with testosterone.
481 This is because while the liver can
convert nandrolone to estradiol, in other more active sites of steroid
aromatization such as adipose tissue nandrolone is far less open to this
process.
482 Consequently, estrogen-related side effects are a much lower concern
with this drug than with testosterone. Elevated estrogen levels may still be
noticed with higher dosing, however, and may cause side effects such as
increased water retention, body fat gain, and gynecomastia. An anti-estrogen
such as clomiphene citrate or tamoxifen citrate may be necessary to prevent
estrogenic side effects if they occur. One may alternately use an aromatase
inhibitor like Arimidex® (anastrozole), which more efficiently controls estrogen
by preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
It is of note that nandrolone has some activity as a progestin in the body.
483
Although progesterone is a c-19 steroid, removal of this group as in 19-
norprogesterone creates a hormone with greater binding affinity for its
corresponding receptor. Sharing this trait, many 19-nor anabolic steroids are
shown to have some affinity for the progesterone receptor as well.
484 The side
effects associated with progesterone are similar to those of estrogen, including
negative feedback inhibition of testosterone production and enhanced rate of fat
storage. Progestins also augment the stimulatory effect of estrogens on
mammary tissue growth. There appears to be a strong synergy between these
two hormones here, such that gynecomastia might even occur with the help of
progestins, without excessive estrogen levels. The use of an anti-estrogen, which
inhibits the estrogenic component of this disorder, is often sufficient to mitigate
gynecomastia caused by nandrolone.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance, especially with higher doses. This may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are warned of the
potential virilizing effects of anabolic/androgenic steroids. These may include a
deepening of the voice, menstrual irregularities, changes in skin texture, facial
hair growth, and clitoral enlargement. Nandrolone is a steroid with relatively low
androgenic activity relative to its tissue-building actions, making the threshold
for strong androgenic side effects comparably higher than with more androgenic
agents such as testosterone, methandrostenolone, or fluoxymesterone. It is also
important to point out that due to its mild androgenic nature and ability to
suppress endogenous testosterone, nandrolone is prone to interfering with libido
in males when used without another androgen.
Note that in androgen-responsive target tissues such as the skin, scalp, and
prostate, the relative androgenicity of nandrolone is reduced by its reduction to
dihydronandrolone (DHN).
485 486 The 5-alpha reductase enzyme is responsible
for this metabolism of nandrolone. The concurrent use of a 5-alpha reductase
inhibitor such as finasteride or dutasteride will interfere with site-specific
reduction of nandrolone action, considerably increasing the tendency of
nandrolone to produce androgenic side effects. Reductase inhibitors should be
avoided with nandrolone if low androgenicity is desired.
Side Effects (Hepatotoxicity):
Nandrolone is not c-17 alpha alkylated, and not known to have hepatotoxic
effects. Liver toxicity is unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Studies
administering 600 mg of nandrolone decanoate per week for 10 weeks
demonstrated a 26% reduction in HDL cholesterol levels.
487 This suppression is
slightly greater than that reported with an equal dose of testosterone enanthate,
and is in agreement with earlier studies showing a slightly stronger negative
impact on HDL/LDL ratio with nandrolone decanoate as compared to
testosterone cypionate.
488 Nandrolone injectables, however, should still have a
significantly weaker impact on serum lipids than c-17 alpha alkylated agents.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production. For
sake of comparison, studies administering 100 mg per week of nandrolone
decanoate for 6 weeks have demonstrated an approximate 57% reduction in
serum testosterone levels during therapy. At a dosage of 300 mg per week, this
reduction reached 70%.
489
It is believed that the progestational activity of
nandrolone notably contributes to the suppression of testosterone synthesis
during therapy, which can be marked in spite of a low tendency for estrogen
conversion.
490 Without the intervention of testosterone-stimulating substances,
testosterone levels should return to normal within 2-6 months of drug secession.
Note that prolonged hypogonadotrophic hypogonadism can develop secondary
to steroid abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
When used for physique-or performance-enhancing purposes, a dose of 200-400
mg per week is most common, taken in cycles 8 to 12 weeks in length. This level
is sufficient for most users to notice measurable gains in lean muscle mass and
strength, which should be accompanied by a low level of estrogenic and
androgenic activity. Although higher doses (450-600 mg) may produce a
stronger anabolic effect, given the relatively low concentration in which this
drug is found (50 mg/mL), doses above 400 mg are not commonly applied.
Instead, the drug is often stacked with another agent, usually an androgen such
as an injectable testosterone, which also helps offset the very low level of
androgenicity of nandrolone. An oral steroid with pronounced androgenicity,
such as methandrostenolone or oxymetholone, is sometimes used as well, but
will also present some hepatotoxicity and have a stronger effect on serum lipids
(negatively).
Administration (Women):
When used for physique-or performance-enhancing purposes, a dosage of 50 mg
per week is most common. Although only slightly androgenic, women are
occasionally confronted with virilization symptoms when taking this compound.
Should virilizing side effects become a concern, nandrolone cypionate should be
discontinued immediately to help prevent their permanent appearance. After a
sufficient period of withdrawal, the shorter-acting nandrolone Durabolin® might
be considered a safer (more controllable) option. This drug stays active for only
several days, greatly reducing the withdrawal time if indicated.
Availability:
The only remaining pure nandrolone cypionate product is Anabolic DN from
Australia, produced only in a 50 mg/mL concentration. It comes in the form of a
10 mL vial, which is contained in an orange tube.
Dynabolon® (nandrolone undecanoate)
Description:
Nandrolone undecanoate is an injectable form of the anabolic steroid
nandrolone. The ester applied here is one carbon atom longer than decanoate,
and consequently forms a very slightly longer-lasting drug deposit at the site of
injection. With proper attention paid to carrier, concentration, volume, and
pharmacokinetics, it would likely even be possible to formulate this steroid into
a very long-acting drug preparation, one similar to testosterone undecanoate
(Nebido) in appearance. Even without a further protracted therapeutic window,
nandrolone undecanoate can be comfortably injected once every 1 to 2 weeks,
which reflects its slow-acting nature. Although no longer available, this agent
was once highly favored by athletes and bodybuilders for its ability to promote
slow steady gains in lean mass with minimal estrogenic or androgenic side
effects.
History:
Nandrolone undecanoate was developed during the 1960’s, and was
subsequently sold as Dynabolon in Italy (Chrinos) and France (Theramex), and
as Psychobolan in Germany (Theramex). The Italian product was moved to the
new Farmasister label years later, but retained the original Dynabolon trade
name. Dynabolon was generally indicated for use in patients suffering from
malnutrition, catabolic states, or recovering from major surgery. It was also used
to combat osteoporosis, including the treatment of androgen-sensitive
populations such as women and the elderly. Nandrolone undecanoate seems to
have exhibited a fair safety record, yet in spite of this, the three known
commercial preparations did not last on their respective prescription drug
markets. Psychobolan from Germany and Dynabolon from Farmasister in Italy
were discontinued many years ago, and Dynabolon from France finally followed
before the close of the 1990’s. Presently, no legitimate pharmaceutical
preparation containing nandrolone undecanoate is known to exist.
How Supplied:
Nandrolone undecanoate is no longer available as a prescription drug product.
When manufactured, it was supplied at a concentration of 80.5 mg/mL dissolved
in oil and sealed in a 1 mL ampule. Each ampule provided the equivalent of 50
mg of nandrolone base.
Structural Characteristics:
Nandrolone undecanoate is a modified form of nandrolone, where a carboxylic
acid ester (undecanoic acid) has been attached to the 17-beta hydroxyl group.
Esterified steroids are less polar than free steroids, and are absorbed more slowly
from the area of injection. Once in the bloodstream, the ester is removed to yield
free (active) nandrolone. Esterified steroids are designed to prolong the window
of therapeutic effect following administration, allowing for a less-frequent
injection schedule compared to injections of free (unesterified) steroid.
Nandrolone undecanoate is designed to provide a slow release of nandrolone for
up to 3 to 4 weeks following injection.
Side Effects (Estrogenic):
Nandrolone has a low tendency for estrogen conversion, estimated to be only
about 20% of that seen with testosterone.
491 This is because while the liver can
convert nandrolone to estradiol, in other more active sites of steroid
aromatization such as adipose tissue nandrolone is far less open to this
process.
492 Consequently, estrogenrelated side effects are a much lower concern
with this drug than with testosterone. Elevated estrogen levels may still be
noticed with higher dosing, however, and may cause side effects such as
increased water retention, body fat gain, and gynecomastia. An anti-estrogen
such as clomiphene citrate or tamoxifen citrate may be necessary to prevent
estrogenic side effects if they occur. One may alternately use an aromatase
inhibitor like Arimidex® (anastrozole), which more efficiently controls estrogen
by preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
It is of note that nandrolone has some activity as a progestin in the body.
493
Although progesterone is a c-19 steroid, removal of this group as in 19-
norprogesterone creates a hormone with greater binding affinity for its
corresponding receptor. Sharing this trait, many 19-nor anabolic steroids are
shown to have some affinity for the progesterone receptor as well.
494 The side
effects associated with progesterone are similar to those of estrogen, including
negative feedback inhibition of testosterone production and enhanced rate of fat
storage. Progestins also augment the stimulatory effect of estrogens on
mammary tissue growth. There appears to be a strong synergy between these
two hormones here, such that gynecomastia might even occur with the help of
progestins, without excessive estrogen levels. The use of an anti-estrogen, which
inhibits the estrogenic component of this disorder, is often sufficient to mitigate
gynecomastia caused by nandrolone.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance, especially with higher doses. This may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are warned of the
potential virilizing effects of anabolic/androgenic steroids. These may include a
deepening of the voice, menstrual irregularities, changes in skin texture, facial
hair growth, and clitoral enlargement. Nandrolone is a steroid with relatively low
androgenic activity relative to its tissue-building actions, making the threshold
for strong androgenic side effects comparably higher than with more androgenic
agents such as testosterone, methandrostenolone, or fluoxymesterone. It is also
important to point out that due to its mild androgenic nature and ability to
suppress endogenous testosterone, nandrolone is prone to interfering with libido
in males when used without another androgen.
Note that in androgen-responsive target tissues such as the skin, scalp, and
prostate, the relative androgenicity of nandrolone is reduced by its reduction to
dihydronandrolone (DHN).
495 496 The 5-alpha reductase enzyme is responsible
for this metabolism of nandrolone. The concurrent use of a 5-alpha reductase
inhibitor such as finasteride or dutasteride will interfere with site-specific
reduction of nandrolone action, considerably increasing the tendency of
nandrolone to produce androgenic side effects. Reductase inhibitors should be
avoided with nandrolone if low androgenicity is desired.
Side Effects (Hepatotoxicity):
Nandrolone is not c-17 alpha alkylated, and not known to have hepatotoxic
effects. Liver toxicity is unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Studies
administering 600 mg of nandrolone decanoate per week for 10 weeks
demonstrated a 26% reduction in HDL cholesterol levels.
497 This suppression is
slightly greater than that reported with an equal dose of testosterone enanthate,
and is in agreement with earlier studies showing a slightly stronger negative
impact on HDL/LDL ratio with nandrolone decanoate as compared to
testosterone cypionate.
498 Nandrolone injectables, however, should still have a
significantly weaker impact on serum lipids than c-17 alpha alkylated agents.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production. For
sake of comparison, studies administering 100 mg per week of nandrolone
decanoate for 6 weeks have demonstrated an approximate 57% reduction in
serum testosterone levels during therapy. At a dosage of 300 mg per week, this
reduction reached 70%.
499
It is believed that the progestational activity of
nandrolone notably contributes to the suppression of testosterone synthesis
during therapy, which can be marked in spite of a low tendency for estrogen
conversion.
500 Without the intervention of testosterone-stimulating substances,
testosterone levels should return to normal within 2-6 months of drug secession.
Note that prolonged hypogonadotrophic hypogonadism can develop secondary
to steroid abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
Nandrolone undecanoate was used clinically at a dose of 1 ampule every 1 to 2
weeks. A total of 3 to 6 ampules were used for a given 6-week period of therapy.
When used for physique-or performance-enhancing purposes, a dose of 3 to 4
ampules (241.5 to 322mg) per week is most common, taken in cycles 8 to 12
weeks in length. This level is sufficient for most users to notice measurable gains
in lean muscle mass and strength, which should be accompanied by a low level
of estrogenic and androgenic activity. Higher doses (400-600 mg per week) will
impart a stronger anabolic effect, but can be difficult given the relatively low
concentration this steroid was manufactured in. Instead, many opted to combine
this agent with other anabolic/androgenic steroids for a stronger effect. Given its
properties, it seems to fit well for both bulking and cutting purposes, and can
reasonably replace Deca-Durabolin in such cycles.
Administration (Women):
Nandrolone undecanoate was used clinically at a dose of 1 ampule every 1 to 2
weeks. A total of 3 to 6 ampules were used for a given 6-week period of therapy.
When used for physique-or performance-enhancing purposes, a dosage of 1
ampule (80.5 mg) every 10 days was most common, which is taken for 4 to 6
weeks. Although only slightly androgenic, women are occasionally confronted
with virilization symptoms when taking this compound. Should virilizing side
effects become a concern, the drug should be discontinued immediately to help
prevent their permanent appearance. After a sufficient period of withdrawal, the
shorter acting nandrolone Durabolin® might be considered a safer (more
controllable) option. This drug stays active for only several days, greatly
reducing the withdrawal time if indicated.
Availability:
Nandrolone undecanoate is no longer available as a prescription drug product.
Some underground preparations are, however, known to exist.
Equipoise® (boldenone undecylenate)
Description:
Boldenone undecylenate is an injectable veterinary steroid that exhibits strong
anabolic and moderately androgenic properties. The undecylenate ester extends
the activity of the drug greatly (the undecylenate ester is only one carbon atom
longer than decanoate), so that injections need to be repeated only once every 3
or 4 weeks. The well-balanced anabolic and androgenic properties of this drug
are greatly appreciated by athletes, who generally consider it to be a stronger,
slightly more androgenic, alternative to Deca-Durabolin®. It is generally
cheaper, and could replace Deca in most cycles without greatly changing the end
result. Boldenone undecylenate is also commonly known as a drug capable of
increasing red blood cell production, although there should be no confusion that
this is an effect characteristic of nearly all anabolic/androgenic steroids.
History:
Ciba reportedly patented boldenone as a synthetic anabolic steroid in 1949.
During the 1950’s and ’60’s, the firm developed several experimental esters of
the drug, and would later release a long-acting form of the agent (briefly) in the
form of boldenone undecylenate. It would be sold under the brand name
Parenabol, which likely referred to its characteristics as a parenteral (injectable)
anabolic agent. Parenabol saw some clinical use during the late ’60’s and early
’70’s, mainly as a lean-tissue-preserving anabolic agent in cases of wasting, and
for the retention of bone mass with osteoporosis. Boldenone undecylenate was a
short-lived preparation on human medical markets, however, and would be
discontinued globally before the end of the 1970’s. Squibb would ultimately be
most famous for introducing this agent in the veterinary market, and would sell it
under its now most famous trade name, Equipoise.
In the veterinary market, boldenone undecylenate is most commonly applied to
horses, although in many regions it is indicated for use in other animals as well.
It generally exhibits a pronounced effect on lean bodyweight, appetite, and
general disposition of the animal. The Equipoise brand was sold under the
Squibb label until 1985, when Solvay acquired Squibb’s U.S. animal health
business. Equipoise would be sold under the Solvay label for the next several
years, until Wyeth finally acquired the animal health division of Solvay in 1995.
The division was formed into Fort Dodge Animal Health, which continues to
market Equipoise in the U.S. and certain markets abroad today. Many other
generic and brand name forms of boldenone undecylenate exist in numerous
international drug markets, owing to the fact that any patents on boldenone
undecylenate have long since expired.
How Supplied:
Boldenone undecylenate is widely available in veterinary drug markets.
Composition and dosage may vary by country and manufacturer; the majority of
products are supplied as multi-dose glass vials containing an oily solution;
usually carrying 25 mg/ml or 50 mg/ml of steroid.
Structural Characteristics:
Boldenone is a modified form of testosterone. It differs by the introduction of a
double bond between carbons 1 and 2, which reduces its relative estrogenicity
and androgenicity. Equipoise® contains boldenone modified with the addition of
carboxylic acid ester (undecylenoic acid) at the 17-beta hydroxyl group.
Esterified steroids are less polar than free steroids, and are absorbed more slowly
from the area of injection. Once in the bloodstream, the ester is removed to yield
free (active) boldenone. Esterified steroids are designed to prolong the window
of therapeutic effect following administration, allowing for a less frequent
injection schedule compared to injections of free (unesterified) steroid.
Boldenone undecylenate is designed to provide a peak release of boldenone
within a few days after injection, and sustain hormone release for approximately
21-28 days.
It is interesting to note that structurally boldenone and methandrostenolone
(Dianabol) are almost identical. In the case of boldenone (as applied here), the
compound uses a 17-beta ester (undecylenate) to facilitate administration, while
methandrostenolone accomplishes this with the use of a 17-alpha alkyl group.
Aside from this, the molecules are the same. Of course they act quite differently
in the body, which goes to show that the 17-methylation affects more than just
the oral efficacy of an anabolic/androgenic steroid.
Side Effects (Estrogenic):
Boldenone is aromatized in the body to estradiol (estrogen). Elevated estrogen
levels can cause side effects such as increased water retention, body fat gain, and
gynecomastia. Boldenone is considered a mildly estrogenic steroid.
Aromatization studies suggest that its rate of conversion to estradiol is roughly
half that of testosterone.
501 The tendency to develop noticeable estrogenic side
effects with boldenone should be slightly higher than nandrolone, but much
lower than with testosterone. Estrogenic side effects are usually not pronounced
unless this drug is taken in doses above 200-400 mg per week. An anti-estrogen
such as clomiphene citrate or tamoxifen citrate might be used to help mitigate
these side effects, should they become present. One may alternately use an
aromatase inhibitor like Arimidex® (anastrozole), although it is considerably
more expensive, and may negatively affect blood lipids.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
common with this substance, especially with higher doses. This may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are also warned of
the potential virilizing effects of anabolic/androgenic steroids. These may
include a deepening of the voice, menstrual irregularities, changes in skin
texture, facial hair growth, and clitoral enlargement.
Note that while boldenone does reduce to a more potent androgen
(dihydroboldenone) via the 5-alpha reductase enzyme in androgen-responsive
target tissues such as the skin, scalp, and prostate, its affinity to do so in the
human body is extremely low.
502 The relative androgenicity of boldenone is,
therefore, not significantly affected by finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Boldenone is not c-17 alpha alkylated, and not known to have hepatotoxic
effects. Liver toxicity is unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction. Boldenone is likely to have a less dramatic impact on
cardiovascular risk factors than synthetic oral anabolic steroids. This is due in
part to its openness to metabolism by the liver, which allows it to have less effect
on the hepatic management of cholesterol. The aromatization of boldenone to
estradiol may also help to mitigate the negative effects of androgens on serum
lipids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
Although it stays active for a much longer time, boldenone undecylenate is
injected at least weekly for physique-or performance-enhancing purposes. It is
most commonly used at a dosage of 200-400 mg (4-8ml,50 mg version) per
week. The dosage schedule can be further divided to reduce the volume of each
injection if necessary, perhaps administering the drug two to three times per
week. One should also take caution to rotate injection sites regularly, so as to
avoid irritation or infection.
Not a rapid mass builder, boldenone undecylenate instead provides a slow but
steady gain of strength and quality muscle mass. The positive effects of this drug
become most apparent when it is used for longer cycles, usually lasting 8 weeks
or more in duration. The muscle gained should also not be the smooth bulk
associated with testosterone, but more defined and solid. Since water bloat is not
contributing greatly to the diameter of the muscle, more of the visible size
gained on a cycle of boldenone undecylenate should be retained after the drug
has been discontinued.
Boldenone undecylenate is a very versatile drug, and can be combined with a
number of other agents depending on the desired result. For mass, it is
commonly stacked with an injectable testosterone such as enanthate or
cypionate. This should produce strong gains in muscle size and strength, without
the same intensity of side effects of using testosterone (at a higher dose) alone.
During a cutting phase, muscle hardness and density can be greatly improved
when combining boldenone undecylenate with a non-aromatizable steroid such
as trenbolone acetate or methenolone enanthate. Oral c-17 alpha alkylated agents
such as fluoxymesterone or stanozolol may also be used, but will present some
level of hepatotoxicity. For some, even the low buildup of estrogen associated
with this compound is enough to relegate its use to bulking cycles only.
Administration (Women):
When used for physique-or performance-enhancing purposes, women take much
lower doses of boldenone undecylenate than men, typically 50-75 mg per week.
Women should take caution with the slow-acting characteristics of this
preparation, which make blood levels difficult to control and slow to decline
should virilization symptoms become present.
Availability:
Boldenone undecylenate remains widely available as a veterinary drug product.
It is produced mainly in the Americas, consistently at a dosage of 25 mg/mL or
50 mg/mL. A small number of preparations are made at a higher dosage
(typically 200 mg/mL), mainly by companies in less regulated markets of Asia
where supply is often dictated by black market demand. In reviewing some of
the more popular products and changes on the global pharmaceutical market, we
have made the following observations.
Brand name Equipoise is no longer available in Canada. This product was
formerly manufactured by Wyeth Animal Health, which following a series of
mergers is now part of Pfizer. The Equipoise product was never manufactured
under the Pfizer label.
Equipoise® is produced in the United States by the Fort Dodge Company. The
Fort Dodge products are sold readily in Mexico, and afterwards smuggled back
into the U.S. Legitimate vials are made of clear glass, and carry a label with a
shiny metallic surface on the under side. Fakes are very abundant of this item.
Ganabol, which is produced in a number of South American countries, is still a
popular brand in international commerce. It is seen in two strengths (25 mg/mL
and 50 mg/mL) and in five sizes (10, 50, 100, 250, and 500 mL). There have
been numerous fakes of this product in the past, so be careful when shopping.
The Legacy brand name product from Tecnoquimicas in Argentina seems to be
reaching the U.S. as of late, at least in small volume. This product carries 50
mg/mL of steroid in a 50 mL vial. At this time the Legacy product is very low on
the radar, and probably can be trusted when located.
The brands Boldenona and Boldegan from Gen-Far are also popular in South
America. These are low-dose (50 mg/mL) preparations. Like Ganabol, they
come in a variety of vial sizes. Counterfeits do not appear to be a big issue at this
time.
Finajet (trenbolone acetate)
Description:
Trenbolone acetate is an injectable (generally) anabolic steroid derived from
nandrolone. Its activity is quite removed from its structural parent, however,
such that direct comparisons between the two are difficult. Trenbolone is a nonestrogenic steroid, and is considerably more anabolic and androgenic than
nandrolone on a milligram for milligram basis. In appearance, it is much more
commonly compared to a stronger androgen such as drostanolone, than it is to
nandrolone. It is also estimated to display about three times more androgenic
potency than testosterone, making it one of the strongest injectable anabolic
steroids ever commercially manufactured. Among athletes, this steroid is highly
valued for its ability to increase muscle hardness, definition, and raw strength,
without unwanted water retention and fat mass gains. It is considered a drug of
choice for contest bodybuilders, yet remains very popular with recreational users
simply looking to refine their physiques.
History:
Trenbolone acetate was first closely studied in 1967, described during a series of
experiments into synthetic anabolic steroids by Roussel-UCLAF.
503 By the early
1970’s, trenbolone acetate was being sold in England by Hoechst as Finajet, and
in France as Finaject by Roussel. Roussel AG in Germany was parent to both
companies. Trenbolone acetate is a drug of veterinary medicine, although a
longer-acting ester of trenbolone (see: Parabolan) was once sold for human
consumption as well. Trenbolone acetate is used, almost exclusively, to increase
the rate of weight gain and improve feed efficiency of cattle shortly before
slaughter. Essentially, the drug is utilized to increase product profitability, as
measured in total pounds of salable meat. It is generally used right up to the
point of slaughter, with no withholding period. Meat products sold in many areas
of the world will often contain small amounts of residual trenbolone metabolites
as a result of this practice.
Trenbolone acetate first became popular among U.S. bodybuilders during the
1980’s, a time when the drug was being smuggled in from Europe in high
volume. It was identified (rightly so) as a powerful anabolic and androgenic
agent, and quickly became a drug of choice among American competitive
bodybuilders. Although extremely hot for a brief period of time, the supply of
trenbolone acetate ended abruptly in 1987, as Hoechst-Roussel decided to
voluntarily discontinue sale of all injectable forms of this medication. Although
unconfirmed, the growing public concern about sports doping likely had much to
do with this decision, as the discontinuation of “controversial” steroids was very
common during the late 1980’s and early 1990’s. This event marked the end of
legitimate medicines containing trenbolone acetate for injection.
Around the same time as we were seeing the demise of Finajet and Finaject,
Hoechst-Roussell was introducing trenbolone acetate to the U.S. market as
Finaplix cattle implant pellets. This came subsequent to the FDA’s approval for
such products in 1987 . The pellets were designed for subcutaneous implantation
into the ear of the cattle with a handheld implant gun, and are far too large to be
implanted in humans without minor surgery. Remarkably, trenbolone acetate
pellets are exempt from U.S. controlled substance laws. This is presumably to
make it easy and affordable for livestock owners to have access to the growthpromoting agent. If a veterinarian were needed every time these products were to
be used, they might be too troublesome or cost prohibitive to consider.
Admittedly, since these products come in the form of pellets, they are not in a
form suitable for human consumption either, making their exemption seem a
little more reasonable than at first glance.
Human administration of Finaplix pellets can be difficult to accomplish, but it is
still widely done. Most commonly, two to four implant pellets are ground up and
mixed with a 50/50 water and DMSO solution, which is applied to the skin daily.
This home-brew transdermal mix is effective, but also tends to carry a strong
odor of garlic (an effect of the DMSO). Others simply grind up a few pellets
with the back of a spoon and inhale (snort) them. Here, the drug enters the blood
stream through the mucous membrane, a poor but still useful means of delivery
for steroid hormones. Those who have tried this often claim it is not as irritating
as they had imagined it would be. Alternately, some athletes opt to simply
consume the drug orally. Although not an ideal mode of delivery, trenbolone
displays a moderate level of oral bioavailability, and can be used in this manner
given adequate dosing.
More adventurous individuals have made it a practice to mix their own injections
with Finaplix. The pellets are ground into a fine powder (usually anywhere from
2 to 6 pellets), and then are added to sterile water, propylene glycol, or an oilbased injectable steroid or veterinary vitamin. This is usually repeated twice
weekly, although some do manage to undertake this practice more frequently.
Since this is not being done in a controlled sterile environment, however, one is
obviously risking infection (or worse) by doing this. Starting in the late 1990’s,
some stores began selling kits that contain all the necessary ingredients to
separate the binders from the active steroid and brew a relatively pure injectable.
These kits have grown in popularity over the years, and are usually reviewed
favorably, although are not considered a substitute for sterile pharmaceutical
medications.
Finaplix® is presently available in the U.S. and some markets abroad, although
it is now being sold by Intervet instead of Hoechst-Roussel Agri-vet. This
product comes in two forms, Finaplix-H and Finaplix-S, which denotes if the
product was intended for a Heifer or a Steer respectively. The total dosages of
both products are different, with the “H” version containing 100 20 mg
trenbolone acetate pellets (2,000 mg) and the “S” version only 70 (1,400 mg).
Ivy Animal Health (U.S.) has introduced two competing products of equivalent
makeup as well, sold as Component-TH and Component-TS. There are also the
Revalor and Synovex+ brands that contain trenbolone acetate with an added
(usually unwanted) dose of estrogen. Additionally, although no other legitimate
medicines containing trenbolone acetate exist, the drug is produced (for injection
and oral use) by a number of export and underground steroid manufacturers.
How Supplied:
Trenbolone acetate is available in select veterinary drug markets. It generally
comes in the form of implant pellets containing 20 mg of trenbolone acetate
each. Injectable preparations containing 30 mg/ml of steroid in oil were formerly
sold.
Structural Characteristics:
Trenbolone is a modified form of nandrolone. It differs by the introduction of
double bonds at carbons 9 and 11, which inhibit aromatization (9-ene), increase
androgen-binding affinity,
504 and slow its metabolism. The resulting steroid is
significantly more potent as both an anabolic and an androgen than its
nandrolone base. Trenbolone acetate contains trenbolone modified with the
addition of carboxylic acid ester (acetic acid) at the 17-beta hydroxyl group, so
that the free steroid is released more slowly from the area of injection.
Side Effects (Estrogenic):
Trenbolone is not aromatized by the body, and is not measurably estrogenic. It is
of note, however, that this steroid displays significant binding affinity for the
progesterone receptor (slightly stronger than progesterone itself ).
505 506 The side
effects associated with progesterone are similar to those of estrogen, including
negative feedback inhibition of testosterone production and enhanced rate of fat
storage. Progestins also augment the stimulatory effect of estrogens on
mammary tissue growth. There appears to be a strong synergy between these
two hormones here, such that gynecomastia might even occur with the help of
progestins, without excessive estrogen levels. The use of an anti-estrogen, which
inhibits the estrogenic component of this disorder, is often sufficient to mitigate
gynecomastia caused by progestational anabolic/androgenic steroids. Note that
progestational side effects are more common when trenbolone is being taken
with other aromatizable steroids.
Side Effects (Androgenic):
Although classified as an anabolic steroid, trenbolone is sufficiently androgenic.
Androgenic side effects are still common with this substance, and may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are also warned of
the potential virilizing effects of anabolic/androgenic steroids. These may
include a deepening of the voice, menstrual irregularities, changes in skin
texture, facial hair growth, and clitoral enlargement. Additionally, the 5-alpha
reductase enzyme does not metabolize trenbolone,
507 so its relative
androgenicity is not affected by finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Trenbolone is not c-17 alpha alkylated, and is generally not considered a
hepatotoxic steroid; liver toxicity is unlikely. This steroid does have a strong
level of resistance to hepatic breakdown, however, and severe liver toxicity has
been noted in bodybuilders abusing trenbolone.
508 Although unlikely,
hepatotoxicity cannot be completely excluded, especially with high doses.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Due to its nonaromatizable nature and strong resistance to metabolism, trenbolone has a
moderate to strong (negative) impact on lipid values and atherogenic risk.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention. In experimental studies, trenbolone
was determined to be approximately three times stronger at suppressing
gonadotropins than testosterone on a milligram for milligram basis.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
Trenbolone acetate was never approved for use in humans. Prescribing
guidelines are unavailable. An effective dosage for physique-or performanceenhancing purposes generally falls in the range of 100-300 mg per week, taken
for 6 to 8 weeks. Due to the short-acting nature of acetate esters, the total week’s
dosage is subdivided into 2-3 smaller applications. Effective oral doses tend to
fall in the range of 100-200 mg per day, taken for no longer than 6-8 weeks to
minimize any potential hepatic strain. This level is sufficient to notice strong
increases in strength and lean tissue mass, with a low level of unwanted side
effects. Lack of estrogenic activity has made trenbolone very appealing for
competitive athletes looking to shed fat, while at the same time trying to avoid
water retention. Here, trenbolone may provide the high androgen content needed
in order to elicit a very hard, defined physique.
While it is a noteworthy hardening agent, this is not the only benefit of
trenbolone acetate. It is also a strong anabolic, with muscle-building properties
often compared to testosterone and Dianabol, but without the same level of
water retention. This may be a little generous of a description, as its lack of
estrogenic activity does seem to hurt this agent in its abilities to promote muscle
mass gains. While trenbolone is often recommended as a great addition to a mass
cycle, it is rarely reported to be a very powerful agent when used alone. Results
are most often reported as moderate lean tissue growth accompanied by
exceptional hardening and fat loss. Although perhaps it is not quite as potent as
the more estrogenic bulking agents if sheer mass is the goal, trenbolone is still a
better builder milligram for milligram than nandrolone, and likely the most
anabolic of all the non-estrogenic commercial steroids.
For stacking, trenbolone is a very versatile steroid, and seems to work
exceptionally well with other agents for both bulking and cutting purposes. For
cutting, bodybuilders often stack it with a mild anabolic like Winstrol® or
Primobolan®. Without extra water beneath your skin, the mix will elicit a very
solid, well-defined hardness to the physique. For lean mass gains, DecaDurabolin® or Equipoise® are popular additions. Here again, trenbolone will
greatly enhance and solidify the new muscle growth. When looking purely for
mass, trenbolone pairs well with testosterone, Anadrol 50®, or Dianabol.The
result is typically the rapid and substantial gain of somewhat solid muscle mass.
In the Underground Steroid Hanbook II, Dan Duchaine describes the mix of
trenbolone, testosterone, and Anadrol as the “Most Effective” stack for men, and
states, “I’ve not encountered any other stack that will put weight and strength on
like this one.” This particular drug combination has subsequently become quite
popular.
Administration (Women):
Trenbolone acetate was never approved for use in humans. Prescribing
guidelines are unavailable. This agent is not recommended for women for
physique-or performance-enhancing purposes due to strong androgenic nature
and tendency to produce virilizing side effects.
Availability:
Pharmaceutical preparations containing trenbolone acetate remain scarce. The
bulk of the supply for this compound comes from underground steroid
manufacturers. In reviewing some of the remaining products and changes in the
global pharmaceutical market, we have made the following observations.
Trenbolone acetate is still produced in the United States, sold in the form of
cattle implant pellets (mainly Finaplix®). This agricultural product is also
exported to some neighboring markets, though is not widely popular outside of
the Americas. These pellets are difficult to administer, and are not commonly the
subject of counterfeiting. This is the only legitimate form of trenbolone acetate
in the U.S.
Most other forms are from underground manufacturers, and therefore are of
unverifiable quality.
Halotestin® (fluoxymesterone)
Description:
Fluoxymesterone is an oral anabolic steroid derived from testosterone. More
specifically, it is a methyltestosterone derivative, differing by the addition of 11-
beta-hydroxy and 9-alpha-fluoro groups. The result is a potent orally active nonaromatizable steroid that exhibits extremely strong androgenic properties.
Fluoxymesterone is considerably more androgenic than testosterone, while at the
same time the anabolic effects of this agent are considered to be moderate in
comparison. This makes fluoxymesterone a great strength drug, but not the most
ideal agent for gaining muscle mass. The predominant effects seen when taking
fluoxymesterone are increased strength, increased muscle density, and increased
definition, with only modest size increases.
History:
Fluoxymesterone was first described in 1956.
509
It was assayed that same year,
and shown to possess approximately 20 times the anabolic potency of
methyltestosterone
510
(its relative anabolic effect in humans would not be quite
as strong in comparison). It was introduced to the U.S. prescription drug market
shortly after under the brand name Halotestin (Upjohn), and soon after that as
Ultandren (Ciba). The drug was initially described as halogenated derivative of
testosterone, possessing up to 5 times greater anabolic and androgenic potency
than methyltestosterone. Early prescribing guidelines recommended its use in
both sexes for the promotion of lean tissue repair and growth following such
conditions as burns, delayed healing of fractures, chronic malnutrition,
debilitating diseases, convalescence, paraplegia, and catabolism induced by
long-term administration of cortisone. It was also used in males to treat
insufficient androgen levels, and in women to treat abnormal bleeding in the
uterus and advanced breast cancer.
By the mid-1970’s, the FDA had been granted much more control over the U.S.
drug market. One of the first major changes with steroid medicine came when
the FDA required strong substantiation for each potential use of a drug. The
prescribing guidelines for fluoxymesterone were soon refined to state that the
drug was “effective” for treating various forms of androgen deficiency in males,
and reducing the severity of postpartum breast pain and treating androgenresponsive inoperable breast cancer in females. It was also listed as “probably
effective” in treating postmenopausal osteoporosis. Current prescribing
guidelines for fluoxymesterone list only the uses of treating androgen deficiency
in males and breast cancer in females.
In recent years, fluoxymesterone has become viewed more and more as a
controversial medication in the eyes of most clinicians. Its hepatotoxicity and
potential negative impact of lipids and cardiovascular risk factors are often cited
as reasons for avoiding the use of this agent in otherwise healthy males for
treating androgen insufficiency. Today, testosterone preparations (injections,
gels, patches, implants, etc.) are preferred for this purpose, and they supplement
the same androgens missing from the body (testosterone, DHT), not more toxic
synthetic derivatives. Fluoxymesterone remains for sale in the U.S. as a generic
drug only. It remains available in only limited supply outside of the United
States.
How Supplied:
Fluoxymesterone is available in select human drug markets. Composition and
dosage may vary by country and manufacturer,although generally contain 2mg,
2.5 mg, 5 mg, or 10 mg per tablet.
Structural Characteristics:
Fluoxymesterone is a modified form of testosterone. It differs by 1) the addition
of a methyl group at carbon 17-alpha, which helps protect the hormone during
oral administration, 2) the introduction of a fluoro group at carbon 9 (alpha) and
3) the attachment of a hydroxyl group at carbon 11 (beta), which inhibits steroid
aromatization. The latter two modifications also greatly enhance the androgenic
and relative biological activity of the steroid over 17-alpha methyltestosterone.
Side Effects (Estrogenic):
Fluoxymesterone is not aromatized by the body, and is not measurably
estrogenic. An anti-estrogen is not necessary when using this steroid, as
gynecomastia should not be a concern even among sensitive individuals. Since
estrogen is the usual culprit with water retention, this steroid instead produces a
lean, quality look to the physique with no fear of excess subcutaneous fluid
retention. This makes it a favorable steroid to use during cutting cycles, when
water and fat retention are major concerns.
Side Effects (Androgenic):
Fluoxymesterone is classified as an androgen. Androgenic side effects are
common with this substance, and may include bouts of oily skin, acne, and
body/facial hair growth. Anabolic/androgenic steroids may also aggravate male
pattern hair loss. Those genetically prone to male pattern hair loss may wish to
opt for a milder, less androgenic, anabolic steroid. As a potent androgen, this
steroid may also increase aggressiveness. Women are additionally warned of the
potential virilizing effects of anabolic/androgenic steroids. These may include a
deepening of the voice, menstrual irregularities, changes in skin texture, facial
hair growth, and clitoral enlargement.
Fluoxymesterone appears to be a good substrate for the 5-alpha reductase
enzyme. This is evidenced by the fact that a large number of its metabolites are
found to be 5-alpha reduced androgens,
511 which coupled with its outward
androgenic nature, suggests that this steroid is converting to a much more active
steroid in androgen responsive target tissues such as the skin, scalp and prostate.
It may be possible to reduce the relative androgenicity of fluoxymesterone by the
concurrent use of finasteride or dutasteride.
It is also of note that fluoxymesterone has been shown to possess usual
androgenic properties. In human studies published back in 1961, the steroid
displayed a much stronger tendency to promote phallic enlargement compared to
other androgenic effects such as hair growth, libido, and changes in vocal
pitch.
512 Fluoxymesterone was offering a somewhat different androgenic profile
compared to testosterone, and as such demonstrated that it was possible, at some
level, to actually tailor drug effect within the broad category of androgenic
action. Fluoxymesterone remains considered an androgen, but studies like the
above suggest that it may not offer a complete biological equivalent to
testosterone where androgenicity is concerned.
Side Effects (Hepatotoxicity):
Fluoxymesterone is a c17-alpha alkylated compound. This alteration protects the
drug from deactivation by the liver, allowing a very high percentage of the drug
entry into the bloodstream following oral administration. C17-alpha alkylated
anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure
may result in liver damage. In rare instances life-threatening dysfunction may
develop. It is advisable to visit a physician periodically during each cycle to
monitor liver function and overall health. Intake of c17-alpha alkylated steroids
is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain.
Studies administering 20 mg of fluoxymesterone to a group of nine male
subjects for two weeks resulted in most patients (6/9) noticing abnormal
sulfobromophthalein (BSP) retention,
513 a marker of liver stress.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Fluoxymesterone
has a strong effect on the hepatic management of cholesterol due to its structural
resistance to liver breakdown and route of administration. Anabolic/androgenic
steroids may also adversely affect blood pressure and triglycerides, reduce
endothelial relaxation, and support left ventricular hypertrophy, all potentially
increasing the risk of cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
Studies administering 10 mg, 20 mg, or 30 mg of fluoxymesterone to nine
healthy male subjects for up to 12 weeks have demonstrated the strong
suppression of endogenous testosterone levels, with inconsistent effects on
gonadotropin levels. Although not fully understood, fluoxymesterone is
proposed to have a direct suppressive effect on testicular steroidogenesis that is
not mediated by the suppression gonadotropins.
514
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
515 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, this steroid should be taken on an empty stomach.
Administration (Men):
To treat androgen insufficiency, early prescribing guidelines for
fluoxymesterone called for a dose of 2-10 mg per day. Modern prescribing
guidelines call for a daily dosage of 5-20 mg. Therapy is usually initiated at the
full 20 mg dosage,which is later adjusted downward to meet the individual needs
of the patient. The drug would be continued long-term unless laboratory tests
(lipids, liver enzymes, etc.) or side effects contraindicate its continued use. For
physique-or performance-enhancing purposes, an effective oral daily dosage
would fall in the range of 10-40 mg, taken in cycles lasting no more than 6-8
weeks to minimize hepatotoxicity. This level is sufficient for measurable
increases in muscle strength, which may be accompanied by modest increases in
lean muscle mass.
Fluoxymesterone is commonly used by athletes in weight-restricted sports like
wrestling, powerlifting, and boxing, due to the fact that strength gained from the
drug is usually not accompanied by great increases in bodyweight. When
properly used, it can allow a competitor to stay within a specified weight range,
yet drastically improve his performance. Fluoxymesterone is also commonly
used for bodybuilding contest preparation. When the competitor has an
acceptably low body fat percentage, the strong androgen level (in absence of
excess estrogen) can elicit an extremely hard and defined (“ripped”) look to the
muscles. The shift in androgen/estrogen ratio additionally seems to bring about a
state in which the body may be more inclined to burn off excess fat and prevent
new fat storage. The “hardening” effect of fluoxymesterone would, therefore, be
somewhat similar to that seen with trenbolone, although it will be without the
same level of mass gain.
In cutting phases, a milder anabolic such as Deca-Durabolin® or Equipoise® is
commonly stacked with fluoxymesterone, as they provide good anabolic effect
without excessive estrogen buildup. Here, fluoxymesterone provides a wellneeded androgenic component, helping to promote a more solid and defined gain
in muscle mass, with less interference with energy and libido, than might be
obtained with a primarily anabolic agent alone. Perhaps Primobolan®-Depot
would be an even better choice, as with such a combination there is no buildup
of estrogen, and likewise even less worry of water and fat retention. For mass,
one might alternately use an injectable testosterone. A mix of 400 mg per week
of testosterone enanthate and 20-30 mg daily of fluoxymesterone, for example,
often provides exceptional increases in strength and lean muscle mass. A more
significant level of androgenic side effects usually accompanies such a
combination, however, as both compounds exhibit strong androgenic activity in
the body.
Administration (Women):
Fluoxymesterone is most often used as a secondary medication during
inoperable androgen-sensitive breast cancer, when other therapies have failed to
produce a desirable effect. The dosage used for this application is 10-40 mg per
day. Virilizing effects are common at doses of only 10-15 mg per day in these
patients. Fluoxymesterone is not recommended for women for physique-or
performance-enhancing purposes due to its strong androgenic nature and
tendency to produce virilizing side effects.
Availability:
Pharmaceutical preparations containing fluoxymesterone remain scarce. The
drug has largely associated with western medical markets, where it has been
falling out of favor for most clinical application. The bulk of the supply
presently comes from underground steroid manufacturers and export-only
products. In reviewing some of the remaining products and changes in the global
pharmaceutical market, we have made the following observations.
Currently, the most popular item found on the black market is the Stenox brand
from Mexico, which is sold in boxes of 20 tablets. Note that the dosage of these
tablets is only 2.5 mg.
Fluoxymesterone remains available in the U.S. as a generic drug by USL
Pharma. It is available in a 10 mg tablet only.
Balkan Pharmaceuticals (Moldova) makes the product Halotest. It is prepared in
2 mg, 5 mg, and 10 mg tablets, with 20 tablets contained in each foil and plastic
strip.
Laurabolin® (nandrolone laurate)
Description:
Nandrolone laurate is an injectable form of the anabolic steroid nandrolone. The
laurate ester applied here is two carbon atoms longer than decanoate, and
consequently this agent forms a slightly longer-lasting drug deposit around the
area of injection than Deca-Durabolin. Given its strong delayed-release
properties, it is possible to administer nandrolone laurate once every three to
four weeks in a medical setting. As a nandrolone injectable, this drug provides a
moderately strong anabolic effect, which is accompanied by a low level of
estrogenic and androgenic properties. Although not widely used, nandrolone
laurate is favored by athletes and bodybuilders for its ability to promote slow
steady gains in lean mass with minimal side effects.
History:
Nandrolone laurate was developed during the 1960’s, a time when many new
nandrolone esters were being synthesized and investigated. This long-acting
ester of nandrolone is usually identified as a veterinary drug, but was actually
prescribed to humans before it was adopted for animal use. The only brand name
of reference is Clinibolin, which was sold for a brief time on the German drug
market around the end of the 1960’s. Nandrolone laurate was ultimately shortlived as a human medication, however, and from this point on would be used
exclusively in veterinary preparations. There is nothing particular that makes the
drug poorly suited for human use, and its discontinuance probably had much
more to do with the dominance of Organon’s Deca-Durabolin, which made
nandrolone laurate fairly superfluous as a prescription drug, than any faults of
the drug itself.
As a veterinary drug, nandrolone laurate is most commonly identified with the
Laurabolin brand name. Laurabolin is manufactured by Intervet, and is found in
a variety of countries including Mexico, Chile, The Netherlands, Australia, and
Colombia. It is used with cats, dogs, horses, pigs and cattle, typically to offset
malnutrition caused by viral or parasitic illness, to treat anemia, counter the
catabolic effects of corticosteroids, and to improve the overall physical condition
of highly active or elderly animals. The Laurabolin brand has also been sold at
one time by Werfft-Chemie in Austria and Vemie in Germany, however these
products have since been discontinued. In addition to the Laurabolin brand
name, the drug had also been marketed in the past under the trade names
Fortadex (Hydro, Germany), Fortabol (Parfam, Mexico), and Lauradrol 250
(Loeffler, Mexico). Today, only the Intervet products are known to exist.
How Supplied:
Nandrolone laurate is available in select veterinary drug markets. Composition
and dosage may vary by country and manufacturer, but usually contain 20
mg/mL or 50 mg/mL of steroid dissolved in oil.
Structural Characteristics:
Nandrolone laurate is a modified form of nandrolone, where a carboxylic acid
ester (lauric acid) has been attached to the 17-beta hydroxyl group. Esterified
steroids are less polar than free steroids, and are absorbed more slowly from the
area of injection. Once in the bloodstream, the ester is removed to yield free
(active) nandrolone. Esterified steroids are designed to prolong the window of
therapeutic effect following administration, allowing for a less frequent injection
schedule compared to injections of free (unesterified) steroid. Nandrolone
laurate is designed to provide a slow release of nandrolone for up to 3 to 4 weeks
following injection.
Side Effects (Estrogenic):
Nandrolone has a low tendency for estrogen conversion, estimated to be only
about 20% of that seen with testosterone.
516 This is because while the liver can
convert nandrolone to estradiol, in other more active sites of steroid
aromatization such as adipose tissue nandrolone is far less open to this
process.
517 Consequently, estrogen-related side effects are a much lower concern
with this drug than with testosterone. Elevated estrogen levels may still be
noticed with higher dosing, however, and may cause side effects such as
increased water retention, body fat gain, and gynecomastia. An anti-estrogen
such as clomiphene citrate or tamoxifen citrate may be necessary to prevent
estrogenic side effects if they occur. One may alternately use an aromatase
inhibitor like Arimidex® (anastrozole), which more efficiently controls estrogen
by preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
It is of note that nandrolone has some activity as a progestin in the body.
518
Although progesterone is a c-19 steroid, removal of this group as in 19-
norprogesterone creates a hormone with greater binding affinity for its
corresponding receptor. Sharing this trait, many 19-nor anabolic steroids are
shown to have some affinity for the progesterone receptor as well.
519 The side
effects associated with progesterone are similar to those of estrogen, including
negative feedback inhibition of testosterone production and enhanced rate of fat
storage. Progestins also augment the stimulatory effect of estrogens on
mammary tissue growth. There appears to be a strong synergy between these
two hormones here, such that gynecomastia might even occur with the help of
progestins, without excessive estrogen levels. The use of an anti-estrogen, which
inhibits the estrogenic component of this disorder, is often sufficient to mitigate
gynecomastia caused by nandrolone.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance, especially with higher doses. This may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are warned of the
potential virilizing effects of anabolic/androgenic steroids. These may include a
deepening of the voice, menstrual irregularities, changes in skin texture, facial
hair growth, and clitoral enlargement. Nandrolone is a steroid with relatively low
androgenic activity relative to its tissue-building actions, making the threshold
for strong androgenic side effects comparably higher than with more androgenic
agents such as testosterone, methandrostenolone, or fluoxymesterone. It is also
important to point out that due to its mild androgenic nature and ability to
suppress endogenous testosterone, nandrolone is prone to interfering with libido
in males when used without another androgen.
Note that in androgen-responsive target tissues such as the skin, scalp, and
prostate, the relative androgenicity of nandrolone is reduced by its reduction to
dihydronandrolone (DHN).
520 521 The 5-alpha reductase enzyme is responsible
for this metabolism of nandrolone. The concurrent use of a 5-alpha reductase
inhibitor such as finasteride or dutasteride will interfere with site-specific
reduction of nandrolone action, considerably increasing the tendency of
nandrolone to produce androgenic side effects. Reductase inhibitors should be
avoided with nandrolone if low androgenicity is desired.
Side Effects (Hepatotoxicity):
Nandrolone is not c-17 alpha alkylated, and not known to have hepatotoxic
effects. Liver toxicity is unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Studies
administering 600 mg of nandrolone decanoate per week for 10 weeks
demonstrated a 26% reduction in HDL cholesterol levels.
522 This suppression is
slightly greater than that reported with an equal dose of testosterone enanthate,
and is in agreement with earlier studies showing a slightly stronger negative
impact on HDL/LDL ratio with nandrolone decanoate as compared to
testosterone cypionate.
523 Nandrolone injectables, however, should still have a
significantly weaker impact on serum lipids than c-17 alpha alkylated agents.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production. For
sake of comparison, studies administering 100 mg per week of nandrolone
decanoate for 6 weeks have demonstrated an approximate 57% reduction in
serum testosterone levels during therapy. At a dosage of 300 mg per week, this
reduction reached 70%.
524
It is believed that the progestational activity of
nandrolone notably contributes to the suppression of testosterone synthesis
during therapy, which can be marked in spite of a low tendency for estrogen
conversion.
525 Without the intervention of testosterone-stimulating substances,
testosterone levels should return to normal within 2-6 months of drug secession.
Note that prolonged hypogonadotrophic hypogonadism can develop secondary
to steroid abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
Nandrolone laurate is not approved for use in humans. Prescribing guidelines are
unavailable. When used for physique-or performance-enhancing purposes, a
dose of 200-400 mg given every 7-10 days is most common, taken in cycles 8 to
12 weeks in length. This level is sufficient for most users to notice measurable
gains in lean muscle mass and strength, which should be accompanied by a low
level of estrogenic and androgenic activity. Higher doses (450-600 mg every 7-
10 days) will impart a stronger anabolic effect, but can be difficult given the
relatively low concentration this steroid is usually found in. Instead, many opt to
combine this agent with other anabolic/androgenic steroids. Given its properties,
it seems to fit well for both bulking and cutting purposes, and can reasonably
replace Deca-Durabolin in cycles.
Administration (Women):
Nandrolone laurate is not approved for use in humans. Prescribing guidelines are
unavailable. When used for physique-or performance-enhancing purposes, a
dosage of 100 mg every 10-14 days is most common, taken for 4 to 6 weeks.
Although only slightly androgenic, women are occasionally confronted with
virilization symptoms when taking this compound. Should virilizing side effects
become a concern, the drug should be discontinued immediately to help prevent
their permanent appearance. After a sufficient period of withdrawal, the shorteracting nandrolone Durabolin® might be considered a safer (more controllable)
option. This drug stays active for only several days, greatly reducing the
withdrawal time if indicated.
Availability:
Pharmaceutical preparations containing nandrolone laurate remain scarce. In
reviewing some of the remaining products and changes in the global
pharmaceutical market, we have made the following observations.
The Intervet brand name Laurabolin product is almost exclusively associated
with this compound. It remains available in select markets of Europe and the
America’s, and is not widely diverted for black market sale.
Masteron® (drostanolone propionate)
Description:
Drostanolone propionate is an injectable anabolic steroid derived from
dihydrotestosterone (DHT). Here, the DHT backbone has been modified with a
2-methyl group to increase its anabolic properties, making this agent
significantly more effective at promoting the growth of muscle tissue than its
non-methylated parent. Drostanolone propionate is described in product
literature as a “steroid with powerful anabolic and anti-estrogenic properties,”
and indeed does seem to share some of both properties. Admittedly, however, its
anabolic properties are more properly described as moderate, especially when
placed in the context of other agents. The drug is most often used by dieting
bodybuilders and athletes in speed sports, where it is highly favored for its
ability to produce solid increases in lean muscle mass and strength, which are
usually accompanied by reductions in body fat level and minimal side effects.
History:
Drostanolone propionate was first described in 1959.
526 Syntex developed the
agent alongside such other well-known steroids as Anadrol and
methyldrostanolone (Superdrol), also first described in the same paper.
Drostanolone propionate would be introduced as a prescription drug product
approximately a decade later. Lilly had an agreement with Syntex to split certain
research and development costs in exchange for the rights to market the results
of that research. Lilly would, therefore, sell drostanolone propionate in the U.S.
under the Drolban brand name, while Syntex would sell/license it in other
markets. Products included Masteron in Belgium (Sarva-Syntex) and Portugal
(Cilag), Masteril in the U.K. and Bulgaria, and Metormon in Spain.
Drostanolone propionate was also found in such popular preparations as
Permastril (Cassenne, France), Mastisol (Shionogi, Japan), and Masterid
(Grunenthal, Germany Democratic Republic).
The U.S. Food and Drug Administration approved drostanolone propionate for
the treatment of advanced inoperable breast cancer in postmenopausal women.
This remained the principle clinical indication for the agent in all international
markets as well. The prescribing literature reminds doctors and female patients
that there is considerably less virilization with drostanolone propionate as
compared to equal doses of testosterone propionate, suggesting this was a much
more comfortable alternative to testosterone injections for the given audience.
Still, the given dosage level (300 mg per week) was relatively high, and the
literature also reminds us that mild virilization symptoms still commonly occur,
such as deepening of the voice, acne, facial hair growth, and enlargement of the
clitoris. It also reports that marked virilization sometimes follows long-term
therapy.
While highly popular among athletes during the 1970’s and ’80’s, drostanolone
propionate ultimately enjoyed limited success as a prescription agent.
Manufacturers began voluntarily discontinuing sale of the agent in various
markets before long, likely due to the advent of more effective therapies for
breast cancer, as well as the slow decline in steroid prescriptions for this phase
of treatment. One of the first preparations to go was the U.S. Drolban, which was
removed from market during the late 1980’s. Permastril and Metormon were
soon dropped as well. The last remaining Western preparation containing
drostanolone propionate was Masteron from Belgium, which disappeared by the
late 1990’s. Drostanolone propionate remains listed on the U.S. Pharmacopias,
suggesting there is presently no legal roadblock to its sale, although its
reemergence as a prescription drug product seems highly unlikely.
How Supplied:
Drostanolone propionate is no longer available as a prescription drug
preparation. When produced, it was supplied in the form of 1 mL and 2 mL
ampules and 10 mL vials containing 50 mg/ml or 100 mg/ml of steroid in oil.
Structural Characteristics:
Drostanolone (also known as dromostanolone) is a modified form of
dihydrotestosterone. It differs by the introduction of a methyl group at carbon-2
(alpha), which considerably increases the anabolic strength of the steroid by
heightening its resistance to metabolism by the 3-hydroxysteroid dehydrogenase
enzyme in skeletal muscle tissue. Drostanolone propionate is a modified form of
drostanolone, where a carboxylic acid ester (propionic acid) has been attached to
the 17-beta hydroxyl group. Esterified steroids are less polar than free steroids,
and are absorbed more slowly from the area of injection. Once in the
bloodstream, the ester is removed to yield free (active) drostanolone. Esterified
steroids are designed to prolong the window of therapeutic effect following
administration, allowing for a less frequent injection schedule compared to
injections of free (unesterified) steroid. The half-life of drostanolone propionate
is approximately two days after injection.
Side Effects (Estrogenic):
Drostanolone is not aromatized by the body, and is not measurably estrogenic.
An anti-estrogen is not necessary when using this steroid, as gynecomastia
should not be a concern even among sensitive individuals. Since estrogen is the
usual culprit with water retention, drostanolone instead produces a lean, quality
look to the physique with no fear of excess subcutaneous fluid retention.This
makes it a favorable steroid to use during cutting cycles, when water and fat
retention are major concerns. As a non-aromatizable DHT derivative,
drostanolone may impart an anti-estrogenic effect, the drug competing with
other (aromatizable) substrates for binding to the aromatase enzyme.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance, especially with higher than normal therapeutic
doses. This may include bouts of oily skin, acne, and body/facial hair growth.
Anabolic/androgenic steroids may also aggravate male pattern hair loss. Women
are warned of the potential virilizing effects of anabolic/androgenic steroids.
These may include a deepening of the voice, menstrual irregularities, changes in
skin texture, facial hair growth, and clitoral enlargement. Drostanolone is a
steroid with relatively low androgenic activity relative to its tissue-building
actions, making the threshold for strong androgenic side effects comparably
higher than with more androgenic agents such as testosterone,
methandrostenolone, or fluoxymesterone. Note that drostanolone is unaffected
by the 5-alpha reductase enzyme, so its relative androgenicity is not affected by
the concurrent use of finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Drostanolone is not c17-alpha alkylated, and not known to have hepatotoxic
properties. Liver toxicity is unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Drostanolone
should have a stronger negative effect on the hepatic management of cholesterol
than testosterone or nandrolone due to its non-aromatizable nature, but a weaker
impact than c-17 alpha alkylated steroids. Anabolic/androgenic steroids may also
adversely affect blood pressure and triglycerides, reduce endothelial relaxation,
and support left ventricular hypertrophy, all potentially increasing the risk of
cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
Drostanolone propionate was not FDA approved for use in men. Prescribing
guidelines are unavailable. For physique-or performance-enhancing purposes,
this drug is usually injected three times per week. The total weekly dosage is
typically 200-400 mg, which is taken for 6-12 weeks. This level of use is
sufficient to provide measurable gains in lean muscle mass and strength.
Drostanolone propionate is often combined with other steroids for an enhanced
effect. Common stacks include an injectable anabolic such as Deca-Durabolin®
(nandrolone decanoate) or Equipoise® (boldenone undecylenate), which can
provide notably enhanced muscle gains without excessive water retention. For
mass gains, it is often combined with an injectable testosterone. The result here
can be solid muscle gain, with a lower level of water retention and other
estrogenic side effects than if these steroids were used alone (usually in higher
doses). Masteron, however, is most commonly applied during cutting phases of
training. Here it is often combined with other non-aromatizable steroids such as
Winstrol®, Primobolan®, Parabolan, or Anavar, which can greatly aid muscle
retention and fat loss, during a period which can be very catabolic without
steroids.
Administration (Women):
The prescribing guidelines for Drolban recommended a dose of 100 mg given
three times per week. Therapy is given for a minimum of 8 to 12 weeks before
an evaluation of its efficacy is made. If successful, the drug may be continued
for as long as satisfactory results are obtained. Note that virilization symptoms
were common at the recommended dosage. When used for physique-or
performance-enhancing purposes, a dosage of 50 mg per week is most common,
taken for 4 to 6 weeks. Virilization symptoms are rare in doses of 100 mg per
week or below. Note that due to the short-acting nature of the propionate ester,
the total weekly dosage is usually subdivided into smaller injections given once
every second or third day.
Availability:
Drostanolone propionate is presently unavailable as a prescription drug product.
All supplies of this drug come from export companies or underground steroid
manufacturers.
Megagrisevit-Mono® (clostebol acetate)
Description:
Clostebol acetate is an anabolic steroid that is derived from testosterone.
Clostebol is 4-chloro-testosterone, a modification that makes this steroid a low
strength anabolic compound with minimal androgenic potency. This analog of
testosterone is also not 17-alpha alkylated and does not aromatize, so there is
little worry of water retention, gynecomastia, or liver toxicity during use. The
hydrogen substitution at the 4 position does not greatly enhance the oral efficacy
of this drug, however, so the injectable is much more potent on a milligram for
milligram basis, and generally preferred. Although a derivative of the potent
androgen testosterone, clostebol is certainly far removed from its parent steroid
in action, and generally favored by athletes for its mildness, not raw power.
History:
Clostebol acetate was first described in 1956.
527
It was developed into a
medicine in Europe, where it was sold as Steranabol (Farmitalia, Germany) and
Turinabol (Jenapharm, GDR). This anabolic steroid had generally been indicated
for the treatment of osteoporosis, although it has reportedly been used with
success for a wide variety of ailments including anorexia and liver disease. Both
oral and injectable forms of the drug were produced, although the injectable was
more popularly used. Clostebol acetate was commonly used with women and the
elderly in European medicine, making clear the relative mildness of this
anabolic. The side effects of anabolic/androgenic steroids can be much more
pronounced in these populations, so typically very weak androgens are shown to
be the most tolerable here.
Although quite favorable in effect and patient comfort, clostebol acetate was
never a widely successful anabolic, and saw only limited use in a small number
of markets. As such, its future would be a tenuous one. The Turinabol product
from Jenapharm would disappear by the reunification of Germany, and the
Steranabol brand would soon be replaced with lower dosed vitamin fortified
versions of the drug sold by Farmitalia under the new Megagrisevit brand name.
Pharmacia would acquire Farmitalia in 1993, although for a short point
thereafter Megagrisevit was still being manufactured under the Pharmacia label.
This did not last long, however, and Pharmacia eventually tightened up its line
and removed this steroid from its offerings. Clostebol acetate had also appeared
for some time in Japan, sold as Macrobin by the firm Teikoku, but this product
too has since been discontinued.
Although the more functional injectable preparations of this steroid are off the
market, clostebol acetate is still manufactured in a number of dermal
preparations. The most recognizable such product has been Alfa-Trofodermin
from Italy, although it has also been sold in such products as Neobol (Mexico),
Trofodermin (Chile, Brazil), and Novaderm (Brazil). Dermal preparations of
clostebol acetate are generally used to treat ulcers and wounds, and often include
some neomycin to help accelerate healing. The doses of steroid used in these
products is generally very small, however, and, combined with poor systemic
delivery, are not of much use to athletes. In addition, this steroid has even been
included in certain ophthalmologic solutions, which are even less practical to use
for performance-enhancing purposes, and of less interest. Given that
Megagrisevit was the last remaining effective oral or injectable steroid product
to contain clostebol acetate, this drug is now essentially a defunct item as far as
the athletic use of steroids are concerned.
How Supplied:
Clostebol acetate is no longer available as a commercial oral or injectable agent.
When produced (Steranabol) it contained 20 mg/ml of steroid in a 2 mL glass
ampule or 15 mg per tablet.
Structural Characteristics:
Clostebol is a modified form of testosterone. It differs by the introduction of a
hydroxyl group at carbon 4, which inhibits aromatization and reduces relative
steroid androgenicity. Clostebol acetate contains clostebol modified with the
addition of carboxylic acid ester (acetic acid) at the 17-beta hydroxyl group, so
that the free steroid is released more slowly from the area of injection.
Side Effects (Estrogenic):
Clostebol is not aromatized by the body, and is not measurably estrogenic. An
anti-estrogen is not necessary when using this steroid, as gynecomastia should
not be a concern even among sensitive individuals. Since estrogen is the usual
culprit with water retention, clostebol instead produces a lean, quality look to the
physique with no fear of excess subcutaneous fluid retention. This makes it a
favorable steroid to use during cutting cycles, when water and fat retention are
major concerns.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance. This may include bouts of oily skin, acne, and
body/facial hair growth. Anabolic/androgenic steroids may also aggravate male
pattern hair loss. Women are also warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement. Additionally, clostebol is not extensively metabolized by the 5-
alpha reductase enzyme, so its relative androgenicity is not greatly altered by the
concurrent use of finasteride or dutasteride. Note that clostebol is a steroid with
low androgenic activity relative to its tissue-building actions, making the
threshold for strong androgenic side effects comparably higher than with more
androgenic agents such as testosterone, methandrostenolone, or
fluoxymesterone.
Side Effects (Hepatotoxicity):
Clostebol is not a c17-alpha alkylated compound, and not known to have
hepatotoxic effects. Liver toxicity is unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Clostebol should
have a stronger negative effect on the hepatic management of cholesterol than
testosterone or nandrolone due to its non-aromatizable nature, but a much
weaker impact than c-17 alpha alkylated steroids. Anabolic/androgenic steroids
may also adversely affect blood pressure and triglycerides, reduce endothelial
relaxation, and support left ventricular hypertrophy, all potentially increasing the
risk of cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
Clostebol acetate is generally used in clinical doses of 30 mg per week by
injection or 15 mg 2-3 times per day orally. The drug is administered for 3
consecutive weeks, followed by a break for 3 weeks. It is resumed at this point if
indicated. Effective doses for physique-or performance-enhancing purposes fall
in the range of 100-300 mg per week, taken for 6-12 weeks. Given the fast-
acting nature of acetate injectables, the weekly dosage is generally subdivided
into injections given at least every third day. With the low dosage of previous
commercial clostebol acetate products, daily injectable were most common.
Given the lower bioavailability and higher price, oral forms of the drug were not
commonly used by athletes. When administered, a daily dosage of 60-90 mg
appeared to be the most common.
The anabolic effect of this drug is fairly weak, so clostebol acetate is most often
utilized in combination with other steroids for a stronger effect. The general
application is to use it for contest preparations with other non-aromatizing
anabolics such as Winstrol® or oxandrolone. Here, a daily dose of 20 mg may
be added in with an average dose (20-30 mg per day) of the oral anabolic, which
together should provide the user a nice muscle building effect without any water
retention. The effect of clostebol would be somewhat similar to that seen with
the old Primobolan® acetate ampules, although Megagrisevit is somewhat
weaker in effect. Some also opt to use this compound in addition with strong
non-aromatizing androgens such as trenbolone, Halotestin®, or Proviron®. The
result in such cases can be an even more pronounced effect of muscle definition,
although this will be accompanied by a much stronger set of side effects.
Administration (Women):
Clostebol acetate is generally used in clinical doses 30 mg per week by injection
or 15 mg 2-3 times per day orally. The drug is administered for 3 consecutive
weeks, followed by a break for 3 weeks. The drug is resumed at this point if
indicated. Effective doses for physique-or performance-enhancing purposes fall
in the range of 50-75 mg per week for the injectable, or 30-60 mg daily for the
oral, taken for no longer than 6 weeks.
Availability:
Clostebol acetate is no longer available as a prescription agent at this time, and is
unavailable on the black market.
Metandren (methyltestosterone)
Description:
Methyltestosterone is an orally available form of the primary male androgen
testosterone. Looking at the structure of this steroid, we see it is basically just
testosterone with an added methyl group at the c-17 alpha position (a c-17 alpha
alkylated substance), which allows for oral administration. The resultant
compound “methylated-testosterone” was among the first functional oral steroids
to be produced. This field of research has consequently improved greatly over
the years, and today methyltestosterone is quite crude in comparison to many of
the other orals that were subsequently developed. The action of this steroid is
moderately anabolic and androgenic, with high estrogenic activity due to its
aromatization to 17-alpha methyl estradiol. This generally makes
methyltestosterone too troublesome (in terms of estrogenic side effects) to use
for muscle-building purposes.
History:
Methyltestosterone was first described in 1935,
528 and was one of the first oral
androgens to be used in clinical medicine (it follows Proviron, the first oral
androgen, by one year). Its main clinical use at the time of development was as
an oral medication to replace testosterone (and its anabolic and/or androgenic
activity) in males when endogenous levels were insufficient (Andropause),
although the drug was adopted for a number of other uses over the years as well.
These include the treatment of cryptorchidism (undescended testicles), breast
cancer in postmenopausal women, excessive lactation and breast pain after
pregnancy in mothers not nursing, osteoporosis, and, more recently, female
menopause (supporting the overall energy and sexual interest of the patient).
In addition to standard tablets and capsules, methyltestosterone has also been
commercially prepared in sublingual or buccal tablets. Metandren Linguets from
Ciba Pharmaceutical Company were perhaps the most recognized, and were
popularly sold from the 1950’s to 1990’s. These tablets were placed under the
tongue or between the gum and cheek and left to dissolve, delivering the drug to
circulation via the mucous membranes, bypassing the liver. Sublingual or buccal
intake approximately doubles the bioavailability of methyltestosterone, and also
provides peak levels of drug rapidly (approximately 1 hour after dosing instead
of 2 hours). Although Ciba’s Metandren Linguets are no longer commercially
available, numerous other sublingual/buccal methyltestosterone tablets are still
in production today.
Methyltestosterone remains a controversial steroid. Although it has a long
history, and arguably a justifiable safety record, it is no longer widely used, and
is even being withdrawn from many drug markets. The German Endocrine
Society made an official statement that methyltestosterone was obsolete in 1981,
and the drug would be removed from German pharmacies some seven years
later. Most European nations followed suit. The drug remains available in the
United States, although most clinicians generally find it to be a poor choice and
don’t prescribe it. Its potential hepatotoxicity is usually cited as a reason,
especially when long-term androgen therapy is contemplated. The one exception
seems to be the growing interest in using oral methyltestosterone in low doses to
treat female menopause. Early success with Estratest (Solvay) seems to indicate
future expansion for this application. Although many markets no longer produce
this drug, especially as a single-ingredient product, methyltestosterone remains
widely produced in many others.
How Supplied:
Methyltestosterone is widely available in human drug markets. Composition and
dosage may vary by country and manufacturer.
Structural Characteristics:
Methyltestosterone is a modified form of testosterone. It differs by the addition
of a methyl group at carbon 17-alpha, which helps protect the hormone during
oral administration. As is typical with c17-alpha alkylation, the resulting steroid
has lower anabolic activity than its parent testosterone.
Side Effects (Estrogenic):
Methyltestosterone is aromatized by the body, and is highly estrogenic due to its
conversion to 17-alpha methylestradiol, a synthetic estrogen with high biological
activity. 17-alpha methylation actually slows the rate of aromatization, although
the potent nature of 17-methylestradiol more than compensates for this.
Gynecomastia is often a concern during treatment, and may present itself quite
early into a cycle (particularly when higher doses are used). At the same time
water retention can become a problem, causing a notable loss of muscle
definition as both subcutaneous water retention and fat levels build. To avoid
strong estrogenic side effects, it may be necessary to use an anti-estrogen such as
Nolvadex®. One may alternately use an aromatase inhibitor like Arimidex®
(anastrozole), which is a more effective remedy for estrogen control. Aromatase
inhibitors, however, can be quite expensive in comparison to standard estrogen
maintenance therapies, and may also have negative effects on blood lipids.
Side Effects (Androgenic):
Methyltestosterone is classified as an androgen. Androgenic side effects are
common with this substance, and may include bouts of oily skin, acne, and
body/facial hair growth. Higher doses are more likely to cause such side effects.
Anabolic/androgenic steroids may also aggravate male pattern hair loss. Those
genetically prone to male pattern hair loss may wish to opt for a milder, less
androgenic, anabolic steroid. As a potent androgen, this steroid may also
increase aggressiveness. Women are additionally warned of the potential
virilizing effects of anabolic/androgenic steroids. These may include a deepening
of the voice, menstrual irregularities, changes in skin texture, facial hair growth,
and clitoral enlargement. Like testosterone, methyltestosterone converts to a
more potent steroid via interaction with the 5-alpha reductase enzyme, in this
case 17-alpha-methyldihydrotestosterone. The relative androgenicity of
methyltestosterone may be reduced, although not completely eliminated, by the
concurrent use of finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Methyltestosterone is a c17-alpha alkylated compound. This alteration protects
the drug from deactivation by the liver, allowing a very high percentage of the
drug entry into the bloodstream following oral administration. C17-alpha
alkylated anabolic/androgenic steroids can be hepatotoxic. Prolonged or high
exposure may result in liver damage. In rare instances life-threatening
dysfunction may develop. It is advisable to visit a physician periodically during
each cycle to monitor liver function and overall health. Intake of c17-alpha
alkylated steroids is commonly limited to 6-8 weeks, in an effort to avoid
escalating liver strain.
Methyltestosterone was the first oral steroid linked to hepatic damage. This may
be, in part, related to the early widespread use of the compound, as the drug
generally displays acceptable safety when used in clinically prescribed dosages
(serious liver toxicity cannot be completely excluded, however, even at clinical
doses). When taken at a dose of 30 mg daily for 5 weeks, hepatotoxicity, as
measured by bromosulphalein (BSP) retention, was low in one study.
529
In a
separate investigation, a majority of patients noticed significant BSP retention
after only 2 weeks of therapy with 67mg daily.
530 Severe liver complications are
rare given the periodic nature in which most people use oral anabolic/androgenic
steroids, although cannot be excluded with methyltestosterone, especially with
high doses and/or prolonged administration periods.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Methyltestosterone has a strong effect on the hepatic management of cholesterol
due to its structural resistance to liver breakdown and route of administration.
Studies have demonstrated an approximate 35% decrease in HDL cholesterol
and a 30% increase in LDL cholesterol with 40 mg per day.
531 These changes
occurred within 2-4 weeks of the initiation of therapy, and persisted for 2 weeks
after discontinuation of the drug. Anabolic/androgenic steroids may also
adversely affect blood pressure and triglycerides, reduce endothelial relaxation,
and support left ventricular hypertrophy, all potentially increasing the risk of
cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
532 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, this steroid should be taken on an empty stomach.
Administration (Men):
To treat androgen insufficiency, prescribing guidelines call for a daily dosage of
10-40 mg. The dose is reduced by 50% when administered in sublingual or
buccal form. The drug would be used for extended periods so long as the
patent’s laboratory results (hepatotoxicity, serum lipids, etc.) do not necessitate
its discontinuance. When used for physique-or performance-enhancing purposes,
a daily dosage of 10-50 mg is most commonly used, taken in cycles lasting no
more than 6-8 weeks in length. Methyltestosterone is most commonly used not
as an anabolic, but to stimulate aggression in the user. Powerlifters,
bodybuilders, and competitive athletes often attempt to harness this effect,
looking for extra intensity in a training session or competition. Aside from this,
methyltestosterone offers little except side effects. It is quite toxic, elevating
liver enzymes and causing acne, gynecomastia, aggression, and water retention
quite easily. Were one to tolerate these side effects, methyltestosterone will offer
only poor quality (bulky) gains. One should also be prepared for a substantial
loss of size and bodyweight at the conclusion of each cycle with
methyltestosterone, due to the high level of water excretion once the drug is
discontinued (during administration water retention will account for a
considerable percentage of the total weight gain).
Administration (Women):
Methyltestosterone is not widely used with women in clinical medicine. When
applied, it is most often used as a secondary medication during inoperable breast
cancer, when other therapies have failed to produce a desirable effect. The
dosage used for this application can be as high as 200 mg per day. Low doses of
methyltestosterone have been used in recent years to treat the symptoms of
menopause. An example is the product Estratest, which contains esterified
estrogens and 2.5 mg of methyltestosterone. A dosage of 1 tablet per day may
improve energy, libido, and overall wellness of the patient, as well as combat
osteoporosis (while estrogen replacement may halt calcium loss in the bones,
testosterone tends to increase calcium stores). Methyltestosterone is generally
not recommended for women for physique-or performance-enhancing purposes
due to its strong androgenic nature and tendency to produce virilizing side
effects.
Availability:
Pharmaceutical preparations containing methyltestosterone are fairly limited. In
reviewing some of the remaining products and changes on the global
pharmaceutical market, we have made the following observations.
Methyltestosterone remains available in the United States. It is sold under the
brand names Android tablets and Testred capsules from Valeant
Pharmaceuticals. A generic is also available from Impax Labs.
Aburaihan makes a generic methyltestosterone product in Iran. It comes in 25
mg tablets, with 10 sealed in each foil and plastic blister.
Methandriol (methylandrostenediol)
Description:
Methylandrostenediol (methandriol for short) is an anabolic steroid derived from
dihydrotestosterone. The drug itself is manufactured in two very distinct forms.
The first is unesterified (straight) methylandrostenediol, which is used when
making an oral medication with this steroid (although an injectable once existed
in the U.S.). It is also found as esterified methylandrostenediol dipropionate,
which is prepared as an injectable. The added propionate esters in the injectable
form extend the activity of the drug for several days. Basically, methandriol
drugs are altered c17-alkylated forms of 5-androstenediol. Methandriol is
classified as a weak anabolic with weak androgenic properties. It also seems to
display some level of estrogenic activity, making this steroid less ideal for
dieting. The drug is generally considered too mild, and is not widely popular
among bodybuilders and athletes. Sometimes, however, it is used in place of
other anabolic/androgenic agents in bulking stacks when available.
History:
Methylandrostenediol was first described in 1935,
533 making this a very old
agent as far as synthetic anabolic steroids are concerned. Methylandrostendiol
was developed into a medicine by Organon, which sold it in the United States
under the Stenediol brand name in both oral (methylandrostenediol) and
injectable (methylandrostendiol dipropionate) forms. Many other generics and
other brands of methylandrostenediol soon followed, and the drug was a popular
anabolic agent in the United States during the 1950’s. Methylandrostenediol was
essentially the first steroid perceived to have a notable separation of anabolic
(higher) and androgenic (lower) effect, a persistent goal of pharmaceutical
developers. Early product literature described it as, “a steroid which has
considerable of the male hormone’s tissue-building action without to the same
extent causing virilization.”
534
It was indicated for use as a, “tissue-builder in
cases of retarded growth or failure to gain weight accompanied by protein
wastage, negative nitrogen balance, or failure to build body proteins.”
Early assessments of methylandrostenediol being primarily anabolic in nature
did not hold up well with later extensive use in humans. It was eventually
determined that in doses sufficient to promote weight gain, its anabolic
properties were accompanied by significant androgenic activity. Ultimately, this
drug would be viewed as one of balanced anabolic and androgenic action, not as
a highly anabolic agent as originally thought. Organon would go on to develop
more effective anabolic agents, such as their 19-nor series of drugs including
Durabolin, Deca-Durabolin, and Maxibolin, and eventually discontinued the
Stenediol products. The other U.S. brand and generic forms of the drug would
follow as well, although methylandrostenediol would persist in the U.S. scene
for some time. Currently, no domestic source of the drug exists, although it is
still found in certain international markets. It seems most prominent in Australia
at the present time, where it remains included in a number of veterinary anabolic
steroid products.
How Supplied:
Methylandrostendiol is available in select human and veterinary drug markets.
Composition and dosage may vary by country and manufacturer.
Structural Characteristics:
Methylandrostendiol is a modified form of dihydrotestosterone. It differs by: 1)
the addition of a methyl group at carbon 17-alpha to protect the hormone during
oral administration and 2) the introduction of a double bond between carbons 5
and 6, which seems to increase the anabolic strength of the steroid (partly by
making it resistant to metabolism by 3-hydroxysteroid dehydrogenase in skeletal
muscle tissue). Methylandrostenediol dipropionate contains
methylandrostenediol modified with the addition of 2 carboxylic acid esters
(propionic acid) at the 3-beta and 17-beta hydroxyl groups, which delay the
release of free methylandrostenediol from the site of injection (depot).
Side Effects (Estrogenic):
Methylandrostendiol is not directly aromatized by the body, although one of its
known metabolites is methyltestosterone, which can aromatize.
Methlyandrostenediol is also believed to have some inherent estrogenic activity.
It is, likewise, considered a weakly to moderately estrogenic steroid.
Gynecomastia is possible during treatment, but generally only when higher
doses are used. Water and fat retention can also become issues, again depending
on dose. Sensitive individuals may need to addition an anti-estrogen such as
Nolvadex® to minimize related side effects.
Side Effects (Androgenic):
Although often classified as an anabolic steroid, methylandrostenediol is
sufficiently androgenic. Androgenic side effects are common with this
substance. This may include bouts of oily skin, acne, and body/facial hair
growth. Anabolic/androgenic steroids may also aggravate male pattern hair loss.
Women are warned of the potential virilizing effects of anabolic/androgenic
steroids. These may include a deepening of the voice, menstrual irregularities,
changes in skin texture, facial hair growth, and clitoral enlargement. Note that
methylandrostenediol is not affected by 5-alpha reductase, so the relative
androgenicity of this steroid is not affected by the concurrent use of finasteride
or dutasteride.
Side Effects (Hepatotoxicity):
Methylandrostenediol is a c17-alpha alkylated compound. This alteration
protects the drug from deactivation by the liver, allowing a very high percentage
of the drug entry into the bloodstream following oral administration. C17-alpha
alkylated anabolic/androgenic steroids can be hepatotoxic. Prolonged or high
exposure may result in liver damage. In rare instances life-threatening
dysfunction may develop. It is advisable to visit a physician periodically during
each cycle to monitor liver function and overall health. Intake of c17-alpha
alkylated steroids is commonly limited to 6-8 weeks, in an effort to avoid
escalating liver strain. Injectable forms of the drug may present slightly less
strain on the liver by avoiding the first pass metabolism of oral dosing, although
may still present substantial hepatotoxicity.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Methylandrostenediol has a strong effect on the hepatic management of
cholesterol due to its structural resistance to liver breakdown and (with the oral)
route of administration. Anabolic/androgenic steroids may also adversely affect
blood pressure and triglycerides, reduce endothelial relaxation, and support left
ventricular hypertrophy, all potentially increasing the risk of cardiovascular
disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability. This is caused by the fat-soluble nature of steroid hormones,
which can allow some of the drug to dissolve with undigested dietary fat,
reducing its absorption from the gastrointestinal tract. For maximum utilization,
oral forms of this steroid should be taken on an empty stomach.
Administration (Men):
Early prescribing guidelines for Stenediol recommend a dosage of 25 mg given 2
to 5 times per week by oral, buccal, or intramuscular route. For physique-or
performance-enhancing purposes, a typical dosage is in the range of 25-50 mg
daily for the oral form, and 200-400 mg per week with the injectable. In order to
keep blood levels more even with the injectable, it is generally administered
once every three to four days. Cycles generally last for no more than 6 to 8
weeks, in an effort to minimize hepatotoxicity and strain on the liver and
cholesterol values. This level of use is sufficient for moderate gains in muscle
size and strength, which may be accompanied by a low level of water retention.
While it may be possible to use methylandrostenediol alone for muscle-building
purposes, it is most often combined with other anabolics for a stronger effect.
Combined with Deca-Durabolin® or Equipoise®, for example, measurable gains
of hard muscle mass, without an extreme level of water retention, may be
noticed. This is the general composition of most Australian vet blends that
include methylandrostenediol. When looking for a more pronounced gain in
mass, a stronger androgen such as testosterone may be added. The resulting
growth can be quite exceptional, but the user will also have to deal with a much
stronger set of estrogenic side effects. The drug sometimes also combines well
with non-aromatizing anabolics such as Winstrol®, Primobolan®, or
oxandrolone. The result here should be a more pronounced effect on muscle
hardness, with a moderate gain of solid lean tissue.
Administration (Women):
Early prescribing guidelines for Stenediol recommend a dosage of 25 mg given 2
to 5 times per week by oral, buccal, or intramuscular route.
Methylandrostenediol is generally not recommended for women for physique-or
performance-enhancing purposes due to its androgenic nature and tendency to
produce virilizing side effects.
Availability:
Pharmaceutical preparations containing methylandrostenediol remain scarce. In
reviewing some of the remaining products and changes in the global
pharmaceutical market, we have made the following observations.
The only place where this steroid is still produced in an volume is Australia,
where a number of veterinary preparations still include methandriol in their
blends. These products are rarely traded in international commerce due to tight
controls on anabolic steroids in that country.
Metribolone (methyltrienolone)
Description:
Methyltrienolone is one of the strongest oral anabolic steroids ever produced.
This agent is a derivative of trenbolone (trienolone), which has been c-17 alpha
alkylated to allow for oral administration. This modification has created a steroid
that is significantly stronger than its non-methylated cousin. Its potency has been
measured to be anywhere from 120-300 times greater than that of
methyltestosterone, with greater dissociation between anabolic and androgenic
effects.
535 536 Milligram for milligram methyltrienolone is a more active steroid
than any agent sold on the commercial market, requiring doses as little as .5-1
milligram per day to notice a strong anabolic effect. Its potency is only matched
by its relative toxicity, however, which has limited its modern use to that of
laboratory research only.
History:
Methyltrienolone was first described in 1965.
537
It was immediately identified as
an extremely potent anabolic agent, far more potent than the commercially
available agents of the time. In spite of its high relative activity, however,
methyltrienolone has seen very limited use in humans. It was used clinically
during the late 1960’s and early ’70’s, most notably in the treatment of advanced
breast cancer. Here, its exceedingly strong anabolic/androgenic action helps the
drug counter the local effects of endogenous estrogens, lending it some efficacy
for slowing or even regressing tumor growth. Such application was not long
lived, however, as more realistic evaluations of the drug’s toxicity soon led to its
abandonment in human medicine.
By the mid-1970’s, methyltrienolone was becoming an accepted standard in
non-human research studies, particularly those pertaining to the study of the
androgen receptor activity. For this purpose the agent is very well suited. Its
sheer potency and resistance to serum-binding proteins makes it an excellent invitro receptor-binding standard to compare other agents to. Being so resistant to
metabolism, active methyltrienolone metabolites are also not going to greatly
interfere with the results of most experiments. Body tissues can metabolize most
steroids fairly easily, which means that even incubation studies can be
complicated with the question of what is causing a particular effect, the steroid
or one of its unidentified metabolites. This is much less of an issue with
methyltrienolone. Today, methyltrienolone remains an agent of research use
only.
How Supplied:
Methyltrienolone is not available as a commercial agent.
Structural Characteristics:
Methyltrienolone is a modified form of nandrolone. It differs by: 1) the addition
of a methyl group at carbon 17-alpha to protect the hormone during oral
administration and 2) the introduction of double bonds at carbons 9 and 11,
which increases its binding affinity and slows its metabolism. The resulting
steroid is significantly more potent than its nandrolone base, and displays a
much longer half-life and lower affinity for serum-binding proteins in
comparison. Methyltrienolone chemically differs from trenbolone only by the
addition of a methyl group at c-17. This alteration changes the activity of
methyltrienolone considerably, however, such that this agent should not simply
be considered an oral form of trenbolone.
Side Effects (Estrogenic):
Methyltrienolone is not aromatized by the body, and is not measurably
estrogenic. It is of note, however, that methyltrienolone displays significant
binding affinity for the progesterone receptor.
538 The side effects associated with
progesterone are similar to those of estrogen, including negative feedback
inhibition of testosterone production and enhanced rate of fat storage. Progestins
also augment the stimulatory effect of estrogens on mammary tissue growth.
There appears to be a strong synergy between these two hormones here, such
that gynecomastia might even occur with the help of progestins, without
excessive estrogen levels. The use of an anti-estrogen, which inhibits the
estrogenic component of this disorder, is often sufficient to mitigate
gynecomastia caused by progestational anabolic/androgenic steroids.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
common with this substance. This may include bouts of oily skin, acne, and
body/facial hair growth. Anabolic/androgenic steroids may also aggravate male
pattern hair loss. Women are also warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement. Additionally, the 5-alpha reductase enzyme does not metabolize
methyltrienolone, so its relative androgenicity is not affected by finasteride or
dutasteride.
Side Effects (Hepatotoxicity):
Methyltrienolone is a c17-alpha alkylated compound. This alteration protects the
drug from deactivation by the liver, allowing a very high percentage of the drug
entry into the bloodstream following oral administration. C17-alpha alkylated
anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure
may result in liver damage. In rare instances life-threatening dysfunction may
develop. It is advisable to visit a physician periodically during each cycle to
monitor liver function and overall health. Intake of c17-alpha alkylated steroids
is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain.
Methyltrienolone is an exceedingly potent oral steroid, with a very high level of
resistance to hepatic metabolism. This makes methyltrienolone exceedingly
liver-toxic, precluding its use as a prescription agent at this time, in any part of
the world. Studies published from the University of Bonn Germany back in 1966
make this very clear.
539
In fact, at this time researchers had deemed this the most
liver-toxic steroid to ever be studied in humans, summing up their findings well
when stating:
“Methyltrienolone… which is orally active as an anabolic agent in a dose less
than 1.0 mg per day in normal adults,has been tested with regard to its influence
on liver function. As measured by multiple parameters (BSP retention; total
bilirubin; activities of transaminases, alkaline phosphates and cholinesterase in
serum; activity of proaccelerin in plasma) methyltrienolone turned out to be very
active as to causing biochemical symptoms of intrahepatic cholestasis. …thus
methyltrienolone at present being the most ‘hepatotoxic’ steroid.”
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Although not
extensively studied in humans, the oral route, high relative potency, and nonaromatizable nature of methyltrienolone suggest that this agent is extremely
prone to negatively altering lipid values and increasing atherogenic risk.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
540 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, methyltrienolone should be taken on an empty stomach.
Administration (Men):
Methyltrienolone is no longer used in clinical medicine due to an unacceptable
level of hepatotoxicity. This agent is generally not recommended for physique-or
performance-enhancing purposes for the same reason. Those absolutely insisting
on its use need to take its level of liver toxicity very seriously. At the very least,
routine blood tests should be conducted to ensure the agent is not imparting
damage. Drug duration should also be very limited, preferably to 4 weeks of use
or less. The relative potency of methyltrienolone is extremely high, requiring
doses as little as .5 milligram per day. Its effective and tolerable range is usually
considered to be .5 to 2mg per day. Dianabol-type doses of 20-30 mg daily are
completely unthinkable, and should never be attempted. Again, this is an
extremely toxic steroid, and all good advice would say to avoid it. Any one of
the many commercially available steroids would be much safer choices.
Administration (Women):
Methyltrienolone is no longer used in clinical medicine due to an unacceptable
level of hepatotoxicity. This agent is not recommended for women for physiqueor performance-enhancing purposes due to its extremely strong toxicity and
tendency to produce virilizing side effects.
Availability:
Methyltrienolone is not produced as a prescription steroid product in any part of
the world. With the rapid expansion of underground steroid manufacturers, this
agent has been released as a black market designer compound. Those
contemplating the use of underground forms of methyltrienolone should
consider that such agents are being released for human use without any
government approval or consideration to its safety.
Miotolan® (furazabol)
Description:
Furazabol is an oral anabolic steroid derived from dihydrotestosterone. This
agent is moderately anabolic, with only mild androgenic properties. This is no
doubt due to the modification of the steroid’s A-ring, which allows the steroid
structure to remain stable and bind receptors in muscle tissue long enough to
provide an anabolic benefit. Dihydrotestosterone, in comparison, is a poor
anabolic, quickly metabolized in muscle tissue to inactive metabolites. The gains
associated with furazabol are not extreme, and would more closely resemble the
quality growth of a mild non-aromatizing anabolic like stanozolol or
drostanolone, instead of the watery bulk of a testosterone. For this reason,
furazabol is most often applied during cutting phases of training, and by athletes
in speed and weight-restricted sports.
History:
Furazabol was first described in 1965.
541 The only modern pharmaceutical
preparation of record containing furazabol, at least known to researchers in the
West, was Miotolan from Daiichi Seiyaku Labs in Japan, which was sold in
Japan mainly during the 1970’s and ’80’s. The agent itself is scarcely mentioned
in the Western medical literature, and consequently a great deal of myth has
come to surround it among athletes. A realistic appraisal sits this agent in a very
similar class to stanozolol, however, with both agents being moderately strong
anabolics with low androgenic activity. Aside from this, it is difficult to ascribe
any drastically unique traits to this drug.
Furazabol was a popular steroid among Olympic athletes during the 1980’s,
when it was quietly known among certain trainers that testing officials had not
yet identified the agent, and therefore could not test for it. Dr. Jamie Astaphan,
the physician that accompanied Ben Johnson to the 1988 Olympics in Seoul,
reportedly was giving Johnson (and numerous other athletes at the time)
furazabol, knowing the drug would not be detectable. It remains uncertain how
Johnson ultimately tested positive for stanozolol, which Dr. Astaphan strongly
denied giving his athletes. Within two years, methods for the detection of
furazabol in urine were published, immediately eliminating any value this agent
formerly possessed as a steroid undetectable to drug screeners.
Today, furazabol is very scarcely known to bodybuilders. The Miotolan brand
from Japan was discontinued many years ago, and no pharmaceutical
preparation containing furazabol has been known to exist since. The drug is
occasionally located on the black market, however, due to the fact that is it still
produced in bulk (as a raw material for product manufacturing) in Asia. From
there it is obtained by underground steroid manufacturing operations in the
West, and produced into oral tablets and capsules. Currently the actual number
of products containing furazabol is small, although could easily be expanded if
market demand for the agent increases. It remains unlikely that an actual
prescription product containing this steroid will ever be seen again.
How Supplied:
Furazabol is no longer available as a prescription drug preparation. When sold it
came in the form of tablets containing 1mg of steroid.
Structural Characteristics:
Furazabol is a modified form of dihydrotestosterone. It differs by: 1) the addition
of a methyl group at carbon 17-alpha, which helps protect the hormone during
oral administration, and 2) the attachment of a furazan group to the A-ring,
replacing the normal 3-keto group. When viewed in the light of 17-alpha
methyldihydrotestosterone, the A-ring modification on furazabol seems to
considerably increase its anabolic strength while reducing its relative
androgenicity.
Side Effects (Estrogenic):
Furazabol is not aromatized by the body, and is not measurably estrogenic. An
anti-estrogen is not necessary when using this steroid, as gynecomastia should
not be a concern even among sensitive individuals. Since estrogen is the usual
culprit with water retention, this steroid instead produces a lean, quality look to
the physique with no fear of excess subcutaneous fluid retention. This makes it a
favorable steroid to use during cutting cycles, when water and fat retention are
major concerns.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance, especially with higher doses. This may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are warned of the
potential virilizing effects of anabolic/androgenic steroids. These may include a
deepening of the voice, menstrual irregularities, changes in skin texture, facial
hair growth, and clitoral enlargement. Furazabol is a steroid with relatively low
androgenic activity relative to its tissue-building actions, making the threshold
for strong androgenic side effects comparably higher than with more androgenic
agents such as testosterone, methandrostenolone, or fluoxymesterone. Note that
furazabol is unaffected by the 5-alpha reductase enzyme, so its relative
androgenicity is not affected by the concurrent use of finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Furazabol is a c17-alpha alkylated compound. This alteration protects the drug
from deactivation by the liver, allowing a very high percentage of the drug entry
into the bloodstream following oral administration. C17-alpha alkylated
anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure
may result in liver damage. In rare instances life-threatening dysfunction may
develop. It is advisable to visit a physician periodically during each cycle to
monitor liver function and overall health. Intake of c17-alpha alkylated steroids
is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Furazabol has a
strong effect on the hepatic management of cholesterol due to its nonaromatizable nature, structural resistance to liver breakdown, and route of
administration. Anabolic/androgenic steroids may also adversely affect blood
pressure and triglycerides, reduce endothelial relaxation, and support left
ventricular hypertrophy, all potentially increasing the risk of cardiovascular
disease and myocardial infarction.
Note that furazabol is often mistakenly described as a steroid with unique
beneficial cholesterol-lowering effects. Such statements usually make reference
of studies conducted in the early 1970’s, which examined the lipid-lowering
effects of the agent.
542 Such a position, however, lacks a modern perspective of
the drug. To draw a parallel, during the early 1970’s there was research done on
oxandrolone, demonstrating a lipid-lowering effect.
543 Upon closer inspection,
however, it was shown that oxandrolone tends to lower HDL (good) cholesterol,
increasing the HDL-LDL ratio and atherogenic risk. General cholesterollowering applications for the drug never materialized. The same is true for
furazabol. Some have gone so far as to recommend this steroid to those with
high cholesterol! Such use absolutely should be avoided.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse,necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
An effective dosage of furazabol seems to begin in the range of 10-20 mg daily
for men, taken for no longer than 6 or 8 weeks. At this level it seems to impart a
measurable muscle-building effect, which is usually accompanied by fat loss and
increased definition. Doses of 30 mg per day or more considerably increase the
anabolic potential of the drug, but at the expense of greater hepatotoxicity. The
muscle-building activity of furazabol could, instead, be further enhanced by the
addition of an injectable anabolic such as Deca-Durabolin® or Equipoise®. In
this case, the combination should provide a noteworthy gain of solid, quality
muscle mass without a loss of definition due to water retention. We could
alternately use a more potent aromatizable androgen such as testosterone,
although here the gains may be accompanies by some level of water retention,
and potentially a decrease in muscle definition.
Administration (Women):
In the athletic arena, an effective oral daily dosage would fall in the range of 2-5
mg, taken in cycles lasting no more than 4-6 weeks to minimize the chance for
virilization. As with all steroids, virilizing side effects are still possible in
women, but remain rare with conservative dosing.
Availability:
Furazabol is no longer produced as a prescription drug product, although
underground preparations containing this steroid may be located.
Myagen (bolasterone)
Description:
Bolasterone is an oral anabolic steroid structurally related to methyltestosterone.
It differs only by the addition of a methyl group at c-7, which accounts for its
given chemical name, 7,17-dimethyltestosterone. The added c-7 methyl group
makes the activity of this steroid far removed from methyltestosterone, however,
such that any direct comparison is difficult to justify. For starters, bolasterone is
a fairly potent steroid, measured in human subjects to have approximately twice
the anabolic effect of methandrostenolone.
544 This is in contrast to
methyltestosterone, which is considerably less potent than methandrostenolone.
Despite being a testosterone derivative, bolasterone is also much more anabolic
than androgenic in nature. At a given therapeutic level, it is much less likely to
cause androgenic/virilizing side effects. It does have one strong similarity to
methyltestosterone, however, which lies in the fact that bolasterone too is quite
estrogenic. Both agents are, therefore, most appropriately used during bulking
phases or training.
History:
Bolasterone was first described in 1959.
545
It was closely evaluated for anabolic
and androgenic effect approximately 3 years later.
546 The drug was developed by
Upjohn, and sold in the U.S. during the 1960’s under the Myagen brand name. It
was mainly indicated for the treatment of advanced breast cancer in women,
although the agent was also investigated for its stimulatory effect on blood cells
and its general anabolic (lean-tissue sparing) activity. Bolasterone was ultimately
a short-lived drug, disappearing from the U.S. market shortly after its release. By
the 1980’s, bolasterone had been out of commerce for so long that it was all but
forgotten among athletes. Although bolasterone is no longer produced, the drug
remains listed in the U.S. Pharmacopeias, suggesting it would not be impossible
to see this agent for sale (legally) in the U.S. again, perhaps under order by a
private compounding pharmacy. The reemergence of an actual commercial
bolasterone compound, however, remains very unlikely.
How Supplied:
Bolasterone is no longer available as a prescription drug product.
Structural Characteristics:
Bolasterone is a modified form of testosterone. It differs by: 1) the addition of a
methyl group at carbon 17-alpha, which helps protect the hormone during oral
administration, and 2) the introduction of a methyl group at carbon 7 (alpha),
which inhibits 5-alpha reduction and shifts the anabolic to androgenic ratio in
favor of the former. 7,17-dimethylated steroids also tend to be very resistant to
metabolism and serum-binding proteins, greatly enhancing their relative
biological activity.
Side Effects (Estrogenic):
Bolasterone is aromatized by the body, and is considered a highly estrogenic
steroid due to its conversion to 7,17-dimethylestradiol (an estrogen with high
biological activity). Gynecomastia may be a concern during treatment, especially
when higher than normal therapeutic doses are used. At the same time water
retention can become a problem, causing a notable loss of muscle definition as
both subcutaneous water retention and fat levels build. To avoid strong
estrogenic side effects, it may be necessary to use an anti-estrogen such as
Nolvadex®. One may alternately use an aromatase inhibitor like Arimidex®
(anastrozole), which is a more effective remedy for estrogen control. Aromatase
inhibitors, however, can be quite expensive in comparison to standard estrogen
maintenance therapies, and may also have negative effects on blood lipids.
Side Effects (Androgenic):
Although bolasterone is classified as an anabolic steroid, androgenic side effects
are still possible with this substance. These may include bouts of oily skin, acne,
and body/facial hair growth. Higher doses are more likely to cause such side
effects. Anabolic/androgenic steroids may also aggravate male pattern hair loss.
Women are additionally warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement. Bolasterone is unaffected by the 5-alpha reductase enzyme, so its
relative androgenicity is not affected by the concurrent use of finasteride or
dutasteride. Note that studies administering 1mg and 2mg of bolasterone per day
have shown no outward androgenic side effects in children and
hypogonadotrophic males, as would be characterized by public hair growth,
genital changes, voice changes, and acne. Higher doses remain likely to induce
androgenic effects. Bolasterone is considered to have a comparable ratio of
anabolic to androgenic effect as oxymetholone and methandrostenolone.
Side Effects (Hepatotoxicity):
Bolasterone is a c17-alpha alkylated compound. This alteration protects the drug
from deactivation by the liver, allowing a very high percentage of the drug entry
into the bloodstream following oral administration. C17-alpha alkylated
anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure
may result in liver damage. In rare instances life-threatening dysfunction may
develop. It is advisable to visit a physician periodically during each cycle to
monitor liver function and overall health. Intake of c17-alpha alkylated steroids
is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain.
Studies administering 1mg and 2mg of bolasterone daily for 6 weeks to 27
patients have demonstrated a trend toward increases in serum alkaline
phosphatase (a marker of liver stress), although no significant untoward effects
on the liver were documented.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Bolasterone has a
strong effect on the hepatic management of cholesterol due to its structural
resistance to liver breakdown and route of administration. Anabolic/androgenic
steroids may also adversely affect blood pressure and triglycerides, reduce
endothelial relaxation, and support left ventricular hypertrophy, all potentially
increasing the risk of cardiovascular disease and myocardial infarction. Studies
administering 1mg and 2mg of bolasterone daily for 6 weeks to 27 patients have
demonstrated a trend toward increased serum cholesterol. Although no HDL and
LDL breakdown was provided, it can be assumed based on the structure and
route of administration that bolasterone significantly shifted the ratio of these
two fractions of cholesterol further apart, measurably increasing atherogenic
risk.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
547 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, this steroid should be taken on an empty stomach.
Administration (Men):
Clinical studies have demonstrated that significant nitrogen retention and weight
gain can be induced with a daily dosage of 1-2mg per day. In the athletic arena,
doses of 2-5 mg daily seem to be most reasonable, taken in cycles lasting no
more than 6-8 weeks in length to minimize hepatotoxicity. This level is
sufficient for strong increases in muscle size and strength, although such gains
will likely be accompanied by significant water retention.
Administration (Women):
Bolasterone was not widely used with women in clinical medicine. When
applied, it was most often used as a secondary medication during inoperable
breast cancer, when other therapies have failed to produce a desirable effect. The
dosage used for this application would be as high as 10 mg per day, a level that
has caused significant virilization among patients. Bolasterone is generally not
recommended for women for physique-or performance-enhancing purposes due
to its very strong nature and tendency to produce virilizing side effects.
Availability:
Bolasterone is no longer produced as a prescription drug, although a handful of
underground laboratories have taken to selling this material.
Nebido (testosterone undecanoate)
Description:
Nebido® is an injectable steroid that contains testosterone undecanoate, a very
slow-acting ester of testosterone. This is the active drug that is used in Andriol,
but in that case it is part of an oral medication, not an injectable. Nebido is being
marketed as a replacement for established injectable testosterone products like
Delatestryl®, Depo-Testosterone®, and Sustanon®, which are actually much
faster acting in comparison. It is designed to offer a much less frequent injection
schedule, and, therefore, much greater comfort for the patient. Nebido is a drug
developed under a similar focus as testosterone buciclate, which is another very
slow-acting injectable ester of testosterone.
History:
Nebido® was developed by international giant Schering AG, Germany (now
Bayer). It first surfaced as a prescription drug in Finland and Germany in
October and November of 2004, respectively. Within a year it had been
approved for sale throughout Europe. Schering/Bayer has since also brought this
product to Mexico, Brazil, Argentina, South Africa, Colombia, Korea,
Venezuela, and various countries in Eastern Europe (86 countries in total). In
July 2005, the U.S. pharmaceuticals firm Indevus purchased the rights to market
Nebido under the Aveed trade name. The FDA has since held up U.S. approval
of the drug, however, focusing on a small number of adverse reports in
Germany. These specifically involve post-injection anaphylactic reactions and
pulmonary oil microembolism. Most of these reactions are likely not due to a
problem with the drug itself, but incorrect administration of the high-volume
injection. Future approval in the U.S. is expected, but unclear.
Nebido® was described by Schering as being the, “first long-acting injection for
the treatment of male hypogonadism.” This may be a matter of perspective, as
other slow-acting esters do exist. Schering, however, is taking the lead to market
in most regions. The applications for Nebido® are extremely narrow, being
approved for use in men as a long-term treatment option for low androgen levels
only. It is not labeled for use in women, or in males for other uses. Given the
growing acceptance of androgen replacement therapy, and the comfort
advantage that Nebido® seems to offer male hormone replacement therapy
patients (esters like enanthate and cypionate generally require between 13 and 26
injections per year), it may very well become a dominant testosterone product in
the years to come, especially with the marketing support of a pharmaceutical
giant like Bayer.
How Supplied:
Testosterone undecanoate (injection) is available in various human drug markets.
All products (Nebido®) contain 250 mg/ml of steroid dissolved in oil; packaged
in 4ml ampules containing 1,000 mg of steroid in total.
Structural Characteristics:
Testosterone undecanoate is a modified form of testosterone, where a carboxylic
acid ester (undecanoic acid) has been attached to the 17-beta hydroxyl group.
Esterified forms of testosterone are less polar than free testosterone, and are
absorbed more slowly from the area of injection. Once in the bloodstream, the
ester is removed to yield free (active) testosterone. Esterified forms of
testosterone are designed to prolong the window of therapeutic effect following
administration, allowing for a less frequent injection schedule compared to
injections of free (unesterified) steroid. Nebido® is designed to maintain
physiological levels of testosterone for up to 14 weeks after injection.
548
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone more likely to require the
concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention
and loss of muscle definition are common with higher doses of testosterone, this
drug is usually considered a poor choice for dieting or cutting phases of training.
Its moderate estrogenicity makes it more ideal for bulking phases, where the
added water retention will support raw strength and muscle size, and help foster
a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
549
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
550 Studies using 300 mg of testosterone ester
(enanthate) per week for twenty weeks without an aromatase inhibitor
demonstrated only a 13% decrease in HDL cholesterol, while at 600 mg the
reduction reached 21%.
551 The negative impact of aromatase inhibition should
be taken into consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less per week, the impact on lipid
profile tends to be noticeable but not dramatic, making an anti-estrogen (for
cardioprotective purposes) perhaps unnecessary. Doses of 600 mg or less per
week have also failed to produce statistically significant changes in LDL/VLDL
cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive protein, and insulin
sensitivity, all indicating a relatively weak impact on cardiovascular risk
factors.
552 When used in moderate doses, injectable testosterone esters are
usually considered to be the safest of all anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone stimulating substances, testosterone
levels should return to normal within 1-4 months after the drug has fully cleared
the body. Note that prolonged hypogonadotrophic hypogonadism can develop
secondary to steroid abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Due to the large injection volume, prescribing guidelines recommend that each
injection be given slowly, taking approximately 60 seconds to administer the full
4ml dose. Nebido® should always be injected deep in the gluteal muscle.
Administration (Men):
To treat androgen insufficiency, the prescribing guidelines for testosterone
undecanoate (Nebido®) call for a dosage of 1,000 mg (4ml) every twelve weeks.
Therapy is usually initiated with a loading phase, which requires that the second
injection of 1,000 mg be given at approximately the six-week mark. For
bodybuilding purposes, supraphysiological (rather than physiological) hormone
levels would require injecting the drug on a more regular basis. The most logical
protocol would be to administer a 4ml injection of Nebido every 2-4 weeks, for
an approximate average weekly dosage of 250-500 mg of testosterone ester. At
this level one could expect results very much in line with other testosterone
esters, albeit with a less frequent injection schedule. The onset of action may,
however, be much slower with Nebido. Some may opt to begin their cycle with a
faster acting ester, such as enanthate or cypionate, which would allow
testosterone levels to reach into supraphysiological ranges sooner. Testosterone
is ultimately very versatile, and can be combined with many other
anabolic/androgenic steroids depending on the desired effect.
Administration (Women):
Testosterone undecanoate is not approved for use with women in clinical
medicine. This drug is not recommended for women for physique-or
performance-enhancing purposes due to its strong androgenic nature, tendency
to produce virilizing side effects, and very slow acting characteristics (making
blood levels difficult to control).
Availability:
Testosterone undecanoate injection continues to increase in prominence as a
pharmaceutical product. It is presently approved for sale in 86 countries
worldwide. In reviewing some of the more popular products and changes on the
global pharmaceutical market, we have made the following observations.
Nebido gained approval for Europe-wide sales in 2005. The product is has since
distributed throughout Europe, and is widely available in this region.
Indevus, a subsidiary of Endo Pharmaceuticals, has continued to push for FDA
approval of Aveed in the United States, but such approval has not yet been
granted.
Nilevar® (norethandrolone)
Description:
Norethandrolone is an anabolic steroid closely related to nortestosterone
(nandrolone) in structure. The activity of this steroid is that of a mild to
moderate oral anabolic steroid, which is accompanied by distinguishable
androgenic and estrogenic components. Although this steroid is essentially
nandrolone modified (alkylated) to make oral dosing viable, it cannot be looked
at simply as an oral alternative to Deca-Durabolin®. Most notably, the greatly
increased estrogenicity caused by 17-alkylation makes norethandrolone much
more problematic when trying to build quality (lean) muscle mass. In
administering an effective amount of steroid in terms of muscle growth, the user
has to deal with much more in terms of estrogenic side effects. The muscle
accumulation with norethandrolone is also going to be accompanied by a high
level of water and (likely) fat retention, not the quality muscularity normally
associated with nandrolone decanoate.
History:
Norethandrolone was first described in 1954.
553
It was developed into a
medicine by Searle, which introduced it into the U.S. prescription drug market
under the Nilevar brand name during the late 1950’s. The drug was originally
sold as an oral tablet, an oral solution (with dropper bottle), and an injectable
solution (in 25 mg ampules). The latter form of norethandrolone has been out of
commerce for so long that few remember it was once also given by injection.
Nilevar was prescribed for a variety of illnesses that were benefited by a protein
sparing anabolic agent, Listed indications included preparation for and recovery
from surgery, severe or prolonged illness, anorexia nervosa, severe burns and
trauma, decubitus ulcers, osteoporosis, bone fracture healing, gastrointestinal
disease, prolonged corticosteroid administration, and various forms of
malnourishment in adults and children.
Norethandrolone ultimately saw only limited success as a prescription anabolic
agent. It did make its way to Europe and certain other markets, but not widely.
The drug was an early functional anabolic, displaying more tissue-building
properties than androgenic effects. But it also remained an agent with a troubling
estrogenic side. This eventually led to norethandrolone being passed over
clinically for more refined compounds as they became available. Searle decided
to discontinue the sale of Nilevar in the U.S. during the 1960’s, and instead
began focusing energies on its newer, more strongly anabolic, and nonestrogenic steroid oxandrolone (sold as Anavar). Most other markets carrying
norethandrolone, either by Searle or other companies, soon began losing this
compound as well. Today, this drug is available on a limited basis, most notably
in Australia where it remains viable on the veterinary drug market.
How Supplied:
Norethandrolone is available in select veterinary drug markets. Composition and
dosage may vary by country and manufacturer, but typically contain 5 or 10 mg
of steroid per tablet.
Structural Characteristics:
Norethandrolone is a modified form of nandrolone. It differs by the addition of
an ethyl group at carbon 17alpha to protect the hormone during oral
administration.
Side Effects (Estrogenic):
Norethandrolone is aromatized by the body, and converts to a synthetic estrogen
with a high level of biological activity (17alpha-ethyl-estradiol). As a result, it is
a highly estrogenic steroid. Gynecomastia is often a concern during treatment,
and may present itself quite early into a cycle (particularly when higher doses
are used). At the same time water retention can become a problem, causing a
notable loss of muscle definition as both subcutaneous water retention and fat
levels build. Sensitive individuals may want to keep the estrogen under control
with the addition of an anti-estrogen such as Nolvadex®. One may alternately
use an aromatase inhibitor like Arimidex® (anastrozole), which is a more
effective remedy for estrogen control. Aromatase inhibitors, however, can be
quite expensive in comparison to standard estrogen maintenance therapies, and
may also have negative effects on blood lipids.
It is of note that norethandrolone has some additional activity as a progestin in
the body.
554 The side effects associated with progesterone are similar to those of
estrogen, including negative feedback inhibition of testosterone production and
enhanced rate of fat storage. Progestins also augment the stimulatory effect of
estrogens on mammary tissue growth. There appears to be a strong synergy
between these two hormones here, such that gynecomastia might even occur
with the help of progestins without excessive estrogen levels being present. The
use of an anti-estrogen, which inhibits the estrogenic component of this disorder,
is often sufficient to mitigate gynecomastia caused by norethandrolone.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
common with this substance. This may include bouts of oily skin, acne, and
body/facial hair growth. Anabolic/androgenic steroids may also aggravate male
pattern hair loss. Individuals sensitive to the androgenic effects of this steroid
may find a milder anabolic such as Deca-Durabolin® to be more comfortable.
Women are additionally warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
Note that in androgen-responsive target tissues such as the skin, scalp, and
prostate, the relative androgenicity of norethandrolone is reduced by its
reduction to dihydronorethandrolone. The 5-alpha reductase enzyme is
responsible for this metabolism. The concurrent use of a 5-alpha reductase
inhibitor such as finasteride or dutasteride will interfere with site-specific
reduction of norethandrolone action, considerably increasing the tendency of the
drug to produce androgenic side effects. Reductase inhibitors should be avoided
with this steroid if maintaining low relative androgenicity is desired.
Side Effects (Hepatotoxicity):
Norethandrolone is a c17-alpha alkylated compound. This alteration protects the
drug from deactivation by the liver, allowing a very high percentage of the drug
entry into the bloodstream following oral administration. C17-alpha alkylated
anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure
may result in liver damage. In rare instances life-threatening dysfunction may
develop. It is advisable to visit a physician periodically during each cycle to
monitor liver function and overall health. Intake of c17-alpha alkylated steroids
is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain.
Severe liver complications are rare given the periodic nature in which most
people use oral anabolic/androgenic steroids, although cannot be excluded with
this steroid, especially with high doses and/or prolonged administration periods.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Norethandrolone
has a strong effect on the hepatic management of cholesterol due to its structural
resistance to liver breakdown and route of administration. Anabolic/androgenic
steroids may also adversely affect blood pressure and triglycerides, reduce
endothelial relaxation, and support left ventricular hypertrophy, all potentially
increasing the risk of cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
555 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, this steroid should be taken on an empty stomach.
Administration (Men):
The original prescribing guidelines for Nilevar called for a daily dosage of 20 to
30 mg. This was to be administered on an intermittent basis, with the drug taken
for no more than 12 consecutive weeks. Thereafter, a break of at least 1 month
was advised before therapy was resumed. When used for physique-or
performance-enhancing purposes, the drug is also used intermittently, with
cycles usually lasting between 6 and 8 weeks in length followed by 6-8 weeks
off. A daily dosage of 20 to 40 mg is most common for such applications. This
level is typically sufficient for rapid gains in strength and muscle mass (bulk).
The high estrogenicity makes norethandrolone of little value in speed and
endurance sports, causing an unwanted retention of water weight. When given
by injection, the same milligram dosage is recommended as when the drug is
given orally.
Administration (Women):
The original prescribing guidelines for Nilevar made no special dosing
recommendations for women, although it did warn that androgenicity is likely on
a high dosage. When used by women for physique-or performance-enhancing
purposes, a daily dosage of 5-10 mg is most common, taken for no longer than 4
weeks. This level is quite effective for promoting new muscle growth. Note that
virilizing side effects are still sometimes noticed at lower doses,and need to be
carefully examined for.
Availability:
Pharmaceutical preparations containing norethandrolone remain scarce, and are
rarely diverted for black market sale. The only region of note where this
compound is still made is Australia.
Omnadren® 250 (testosterone blend)
Description:
Omnadren® 250 (in its original formulation), was an oil-based injectable
testosterone blend that contained four different testosterone esters: testosterone
propionate (30 mg); testosterone phenylpropionate (60 mg); testosterone
isocaproate (60 mg); and testosterone caproate (100 mg). Being a fourcomponent testosterone blend, this preparation was most commonly compared to
Sustanon® 250. While it did contain testosterone propionate, phenylpropionate,
and isocaproate in the same strengths as Sustanon®, the last ester is different. It
was a slightly shorter-acting drug, making Omnadren® more analogous to
Testoviron® (the caproate ester is one carbon shorter than enanthate) than
Sustanon® 250. Please note that there were even older versions of Omnadren®
listing isohexanoate and hexanoate as the final two ingredients, which are simply
different words for isocaproate and caproate.
History:
Omnadren® 250 was developed in Poland by Polfa during the years of Soviet
control. Its formulation (original) is very similar to that of Sustanon® 250,
barring the substitution of one of the component esters. This was likely done to
avoid patent issues with the international pharmaceutical giant Organon, which
exclusively controlled the global supply of Sustanon® 250. In clinical medicine,
Omnadren® 250 was used most commonly to treat adult men suffering from low
androgen levels, usually noticing symptoms of impotence or hormonal
disturbance of spermatogenesis. This drug was also used on occasion to treat
adolescents with delayed puberty, and women with advanced breast or
endometrial cancer.
The manufacture of Omnadren® 250 under the Polfa label was discontinued in
1994. That year, the newly privatized Polfa firm was renamed Jelfa, mainly to
distinguish itself from other firms that use a Polfa prefix as part of their names.
Jelfa continued to produce Omnadren® 250 for the domestic market, which
remained available without interruption in the same familiar 5-pack of ampules
(albeit with a new company label and logo) for years after. Today, Jelfa
continues to market Omnadren® 250 in Poland, as well as in many neighboring
markets including Russia, Ukraine, Kazakhstan, Uzbekistan, Kurdistan,
Kyrgyzstan, Armenia, Moldavia, Latvia, Lithuania, Azerbaijan, Georgia, and
Belarus, however the formulation has recently changed. All Omnadren 250 sold
today carries the same exact formulation as Sustanon 250. This profile refers to
the original formulation only, which is now unavailable worldwide.
How Supplied:
Omnadren® 250 (original formulation) in no longer available. When
manufactured, it was supplied in 1 mL glass ampules containing an oily solution;
sold in boxes of 5 ampules.
Structural Characteristics:
Omnadren® 250 contains a mixture of four testosterone compounds, which
where modified with the addition of carboxylic acid esters (propionic, propionic
phenyl ester, isocaproic, and caproic acids) at the 17-beta hydroxyl group.
Esterified forms of testosterone are less polar than free testosterone, and are
absorbed more slowly from the area of injection. Once in the bloodstream, the
ester is removed to yield free (active) testosterone. Esterified forms of
testosterone are designed to prolong the window of therapeutic effect following
administration, allowing for a less frequent injection schedule compared to
injections of free (unesterified) steroid. Omnadren® 250 is designed to provide a
rapid peak in testosterone levels (24-48 hours after injection), and maintain
physiological concentrations for approximately 14 days.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone more likely to require the
concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention
and loss of muscle definition are common with higher doses of testosterone, this
drug is usually considered a poor choice for dieting or cutting phases of training.
Its moderate estrogenicity makes it more ideal for bulking phases, where the
added water retention will support raw strength and muscle size, and help foster
a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
556
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
557 Studies using 300 mg of testosterone ester
(enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated
only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached
21%.
558 The negative impact of aromatase inhibition should be taken into
consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less of testosterone per week, the
impact on lipid profile tends to be noticeable but not dramatic, making an antiestrogen (for cardioprotective purposes) perhaps unnecessary. Doses of 600 mg
or less per week have also failed to produce statistically significant changes in
LDL/VLDL cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive
protein, and insulin sensitivity, all indicating a relatively weak impact on
cardiovascular risk factors.
559 When used in moderate doses, injectable
testosterone esters are usually considered to be the safest of all
anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Testosterone propionate is often regarded as a painful injection. This is due to
the very short carbon chain of the propionic acid ester, which can be irritating to
tissues at the site of injection. Many sensitive individuals choose to stay away
from this steroid completely, their bodies reacting with a pronounced soreness
and low-grade fever that may last for a few days after each injection.
Administration (Men):
Depending on the application, the prescribing guidelines for Omnadren® 250
call for a dosage of 250 mg (1 ampule) to be injected every 3 to 4 weeks.
Although active in the body for a longer time, Omnadren® 250 is usually
administered on a weekly basis for muscle-building purposes. This schedule will
allow for the higher doses most commonly applied by athletes, and more stable
elevations in hormone level. The usual dosage among male athletes is in the
range of 250-750 mg per injection, taken in cycles 6 to 12 weeks in length. This
level is sufficient for most users to notice exceptional gains in muscle size and
strength. Some bodybuilders have been known to use excessively high dosages
of this drug (1,000 mg per week or more), although this practice is generally not
advised due to the higher incidence of side effects. Testosterone is ultimately
very versatile, and can be combined with many other anabolic/androgenic
steroids to tailor the desired effect.
Administration (Women):
Omnadren® 250 is rarely used with women in clinical medicine. When applied,
it is most often used to treat inoperable breast or endometrial cancer.
Omnadren® 250 is not recommended for women for physique-or performanceenhancing purposes due to its strong androgenic nature, tendency to produce
virilizing side effects, and slow-acting characteristics (making blood levels
difficult to control).
Availability:
The original Omnadren 250 formulation is no longer available. Jelfa continues to
use the trade name to market a steroid product, but it is now equivalent in
makeup to Sustanon 250. See the Sustanon 250 profile for more information.
Orabolin® (ethylestrenol)
Description:
Ethylestrenol is an oral anabolic steroid derived from nandrolone. As is typical
for many 19-nor steroids, this agent exhibits far greater anabolic properties than
androgenic, is only weakly estrogenic, and is strongly progestational.
Structurally, ethylestrenol most closely resembles Nilevar (norethandrolone).
The two differ only by the absence of an oxygen atom at the c3 position of
ethylestrenol, and in the body ethylestrenol actually has a notable affinity to
convert to norethandrolone.
560 This path of metabolism is responsible for much
of the anabolic, androgenic, and estrogenic activity we see with this compound,
and in most regards ethylestrenol can be viewed as a pro-drug to
norethandrolone. Although ethylestrenol is strongly anabolic relative to its
androgenicity, athletes generally find this steroid to be extremely weak. The
level of muscle growth obtained with this steroid is generally much less
noticeable than that expected with either Nilevar or Deca-Durabolin®, and it is
considerably less effective than both stanozolol and oxandrolone on a milligram
for milligram basis.
History:
Ethylestrenol was first described in 1959.
561
It was developed into an oral
medicine by Organon (now Merck/MSD), appearing in most markets between
1961 and 1964. Organon sold the tablets under the trade name Maxibolin in the
U.S., and as Orabolin, Orgabolin, and Durabolin-O in other markets. The latter
name is a compressed form of “Durabolin-Oral,” noting that the drug is an oral
cousin to Durabolin (nandrolone phenylpropionate). Organon also produced oral
ethylestrenol solutions, such as Maxibolin Elixir (U.S.) and Fertabolin (India,
Philippines). Ethylestrenol was initially indicated for several uses, mainly
focused on preserving lean mass. Early U.S. product literature states,“… along
with a good dietary regimen, Maxibolin promotes tissue-building and weight
gain, stimulation of appetite and sense of wellbeing, renewal of vigor, is an aid
in bone matrix reconstruction and in combating the depression and weakness of
chronic illness or prolonged convalescence. It can also prevent or reverse certain
catabolic effects associated with corticosteroid therapy.”
Ethylesterenol became a steroid of great controversy during the early 1980’s,
when Western media attention was given to the marketing of the drug to
malnourished children in Third-World markets such as India, Bangladesh, and
the Philippines. Advertising on Fertabolin in India claimed the drug would “help
children gain full weight and height,” “simulates physiological appetite,” and
“ensures optimal assimilation of food.” It also described a “delicious [raspberry]
syrup flavor children love.” The main point of contention was the promotion of
an anabolic steroid to treat the lack of adequate food supply, the real issue at
hand. Many viewed Organon’s actions as potentially dangerous and highly
unethical, and the company soon discontinued Fertabolin and related marketing
practices. Maxibolin and Maxibolin Elixir were voluntarily withdrawn from the
U.S. market during the late 1980’s as well, and most Western ethylestrenol
products from Organon soon followed. Today, Merck/MSD retains only a
limited interest in the drug. Ethylestrenol is currently a rare find, as it is only
manufactured (as a generic drug or under other brand names) is a select few
countries.
How Supplied:
Ethylestrenol is available in select human and veterinary drug markets.
Composition and dosage may vary by country and manufacturer, but typically
contains 2mg of steroid per tablet. Oral solutions have also been produced in the
past, such as Maxibolin Elixir, which contained 2mg/5 mL in a 4 ounce bottle.
Fertabolin for children contained .2mg/2 mL of solution.
Structural Characteristics:
Ethylestrenol is a modified form of nandrolone. It differs by: 1) the addition of
an ethyl group at carbon 17alpha to protect the hormone during oral
administration and 2) the removal of the 3-oxygen.
Side Effects (Estrogenic):
Ethylestrenol is aromatized by the body, and converts to a synthetic estrogen
with a high level of biological activity (17alpha-ethyl-estradiol). Rate of
aromatization is so low, however, that it remains classified as a weakly
estrogenic steroid. Gynecomastia is possible during treatment, but generally only
when higher doses are used. Water and fat retention can also become issues,
again depending on dose. Sensitive individuals may need to addition an antiestrogen such as Nolvadex®. One may alternately use an aromatase inhibitor
like Arimidex® (anastrozole), which is a more effective remedy for estrogen
control. Aromatase inhibitors, however, can be quite expensive in comparison to
standard estrogen maintenance therapies, and may also have negative effects on
blood lipids.
It is of note that ethylestrenol has strong activity as a progestin in the body.
562
The side effects associated with progesterone are similar to those of estrogen,
including negative feedback inhibition of testosterone production and enhanced
rate of fat storage. Progestins also augment the stimulatory effect of estrogens on
mammary tissue growth. There appears to be a strong synergy between these
two hormones here, such that gynecomastia might even occur with the help of
progestins without excessive estrogen levels being present. The use of an antiestrogen, which inhibits the estrogenic component of this disorder, is often
sufficient to mitigate gynecomastia caused by this steroid.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
common with this substance. This may include bouts of oily skin, acne, and
body/facial hair growth. Anabolic/androgenic steroids may also aggravate male
pattern hair loss. Individuals sensitive to the androgenic effects of this steroid
may find a milder anabolic such as Deca-Durabolin® to be more comfortable.
Women are additionally warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
Note that in androgen-responsive target tissues such as the skin, scalp, and
prostate, the relative androgenicity of ethylestrenol is reduced by its reduction to
weaker “dihidyo” metabolites. The 5-alpha reductase enzyme is responsible for
this metabolism. The concurrent use of a 5-alpha reductase inhibitor such as
finasteride or dutasteride will interfere with site-specific reduction of
ethylestrenol action, increasing the tendency of the drug to produce androgenic
side effects. Reductase inhibitors should be avoided with this steroid if
maintaining low relative androgenicity is desired.
Side Effects (Hepatotoxicity):
Ethylestrenol is a c17-alpha alkylated compound. This alteration protects the
drug from deactivation by the liver, allowing a very high percentage of the drug
entry into the bloodstream following oral administration. C17-alpha alkylated
anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure
may result in liver damage. In rare instances life-threatening dysfunction may
develop. It is advisable to visit a physician periodically during each cycle to
monitor liver function and overall health. Intake of c17-alpha alkylated steroids
is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain.
Severe liver complications are rare given the periodic nature in which most
people use oral anabolic/androgenic steroids, although cannot be excluded with
this steroid, especially with high doses and/or prolonged administration periods.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Ethylestrenol has a
strong effect on the hepatic management of cholesterol due to its structural
resistance to liver breakdown and route of administration. Anabolic/androgenic
steroids may also adversely affect blood pressure and triglycerides, reduce
endothelial relaxation, and support left ventricular hypertrophy, all potentially
increasing the risk of cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
563 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, this steroid should be taken on an empty stomach.
Administration (Men):
Original prescribing guidelines recommend a dosage of 4 mg to 8 mg per day,
taken for no more than 6 consecutive weeks. After a break for 4 weeks, the drug
is resumed for an additional 6 weeks if indicated. When used for physique-or
performance-enhancing purposes, a daily dosage of 20 mg to 40 mg is most
common, which equates to ten to twenty 2mg tablets.The drug is typically used
in cycles lasting no longer than 6-8 weeks, in an effort to minimize hepatic
strain. This level is sufficient for some measurable gains in muscle size and
strength, although experienced steroid users are likely to still be disappointed
with the results. Instead of increasing the dosage, most opt to add a second
steroid to the cycle, usually an injectable such as testosterone cypionate or
enanthate, boldenone undecylenate, or methenolone enanthate (usually at a dose
of 200-400 mg per week), which do not provide additional liver toxicity.
Administration (Women):
Original prescribing guidelines recommend a dosage of 4 mg to 8mg per day,
taken for no more than 6 consecutive weeks. After a break for 4 weeks, the drug
is resumed for an additional 6 weeks if indicated. When used for physique-or
performance-enhancing purposes, a daily dosage of 10 mg to 16 mg is most
common, taken for no longer than 4 weeks.This level seems to be fairly effective
for promoting new muscle growth. Higher doses are likely to produce virilizing
side effects, and are not recommended. Note that virilizing side effects are still
sometimes noticed at lower doses.
Availability:
Pharmaceutical preparations containing ethylestrenol remain scarce. In
reviewing some of the remaining products and changes in the global
pharmaceutical market, we have made the following observations.
At the present time, the legitimate supply of ethylestrenol appears to be isolated
to Australia, where it is found in a small number of veterinary compounds
including Nandoral tablets and Nitrotain paste.
Oral Turinabol (chlorodehydromethyltestosterone)
Description:
Chlorodehydromethyltestosterone is a potent derivative of Dianabol. This oral
steroid is structurally a cross between methandrostenolone and clostebol (4-
chlorotestosterone), having the same base structure as Dianabol with the added
4-chloro alteration of clostebol. This alteration makes
chlorodehydromethyltestosterone a milder cousin of Dianabol, the new steroid
displaying no estrogenic and a much less androgenic activity in comparison to its
more famous counterpart. The anabolic activity of
chlorodehydromethyltestosterone is somewhat lower than that of Dianabol as
well, but it does maintain a much more favorable balance of anabolic to
androgenic effect. This means that at any given level of muscle-building activity,
chlorodehydromethyltestosterone will be less likely to produce androgenic side
effects.
History:
Chlorodehydromethyltestosterone was first described in 1962.
564 Jenapharm
(Jena, Germany) soon after released the drug for sale in the East German
prescription drug market, under the brand name Oral Turinabol. The drug was
favored by clinicians for its highly anabolic and low anabolic nature, lending
itself to use in not only adult males, but women and children as well. The
product was manufactured in two strengths, containing 1 mg and 5 mg of drug
per tablet, so that a lower-dosed version was available for the more sensitive
populations. Chlorodehydromethyltestosterone was applied for a number of
medical uses; mainly those focusing on the building or preservation of lean
muscle tissue and bone mass.
Oral Turinabol became a steroid of infamy during the 1990’s, when it was
revealed that chlorodehydromethyltestosterone had been one of the closely held
secrets inside the “East German Doping Machine.” This is referring to the statesponsored doping program, called “State Plan Research Theme 14.25,” that
operated in East Germany between 1974 and 1989. It was an aggressive anabolic
steroid administration program, designed with one goal in mind: cheating the
Olympic drug test. In many cases, the Olympic athletes, both male and female,
were unwitting participants, simply told by their trainers and coaches that they
were being given “vitamins.” Many of these blue vitamins turned out to be Oral
Turinabol, a potent and undetectable (at the time) anabolic steroid. As many as
10,000 athletes were given anabolic steroids during the time the program was
active, many of them taking Oral Turinabol. For a more in-depth look at this
dramatic historic event, including the trials of several former East German
officials for their participation, I recommend you look at the book “Faust's Gold:
Inside the East German Doping Machine” by Steven Ungerleider.
In spite of an arguably favorable profile of activity and safety record, Jenapharm
discontinued Oral Turinabol in 1994. This was at a time when a great deal of
negative attention was being given to sports doping, lending credibility to the
speculation that this decision was one based on public relations, and not
necessarily finances or health concerns over the drug. Regardless, Jenapharm
was acquired by Schering AG (Germany) in 1996, a company with no interest in
reliving the controversies of the past (Schering had already discontinued many
of its controversial anabolic steroid products as well). Before or since, no other
brand of chlorodehydromethyltestosterone has existed as a prescription drug
product. Today, this agent is still available, but is only produced by a small
number of underground manufacturers and export-only suppliers.
How Supplied:
Chlorodehydromethyltestosterone is not available as a prescription drug product.
When manufactured, it was found in 1 mg and 5 mg tablets, sold in
Germany/German Democratic Republic.
Structural Characteristics:
Chlorodehydromethyltestosterone is a modified form of testosterone. It differs
by: 1) the addition of a methyl group at carbon 17-alpha, which helps protect the
hormone during oral administration, 2) the introduction of a double bond
between carbons 1 and 2 (1-ene), which shifts the anabolic to androgenic ratio in
favor of the former, and 3) the attachment of a chloro group at carbon 4, which
inhibits steroid aromatization and reduces relative androgenicity.
Side Effects (Estrogenic):
Chlorodehydromethyltestosterone is not aromatized by the body, and is not
measurably estrogenic. An anti-estrogen is not necessary when using this steroid,
as gynecomastia should not be a concern even among sensitive individuals.
Since estrogen is the usual culprit with water retention, this steroid instead
produces a lean, quality look to the physique with no fear of excess
subcutaneous fluid retention. This makes it a favorable steroid to use during
cutting cycles, when water and fat retention are major concerns.
Side Effects (Androgenic):
Although chlorodehydromethyltestosterone is classified as an anabolic steroid,
androgenic side effects are still possible with this substance. These may include
bouts of oily skin, acne, and body/facial hair growth. Doses higher than normally
prescribed are more likely to cause such side effects. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are additionally
warned of the potential virilizing effects of anabolic/androgenic steroids. These
may include a deepening of the voice, menstrual irregularities, changes in skin
texture, facial hair growth, and clitoral enlargement.
Chlorodehydromethyltestosterone is not extensively metabolized by the 5-alpha
reductase enzyme, so its relative androgenicity is not greatly altered by the
concurrent use of finasteride or dutasteride
Side Effects (Hepatotoxicity):
Chlorodehydromethyltestosterone is a c17-alpha alkylated compound. This
alteration protects the drug from deactivation by the liver, allowing a very high
percentage of the drug entry into the bloodstream following oral administration.
C17-alpha alkylated anabolic/androgenic steroids can be hepatotoxic. Prolonged
or high exposure may result in liver damage. In rare instances life-threatening
dysfunction may develop. It is advisable to visit a physician periodically during
each cycle to monitor liver function and overall health. Intake of c17-alpha
alkylated steroids is commonly limited to 6-8 weeks, in an effort to avoid
escalating liver strain. The use of a liver detoxification supplement such as Liver
Stabil, Liv-52, or Essentiale Forte is advised while taking any hepatotoxic
anabolic/androgenic steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Chlorodehydromethyltestosterone has a strong effect on the hepatic management
of cholesterol due to its non-aromatizable nature, structural resistance to liver
breakdown, and route of administration. Anabolic/androgenic steroids may also
adversely affect blood pressure and triglycerides, reduce endothelial relaxation,
and support left ventricular hypertrophy, all potentially increasing the risk of
cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
565 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, this steroid should be taken on an empty stomach.
Administration (Men):
A common clinical dose of chlorodehydromethyltestosterone is estimated to be 5
mg per day; actual prescribing guidelines are unavailable. In the athletic arena,
an effective oral daily dosage falls in the range of 15-40 mg, taken in cycles
lasting no more than 6-8 weeks to minimize hepatotoxicity. This level is
sufficient for measurable increases in lean muscle mass and strength. This agent
is most often applied as a pre-contest or cutting steroid for bodybuilding
purposes, and is not viewed as an ideal bulking agent due to its lack of
estrogenicity. Athletes in sports where speed tends to be a primary focus also
find strong favor in chlorodehydromethyltestosterone, obtaining a strong
anabolic benefit without having to carry around any extra water or fat weight.
Administration (Women):
A common clinical dose of chlorodehydromethyltestosterone is estimated to be
1-2.5 mg per day; actual prescribing guidelines are unavailable. In the athletic
arena, women would commonly take a single 5 mg tablet per day, taken in
cycles lasting no more than 4-6 weeks to minimize hepatotoxicity. Virilizing
effects are unlikely at this level of use. Much higher doses were often used with
female athletes in the former GDR doping program, but often to detriment of
strong virilizing side effects.
Availability:
Chlorodehydromethyltestosterone has been unavailable as a prescription drug
product in Germany (the sole country of manufacture for most of its history)
since 1994. A very small number of pharmaceutical companies have marketed
the drug since, mainly in less regulated markets of Eastern Europe and Asia,
where black market demand still influences production. In reviewing some of the
remaining pharmaceutical products and recent changes on the global
pharmaceutical market, we have made the following observations.
Balkan Pharmaceuticals (Moldova) makes the product Turanabol. It is prepared
in 10 mg tablets, 20 tablets per foil and plastic strip.
Oreton (testosterone propionate)
Description:
Testosterone propionate is a commonly manufactured injectable form of the
primary male androgen testosterone. The added propionate ester will slow the
rate in which testosterone is released from the injection site, but only for a few
days. Testosterone propionate is, therefore, comparatively much faster-acting
than other testosterone esters such as cypionate or enanthate, and requires a
much more frequent dosing schedule. By most accounts testosterone propionate
is an older and cruder form of injectable testosterone, made obsolete by the
slower-acting and more comfortable esters that were developed subsequent to it.
Still, those who are not bothered by the frequent injection schedule find
testosterone propionate every bit as acceptable. As an injectable testosterone, it
is a powerful mass-building drug, capable of producing rapid gains in both
muscle size and strength.
History:
Testosterone propionate was first described in 1935, during a series of
experiments that set out to increase the therapeutic usefulness of testosterone by
slowing its release into the bloodstream.
566 Two years later, Schering AG in
Germany would introduce the first testosterone propionate product under the
brand name Testoviron®. Propionate was also the first commercially available
injectable ester of testosterone on the U.S. prescription drug market, and
remained the dominant form of testosterone globally before 1960. Back during
the early 1950’s, for example, when steroids were first being experimented with
by small numbers of American athletes, the only readily available
anabolic/androgenic steroids were methyltestosterone, testosterone propionate,
and testosterone suspension. Interesting enough, during this time testosterone
propionate was also available in orally administered (Buccal) preparations, but
they disappeared from the U.S. market during the 1980’s.
Early prescribing guidelines for testosterone propionate called for a number of
therapeutic uses. It was mainly applied to cases of male androgen insufficiency,
and those issues normally surrounding low testosterone levels such as reduced
sex drive and impotence in adults, and cryptorchidism (undescended testicles) in
teenagers and young adults. But it also had such other uses as treating
menopause, menorrhagia (heavy menstrual bleeding), menstrual tension, chronic
cystic mastitis (fibrocystic breasts), endometriosis, and excessive lactation,
covering a wide range of situations in which the male hormone testosterone was
being applied to female patients. Over the years these wide guidelines were
narrowed by the U.S. Food & Drug Administration, however, and by the 1980’s,
testosterone propionate was being largely applied only to male patients.
Testosterone propionate has a long history of availability in the U.S. and abroad,
and remains a very common form of testosterone on the global market to this
day. It must be emphasized, however, that its ability to remain on the market is
more a product of history than unique application. Testosterone propionate was
the first acceptable ester of testosterone, and consequently has many decades of
history as a useable therapeutic agent. Many companies have sold it for decades
now, and so long as it is still in demand will continue to do so. But other (more
modern) forms of testosterone such as enanthate and cypionate are much more
popular today, as they are much slower-acting still, and allow for far more
comfortable administration schedules. Testosterone propionate is still approved
for sale in the United States, although its ultimate market future here remains
questionable.
Bodybuilders commonly consider propionate to be the mildest testosterone ester,
and the preferred form of this hormone for dieting/cutting phases of training.
Some will go so far as to say that propionate will harden the physique, while
giving the user less water and fat retention than one typically expects to see with
a testosterone like enanthate, cypionate or Sustanon. Realistically, however,
these advantages do not hold up to close scrutiny. The propionate ester is
actually removed before the testosterone it carries is active in the body, and
ultimately has little effect outside of slowing steroid release. It all really boils
down to how much testosterone you are getting into your blood with each
particular esterified compound. Otherwise, there are no real functional
differences between them.
How Supplied:
Testosterone propionate is widely available in human and veterinary drug
markets. Composition and dosage may vary by country and manufacturer, but
usually contain 25 mg/ml, 50 mg/ml, or 100 mg/ml of steroid dissolved in oil.
Structural Characteristics:
Testosterone propionate is a modified form of testosterone, where a carboxylic
acid ester (propionic acid) has been attached to the 17-beta hydroxyl group.
Esterified forms of testosterone are less polar than free testosterone, and are
absorbed more slowly from the area of injection. Once in the bloodstream, the
ester is removed to yield free (active) testosterone. Esterified forms of
testosterone are designed to prolong the window of therapeutic effect following
administration, allowing for a less frequent injection schedule compared to
injections of free (unesterified) steroid. The half-life of testosterone propionate is
approximately two days after injection.
Figure 1. Pharmacokinetics of 25 mg labeled testosterone propionate
injection. Source: Pharmacokinetic properties of testosterone propionate in
normal men. Fujioka M, Shinohara Y,Baba S. et.Al. J Clin Endocrinol
Metab 63 (1986):1361-4.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone propionate more likely to
require the concurrent use of an anti-estrogen or aromatase inhibitor. Since water
retention and loss of muscle definition are common with higher doses of
testosterone, this drug is usually considered a poor choice for dieting or cutting
phases of training. Its moderate estrogenicity makes it more ideal for bulking
phases, where the added water retention will support raw strength and muscle
size, and help foster a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that both anabolic and
androgenic effects are mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
567
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
568 Studies using 300 mg of testosterone ester
(enanthate) per week for twenty weeks without an aromatase inhibitor
demonstrated only a 13% decrease in HDL cholesterol, while at 600 mg the
reduction reached 21%.
569 The negative impact of aromatase inhibition should
be taken into consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less of testosterone per week, the
impact on lipid profile tends to be noticeable but not dramatic, making an antiestrogen (for cardioprotective purposes) perhaps unnecessary. Doses of 600 mg
or less per week have also failed to produce statistically significant changes in
LDL/VLDL cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive
protein, and insulin sensitivity, all indicating a relatively weak impact on
cardiovascular risk factors.
570 When used in moderate doses, injectable
testosterone esters are usually considered to be the safest of all
anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Testosterone propionate is often regarded as a painful injection. This is due to
the very short carbon chain of the propionic acid ester, which can be irritating to
tissues at the site of injection. Many sensitive individuals choose to stay away
from this steroid completely, their bodies reacting with a pronounced soreness
and low-grade fever that may last for a few days after each injection. Even the
mild soreness that is experienced by most users can be quite uncomfortable,
especially when you take into account that the drug is being administered
multiple times each week for a number of consecutive weeks.
Administration (Men):
To treat androgen insufficiency, early prescribing guidelines recommended a
dosage of 25 mg given two to three times per week. Modern product literature
usually recommends 25 mg to 50 mg given two to three times per week for the
same purpose. The usual dosage among male athletes is in the range of 50-100
mg per injection, which is given every second or third day. Similar to other
esters of testosterone, testosterone propionate is commonly used at a weekly
cumulative dosage between 200 mg to 400 mg. This level is sufficient for most
users to notice exceptional gains in muscle size and strength.
Testosterone propionate is usually incorporated into bulking phases of training,
when added water retention will be of little consequence, the user more
concerned with raw mass than definition. Some do incorporate this drug into
cutting cycles as well, but typically in lower doses (100-200 mg per week)
and/or when accompanied by an aromatase inhibitor to keep estrogen levels
under control. Testosterone propionate is a very effective anabolic drug, and is
often used alone with great benefit. Some, however, find a need to stack it with
other anabolic/androgenic steroids for a stronger effect, in which case an
additional 200-400 mg per week of boldenone undecylenate, methenolone
enanthate, or nandrolone decanoate should provide substantial results with no
significant hepatotoxicity. Testosterone is ultimately very versatile, and can be
combined with many other anabolic/androgenic steroids to tailor the desired
effect.
Administration (Women):
Testosterone propionate is rarely used with women in clinical medicine. When
applied, it is most often used as a secondary medication during inoperable breast
cancer, when other therapies have failed to produce a desirable effect and
suppression of ovarian function is necessary. Testosterone propionate is not
recommended for women for performance-enhancing purposes due to its strong
androgenic nature and tendency to produce virilizing side effects. Female
bodybuilders who insist on using testosterone, however, often choose
propionate, as blood levels are easier to control with this ester compared to
cypionate or enanthate. Should virilization symptoms develop, hormone levels
will decline in a matter of days, instead of weeks, following drug cessation. The
administration schedule is often more conservative as well, with a small
injection (25 mg at most) given every 5 to 7 days, and cycle duration limited to
6-8 weeks or less.
Availability:
Testosterone propionate is subject to decreasing supply as a pharmaceutical
product. Longer acting esters such as cypionate and enanthate are much better
suited for virtually every clinical application. As such, most physicians and
pharmaceutical companies have abandoned this old ester of testosterone. With a
few exceptions in the west, the remaining legitimate supply largely comes from
manufacturers in loosely regulated markets of Asia, where black market demand
continues to drive production. In reviewing some of the remaining products and
changes in the global pharmaceutical market, we have made the following
observations.
Tesotsterone propionate is unavailable in the United States as a prescription
product. Watson, Lilly, Bel Mar, and Rigby made some of the last known
products, but all have been removed from market for some time. Given that the
FDA never officially withdrew the drug, it can still be specially ordered through
a small number of compounding pharmacies.
Brovel in Mexico makes a testosterone propionate in a 50 mg/mL dosage for
veterinary use. Counterfeits are not commonly a problem.
Testolic is made in Thailand by T.P. Drug Laboratories. This product comes in
the form of 2 mL ampules, each holding 50 mg/mL of steroid.
Propiobolic from Asia Pharma (Malaysia) is now approved for sale through
pharmacies in Thailand. Each box should carry a scratch-off security sticker,
which will display a code that can be validated on the company website.
Misr (Egypt) have updated the packaging to Testone-E. The new box carries a
white green blue pattern similar to other Egyptian steroids including Cidoviron
and Cidoteston.
Balkan Pharmaceuticals (Moldova) makes the product Testosterona P. It is
prepared in both 1 mL ampules and multi-dose vials.
Testosteron is a popular brand from Bulgaria, and is commonly exported to other
markets in high volume. It comes in the form of 1 mL glass ampules containing
50 mg/mL of steroid.
A generic made by the company Farmak is popularly exported from the Ukraine.
This also comes in the form of 1 mL glass ampules containing 50 mg of steroid.
Jelfa makes Testosteronum Propionicum in Poland, which makes its way most
often to the European black market. However, it only contains 25 mg of steroid
in each 1 mL ampule.
Virormone is still manufactured in the UK, most recently by the firm
Nordic.This product contains 2 mL per ampule, with 100 mg of steroid held in
each.
Testogan is made by Laquinsa in Costa Rica. This product contains only 25
mg/mL of steroid, but is distributed in a 50 mL multi-dose vial. This makes it
one of the largest volume testosterone propionate products available in
commerce.
Parabolan® (trenbolone hexahydrobenzylcarbonate)
Description:
Trenbolone hexahydrobenzylcarbonate is a slow-acting injectable ester of the
potent anabolic steroid trenbolone. Trenbolone appears most commonly as
trenbolone acetate, which is a much faster-acting form of the drug (see: Finajet).
The hexahydrobenzylcarbonate ester used here extends the release of trenbolone
for more than 2 weeks, which has always been thought of as more suitable for
human use due to the less frequent injection schedule. The base steroid
trenbolone is roughly three times more androgenic than testosterone, making it a
fairly potent androgen. It also displays about 3 times greater tissue-building
activity in comparison to its androgenic properties, making its official
classification as that of an anabolic steroid. The muscle-building effect of
trenbolone is often compared to such popular bulking agents as testosterone or
Dianabol, but without the same estrogenrelated side effects. It is most commonly
identified as a lean-mass-building drug, and is extremely popular with athletes
for its ability to promote the rapid buildup of strength, muscle size, and
definition.
History:
The first long-acting trenbolone ester (undecanoate) was studied in 1967,
described during a series of experiments into synthetic anabolic steroids by
Roussel-UCLAF.
571 Trenbolone hexahydrobenzylcarbonate was a subsequent
and uniquely French slant to this long-acting anabolic steroid, possessing an
unusual but roughly equivalent compound. Trenbolone
hexahydrobenzylcarbonate was developed into a medicine by Negma
Laboratoires in France, which sold the drug under the Parabolan trade name. It
was also sold for a period of time as Hexabolan, a name that referred to the
unusual ester it possesses. Trenbolone hexahydrobenzylcarbonate is the only
known form of trenbolone ever produced as a medicine for human consumption.
The most notable appearance of trenbolone comes as trenbolone acetate, which
is used widely and exclusively in veterinary medicine.
Parabolan was prescribed in France as a protein-sparing anabolic agent in cases
of cachexia (lean body mass wasting) and malnutrition, as well as to combat
certain forms of osteoporosis. Its prescribing guidelines included
recommendations for the treatment of androgen-sensitive populations, such as
women and the elderly. Owing to its moderate androgenic properties, however,
the drug was contraindicated in children, especially young females. Parabolan
remained on the French market for a very long time, although it was finally
discontinued (voluntarily) by Negma in 1997. For a brief period of time it
seemed that the demise of Parabolan would mark the end of human-use
trenbolone preparations, as no other medicine approved for human use was
known to exist worldwide at the time. A very small number of Parabolan
preparations have been brought to market since, however, so while the drug is
still poorly available, it is not completely defunct.
How Supplied:
Trenbolone hexahydrobenzylcarbonate is no longer produced as a prescription
drug product. When manufactured in France it came in the form of a 1.5 mL
ampule containing 76 mg of steroid (product information lists this as equivalent
to 50 mg of base trenbolone).
Structural Characteristics:
Trenbolone is a modified form of nandrolone. It differs by the introduction of
double bonds at carbons 9 and 11, which inhibit aromatization (9-ene), increase
androgen-binding affinity,
572 and slows its metabolism. The resulting steroid is
significantly more potent as both an anabolic and an androgen than its
nandrolone base. The trenbolone here is modified with a
hexahydrobenzylcarbonate ester at the 17-beta hydroxyl group, so that the free
steroid is released more slowly from the area of injection.
Side Effects (Estrogenic):
Trenbolone is not aromatized by the body, and is not measurably estrogenic. It is
of note, however, that this steroid displays significant binding affinity for the
progesterone receptor (slightly stronger than progesterone itself ).
573 574 The side
effects associated with progesterone are similar to those of estrogen, including
negative feedback inhibition of testosterone production and enhanced rate of fat
storage. Progestins also augment the stimulatory effect of estrogens on
mammary tissue growth. There appears to be a strong synergy between these
two hormones here, such that gynecomastia might even occur with the help of
progestins, without excessive estrogen levels. The use of an anti-estrogen, which
inhibits the estrogenic component of this disorder, is often sufficient to mitigate
gynecomastia caused by progestational anabolic/androgenic steroids. Note that
progestational side effects are more common when trenbolone is being taken
with other aromatizable steroids.
Side Effects (Androgenic):
Although classified as an anabolic steroid, trenbolone is sufficiently androgenic.
Androgenic side effects are still common with this substance, and may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are also warned of
the potential virilizing effects of anabolic/androgenic steroids. These may
include a deepening of the voice, menstrual irregularities, changes in skin
texture, facial hair growth, and clitoral enlargement. Additionally, the 5-alpha
reductase enzyme does not metabolize trenbolone
575
, so its relative
androgenicity is not affected by finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Trenbolone is not c-17 alpha alkylated, and is generally not considered a
hepatotoxic steroid; liver toxicity is unlikely. This steroid does have a strong
level of resistance to hepatic breakdown, however, and severe liver toxicity has
been noted in bodybuilders abusing trenbolone.
576 Although unlikely,
hepatotoxicity cannot be completely excluded, especially with high doses.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Due to its nonaromatizable nature and strong resistance to metabolism, trenbolone has a
moderate to strong (negative) impact on lipid values and atherogenic risk.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention. In experimental studies, trenbolone
was determined to be approximately three times stronger at suppressing
gonadotropins than testosterone on a milligram for milligram basis.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
Trenbolone hexahydrobenzylcarbonate was generally administered in a clinical
dosage of 3 ampules per month. Therapy was initiated the first month with all 3
ampules given over the first 15 days. During the subsequent 3 months, one
injection (76 mg) was given every 10 days. For physique-or performanceenhancing purposes, trenbolone hexahydrobenzylcarbonate is most often
administered at a dosage of 152-220 mg per week. The drug would be taken in
cycles ranging from 6 to 12 weeks. Although a weekly administration schedule
would be more than sufficient, athletes usually injected a single ampule (76mg)
at a time, and the total amount would be spread evenly throughout the week.
Although not necessary, this type of schedule helps to reduce injection volume
per application. The results with the use of trenbolone
hexahydrobenzylcarbonate should be a visibly more muscular physique (larger,
leaner), and, if body fat levels are low enough, that hard ripped look most valued
by dieting and competitive bodybuilders.
While this drug is quite potent when used alone, it is sometimes combined with
other steroids for an even greater effect. Leading up to a show one could
successfully add a non-aromatizing anabolic such as Winstrol® or Primobolan®.
Such combinations will elicit a greater level of density and hardness to the build,
often proving dramatic for a stage appearance. We could also look for bulk with
this drug, and addition stronger compounds like Dianabol or Testosterone. While
the mass gain would be quite formidable with such a stack, some level of water
retention would probably also accompany it. Moderately effective anabolics
such Deca-Durabolin® or Equipoise® would be somewhat of a halfway point,
providing extra strength and mass but without the same level of water bloat we
see with more readily aromatized steroids.
Administration (Women):
Trenbolone hexahydrobenzylcarbonate was generally administered in a clinical
dosage of 3 ampules per month. Therapy was initiated the first month with all 3
ampules given over the first 15 days. During the subsequent 3 months, one
injection (76mg) was given every 10 days. Given the risk of virilization, lower
doses were likely used by physicians with many female patients. This agent is
generally not recommended for women for physique-or performance-enhancing
purposes due to strong androgenic nature and tendency to produce virilizing side
effects.
Availability:
Pharmaceutical preparations containing trenbolone hexahydrobenzylcarbonate
remain scarce. In reviewing some of the remaining products and changes in the
global pharmaceutical market, we have made the following observations.
Balkan Pharmaceuticals (Moldova) makes the product Parabolan. It contains 100
mg/mL of steroid, and is packaged in 1 mL ampules and multi-dose vials of 5
mL and 10 mL.
Primobolan® (methenolone acetate)
Description:
Primobolan® is a brand name for the anabolic steroid methenolone acetate. This
agent is very similar in action to Primobolan® Depot (methenolone enanthate),
except here the drug is designed for oral administration instead of injection.
Methenolone acetate is a non-c17-alpha-alkylated oral steroid, one of only a few
commercially available oral agents that presents limited liver toxicity to the user.
It is also highly favored for its properties as a moderately effective anabolic with
low androgenic and no estrogenic properties. It is, likewise, commonly used
during cutting phases of training, when lean tissue growth and solid muscularity,
not raw bulk, are the key objectives.
History:
Methenolone was first described in 1960.
577 Squibb would introduce the drug (as
methenolone acetate) to the United States in 1962.
578 This agent was sold for a
very short time as a 20 mg tablet, under the brand name of Nibal®. Schering in
West Germany (now Bayer) would be granted rights to the drug that same year,
and would sell it under the Primobolan® name. Nibal® was soon removed from
the U.S. market, never to return as a commercial product. Schering now had
exclusive patent rights to produce methenolone acetate, and would continue to
sell the drug uninterrupted since 1962, and consumers had naturally come to
identify methenolone acetate as a product of Schering.
Primobolan® has always been identified as a European steroid, and during the
1960’s and ’70’s was being offered for sale in such countries as Germany,
Austria, Belgium, France, the Netherlands, and Finland. At one time Schering
also manufactured a 20 mg/ml oil-based injectable of methenolone acetate in
limited markets (called Primobolan® Acetate), but it has been out of
manufacture since 1993. Injectable methenolone acetate proved to be very
popular for pre-contest cutting use, and was gravely missed among European
competitors when discontinued. Although we still have the acetate in oral form,
it is a close, but not equal, substitute (injection is a much more efficient form of
delivery for this steroid).
Primobolan® is prescribed as a lean tissue building anabolic agent, often used in
cases where body wasting has occurred secondary to major surgery, infection,
wasting disease, aggressive corticosteroid administration, or malnutrition. (Some
clinicians also prescribe this agent for treating osteoporosis and sarcopenia, or
the natural loss of muscle mass with aging). This steroid has also been used to
promote weight gain in underweight premature infants and children in clinical
studies, and was able to do so effectively and without signs of toxicity or
undesirable effects.
579 Athletes have long favored the combined strong anabolic,
weak androgenic, and non-estrogenic nature of this drug, which makes it very
desirable for building lean muscularity without side effects.
Although Primobolan® demonstrated a good record of clinical safety, Schering
had withdrawn this drug from most markets by the early 2000s. No 50 mg
versions are still in manufacture, and at most a select couple of products
containing 5 mg or 25 mg may still be in circulation. The only confirmed
sources for oral brand name Primobolan in recent years were in Japan and South
Africa, and these were sold under the Schering name. It is unknown if any such
products have been brought over to the new Bayer label. Aside from this, a very
small number of pharmaceutical preparations containing methenolone acetate
may still be in production.
How Supplied:
All forms of Schering Primobolan® contain 5 mg, 25 mg, or 50 mg (no longer
available) of methenolone acetate per tablet. Composition and dosage of other
brands may vary by country and manufacturer.
Structural Characteristics:
Methenolone is a derivative of dihydrotestosterone. It contains one additional
double bond between carbons 1 and 2, which helps to stabilize the 3-keto group
and increase the steroid’s anabolic properties, and an additional 1-methyl group,
which protects the steroid against hepatic metabolism. Primobolan makes use of
methenolone with a carboxylic acid ester (acetic acid) attached to the 17-beta
hydroxyl group to further help protect it from oxidation during oral
administration. Studies have demonstrated the methenolone is an effective oral
anabolic agent in both the acetate and unesterified forms.
580 581
Side Effects (Estrogenic):
Methenolone is not aromatized by the body,
582 and is not measurably estrogenic.
Estrogen-linked side effects should not be seen when administering this steroid.
Sensitive individuals need not worry about developing gynecomastia, nor should
they be noticing any appreciable water retention with this drug. The increase
seen with methenolone should be quality muscle mass, not the smooth bulk that
often accompanies steroids open to aromatization. During a cycle, the user
should additionally not notice strong elevations in blood pressure, as this effect
is also related (generally) to estrogen and water retention. Methenolone is a
steroid most favored during cutting phases of training, when water and fat
retention are major concerns, and sheer mass not the central objective.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance. This may include bouts of oily skin, acne, and
body/facial hair growth. Anabolic/androgenic steroids may also aggravate male
pattern hair loss. Women are warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement. Methenolone is still a very mild steroid, however, and strong
androgenic side effects are typically related to higher doses. Women often find
this preparation an acceptable choice, observing it to be a very comfortable and
effective anabolic.
Side Effects (Hepatotoxicity):
Methenolone is not considered a hepatotoxic steroid; liver toxicity is unlikely.
Studies have failed to produce appreciable changes in markers of hepatic stress
when the drug was given in therapeutic levels.
583 This steroid does have some
resistance to hepatic breakdown, however, and liver toxicity, failure, and death
was reported in one elderly patient receiving oral methenolone acetate.
584
Although unlikely, hepatotoxicity cannot be completely excluded, especially
with very high oral doses.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Methenolone
should have a stronger negative effect on the hepatic management of cholesterol
than testosterone or nandrolone due to its non-aromatizable nature, but a much
weaker impact than c-17 alpha alkylated steroids. Due to the route of delivery,
oral methenolone will have a slightly stronger negative effect on lipids compared
to methenolone enanthate injections. Anabolic/androgenic steroids may also
adversely affect blood pressure and triglycerides, reduce endothelial relaxation,
and support left ventricular hypertrophy, all potentially increasing the risk of
cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention. Primobolan® is generally described as
having a low impact on endogenous testosterone production. While this may be
true in small clinical doses (20-25 mg daily), this may not be a major distinction
when used for physique-or performance-enhancing purposes. In one study, more
than half of the patients receiving only 30-45 mg per day noticed a 15-65%
suppression of gonadotropin levels.
585 While this is far from having no hormonal
impact, the suppression caused by methenolone acetate may still be less
pronounced than with many other agents. If Primobolan® is used at moderate
doses for less than 8 weeks, hormonal recovery should not be a protracted
experience.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
586 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, this steroid should be taken on an empty stomach.
Administration (Men):
The prescribing guidelines for Primobolan® recommend a maximum daily
dosage of 100-150 mg per day. The usual administration protocols for physiqueor performance-enhancing purposes call for 75-150 mg daily, which is taken for
6 to 8 weeks. This level is sufficient to impart a measurable anabolic effect,
although one usually doesn’t expect to achieve great gains in muscle mass with
this drug. Instead, Primobolan® is utilized when the athlete has a specific need
for a mild anabolic agent, most notably in cutting phases of training.
Due to its mild nature, Primobolan® is often used in conjunction with other
steroids for a stronger effect. In such cases, a slightly lower dose is often used
(50-100 mg per day). During a dieting or cutting phase, thought to be its primary
application, a non-aromatizing androgen like Halotestin® or trenbolone is often
added. Such combinations would enhance the physique without water retention,
and help bring out a harder and more defined look of muscularity. Nonaromatizing androgen/anabolic stacks like this are very popular among
competing bodybuilders, and prove quite reliable for rapidly improving the
contest form. This compound is also occasionally used with more potent
androgens during bulking phases of training. The addition of testosterone,
Dianabol or Anadrol 50® is common, although the gains are often accompanied
by some level of smoothness due to the added estrogenic component, as well as
hepatotoxicity in the case of the latter two agents.
Administration (Women):
The prescribing guidelines for Primobolan® do not offer separate dosing
recommendations for women, although it is indicated that women who are
pregnant, or may become pregnant, should not use the drug. Female athletes
generally respond well to 50-75 mg daily, with no signs of virilization
symptoms. One would not expect a tremendous amount of muscle mass with this
drug, and instead find a slow and steady (quality) increase. Some women choose
to further add-in other anabolics such as Winstrol® or oxandrolone, in an effort
to increase the muscle-building effectiveness of a cycle. While both of these
compounds are quite tolerable, one must be sure not to use too high an
accumulated dosage. Taken at too high a dosage, these weak anabolics can
quickly cause masculinizing side effects.
Availability:
Pharmaceutical preparations containing methenolone acetate remain scarce. The
drug has been unavailable in western nations for many years now, and the bulk
of the supply presently comes from underground steroid manufacturers. In
reviewing some of the remaining products and changes in the global
pharmaceutical market, we have made the following observations.
Balkan Pharmaceuticals produces Primobol in Moldova. It comes in 50 mg
tablets, with 20 sealed in each foil and plastic strip.
Primobolan® Depot (methenolone enanthate)
Description:
Primobolan® Depot is an injectable version of the steroid methenolone. This is
the same constituent in Primobolan® orals (methenolone acetate), although here
an enanthate ester is used to slow the steroid’s release from a site of injection.
Methenolone enanthate offers a similar pattern of steroid release as testosterone
enanthate, with blood hormone levels remaining markedly elevated for
approximately 2 weeks. Methenolone itself is a moderately strong anabolic
steroid with very low androgenic properties. Its anabolic effect is considered to
be slightly less than Deca-Durabolin® (nandrolone decanoate) on a milligram
for milligram basis. Methenolone enanthate is most commonly used during
cutting cycles, when lean mass gain, not a raw mass increase, is the main
objective.
History:
Methenolone was first described in 1960.
567 Squibb introduced the drug (as
methenolone enanthate) to the U.S. prescription drug market in 1962,
568 sold for
a very short time in the U.S. under the brand name of Nibal® Depot. Rights to
the drug were given to Schering in West Germany (now Bayer) that same year,
and Nibal® Depot soon disappeared from the U.S. market. Schering would sell
methenolone enanthate under its new and ultimately most recognizable brand
name, Primobolan® Depot. During the 1960s and ’70’s Primobolan® Depot was
available mainly in Europe, including such countries as Switzerland, Italy,
Germany, Austria, Belgium, France, Portugal, and Greece.
Schering maintained patent control over methenolone enanthate until the late
1970s. Before its patents expired, Schering had rigorously protected its
intellectual property rights against any potential infringement, even in the U.S.
market, where the company had not been marketing Primobolan Depot.
Although methenolone enanthate has not been available for commercial sale in
the United States for decades, it has technically retained its status as an FDAapproved drug.
Primobolan Depot is typically prescribed as a lean tissue building anabolic
agent, often used in cases where body wasting has occurred secondary to an
operation, prolonged infection, wasting disease, aggressive corticosteroid
administration, or convalescence. Some clinicians also prescribe this agent for
treating osteoporosis, sarcopenia (the natural loss of muscle mass with aging),
certain cases of chronic hepatitis, and breast carcinoma (usually as a secondary
medication following other therapies). The steroid has also been used to promote
weight gain in underweight premature infants and children in clinical studies,
and was able to do so effectively and without signs of toxicity or undesirable
effects.
569 Athletes have long favored the combined strong anabolic, weak
androgenic, and non-estrogenic nature of this drug, which makes it very
desirable for building lean muscularity without side effects.
Although Primobolan Depot demonstrated a good record of clinical safety, by
the 1990s Schering had grown to be a multinational pharmaceutical giant, and
was inevitably forced to reexamine its global steroid offerings in light of public
concerns about sports doping. Primobolan Depot would be voluntarily
withdrawn from most of the countries that had originally sold it. Today, the
brand is sold in just a handful of countries including Spain, Turkey, Japan,
Paraguay, and Ecuador. In spite of its limited supply, Bayer has remained
(nearly) the exclusive producer of methenolone enanthate in the human drug
business worldwide. In recent years, however, methenolone enanthate has shown
up in a small number of other preparations, most from underground or exportonly companies.
How Supplied:
All forms of Bayer Primobolan® Depot are packaged in 1 mL glass ampules and
contain 100 mg of methenolone enanthate. Composition and dosage of other
brands may vary by country and manufacturer.
Structural Characteristics:
Methenolone is a derivative of dihydrotestosterone. It contains one additional
double bond between carbons 1 and 2, which helps to stabilize the 3-keto group
and increase the steroid’s anabolic properties, and an additional 1-methyl group,
which gives the steroid some protection against hepatic metabolism. Primobolan
Depot makes use of methenolone with a carboxylic acid ester (enanthoic acid)
attached to the 17-beta hydroxyl group. Esterified steroids are less polar than
free steroids, and are absorbed more slowly from the area of injection. Once in
the bloodstream, the ester is removed to yield free (active) methenolone.
Esterified steroids are designed to prolong the window of therapeutic effect
following administration, allowing for a less frequent injection schedule
compared to injections of free (unesterified) steroid.
Side Effects (Estrogenic):
Methenolone is not aromatized by the body,
570 and is not measurably estrogenic.
Estrogen-linked side effects should not be seen when administering this steroid.
Sensitive individuals need not worry about developing gynecomastia, nor should
they be noticing any appreciable water retention with this drug. The increase
seen with methenolone should be quality muscle mass, not the smooth bulk that
often accompanies steroids open to aromatization. During a cycle, the user
should additionally not notice strong elevations in blood pressure, as this effect
is also related (generally) to estrogen and water retention. Methenolone is a
steroid most favored during cutting phases of training, when water and fat
retention are major concerns, and sheer mass not the central objective.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
possible with this substance. This may include bouts of oily skin, acne, and
body/facial hair growth. Anabolic/androgenic steroids may also aggravate male
pattern hair loss. Women are warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement. Methenolone is still a very mild steroid, however, and strong
androgenic side effects are typically related to higher doses. Women often find
this preparation an acceptable choice, observing it to be a very comfortable and
effective anabolic.
Side Effects (Hepatotoxicity):
Methenolone is not considered a hepatotoxic steroid; liver toxicity is unlikely.
Studies have failed to produce appreciable changes in markers of hepatic stress
when the drug was given in therapeutic levels.
571
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Methenolone
should have a stronger negative effect on the hepatic management of cholesterol
than testosterone or nandrolone due to its non-aromatizable nature, but a much
weaker impact than c-17 alpha alkylated steroids. Anabolic/androgenic steroids
may also adversely affect blood pressure and triglycerides, reduce endothelial
relaxation, and support left ventricular hypertrophy, all potentially increasing the
risk of cardiovascular disease and myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention. At a moderate dosage of 100-200 mg
weekly, methenolone should offer measurably less testosterone suppression than
an equal dose of nandrolone or testosterone, due to its non-aromatizable nature.
If used for less than eight weeks, hormonal recovery should not be a protracted
experience.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
The prescribing guidelines for Primobolan Depot recommend a maximum
dosage of 200 mg at the onset of therapy, and a continuing dosage of 100 mg
every week. Prolonged administration protocols generally call for a 100 mg
dosage every 1-2 weeks, or 200 mg every 2-3 weeks. The usual administration
protocols among male athletes call for a 200-400 mg per week dosage, which is
taken for 6 to 12 weeks, which is sufficient to promote very noticeable increases
in lean muscle tissue. It is, however, not unusual to see the drug taken in doses
as high as 600 mg per week or more, although such amounts are likely to
highlight a more androgenic side of methenolone, as well as exacerbate its
negative effects on serum lipids.
Methenolone enanthate is often stacked with other (typically stronger) steroids in
order to obtain a faster and more enhanced effect. During a dieting or cutting
phase, a non-aromatizing androgen like Halotestin® or trenbolone can be added.
The stronger androgenic component here should help to bring about an added
density and hardness to the muscles. On the other hand, one might add another
mild anabolic steroid such as stanozolol. The result of such a combination
should again be a notable increase in muscle mass and hardness, which still
should not be accompanied by greatly increased side effects. Methenolone
enanthate is also used effectively during bulking phases of training. In such a
scenario, the addition of testosterone or boldenone would prove quite effective
for adding new muscle mass without presenting any notable hepatotoxicity to the
user.
Administration (Women):
The prescribing guidelines for Primobolan® Depot do not offer separate dosing
recommendations for women, although it was indicated that women who were
pregnant, or may become pregnant, should not use the drug. Female athletes
generally respond well to a dosage of 50-100 mg per week. If both oral and
injectable versions are available, the oral is often given preference, as it allows
for greater control over blood hormone levels. Additionally, some women
choose to include Winstrol® Depot (25 mg twice per week) or Oxandrolone
(7.5-10 mg daily), and with it receive a greatly enhanced anabolic effect.
Androgenic activity can be a concern with such dosing, however, and should be
monitored closely. If stacking, it would be best to use a much lower starting
dosage for each drug than if they were to be used alone. This is especially good
advice if you are unfamiliar with the effect such a combination may have on
you. A popular recommendation would also be to first experiment by stacking
with oral Primobolan®, and later venture into the injectable if this is still
necessary.
Availability:
Pharmaceutical preparations containing methenolone enanthate remain scarce.
The bulk of the supply for this compound comes from underground steroid
manufacturers. In reviewing some of the remaining products and changes in the
global pharmaceutical market, we have made the following observations.
Bayer took control of Schering AG in December 2006. Following this
acquisition, the Schering Primobolan Depot products were transitioned over to
the Bayer brand and logo. The company produces the drug in limited markets
only, most notably Turkey and Spain. These products have historically been the
subject of large volume counterfeiting, however, so consumers should be
especially careful with brand name Primobolan Depot products.
Balkan Pharmaceuticals (Moldova) makes the product Primobol. It is prepared
in both 1 mL ampules and multi-dose vials.
Proviron® (mesterolone)
Description:
Proviron® is Schering’s (now Bayer’s) brand name for the oral androgen
mesterolone (1-methyl dihydrotestosterone). Similar to dihydrotestosterone,
mesterolone is a strong androgen with only a weak level of anabolic activity.
This is due to the fact that like dihydrotestosterone, mesterolone is rapidly
reduced to inactive diol metabolites in muscle tissue where concentrations of the
3-hydroxysteroid dehydrogenase enzyme are high. The belief that the weak
anabolic nature of this compound indicates a tendency to block the androgen
receptor in muscle tissue, thereby reducing the gains of other more potent
muscle-building steroids, should likewise not be taken seriously. In fact, due to
its extremely high affinity for plasma binding proteins such as SHBG,
mesterolone may actually work to potentate the activity of other steroids by
displacing a higher percentage into a free, unbound state. Among athletes,
mesterolone is primarily used to increase androgen levels when dieting or
preparing for a contest, and as an anti-estrogen due to its intrinsic ability to
antagonize the aromatase enzyme.
History:
According to company literature, Schering developed Proviron® in 1934,
making this is an extremely old medication as far as anabolic/androgenic
steroids. Schering also states that it was the first medication put into clinical
practice for the treatment of “hormone-related diseases and complaints in men.
”Accordingly, mesterolone would have been developed around the same time as
methyltestosterone (1935) and testosterone propionate (1937), which are both
very old agents generally considered obsolete by today’s standards. In spite of its
age, Proviron has a long history of clinical effectiveness and safety, and remains
in widespread clinical use today. It is generally prescribed to males for the
treatment of declining physical and mental capacity caused by age and
subnormal androgen levels, low libido caused by insufficient androgen levels,
hypogonadism (in pre-and post-pubescent males), and infertility (in certain
situations mesterolone increases the quality and quantity of sperm).
The use of mesterolone as a fertility aid is perhaps one of the most controversial
indications for this drug considering that anabolic/androgenic steroids are
generally linked to infertility. It is also a use of mesterolone that is quite often
misunderstood by athletes. Mesterolone is applicable here because it is an
effective androgen that offers minimal suppression of gonadotropins in normal
therapeutic doses, not because it increases LH output. Absent gonadotropin
suppression, the drug may supplement androgenicity necessary for sperm
production. It is well understood that androgens have direct stimulatory effects
on spermatogenesis, and also influence the transportation and maturation of
sperm via effects on the epididymis, ductus deferens, and seminal vesicles. So
the role of these hormones is not entirely suppressive. Mesterolone seems to
have a unique positive influence on certain cases of male fertility because its
potential stimulatory effects on sperm quantity and quality are not overridden by
the suppression of gonadotropins.
Mesterolone is widely manufactured by Bayer (formerly Schering), which
currently sells the drug in more than thirty countries worldwide. The most
common brand name used for its sale is Proviron, although Schering/Bayer has
sold the agent under other names in certain markets, including Mestoranum and
Provironum. Additionally, other manufacturers have sold mesterolone over the
years, appearing under such brand names as Pluriviron (Asche, Germany),
Vistimon (Jenepharm, Germany), and Restore (Brown & Burke, India). In spite
of its long track record of safety and efficacy, mesterolone was never approved
for sale in the United States. It remains available in many Western nations,
however. Bayer remains the major (almost exclusive) global supplier of
mesterolone today, although on rare occasion other brands of the drug can be
located.
How Supplied:
Mesterolone is widely available in human drug markets. Composition and
dosage may vary by country and manufacturer; preparations generally contain 25
mg or 50 mg of steroid per tablet.
Structural Characteristics:
Mesterolone is a modified form of dihydrotestosterone. It differs by the addition
of a methyl group at carbon 1, which helps protect the hormone from hepatic
metabolism during oral administration. The same structural modification is also
used with oral Primobolan® (methenolone) tablets. Alkylation at the one
position slows hepatic metabolism of the steroid during the first pass, although
much less profoundly than c-17 alpha alkylation. Mesterolone is resistant
enough to breakdown to allow therapeutically beneficial blood levels to be
achieved, although the overall bioavailability remains much lower than c-17
alpha alkylated oral steroids. Mesterolone also has a very strong binding affinity
for Sex Hormone Binding Globulin.
572 This may act to displace other steroids
more weakly bound to SHBG into a free (active) state.
Side Effects (Estrogenic):
Mesterolone is not aromatized by the body, and is not measurably estrogenic. An
anti-estrogen is not necessary when using this steroid, as the drug is unlikely to
induce gynecomastia, water retention, or other estrogen-related side effects.
Mesterolone is actually believed to act as an anti-aromatase in the body,
preventing or slowing the conversion of steroids into estrogen. The result is
somewhat comparable to Arimidex®, although less profound. The antiestrogenic properties of mesterolone are not unique, and a number of other
steroids have demonstrated similar activity. Dihydrotestosterone and Masteron
(2-methyl-dihydrotestosterone), for example, have been successfully used as
therapies for gynecomastia and breast cancer due to their strong androgenic and
potentially anti-estrogenic effect. It has also been suggested that nandrolone may
even lower aromatase activity in peripheral tissues where it is more resistant to
estrogen conversion (the most active site of nandrolone aromatization seems to
be the liver). The anti-estrogenic effect of all of these compounds is presumably
caused by their ability to compete with other substrates for binding to the
aromatase enzyme. With the aromatase enzyme bound to the steroid, yet being
unable to alter it, an inhibiting effect is achieved as it is temporarily blocked
from interacting with other hormones.
Side Effects (Androgenic):
Mesterolone is classified as an androgenic steroid. Androgenic side effects are
common with this substance, especially with higher doses. This may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are also warned of
the potential virilizing effects of anabolic/androgenic steroids. These may
include a deepening of the voice, menstrual irregularities, changes in skin
texture, facial hair growth, and clitoral enlargement. Additionally, the 5-alpha
reductase enzyme does not metabolize mesterolone, so its relative androgenicity
is not affected by finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Mesterolone is not c17-alpha alkylated, and not known to produce hepatotoxic
effects; liver toxicity is unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Mesterolone is an
oral non-aromatizable androgen, and expected to have a notable negative effect
on lipids. Studies administering 100 mg of mesterolone per day to hypogonadal
men for approximately 6 months demonstrated a significant increase in total
cholesterol (18.8%) and LDL cholesterol (65.2%), accompanied by a significant
decrease in HDL cholesterol (-35.7%).
573
Mesterolone should not be used when cardiovascular risk factors preclude the
use of other oral steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
Mesterolone has a very weak suppressive effect on gonadotropins and serum
testosterone. Studies show that when given in moderate doses (150 mg per day
or less), significant suppression of testosterone levels does not occur.
574
In
studies with higher doses (300 mg per day and above), the agent strongly
suppressed serum testosterone.
575
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
To treat androgen insufficiency, mesterolone is usually given in a dose of 1
tablet (25 mg) three times per day at the initiation of therapy. The drug is later
continued at a lower maintenance dose, which usually consists of taking 1 tablet
(25 mg) one to two times per day. Similar doses are used to support male
fertility, usually in conjunction with other fertility drugs like injectable FSH. The
usual dosage among male athletes is between 50 mg and 150 mg of mesterolone
per day, or two to six 25 mg tablets. The drug is typically taken in cycles of 6-12
weeks in length, which is usually a sufficient period of time to notice the
benefits of drug therapy.
Many bodybuilders favor the use of mesterolone during dieting phases or contest
preparation, when low estrogen and high androgen levels are particularly
desirable. This is especially beneficial when anabolics like Winstrol®, Anavar,
or Primobolan® are being used alone, as the androgenic content of these drugs is
relatively low. Mesterolone can be effectively used here to adjust the androgen
to estrogen ratio upwards, bringing about an increase in the hardness and density
of the muscles, supporting libido and general sense of well being, and increasing
the tendency to burn body fat. It is also commonly used (at a similar dosage) to
prevent gynecomastia when other aromatizable steroids are being administered,
often in conjunction with 10-20 mg per day of Nolvadex.
Administration (Women):
Mesterolone is not approved for use in women. This agent is not recommended
for women for physique-or performance-enhancing purposes due to its strong
androgenic nature and tendency to produce virilizing side effects. Some women
do favor the drug, however, and find a single 25 mg tablet enough to efficiently
shift the hormone balance in the body, greatly impacting the look of definition to
the physique. Intake is usually limited to no longer than four or five weeks in
such situations to minimize the chance of developing lasting virilizing effects.
One tablet used in conjunction with 10 or 20 mg of Nolvadex® can be even
more efficient for muscle hardening, creating an environment here the body is
much more inclined to burn off extra body fat, especially in female trouble areas
like the hips and thighs. Extreme caution should be taken with such use,
however.
Availability:
Mesterolone remains widely available, the vast majority of products made by or
under license from Schering (now Bayer). In reviewing some of the more
popular products and changes on the global pharmaceutical market, we have
made the following observations.
Bayer took control of Schering AG in December 2006. Following this
acquisition, the Schering Proviron products have been transitioned over to the
Bayer brand and logo.
Bayer no longer markets Proviron in Egypt. The drug remains available under
the Cidoviron name, produced by the domestic firm CID (Chemical Industries
Development).
Unigen markets the product Mesviron in Thailand. It contains 25 mg per tablet,
and is packaged in foil and plastic strips of 10 tablets each (5 strips per box).
Due to its limited demand, mesterolone products have traditionally not been the
subjects of high volume counterfeiting. When located on the black market, they
can usually be trusted so long as they are properly packaged from a known
manufacturer.
Sten (testosterone cypionate & propionate)
Description:
Sten is a two-component testosterone blend from Mexico that contains a mixture
of testosterone propionate (25 mg), testosterone cypionate (75 mg), and DHEA
(dehydroepiandrosterone; 20 mg) in a 2 mL ampule. Some references incorrectly
list this product as containing 20 mg of DHT (dihydrotestosterone), which would
be a third androgen. This is, however, just a confusion of the Spanish word for
DHEA (dehidroisoandrosterona), which at a quick glance looks similar to
“dihydrotestosterona.” More recent packaging lists this ingredient as the less
confusing “prasterona”(prasterone; another accepted term for DHEA). Holding
the DHEA irrelevant at the moment, this steroid product contains a simple 50
mg/ml mixture of two common testosterone esters.
Many consider Sten to be a low-budget alternative to Sustanon® 250. While it
does contain a blend of two testosterone esters, Sten is not as slow-acting in
comparison. The longest ester of testosterone it uses is cypionate, which allows
testosterone levels to return to baseline approximately 2 weeks after injection.
Testosterone cypionate is also not a delayed-onset drug, so Sten doesn’t offer
much advantage in regards to a “sustained-release” effect. The testosterone
propionate only compounds the initial testosterone spike, making its
pharmacokinetic profile more uneven than if testosterone cypionate were used
alone. Of course Sten and Sustanon® are both testosterone products, so given
equivalently dosed weekly injections the end result should not be very different
between the two.
History:
Sten is made in Mexico by the pharmaceutical firm Atlantis, S.A. de C.V. This
agent is used primarily to correct low androgen levels in males, for the treatment
of hypogonadism, andropause, and impotence. It is also sometimes prescribed to
women for excessive lactation, advanced breast cancer, and low sex drive. Sten
has a long history of sale on the Mexican market, where it is one of the country’s
more inexpensive human-use testosterone products. It has consequently
remained a somewhat popular item there, even if its formulation may not be the
most properly suited for the higher-dosed requirements of athletic use.
How Supplied:
Sten is available on the human drug market in Mexico. It contains a blend of 25
mg/75 mg testosterone propionate and testosterone cypionate (respectively) per
2-milliliter ampule.
Structural Characteristics:
Sten contains a mixture of two testosterone compounds, which where modified
with the addition of carboxylic acid esters (propionic and cyclopentylpropionic
acids) at the 17-beta hydroxyl group. Esterified forms of testosterone are less
polar than free testosterone, and are absorbed more slowly from the area of
injection. Once in the bloodstream, the ester is removed to yield free (active)
testosterone. Esterified forms of testosterone are designed to prolong the window
of therapeutic effect following administration, allowing for a less frequent
injection schedule compared to injections of free (unesterified) steroid. Sten is
designed to provide a rapid peak in testosterone levels (24-48 hours after
injection), and maintain physiological concentrations for approximately 14 days.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone more likely to require the
concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention
and loss of muscle definition are common with higher doses of testosterone, this
drug is usually considered a poor choice for dieting or cutting phases of training.
Its moderate estrogenicity makes it more ideal for bulking phases, where the
added water retention will support raw strength and muscle size, and help foster
a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
576
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely effect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
577 Studies using 300 mg of testosterone ester
(enanthate) per week for twenty weeks without an aromatase inhibitor
demonstrated only a 13% decrease in HDL cholesterol, while at 600 mg the
reduction reached 21%.
578 The negative impact of aromatase inhibition should
be taken into consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less per week, the impact on lipid
profile tends to be noticeable but not dramatic, making an anti-estrogen (for
cardioprotective purposes) perhaps unnecessary. Doses of 600 mg or less per
week have also failed to produce statistically significant changes in LDL/VLDL
cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive protein, and insulin
sensitivity, all indicating a relatively weak impact on cardiovascular risk
factors.
579 When used in moderate doses, injectable testosterone esters are
usually considered to be the safest of all anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Testosterone propionate is often regarded as a painful injection. This is due to
the very short carbon chain of the propionic acid ester, which can be irritating to
tissues at the site of injection. Many sensitive individuals choose to stay away
from this steroid completely, their bodies reacting with a pronounced soreness
and low-grade fever that may last for a few days after each injection.
Administration (Men):
For the treatment of low androgen levels, the prescribing guidelines for Sten
recommend one injection of one 2 mL ampule (100 mg testosterone esters; 20
mg DHEA) every 15-30 days. For bodybuilding purposes, this drug is usually
injected on a weekly basis, in a dosage of 2-4 ampules (200-400 mg of
testosterone esters in total). This level is sufficient to provide excellent gains in
muscle size and strength. Higher doses are possible, but even the injection
volume needed with 4 ampules per week (8ml) can become too uncomfortable
for many. Testosterone drugs are ultimately very versatile, and can be combined
with many other anabolic/androgenic steroids depending on the desired effect.
Administration (Women):
The prescribing guidelines for Sten do not make special dosing
recommendations for women, except to say that androgenic symptoms may
occur, and in certain scenarios therapy should be suspended until symptoms
resolve, and after a lower dose used. This drug is not recommended for women
for physique-or performance-enhancing purposes due to its strong androgenic
nature, tendency to produce virilizing side effects, and slow acting
characteristics (making blood levels difficult to control).
Availability:
Sten is commonly found in Mexico, where 2 pre-loaded syringes are packaged in
a box and usually sell for about $10 in the pharmacy.
Striant® (testosterone)
Description:
Striant® is a mucoadhesive buccal testosterone delivery system. It is prepared in
the form of a small (aspirin-sized) tablet, which contains 30 mg of (free)
testosterone. The tablet is not taken orally, but is affixed to the gums, where it
transfers testosterone across the inner lining of the cheek and into the
bloodstream. The buccal delivery of anabolic/androgenic steroids is not new, and
has been used in the past (with limited success) on agents like
methyltestosterone and testosterone propionate. The adhesive Striant system,
however, is an improvement over the old rapidly dissolving buccal tablets, as it
is much more stable in the mouth (it stays affixed for 12 hours and needs to be
removed). As such, it provides a much more prolonged and efficacious delivery
of hormone in comparison. Twice daily dosing is enough to maintain
physiological hormone levels over a 24-hour period.
History:
Striant® was developed in the United States by Columbia Laboratories. It was
approved by the FDA for sale as a prescription drug in June of 2003, and is
indicated for use in men with conditions associated with a deficiency or absence
of endogenous testosterone. With this product, Columbia was likely trying to
target those hormone replacement therapy (HRT) consumers that do not
welcome biweekly injections, and find patches and gels uncomfortable or
cosmetically objectionable. Striant was shipped to pharmacies in late 2003, and
quickly met with mixed reviews. Some patients find it a very convenient option
for HRT, while others find the oral tablets too uncomfortable to use for long
periods of time. Striant was released in the UK in 2004 under the Striant SR
(Sustained Release) brand name, licensed and sold by Ardana Bioscience.
Columbia’s partnership with Ardana expects to see sale of Straint in 18
European markets.
How Supplied:
Striant® mucoadhesive buccal testosterone delivery system is available in
various human drug markets. Product comes in the form of a small buccal tablet;
usually packaged in strips of 10 tablets, 6 strips to a box.
Structural Characteristics:
Striant® mucoadhesive buccal testosterone delivery system is a buccal tablet
containing 30 mg of (free) testosterone. The system is adhered to the inside of
the mouth, where the gum meets the upper lip above the incisor teeth.With
exposure to saliva the tablet softens into a gel-like consistency, which can stay in
place for 12 hours. The product delivers physiological concentrations of
testosterone through the mucous membrane, where it is absorbed into the
bloodstream via the superior vena cava (major blood vessel), bypassing the liver.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. Exceeding therapeutic doses will increase the
likelihood of estrogenic side effects. In such cases, an anti-estrogen such as
clomiphene citrate or tamoxifen citrate is commonly applied to prevent
estrogenic side effects. One may alternately use an aromatase inhibitor like
Arimidex® (anastrozole), which more efficiently controls estrogen by
preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Exceeding normal therapeutic doses is
likely to produce androgenic side effects including oily skin, acne, and
body/facial hair growth. Men with a genetic predisposition for hair loss
(androgenetic alopecia) may notice accelerated male pattern balding. Women are
warned of the potential virilizing effects of anabolic/androgenic steroids,
especially with a strong androgen such as testosterone. These may include
deepening of the voice, menstrual irregularities, changes in skin texture, facial
hair growth, and clitoral enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
580
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction. Therapeutic doses of testosterone used to correct
insufficient androgen production in otherwise healthy aging men are unlikely to
increase atherogenic risk, and may actually reduce the risk of cardiovascular
mortality.
581
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
The Striant mucoadhesive buccal testosterone delivery system is placed on the
gums just above the incisor tooth. It is left affixed for 12 hours, at which point it
is carefully removed. The product is usually administered twice daily. The
application site should be rotated between left and right sides of the mouth with
each dose.
Administration (Men):
To treat androgen insufficiency, the prescribing guidelines for Striant
recommend administering one buccal tablet twice daily. Doses are given once in
the morning and once at night, 12 hours apart. For physique-or performanceenhancing purposes, higher doses would be necessary to achieve
supraphysiological levels of testosterone. This will be difficult, if not
impractical, given the method of delivery. Such use would require a minimum of
4 systems per day, a level sufficient for most users to notice significant gains in
muscle size and strength, but not much comfort. Lower (therapeutic) doses may
be effective when accompanied by other anabolic/androgenic steroids.
Testosterone is ultimately very versatile, and can be combined with many other
anabolic/androgenic steroids to tailor the desired effect.
Administration (Women):
The Striant mucoadhesive buccal testosterone delivery system is not FDAapproved for use in women. Testosterone is not recommended for women for
physique-or performance-enhancing purposes due to its strong androgenic nature
and tendency to produce virilizing side effects.
Availability:
Given its high relative price and low delivery of testosterone, Striant is not
commonly traded on the black market. Counterfeits have not yet been reported.
Sustanon® 100 (testosterone blend)
Description:
Sustanon® 100 is an oil-based injectable testosterone blend that contains three
different testosterone esters: testosterone propionate (20 mg); testosterone
phenylpropionate (40 mg); and testosterone isocaproate (40 mg). This product is
manufactured by Organon, and is essentially a lower dosed version of their
Sustanon® 250. Like Sustanon® 250, Sustanon® 100 makes use of multiple
esters of testosterone to produce a desired slow-acting effect. The different esters
have different levels of oil solubility, and likewise rates of release from the site
of injection. The design is such that the rapid distribution of testosterone is
followed by a sustained release of hormone. Sustanon® 100 is shorter acting
than Sustanon® 250, as it lacks the longer decanoate ester, and is usually
administered on a biweekly basis. This drug is ultimately very similar to
testosterone cypionate or enanthate, but with a slightly shorter window of
therapeutic effect.
History:
Sustanon® 100 is a modern adaptation of the well-known injectable testosterone
blend Sustanon® 250, both of which were developed by the international
pharmaceutical giant Organon (now Merck/MSD). Sustanon® 100 is essentially
a lower dosed equivalent of Sustanon® 250, supplying the same hormone in a
similar (though not exact) time-released fashion. Sustanon® 100 is
recommended for the same medical uses as Sustanon® 250, namely treating
male androgen insufficiency, which can manifest itself with such symptoms as
reduced sex drive, impotence, infertility, and bone loss. Increased adiposity (fat
mass) and reduced lean mass are also common with patients suffering from low
androgen levels. In addition to these uses, Sustanon® 100 is also recommended
to induce masculinization in female-to-male transsexuals. Sustanon® 100 is
produced only in a handful of countries at this time, and is not widely available.
How Supplied:
Sustanon® 100 is available in select human drug markets. All products are
supplied in 1 mL glass ampules.
Structural Characteristics:
Sustanon® 100 contains a mixture of three testosterone compounds, which
where modified with the addition of carboxylic acid esters (propionic, propionic
phenyl ester, and isocaproic acids) at the 17-beta hydroxyl group. Esterified
forms of testosterone are less polar than free testosterone, and are absorbed more
slowly from the area of injection. Once in the bloodstream, the ester is removed
to yield free (active) testosterone. Esterified forms of testosterone are designed
to prolong the window of therapeutic effect following administration, allowing
for a less frequent injection schedule compared to injections of free
(unesterified) steroid. Sustanon 100 is designed to provide a rapid peak in
testosterone levels (24-48 hours after injection), and maintain physiological
concentrations for approximately 14 days.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone more likely to require the
concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention
and loss of muscle definition are common with higher doses of testosterone, this
drug is usually considered a poor choice for dieting or cutting phases of training.
Its moderate estrogenicity makes it more ideal for bulking phases, where the
added water retention will support raw strength and muscle size, and help foster
a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
582
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
583 Studies using 300 mg of testosterone ester
(enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated
only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached
21%.
584 The negative impact of aromatase inhibition should be taken into
consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less of testosterone per week, the
impact on lipid profile tends to be noticeable but not dramatic, making an antiestrogen (for cardioprotective purposes) perhaps unnecessary. Doses of 600 mg
or less per week have also failed to produce statistically significant changes in
LDL/VLDL cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive
protein, and insulin sensitivity, all indicating a relatively weak impact on
cardiovascular risk factors.
585 When used in moderate doses,injectable
testosterone esters are usually considered to be the safest of all
anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Testosterone propionate is often regarded as a painful injection. This is due to
the very short carbon chain of the propionic acid ester, which can be irritating to
tissues at the site of injection. Many sensitive individuals choose to stay away
from this steroid completely, their bodies reacting with a pronounced soreness
and low-grade fever that may last for a few days after each injection.
Administration (Men):
To treat androgen insufficiency, the prescribing guidelines for Sustanon® 100
call for a dosage of 100 mg (1 ampule) every 2 weeks. Although active in the
body for a longer time, Sustanon® 100 is usually injected every 7 to 10 days for
muscle-building purposes. This schedule will allow for the higher doses most
commonly applied by athletes, and more stable elevations in hormone level. The
usual dosage among male athletes is in the range of 200-600 mg per week, taken
in cycles 6 to 12 weeks in length. This level is sufficient for most users to notice
exceptional gains in muscle size and strength. Testosterone is ultimately very
versatile, and can be combined with many other anabolic/androgenic steroids
depending on the desired effect.
Administration (Women):
Sustanon® 100 is rarely used with women in clinical medicine. When applied, it
is most often used to induce masculinization in female to male transsexuals.
Sustanon® 100 is not recommended for women for physique-or performanceenhancing purposes due to its strong androgenic nature, tendency to produce
virilizing side effects, and slow-acting characteristics (making blood levels
difficult to control).
Availability:
Sustanon® 100 is less widely distributed on the black market than Sustanon®
250, due to the fact that source countries producing this drug are limited. The
moderate total amount of drug contained in each ampule (100 mg) also makes
this product far less desirable to consumers than Sustanon® 250. Sustanon® 100
is mainly located in the Netherlands, Egypt, and the United Kingdom.
Sustanon® 250 (testosterone blend)
Description:
Sustanon® 250 is an oil-based injectable testosterone blend that contains four
different testosterone esters: testosterone propionate (30 mg); testosterone
phenylpropionate (60 mg); testosterone isocaproate (60 mg); and testosterone
decanoate (100 mg). Sustanon® is designed to provide a fast yet extended
release of testosterone, usually requiring injections once every 3 to 4 weeks in a
clinical setting. This is an improvement from standard testosterones such as
cypionate or enanthate, which provide a shorter duration of activity. As with all
testosterone products, Sustanon® 250 is a very strong anabolic drug with
pronounced androgenic activity. It is most commonly used in bulking cycles,
providing exceptional gains in strength and muscle mass. A shorter-acting
version of Sustanon®, called Sustanon® 100, is also made in certain areas
(see:Sustanon 100).
History:
Sustanon® 250 first appeared on international drug markets during the early
1970’s. It was developed by the international pharmaceutical giant Organon
(now Merck/MSD), also responsible for such steroids as Durabolin®, DecaDurabolin®, and Andriol®. Sustanon® 250 was designed to offer a therapeutic
advantage over existing single esters of testosterone, which need to be injected
more frequently (cited advantages in hormone stability are probably not valid).
In spite of this advantage, however, Sustanon® 250 has never been approved for
sale in the United States, although around the world it is one of the most popular
brands of testosterone available. The lack of U.S. availability is probably due to
the high costs associated with the FDA approval process and the availability of
other somewhat comparable agents.
Over the past 25 years, Sustanon® 250 has probably been the most sought-after
injectable testosterone among athletes. It must be emphasized, however, that this
is not due to an unusual potency of this testosterone combination (esters really
only affect the release of testosterone). This is simply due to the fact that a stack
of four different testosterone compounds is a very good selling point; it is
perceived to have more value. In most instances you will actually get a lot more
for your money with testosterone enanthate or cypionate. The advantages to be
found in Sustanon® 250 are for the medical user only. If you were tied to your
doctor for regular injections, then Sustanon® 250 would allow you to visit him
or her less frequently. This equates to a clear improvement in patient comfort.
But if you are a bodybuilder injecting the drug every week, blood levels will
build to the same extremes with either type of testosterone, and the added
expense is probably not warranted.
How Supplied:
Sustanon® 250 is widely available in human and (select) veterinary drug
markets. Packaging volume may vary by country and manufacturer; the majority
of products are supplied as 1 mL glass ampules.
Structural Characteristics:
Sustanon® 250 contains a mixture of four testosterone compounds, which where
modified with the addition of carboxylic acid esters (propionic, propionic phenyl
ester, isocaproic, and decanoic acids) at the 17-beta hydroxyl group. Esterified
forms of testosterone are less polar than free testosterone, and are absorbed more
slowly from the area of injection. Once in the bloodstream, the ester is removed
to yield free (active) testosterone. Esterified forms of testosterone are designed
to prolong the window of therapeutic effect following administration, allowing
for a less frequent injection schedule compared to injections of free
(unesterified) steroid. Sustanon 250 is designed to provide a rapid peak in
testosterone levels (24-48 hours after injection), and maintain physiological
concentrations for approximately 21 days.
586 Each 250 mg ampule provides
176mg of testosterone.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of Sustanon® 250 more likely to require the
concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention
and loss of muscle definition are common with higher doses of testosterone, this
drug is usually considered a poor choice for dieting or cutting phases of training.
Its moderate estrogenicity makes it more ideal for bulking phases, where the
added water retention will support raw strength and muscle size, and help foster
a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
587
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
588 Studies using 300 mg of testosterone ester
(enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated
only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached
21%.
589 The negative impact of aromatase inhibition should be taken into
consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less of testosterone per week, the
impact on lipid profile tends to be noticeable but not dramatic, making an antiestrogen (for cardioprotective purposes) perhaps unnecessary. Doses of 600 mg
or less per week have also failed to produce statistically significant changes in
LDL/VLDL cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive
protein, and insulin sensitivity, all indicating a relatively weak impact on
cardiovascular risk factors.
590 When used in moderate doses, injectable
testosterone esters are usually considered to be the safest of all
anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production.Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Testosterone propionate is often regarded as a painful injection. This is due to
the very short carbon chain of the propionic acid ester, which can be irritating to
tissues at the site of injection. Many sensitive individuals choose to stay away
from this steroid completely, their bodies reacting with a pronounced soreness
and low-grade fever that may last for a few days after each injection.
Administration (Men):
To treat androgen insufficiency, the prescribing guidelines for Sustanon® 250
call for a dosage of 250 mg every 3 weeks. Although active in the body for a
longer time, Sustanon® 250 is usually injected every 7 to 10 days for musclebuilding purposes. This schedule will allow for the higher doses most commonly
applied by athletes, and more stable elevations in hormone level. The usual
dosage among male athletes is in the range of 250-750 mg per injection, taken in
cycles 6 to 12 weeks in length. This level is sufficient for most users to notice
exceptional gains in muscle size and strength.
Sustanon® 250 is usually incorporated into bulking phases of training, when
added water retention will be of little consequence, the user more concerned
with raw mass than definition. Some do incorporate this drug into cutting cycles
as well, but typically in lower doses (125-250 mg every 7-10 days) and/or when
accompanied by an aromatase inhibitor to keep estrogen levels under control.
Sustanon® 250 is a very effective anabolic drug, and is often used alone with
great benefit. Some, however, find a need to stack it with other
anabolic/androgenic steroids for a stronger effect, in which case an additional
200-400 mg per week of boldenone undecylenate, methenolone enanthate, or
nandrolone decanoate should provide substantial results with no significant
hepatotoxicity. Testosterone is ultimately very versatile, and can be combined
with many other anabolic/androgenic steroids to tailor the desired effect.
Some bodybuilders have been known to use excessively high dosages of this
drug (1,000 mg per week or more), although this practice is generally not
advised. At dosages above 750 mg per week, water retention will likely account
for more of the additional weight gain than new muscle tissue. The practice of
“megadosing” is inefficient (not to mention potentially dangerous), especially
when we take into account the typical high cost of Sustanon 250. Such use is
usually not justified outside of aggressive bodybuilding regimens.
Administration (Women):
Sustanon® 250 is rarely used with women in clinical medicine. When applied, it
is most often used to induce masculinization in female to male transsexuals.
Sustanon® 250 is not recommended for women for physique-or performanceenhancing purposes due to its strong androgenic nature, tendency to produce
virilizing side effects, and slow-acting characteristics (making blood levels
difficult to control).
Availability:
Sustanon remains a popular testosterone product in many countries outside of
the United States. The vast majority of products in western markets are made by
or under license from Organon (now Merck/MSD), though many “clone”
products are also manufactured in less regulated markets of Asia. In reviewing
some of the products and changes in the global pharmaceutical market, we have
made the following observations.
In November 2007, Organon was purchased by Schering-Plough. In the two
years following this acquisition, the company was slowly transitioning the
Organon products over to the Schering-Plough label. In November 2009,
Schering-Plough merged with Merck & Co, Inc. Sustanon is expected to
transition over to the new Merck/MSD label in all markets, though packaging
bearing the new company has not yet been located for photographing purposes.
It is unknown what (if any) changes to expect in the global distribution of
Sustanon.
In Brazil, Durateston in now widely available under the Schering-Plough label.
The product is still produced in its familiar clear glass ampule with red and
yellow band on the tip. Given the recent merger with MSD, it is expected that
Durateston will soon be subject to another packaging change.
Omnadren from Jelfa (Poland) recently had its packaging updated. The new
boxes have a more colorful pink gradient to them, but otherwise the presentation
remains similar to the old product (a set of five 1 mL ampules in a rectangular
box with ampule tray).
Unigen markets the product Test-Comp 250 in Thailand. It contains the standard
250 mg/mL dosage in a 10 mL multi-dose vial. Each product should carry a
unique product ID code that can be verified with the company for authenticity.
Sustabolic from Asia Pharma (Malaysia) is now approved for sale through
pharmacies in Thailand. Each box should carry a scratch-off security sticker,
which will display a code that can be validated on the company website.
Balkan Pharmaceuticals (Moldova) makes the product Sustamed. It is prepared
in both 1 mL ampules and multi-dose vials.
Sostenon 250 redi-jects manufactured by Organon/MSD in Mexico are also still
found, although much less commonly in recent years. Due to the sophisticated
packaging, this steroid has never been successfully counterfeited.
Less common, but still seen on the U.S. black market, are the European versions
of Sustanon from countries like Italy, Portugal, Belgium, and England. All of
these products use ampules that are scored, carry colored (yellow and red) rings
on the tip, and have white paper labels.
Sustanon 250 from Karachi Pakistan is also popular as of late. These ampules
are clear glass with yellow silk-screen printing. This is one of the few versions
of this steroid product sold by Organon/MSD globally that does not carry a
paper label. Fakes are circulating in high volume at this time. Note that the
current real product has its lot numbers printed on with electronic equipment,
and are not silk-screened on the glass at the same time as the rest of the lettering.
Synovex® (testosterone propionate & estradiol)
Description
Synovex is a blended-ingredient steroid implant preparation, which is available
only as a veterinary item for use in cattle.The implant comes in the form of small
pellets, which are pushed into the ear of an animal with a very large implant gun.
Once implanted, the pellets slowly dissolve, providing an extended release of
steroids for many weeks. The hormone content of Synovex is mixed, with each
pellet containing 25 mg testosterone propionate and 2.5 mg estradiol benzoate.
This 10:1 ratio has been demonstrated to provide an added anabolic/weight
gaining effect in feed animals, improving the value of the livestock. Given its
estrogen content, Synovex is clearly not an ideal steroid for humans. Most
athletes have only become attracted to this product out of sheer desperation for
legitimate anabolics, as cattle implants like this are not regulated as controlled
substances in the U.S. to spite their steroid content. Otherwise, a pure
testosterone propionate product would be much more appropriate.
History:
Testosterone propionate plus estrogen implant pellets were first approved by the
U.S. Food and Drug administration for use in heifers in 1958.
591
Diethylstilbestrol, a potent estrogen often used to increase animal carcass
weight, had been approved four years earlier for use in cattle, however, and
would remain the leading product for many years. Syntex introduced their
version of testosterone/estrogen pellets (Synovex) during the early 1970’s, as
part of the company’s new Animal Health division. This was during a time a
time when diethylstilbestrol was getting a great deal of negative publicity.
Synovex became a huge seller when the FDA banned the use of diethylstilbestrol
in 1973, the product quickly capturing more than 50% of the market for growthpromoting implants. The popularity of Synovex soon caught the attention of
other companies, a number of which soon started making their own blended
testosterone/estrogen implants. Popular brand names in the U.S. have included
F-TO (Upjohn), Heifer-oid (Boehringer), and Implus (Upjohn). Synovex and
other testosterone/estrogen pellets remain widely available in the U.S. and
abroad today, although are not highly popular with athletes given their estrogen
content.
How Supplied:
Synovex contains 25 mg of testosterone propionate and 2.5 mg of estradiol
benzoate in a small sterile implantation pellet. The number of pellets in each
cartridge dose will vary depending on the intended target animal. Implants
denoted “H” for heifer will carry the most; in the case of U.S. Synovex-H it is 80
pellets (10 doses consisting each of 8 pellets). We will see a slightly lower pellet
count in the “S” implants (steer) and “C” (calf ) cartridges.
Structural Characteristics:
Testosterone propionate is a modified form of testosterone, where a carboxylic
acid ester (propionic acid) has been attached to the 17-beta hydroxyl group to
slow the release of testosterone from the area of implantation. This preparation
also contains an ester (benzoic acid) of estradiol.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen).
Additionally, this preparation contains an active estrogen. Elevated estrogen
levels can cause side effects such as increased water retention, body fat gain, and
gynecomastia. This steroid preparation is considered to be highly estrogenic. An
anti-estrogen such as clomiphene citrate or tamoxifen citrate may be necessary
to prevent estrogenic side effects. One may alternately use an aromatase
inhibitor like Arimidex® (anastrozole), although it will not have an affect on the
additional estrogen present in the preparation. Since water retention and loss of
muscle definition are common with highly estrogenic steroid products, this drug
is usually considered a poor choice for dieting or cutting phases of training. It
would only be appropriate during bulking phases, where the added water
retention will support raw strength and muscle size, and help foster a stronger
anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
Side Effects (Hepatotoxicity):
Testosterone and estrogen do not have hepatotoxic effects; liver toxicity is
unlikely.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Testosterone tends
to have a much less dramatic impact on cardiovascular risk factors than synthetic
steroids. This is due in part to its openness to metabolism by the liver, which
allows it to have less effect on the hepatic management of cholesterol. The
aromatization of testosterone to estradiol also helps to mitigate the negative
effects of androgens on serum lipids. The added estrogen in this product may
further help to offset some of the androgenic effect on lipid values, and the
preparation may, therefore, have a weaker impact on cholesterol than a
comparably dosed straight testosterone product. Anabolic/androgenic steroids
may also adversely affect blood pressure and triglycerides, reduce endothelial
relaxation, and support left ventricular hypertrophy, all potentially increasing the
risk of cardiovascular disease and myocardial infarction.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. The added estrogen will also provide
negative-feedback suppression. This preparation should have a strong effect on
the hypothalamic regulation of natural steroid hormones. Without the
intervention of testosterone stimulating substances, testosterone levels should
return to normal within 1-4 months of drug secession. Note that prolonged
hypogonadotrophic hypogonadism can develop secondary to steroid abuse,
necessitating medical intervention.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Synovex implant pellets were not designed for human consumption. To make
use of these pellets, they must be converted into another (more suitable) delivery
form. To do this, an athlete will typically grind them up and rub them on the skin
in a 50/50 mixture of DMSO and water to facilitate transdermal delivery.
Alternately, one may mix up a homebrew injection with the pellets. This is done
by grinding them into a fine powder and introducing the powder into filtered oil
or an oil-based steroid. One should remember that the practice of preparing
Synovex for injection is not going to be sterile, and as such could be potentially
dangerous. Note that some methods have additionally been published for
removing the estrogen from the pellets, to make the drug more comfortable to
use. They generally involve the use of highly flammable materials, take a
number of different steps to complete, and leave some estrogen when the process
is over, however, usually making the process more trouble than it is worth.
Administration (Men):
Synovex is not approved for use in humans. Prescribing guidelines are
unavailable. When used for physique-or performance-enhancing purposes (very
rarely), the dose is calculated based on the route of administration. When given
by transdermal delivery, a bioavailability rate of no more than 10% is assumed.
A daily dosage of 4 pellets (100 mg) would, therefore, provide the equivalent of
70 mg per week of testosterone propionate (as given by injection). When given
by injection a dose of 100 mg every second or third day is most common. The
drug is generally taken for no more than 8 weeks, and is used almost exclusively
during bulking phases of training. Those who have experimented with this
product have been generally disappointed with the results, as the added estrogen
has often resulted in rapid gynecomastia, noticeable body fat accumulation, and
severe water retention. In many cases the water retained has caused an unsightly
bloated look (extreme loss of definition).
Administration (Women):
Synovex is not approved for use in humans. Prescribing guidelines are
unavailable. Synovex is not recommended for women for physique-or
performance-enhancing purposes due to its strong androgenic nature and
tendency to produce virilizing side effects.
Availability:
Synovex is rarely found on the black market, given that the product is in poor
demand and generally can be obtained through legitimate Agricultural or
Veterinary supply stores. No counterfeits have ever been known to exist.
Testoderm® (testosterone)
Description:
Testoderm® and Testoderm® TTS are testosterone delivery systems that utilize
a “patch” to deliver the hormone transdermally. Both products were designed to
deliver an approximate 5 mg dose of testosterone to the body over a 24-hour
period, after which point the patch is replaced with a fresh one. Testoderm is an
older matrix-type skin patch, which uses no penetration enhancers, so it must be
applied on the scrotum, where the skin is much more permeable to testosterone.
Testoderm TTS is a newer reservoir-type skin patch containing an alcoholic gel
of testosterone, which can be placed on the arm, back, or upper buttocks.
Testoderm and Testoderm TTS are designed to mimic the natural circadian
rhythm of testosterone release in healthy young men, higher during the first 12
hours and lower during the next 12 hours of each day. The clinical significance
of this, if any, is not known.
Figure 1. Mean serum testosterone concentrations (ng/dL) measured during
application of Testoderm TTS to 32 hypogonadal men. Source:
Transdermal testosterone administration in hypogonadal men: comparison
of pharmacokinetics at different sites of application and at the first and 5ths
days of application.J Clin Pharmacol 37: 1129-38.
Testoderm® was developed in the United States by Alza Corporation, and
introduced for sale in 1998. The drug is FDA-approved for testosterone
replacement therapy in men with a deficiency or absence of endogenous
testosterone. The Testoderm system itself did not make use of any penetration
enhancers, and consequently is applied to an area of shaved scrotal skin, which
is about 5 times more permeable to testosterone than normal body skin. Lacking
an integrated adhesive, Alza soon released an updated version of Testoderm
called simply Testoderm With Adhesive. Testoderm was an effective androgen
replacement product, but did have the slight disadvantage of elevating DHT
levels in many patients due to the prominence of 5-alpha reductase in the
scrotum.
592
Testoderm was ultimately the first testosterone patch to be developed for
commercial sale. While it was deemed a success initially, it was soon obsolete
next to the newer and less intrusive Androderm patch (FDA approved in 1995).
Alza released Testoderm TTS in 1998, in an effort to retain its share of the male
androgen replacement market. The new updated patch can be placed on three
types of skin (back, arms,and upper buttocks), and has the advantage of causing
less skin irritation next to Androderm. It also does not require that the patient
rotate application sites each day. Since its approval in the U.S., Testoderm TTS
has also been approved in select markets abroad, although not widely.
How Supplied:
Testoderm, Testoderm With Adhesive, and Testoderm TTS transdermal
testosterone systems are available in select human drug markets. Each comes in
the form of a transdermal patch system, which delivers approximately 5 mg of
testosterone each.
Structural Characteristics:
Testoderm® is a matrix-type transdermal drug delivery system that contains
testosterone (free) enclosed in a skin-applied patch. Testoderm® TTS is
reservoir-type transdermal drug delivery system that contains testosterone (free)
enclosed in a skin-applied adhesive patch. Both are designed to provide steady
but varying levels of testosterone transdermally during each 24-hour period of
application.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. Exceeding therapeutic doses will increase the
likelihood of estrogenic side effects. In such cases, an anti-estrogen such as
clomiphene citrate or tamoxifen citrate is commonly applied to prevent
estrogenic side effects. One may alternately use an aromatase inhibitor like
Arimidex® (anastrozole), which more efficiently controls estrogen by
preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Exceeding therapeutic doses is likely to
produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
593
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction. Therapeutic doses of testosterone used to correct
insufficient androgen production in otherwise healthy aging men are unlikely to
increase atherogenic risk, and may actually reduce the risk of cardiovascular
mortality.
594
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Testoderm is applied daily (in the morning) to intact, clean, shaven dry skin of
the scrotum. Testoderm TTS is applied daily (in the morning) to intact, clean,
dry skin of the back, arms, or upper buttocks. Many OTC ointments will
significantly reduce the penetration of testosterone when applied to the skin
before use, and should be avoided.
Administration (Men):
To treat androgen insufficiency, the prescribing guidelines for Testoderm and
Testoderm TTS recommend the application of one patch daily, which delivers
approximately 5 mg of testosterone systemically. For physique-or performance-
enhancing purposes, higher doses would be necessary to achieve
supraphysiological levels of testosterone. This would require at least three or
four patches per day, delivering approximately 15-20 mg of testosterone. This
level is sufficient for most users to notice gains in muscle size and strength,
although this is not a very realistic idea in a practical sense. Lower doses may be
used, but typically when accompanied by other anabolic/androgenic steroids.
Testosterone is ultimately very versatile, and can be combined with many other
anabolic/androgenic steroids to tailor the desired effect.
Administration (Women):
Testoderm and Testoderm TTS are not FDA-approved for use in women.
Testosterone is not recommended for women for physique-or performanceenhancing purposes due to its strong androgenic nature and tendency to produce
virilizing side effects.
Availability:
Given their high relative price and low delivery of testosterone, Testoderm and
Testoderm TTS are not commonly traded on the black market. Counterfeits have
not yet been reported.
Testolent (testosterone phenylpropionate)
Description:
Testolent is an injectable testosterone preparation containing the fast-acting
phenylpropionate ester of testosterone. Testosterone phenylpropionate is one of
the constituents in Sustanon®, although this profile concerns its use as a standalone ingredient. The activity of Testolent is ultimately very similar to
testosterone propionate, supplying the same hormone over at best a slightly
longer duration of release. While propionate is injected every second or third
day, phenylpropionate might be stretched out to every fourth day. Testolent
might be more comfortable to use, as testosterone propionate is notoriously very
painful at the site of injection, but otherwise there is really no strong advantage
to this preparation in comparison.
History:
Testosterone phenylpropionate was first described in a French medical journal in
1955.
595 A few isolated commercial products containing testosterone
phenylpropionate were developed in the years following, although this never
was a popular item. Testolent was the most recent preparation of testosterone
phenylpropionate known to be on the global steroid market, and was marketed in
Romania by Sicomed. This agent was used primarily to correct low androgen
levels in males, but as also occasionally prescribed in females for the treatment
of advanced breast cancer, osteoporosis, uterine neoplasm, and low sex drive.
Sicomed recently discounted its sale, however, and no other products containing
only testosterone phenylpropionate are currently known to exist.
How Supplied:
Testosterone phenylpropionate is no longer available as a stand-alone
commercial drug product. When produced in Romania, the Testolent brand
contained 100 mg of testosterone phenylpropionate in a 1-milliliter ampule.
Structural Characteristics:
Testosterone phenylpropionate is a modified form of testosterone, where a
carboxylic acid ester (propionic acid phenyl ester) has been attached to the 17-
beta hydroxyl group. Esterified forms of testosterone are less polar than free
testosterone, and are absorbed more slowly from the area of injection. Once in
the bloodstream, the ester is removed to yield free (active) testosterone.
Esterified forms of testosterone are designed to prolong the window of
therapeutic effect following administration, allowing for a less frequent injection
schedule compared to injections of free (unesterified) steroid.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone more likely to require the
concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention
and loss of muscle definition are common with higher doses of testosterone, this
drug is usually considered a poor choice for dieting or cutting phases of training.
Its moderate estrogenicity makes it more ideal for bulking phases, where the
added water retention will support raw strength and muscle size, and help foster
a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
596
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
597 Studies using 300 mg of testosterone ester
(enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated
only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached
21%.
598 The negative impact of aromatase inhibition should be taken into
consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less per week, the impact on lipid
profile tends to be noticeable but not dramatic, making an anti-estrogen (for
cardioprotective purposes) perhaps unnecessary. Doses of 600 mg or less per
week have also failed to produce statistically significant changes in LDL/VLDL
cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive protein, and insulin
sensitivity, all indicating a relatively weak impact on cardiovascular risk
factors.
599 When used in moderate doses, injectable testosterone esters are
usually considered to be the safest of all anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
For the treatment of low androgen levels, the prescribing guidelines for Testolent
recommend administering a dose of 100 mg every 25 days. For physique-or
performance-enhancing purposes, this drug is usually injected twice per
week.The total weekly dosage is typically 200-600 mg, which is sufficient to
provide excellent gains in muscle size and strength. Testosterone drugs are
ultimately very versatile, and can be combined with many other
anabolic/androgenic steroids depending on the desired effect.
Administration (Women):
The prescribing guidelines for Testolent do not make special dosing
recommendations for women. This drug is not recommended for women for
physique-or performance-enhancing purposes due to its strong androgenic
nature, tendency to produce virilizing side effects, and slow acting
characteristics (making blood levels difficult to control).
Availability:
Testolent is no longer available as a prescription drug product.
Testopel® (testosterone)
Description:
Testopel® is a testosterone delivery system comprised of small cylindrical
pellets of pressed testosterone. The pellets are sterile, and are comprised almost
purely of testosterone, barring a small amount of added binders for stability.
These pellets are implanted subcutaneously, and provide the patient a continuous
and very even release of hormone for several months. Testosterone pellets have
the advantage of allowing the patient to not think about their hormone
replacement therapy on a daily, weekly, or monthly basis as with many other
hormone delivery systems, and provide a much more even release of hormone
(less highs and lows) than popular injections. Testosterone implant pellets,
however, have the disadvantage of requiring that the patient undergo minor
office surgery twice to several times per year.
History:
Soon after the oral delivery of testosterone was deemed impractical due to rapid
first pass metabolism, it was realized that pressed pellets of surgically implanted
sterile testosterone could provide physiological androgen levels for extended
periods of time to patients in need of such therapy. Implanted testosterone pellets
were accepted very early as viable options for delivering testosterone, and
various such commercial preparations have been introduced and prescribed over
the years (although historically injectable esters and suspensions of testosterone
have been the norm in this field of medicine).
Currently, Bartor Pharmacal produces the only commercially available brand of
testosterone pellet in the U.S., sold as Testopel. Each pellet contains 75 mg of
(free) testosterone. It is FDA-approved for use in adult males with conditions
associated with a deficiency or absence of endogenous testosterone. This
includes cases of primary hypogonadism caused by cryptorchidism, bilateral
torsion, orchitis, vanishing testis syndrome, orchiectomy, Klinefelter’s
syndrome, chemotherapy, or alcohol/heavy metal toxicity. It is also prescribed to
treat hypogonadotrophic hypogonadism caused by tumors, injury, or radiation.
FDA laws also allow certain private compounding pharmacies to manufacture
generic testosterone implant pellet preparations. Testosterone implant pellets are
not commonly made outside the U.S., but can be located in certain markets.
How Supplied:
Testosterone implant pellets are available in select human drug markets.
Composition and dosage may vary by country or manufacturer, but generally
contain approximately 98.5% pure testosterone (along with some inert binders)
in a small cylindrical pressed pellet.
Structural Characteristics:
Sterile testosterone pellets for implantation contain (free) testosterone in a
pressed pellet. The pellets are implanted subcutaneously with a minor surgical
procedure, and slowly dissolve over time, releasing testosterone into the blood.
Testosterone pellets are designed to provide testosterone for approximately 4-6
months following implantation.
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. Exceeding therapeutic doses will increase the
likelihood of estrogenic side effects. In such cases, an anti-estrogen such as
clomiphene citrate or tamoxifen citrate is commonly applied to prevent
estrogenic side effects. One may alternately use an aromatase inhibitor like
Arimidex® (anastrozole), which more efficiently controls estrogen by
preventing its synthesis. Aromatase inhibitors can be quite expensive in
comparison to anti-estrogens, however, and may also have negative effects on
blood lipids.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Exceeding normal therapeutic doses is
likely to produce androgenic side effects including oily skin, acne, and
body/facial hair growth. Men with a genetic predisposition for hair loss
(androgenetic alopecia) may notice accelerated male pattern balding. Women are
warned of the potential virilizing effects of anabolic/androgenic steroids,
especially with a strong androgen such as testosterone. These may include
deepening of the voice, menstrual irregularities, changes in skin texture, facial
hair growth, and clitoral enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
600
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction. Therapeutic doses of testosterone used to correct
insufficient androgen production in otherwise healthy aging men are unlikely to
increase atherogenic risk, and may actually reduce the risk of cardiovascular
mortality.
601
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of the drug leaving the body.
Note that prolonged hypogonadotrophic hypogonadism can develop secondary
to steroid abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Sterile testosterone pellets are implanted subdermally in the lower abdominal
wall. Prior to insertion, the skin is cleaned with alcohol and draped with a 2%
xylocaine solution. A 2-cm incision is made through anaesthetized skin, and the
pellets administered with the aid of a cannula. The incision site is covered with a
sterile Band-Aid and a waterproof dressing for 1 week, and should not require
stitching.
Administration (Men):
To treat androgen insufficiency, the prescribing guidelines for Testopel
recommend implanting a row of 4-6 pellets (300-450 mg of testosterone) once
every 4-6 months. For physique-or performance-enhancing purposes, higher
doses would be necessary to achieve supraphysiological levels of testosterone.
This would be in the range of 12-18 pellets per application, which is not highly
practical given the higher volume and surgical requirements for implantation.
Administration (Women):
Testopel is not FDA-approved for use in women. Testosterone implant pellets
are not recommended for women for physique-or performance-enhancing
purposes due to their strong androgenic nature, tendency to produce virilizing
side effects, and very slow-acting characteristics.
Availability:
Due to the relative impracticality of general private use, Testopel is not
commonly traded on the black market.
Testoviron® (testosterone propionate/enanthate blend)
Description:
Testoviron® is a mixed testosterone injectable, containing varying amounts of
testosterone propionate and testosterone enanthate. The faster-acting propionate
ester is included to support testosterone release during the early days of therapy,
while the longer-acting ester is included to support the latter part of the
therapeutic window. Together, the two are supposed to result in a rapid increase
in testosterone level, followed by a sustained hormone elevation for
approximately 2 weeks. The design of this steroid is therefore very similar to
Sustanon®, although lacking the decanoate ester Testoviron® will remain active
in the body for a shorter duration. Testoviron® was originally marketed as an
improvement over single-ester preparations like testosterone enanthate, said to
provide a much more balanced release of hormone in comparison.
Upon close analysis, the pharmacokinetic properties of Testoviron® are not as
ideal as initially described. The problem lies in the fact that testosterone
enanthate is not a delayed-onset drug, but actually provides a sharp spike in
testosterone levels 24-48 hours after administration. Adding a fast-acting ester
like testosterone propionate to a formulation of testosterone enanthate only
compounds the initial testosterone spike. See the provided computer simulation
of the release pattern. It shows an even sharper early testosterone peak compared
to the use of testosterone enanthate alone, providing the user with a greater
imbalance between the early and latter days of the administration window. A
study administering a blend of 115.7mg of testosterone enanthate and 20 mg of
testosterone propionate confirms this tendency; demonstrating maximal
increases in serum testosterone the first day following injection.
602
History:
Testoviron® was developed by international pharmaceutical giant Schering in
Germany (now Bayer), and marketed at one time in many of the European
markets including Germany, Austria, Italy, Spain, Ireland, Greece, Switzerland,
Netherlands, Denmark, and Sweden. This product is, likewise, usually identified
as a European item, although it was produced scarcely in Eastern Europe and the
Caribbean as well. Schering has also used the Testoviron® brand for its pure
testosterone enanthate products, which are generally used for the same medical
applications (generally male androgen replacement therapy), and have always
been much more widely distributed.
The Schering Testoviron® products first surfaced in Europe during the early
1950’s, and have since been duplicated in one form or another by numerous
different drug manufacturers in many different parts of the world. Although
scarcely remembered, blended enanthate and propionate products were once
even available commercially in the U.S. Most notable was the brand Testoject
E.P. from Mayrand, which contained 200 mg of testosterone enanthate and 25
mg of testosterone propionate in a 1 mL vial. Today, however, no such
commercial product exists. Blended ester products like this are still prescribed in
the United States, but lack of a commercial item means they are only dispensed
by private compounding pharmacies.
Schering/Bayer has been refining its steroid product line a great deal since the
1990’s, eliminating many unprofitable or controversial items. This has resulted
in their discontinuing the sale of blended ester Testoviron® compounds in most
markets. At this time these products remain in extremely limited production
globally. The only known product left on the European market is Testoviron®
Depot 100, which contains 110 mg of testosterone enanthate and 25 mg
testosterone propionate, for a 100 mg total dose of (free) testosterone. As
mentioned earlier, blended testosterone enanthate and propionate products are
produced by many other companies, and can still be located in a wide variety of
human and veterinary drug markets.
How Supplied:
Testosterone propionate and testosterone enanthate blends are available in
various human and veterinary drug markets. Composition and dosage may vary
by country and manufacturer. Schering Testoviron® products contained a blend
of 20 mg/55 mg, 25 mg/110 mg, or 50 mg/200 mg of testosterone propionate and
enanthate (respectively) per milliliter; packaged in 1 mL ampules.
Structural Characteristics:
Testoviron® contains a mixture of two testosterone compounds, which where
modified with the addition of carboxylic acid esters (propionic and enanthoic
acids) at the 17-beta hydroxyl group. Esterified forms of testosterone are less
polar than free testosterone, and are absorbed more slowly from the area of
injection. Once in the bloodstream, the ester is removed to yield free (active)
testosterone. Esterified forms of testosterone are designed to prolong the window
of therapeutic effect following administration, allowing for a less frequent
injection schedule compared to injections of free (unesterified) steroid.
Testoviron® is designed to provide a rapid peak in testosterone levels (24-48
hours after injection), and maintain physiological concentrations for
approximately 14 days.
Figure 1. Proposed pharmacokinetics of Testoviron® injection (110 mg
testosterone enanthate, 25 mg testosterone propionate) based on an analysis
of the published properties of testosterone propionate and enanthate.
Source: Testosterone Action Deficiency Substitution 2nd Edition. E.
Nieschlag H.M. Behre (Eds.) Springer-Verlag Berlin Heidelberg New York
(1998)
Side Effects (Estrogenic):
Testosterone is readily aromatized in the body to estradiol (estrogen). The
aromatase (estrogen synthetase) enzyme is responsible for this metabolism of
testosterone. Elevated estrogen levels can cause side effects such as increased
water retention, body fat gain, and gynecomastia. Testosterone is considered a
moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or
tamoxifen citrate may be necessary to prevent estrogenic side effects. One may
alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more
efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors
can be quite expensive in comparison to anti-estrogens, however, and may also
have negative effects on blood lipids.
Estrogenic side effects will occur in a dose-dependant manner, with higher doses
(above normal therapeutic levels) of testosterone more likely to require the
concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention
and loss of muscle definition are common with higher doses of testosterone, this
drug is usually considered a poor choice for dieting or cutting phases of training.
Its moderate estrogenicity makes it more ideal for bulking phases, where the
added water retention will support raw strength and muscle size, and help foster
a stronger anabolic environment.
Side Effects (Androgenic):
Testosterone is the primary male androgen, responsible for maintaining
secondary male sexual characteristics. Elevated levels of testosterone are likely
to produce androgenic side effects including oily skin, acne, and body/facial hair
growth. Men with a genetic predisposition for hair loss (androgenetic alopecia)
may notice accelerated male pattern balding. Those concerned about hair loss
may find a more comfortable option in nandrolone decanoate, which is a
comparably less androgenic steroid. Women are warned of the potential
virilizing effects of anabolic/androgenic steroids, especially with a strong
androgen such as testosterone. These may include deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement.
In androgen-responsive target tissues such as the skin, scalp, and prostate, the
high relative androgenicity of testosterone is dependant on its reduction to
dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this
metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor
such as finasteride or dutasteride will interfere with site-specific potentiation of
testosterone action, lowering the tendency of testosterone drugs to produce
androgenic side effects. It is important to remember that anabolic and androgenic
effects are both mediated via the cytosolic androgen receptor. Complete
separation of testosterone’s anabolic and androgenic properties is not possible,
even with total 5-alpha reductase inhibition.
Side Effects (Hepatotoxicity):
Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One
study examined the potential for hepatotoxicity with high doses of testosterone
by administering 400 mg of the hormone per day (2,800 mg per week) to a group
of male subjects. The steroid was taken orally so that higher peak concentrations
would be reached in hepatic tissues compared to intramuscular injections. The
hormone was given daily for 20 days, and produced no significant changes in
liver enzyme values including serum albumin, bilirubin, alanine-aminotransferase, and alkaline phosphatases.
603
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Testosterone tends to have a much less dramatic impact on cardiovascular risk
factors than synthetic steroids. This is due in part to its openness to metabolism
by the liver, which allows it to have less effect on the hepatic management of
cholesterol. The aromatization of testosterone to estradiol also helps to mitigate
the negative effects of androgens on serum lipids. In one study, 280 mg per week
of testosterone ester (enanthate) had a slight but not statistically significant effect
on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor
a strong (25%) decrease was seen.
604 Studies using 300 mg of testosterone ester
(enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated
only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached
21%.
605 The negative impact of aromatase inhibition should be taken into
consideration before such drug is added to testosterone therapy.
Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or
clomiphene citrate are preferred to aromatase inhibitors for those concerned with
cardiovascular health, as they offer a partial estrogenic effect in the liver. This
allows them to potentially improve lipid profiles and offset some of the negative
effects of androgens. With doses of 600 mg or less per week, the impact on lipid
profile tends to be noticeable but not dramatic, making an anti-estrogen (for
cardioprotective purposes) perhaps unnecessary. Doses of 600 mg or less per
week have also failed to produce statistically significant changes in LDL/VLDL
cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive protein, and insulin
sensitivity, all indicating a relatively weak impact on cardiovascular risk
factors.
606 When used in moderate doses, injectable testosterone esters are
usually considered to be the safest of all anabolic/androgenic steroids.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Testosterone is the primary male androgen, and offers strong negative feedback
on endogenous testosterone production. Testosterone-based drugs will, likewise,
have a strong effect on the hypothalamic regulation of natural steroid hormones.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Testosterone propionate is often regarded as a painful injection. This is due to
the very short carbon chain of the propionic acid ester, which can be irritating to
tissues at the site of injection. Many sensitive individuals choose to stay away
from this steroid completely, their bodies reacting with a pronounced soreness
and low-grade fever that may last for a few days after each injection.
Administration (Men):
For the treatment of low androgen levels, prescribing guidelines for Testoviron®
call for a dosage of 250 mg once every 3-6 weeks. For bodybuilding purposes,
this drug is usually injected on a weekly basis, in a dosage of 250-500 mg.
Cycles are generally between 6 and 12 weeks in length. This level is sufficient to
provide excellent gains in muscle size and strength. Given the poor
pharmacokinetics and higher price of Testoviron® and related products,
testosterone enanthate or cypionate are often given preference. Testosterone
drugs are ultimately very versatile, and can be combined with many other
anabolic/androgenic steroids depending on the desired effect.
Administration (Women):
Testoviron® is not commonly prescribed to women in clinical medicine. It is
occasionally used to treat a declining sex drive with age, in which case a low
dose (50 mg) may be given every 5-6 weeks. It is also sometimes used to treat
advanced inoperable breast cancer, at a dose of 250 mg every 2-4 weeks
(virilizing effects are expected at such dosing). This drug is not recommended
for women for physique-or performance-enhancing purposes due to its strong
androgenic nature, tendency to produce virilizing side effects, and slow-acting
characteristics (making blood levels difficult to control).
Availability:
Schering (now Bayer) has discontinued manufacture of its blended Testoviron
product in most parts of the world.
Testoprim-D from Mexico is one of the most commonly located products. This
item comes in a light resistant ampule that is packaged in a red box bearing
white print. The writing is printed directly on the glass surface of the ampule.
The ink used is a white/grayish color that does not smear with a good thumb rub.
Aratest from Aranda (Mexico) appears to still be circulating. This product comes
in a 10 mL multi-dose vial.
Bi Testo is made by Cimol in Argentina. This product comes in a multi-dose
vial. There are no security features to deter counterfeiting, although copies are
not known to be a problem.
Trenabol® (trenbolone enanthate)
Description:
Trenbolone enanthate is an injectable form of the strong anabolic steroid
trenbolone. Given the use of an enanthate ester, this drug will exhibit virtually
identical pharmacokinetics to testosterone enanthate, providing a peak release of
its steroid within the first several days after injection, followed by declining
levels for approximately 2 weeks. The base steroid here (trenbolone) is a
derivative of nandrolone, and exhibits strong anabolic and androgenic properties.
On a milligram for milligram basis it is considerably more potent than
testosterone as both an anabolic and androgenic agent, though it does carry a
more favorable balance (toward anabolism). Trenbolone is also unable to
convert to estrogen, however it does exhibit notable progestational activity,
which may mimic estrogenic side effects given the right physiological
conditions. Trenbolone enanthate is virtually interchangeable with Parabolan
(trenbolone hexahydrobenzylcarbonate), capable of promoting strong gains in
lean muscle mass, often with an accompanying increase in relative hardness and
definition.
History:
Slow-acting trenbolone esters were first studied in 1967, during a series of
experiments into synthetic anabolic steroids by Roussel-UCLAF.
607 Roussel did
not specifically investigate Trenbolone enanthate, although the drug would have
remained an obvious possibility once trenbolone was released given the
widespread application of steroid esters (including enanthate) by the 1960’s. The
drug would not see the light of day for many decades, however, and was only
first released for commercial sale in 2004. It was introduced by British Dragon,
an underground manufacturer. British Dragon would sell it under the trade name
Trenabol, in 200 mg/mL strength.
Although it was not for sale through pharmacies nor approved for human or
veterinary use, Trenabol was widely distributed throughout the world, and
became an extremely popular product with athletes and bodybuilders. Much of
this had to do with the fact that it was unique, in that it was one of but a few
options for injectable trenbolone that used slow-acting esters. At the time of its
introduction, trenbolone acetate products were by and large the dominant form
of trenbolone, and remain the dominant form of the drug to this day. Although
British Dragon was perhaps the largest and most well known underground
steroid manufacturer in the world, the company abruptly collapsed at the end of
2006. The brand has since re-emerged under new ownership. Trenbolone
enanthate continues to be sold by a number of underground labs, though no
registered drug company has yet introduced it to a legitimate drug market.
How Supplied:
Trenbolone enanthate is not available as a prescription drug product.
Structural Characteristics:
Trenbolone is a modified form of nandrolone. It differs by the introduction of
double bonds at carbons 9 and 11, which inhibit aromatization (9-ene), increase
androgen-binding affinity,
608 and slows its metabolism. The resulting steroid is
significantly more potent as both an anabolic and an androgen than its
nandrolone base. The trenbolone here is modified with an enanthate ester at the
17-beta hydroxyl group, so that the free steroid is released more slowly from the
area of injection.
Side Effects (Estrogenic):
Trenbolone is not aromatized by the body, and is not measurably estrogenic. It is
of note, however, that this steroid displays significant binding affinity for the
progesterone receptor (slightly stronger than progesterone itself ).
609 610 The side
effects associated with progesterone are similar to those of estrogen, including
negative feedback inhibition of testosterone production and enhanced rate of fat
storage. Progestins also augment the stimulatory effect of estrogens on
mammary tissue growth. There appears to be a strong synergy between these
two hormones, such that gynecomastia might even occur with the help of
progestins, without excessive estrogen levels. The use of an anti-estrogen, which
inhibits the estrogenic component of this disorder, is often sufficient to mitigate
gynecomastia caused by progestational anabolic/androgenic steroids. Note that
progestational side effects are more common when trenbolone is being taken
with other aromatizable steroids.
Side Effects (Androgenic):
Although classified as an anabolic steroid, trenbolone is sufficiently androgenic.
Androgenic side effects are still common with this substance, and may include
bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic
steroids may also aggravate male pattern hair loss. Women are also warned of
the potential virilizing effects of anabolic/androgenic steroids. These may
include a deepening of the voice, menstrual irregularities, changes in skin
texture, facial hair growth, and clitoral enlargement. Additionally, the 5-alpha
reductase enzyme does not metabolize trenbolone,
611 so its relative
androgenicity is not affected by finasteride or dutasteride.
Side Effects (Hepatotoxicity):
Trenbolone is not c-17 alpha alkylated, and is generally not considered a
hepatotoxic steroid; liver toxicity is unlikely. This steroid does have a strong
level of resistance to hepatic breakdown, however, and severe liver toxicity has
been noted in bodybuilders abusing trenbolone.
612 Although unlikely,
hepatotoxicity cannot be completely excluded, especially with high doses.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Due to its non-
aromatizable nature and strong resistance to metabolism, trenbolone has a
moderate to strong (negative) impact on lipid values and atherogenic risk.
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Without the intervention of testosterone-stimulating substances, testosterone
levels should return to normal within 1-4 months of drug secession. Note that
prolonged hypogonadotrophic hypogonadism can develop secondary to steroid
abuse, necessitating medical intervention. In experimental studies, trenbolone
was determined to be approximately three times stronger at suppressing
gonadotropins than testosterone on a milligram for milligram basis.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (Men):
Trenbolone enanthate was never approved for use in humans. Prescribing
guidelines are unavailable. Common doses for physique-and performanceenhancing purposes fall in the range of 150-300 mg per week, which is usually
taken for 6-10 consecutive weeks. This level is sufficient to produce
considerable increases in lean muscle mass and strength, which are usually
combined with notable fat loss and increased muscle definition. As with all
trenbolone injectables, this product is fairly versatile, and can be combined with
many other agents depending on the desired results.
Administration (Women):
Trenbolone enanthate was never approved for use in humans. Prescribing
guidelines are unavailable.This agent is generally not recommended for women
for physique-or performance-enhancing purposes due to strong androgenic
nature and tendency to produce virilizing side effects.
Availability:
Trenbolone enanthate is currently made by underground steroid manufacturers
only.
Winstrol® (stanozolol)
Description:
Winstrol is the most widely recognized trade name for the drug stanozolol.
Stanozolol is a derivative of dihydrotestosterone, chemically altered so that the
hormone’s anabolic (tissue-building) properties are greatly amplified and its
androgenic activity minimized. Stanozolol is classified as an “anabolic” steroid,
and exhibits one of the strongest dissociations of anabolic to androgenic effect
among commercially available agents. It also cannot be aromatized into
estrogens. Stanozolol is the second most widely used oral steroid, succeeded in
popularity only by Dianabol (methandrostenolone). It is favored for its ability to
promote muscle growth without water-retention, making it highly valued by
dieting bodybuilders and competitive athletes.
History:
Stanozolol was first described in 1959.
613
It was developed into a medicine by
Winthrop Laboratories in Great Britain. Parent firm (Sterling) filed for U.S.
patent on the agent in 1961.
614 Stanozolol was officially released to the U.S.
prescription drug market in 1962 under the brand name Winstrol. Stanozolol was
initially prescribed for a variety of medical purposes, including the induction of
appetite and lean tissue gain in cases of weight loss associated with many
malignant and non-malignant diseases, the preservation of bone mass during
osteoporosis, the promotion of liner growth in children with growth failure, as an
anti-catabolic during prolonged corticosteroid therapy or for post-operative and
post-trauma (burns, fractures) patients, and even to treat debility in the elderly.
The FDA’s control over the prescription drug market had tightened by the mid1970’s, and the indicated uses for Winstrol were soon narrowed. During this
time the FDA officially supported that Winstrol was “Probably Effective” as an
adjunct therapy for treating osteoporosis, and for promoting growth in pituitarydeficient dwarfism. With this position, Winthrop was given more time to sell and
study the agent. Winthrop was able to continually satisfy the FDA regarding
Winstrol’s validity as a therapeutic agent, and it remained in the U.S. throughout
the 1980’s and 1990’s, a time when many other anabolic steroids were
disappearing from the marketplace. Stanozolol was also showing some promise
during this period for improving red blood cell concentrations, combating breast
cancer, and (more recently) treating angioedema, a disorder characterized by the
swelling of subdermal tissues, often with hereditary causes.
Winthrop went through a number of corporate changes during the 1990’s,
including a 1991 merger with Elf Sanofi to form Sanofi Winthrop. Sanofi
Winthrop continued on to sell Winstrol in the U.S. for approximately 10 more
years, before finally discontinuing the medication because of “manufacturing
issues” (Searle was actually making the product for Sanofi at the time, and had
reportedly ceased production). In 2003, the rights to Winstrol were officially
transferred to Ovation Pharmaceuticals. Winstrol remains an approved drug on
the U.S. pharmaceutical market, although is not under active production by
Ovation label. All forms of Winstrol are presently unavailable in the U.S.,
although the Winstrol brand remains available in Spain. Numerous other brands
and generic forms of the drug are produced in other countries, in both human
and veterinary drug markets.
How Supplied:
Stanozolol is widely available in both human and veterinary drug markets.
Composition and dosage may vary by country and manufacturer. Stanozolol was
originally designed as an oral anabolic steroid, containing 2mg of drug per tablet
(Winstrol). Other brands commonly contain 5 mg or 10 mg per tablet. Stanozolol
can also be found in injectable preparations. These are most commonly waterbased suspensions carrying 50 mg/ml of steroid.
Structural Characteristics:
Stanozolol is a modified form of dihydrotestosterone. It differs by: 1) the
addition of a methyl group at carbon 17-alpha to protect the hormone during oral
administration and 2) the attachment of a pyrazol group to the A-ring, replacing
the normal 3-keto group (this gives stanozolol the chemical classification of a
heterocyclic steroid). When viewed in the light of 17-alpha
methyldihydrotestosterone, the A-ring modification on stanozolol seems to
considerably increase its anabolic strength while reducing its relative
androgenicity.
Stanozolol has a much weaker relative binding affinity for the androgen receptor
than testosterone or dihydrotestosterone. At the same time it displays a much
longer half-life and lower affinity for serum binding proteins in comparison.
These features (among others) allow stanozolol to be a very potent anabolic
steroid in spite of a weaker affinity for receptor binding. Recent studies have
additionally confirmed that its primary mode if action involves interaction with
the cellular androgen receptor.
615 Although not fully elucidated, stanozolol may
have additional (some potentially unique) properties with regard to antagonism
of the progesterone receptor, Low Affinity Glucocorticoid-binding Site
interaction, and AR/PR/GR independent activities.
616 617 618
In therapeutic doses
stanozolol does not have significant progestational activity.
619
Stanozolol is known to strongly suppress levels of SHBG (sex hormone-binding
globulin). This trait is characteristic of all anabolic/androgenic steroids, although
its potency and form of administration make oral Winstrol® particularly
effective in this regard. One study with a group of 25 normal males
demonstrated a 48.4% reduction in SHBG after only 3 days of use.
620 The dose
administered was .2mg/kg, or roughly 18mg for a person weighing 200lbs.
Plasma binding proteins such as SHBG act to temporarily constrain steroid
hormones from exerting activity in the body, and effectively reduce the available
percentage of free (active) steroid. Oral stanozolol may be useful for providing a
greater percentage of unbound steroid in the body, especially when taken in
combination with a hormone that is more avidly bound by SHBG, such as
testosterone.
Side Effects (Estrogenic):
Stanozolol is not aromatized by the body, and is not measurably estrogenic. An
anti-estrogen is not necessary when using this steroid, as gynecomastia should
not be a concern even among sensitive individuals. Since estrogen is the usual
culprit with water retention, stanozolol instead produces a lean, quality look to
the physique with no fear of excess subcutaneous fluid retention. This makes it a
favorable steroid to use during cutting cycles, when water and fat retention are
major concerns. Stanozolol is also very popular among athletes in combination
strength/speed sports such as Track and Field. In such disciplines one usually
does not want to carry around excess water weight, and may find the raw
muscle-growth brought about by stanozolol to be quite favorable over the lower
quality mass gains of aromatizable agents.
Side Effects (Androgenic):
Although classified as an anabolic steroid, androgenic side effects are still
common with this substance. This may include bouts of oily skin, acne, and
body/facial hair growth. Anabolic/androgenic steroids may also aggravate male
pattern hair loss. Women are also warned of the potential virilizing effects of
anabolic/androgenic steroids. These may include a deepening of the voice,
menstrual irregularities, changes in skin texture, facial hair growth, and clitoral
enlargement. Additionally, the 5-alpha reductase enzyme does not metabolize
stanozolol, so its relative androgenicity is not affected by finasteride or
dutasteride. Stanozolol is a steroid with relatively low androgenic activity in
relation to its tissue-building actions, making the threshold for strong androgenic
side effects comparably higher than more androgenic agents such as
testosterone, methandrostenolone, or fluoxymesterone.
Side Effects (Hepatotoxicity):
Stanozolol is a c17-alpha alkylated compound. This alteration protects the drug
from deactivation by the liver, allowing a very high percentage of the drug entry
into the bloodstream following oral administration. C17-alpha alkylated
anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure
may result in liver damage. In rare instances life-threatening dysfunction may
develop. It is advisable to visit a physician periodically during each cycle to
monitor liver function and overall health. Intake of c17-alpha alkylated steroids
is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain.
Stanozolol appears to offer less hepatic stress than an equivalent dose of
Dianabol (methandrostenolone). Studies giving 12mg of stanozolol per day for
27 weeks failed to demonstrate clinically-significant changes in markers of liver
function, including serum aspartate amino-transferase, alanine amino-
transferase, gamma-glutamyltransferase, bilirubin, and alkaline phosphatase.
621
Relative hepatotoxicity increases as the dosage escalates, so hepatic dysfunction
should still be a concern. In rare instances, high doses (alone or in combination
with other steroids) have been implicated in cases of serious life-threatening
hepatotoxicity in bodybuilders. Injectable stanozolol has also been implicated in
severe hepatotoxicity in an otherwise healthy bodybuilder,
622 and should not be
used as an alternative medication when liver toxicity precludes oral stanozolol
use.
The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or
Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic
steroids.
Side Effects (Cardiovascular):
Anabolic/androgenic steroids can have deleterious effects on serum cholesterol.
This includes a tendency to reduce HDL (good) cholesterol values and increase
LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a
direction that favors greater risk of arteriosclerosis. The relative impact of an
anabolic/androgenic steroid on serum lipids is dependant on the dose, route of
administration (oral vs. injectable), type of steroid (aromatizable or nonaromatizable), and level of resistance to hepatic metabolism. Stanozolol has a
strong effect on the hepatic management of cholesterol due to its structural
resistance to liver breakdown, non-aromatizable nature, and route of
administration. Studies using an oral dose of 6 mg per day for six weeks
demonstrated a mean serum HDL reduction of 33% in healthy male weighttraining subjects, which was combined with a 29% increase in serum LDL.
623
Anabolic/androgenic steroids may also adversely affect blood pressure and
triglycerides, reduce endothelial relaxation, and support left ventricular
hypertrophy, all potentially increasing the risk of cardiovascular disease and
myocardial infarction.
Injectable stanozolol has also been documented to produce strong negative
changes in serum lipids. One study was carried out on a group of 12 healthy
male subjects, and demonstrated a measurable reduction in HDL cholesterol
values, as well as an increase in LDL and total cholesterol values, following a
single injection of 50 mg.
624 These changes persisted for 4 weeks after the drug
was administered, and represent a potential increased risk for developing
arteriosclerosis. Injectable stanozolol should not be used as an alternative
medication when cardiovascular risk factors preclude oral stanozolol use.
To help reduce cardiovascular strain it is advised to maintain an active
cardiovascular exercise program and minimize the intake of saturated fats,
cholesterol, and simple carbohydrates at all times during active AAS
administration. Supplementing with fish oils (4 grams per day) and a natural
cholesterol/antioxidant formula such as Lipid Stabil or a product with
comparable ingredients is also recommended.
Side Effects (Testosterone Suppression):
All anabolic/androgenic steroids when taken in doses sufficient to promote
muscle gain are expected to suppress endogenous testosterone production.
Stanozolol is no exception, and is noted for its strong influence on the
hypothalamic-pituitary-testicular axis. Clinical studies giving 10 mg per day to
healthy male subjects for 14 days caused the mean plasma testosterone level to
fall by 55%.
625 Without the intervention of testosterone-stimulating substances,
testosterone levels should return to normal within 1-4 months of drug secession.
Note that prolonged hypogonadotrophic hypogonadism can develop secondary
to steroid abuse, necessitating medical intervention.
The above side effects are not inclusive. For more detailed discussion of
potential side effects, see the Steroid Side Effects section of this book.
Administration (General):
Studies have shown that taking an oral anabolic steroid with food may decrease
its bioavailability.
626 This is caused by the fat-soluble nature of steroid
hormones, which can allow some of the drug to dissolve with undigested dietary
fat, reducing its absorption from the gastrointestinal tract. For maximum
utilization, oral forms of stanozolol should be taken on an empty stomach.
There can be large discrepancies in the steroid particle size between injectable
stanozolol preparations. For example, Winstrol from Zambon (Spain) was
designed for human use, and uses a refined powder that will pass through a 27-
gauge needle. Winstrol®-V is a veterinary product in the U.S. and Canada, and
has larger particles that will jam in needles smaller than 22-gauge. Solutions that
utilize a larger particle size may also cause more discomfort at the site of
injection. Injectable forms of stanozolol can be taken in measured oral doses
should injection prove intolerable.
Administration (Men):
The original prescribing guidelines for Winstrol called for a daily dosage of 6
mg, which was administered on a schedule of one 2 mg tablet three times per
day. The usual dosage for physique-or performance-enhancing purposes is
between 15 mg and 25 mg per day, or three to five 5 mg tablets, taken for no
longer than 6-8 weeks. Injectable Winstrol is generally recommended at a
clinical dosage of one 50 mg injection every 2-3 weeks. When used for
physique-or performance-enhancing purposes, a dosage of 50 mg every other
day is most commonly applied. Veterinary stanozolol preparations with a larger
particle size will be more slowly dispersed by the body, and are commonly given
at 75 mg every third day. Doses of 50 mg per day with injectable stanozolol are
not uncommon, although probably not advised. Note that injectable forms of the
drug are expected to have, milligram for milligram, a greater anabolic effect than
oral.
627
Stanozolol is often combined with other steroids for a more dramatic result. For
example, while bulking one might opt to add in 200-400 mg of a testosterone
ester (cypionate, enanthate, or propionate) per week. The result should be a
considerable gain in new muscle mass, with a more comfortable level of water
and fat retention than if taking a higher dose of testosterone alone. For dieting
phases, one might alternately combine stanozolol with a non-aromatizing steroid
such as 150 mg per week of a trenbolone ester or 200-300 mg of Primobolan®
(methenolone enanthate). Such stacks are highly favored for increasing
definition and muscularity. An in-between (lean mass gain) might be to add in
200-400 mg of a low estrogenic compound like Deca-Durabolin® (nandrolone
decanoate) or Equipoise® (boldenone undecylenate).
Administration (Women):
The original prescribing guidelines for Winstrol called for a daily dosage of 4
mg (one 2mg tablet twice daily) with young women particularly susceptible to
the androgenic effects of anabolic steroids. This dosage was increased to 6mg
(the same as the recommended dose for males) when necessary. When used for
physique-or performance-enhancing purposes, a dosage of 5 mg to 10 mg daily
is most common, taken for no longer than 4-6 weeks. Injectable Winstrol is
generally recommended at a clinical dose of 50 mg every 2-3 weeks. The
injectable is usually not advised with women for physique-or performanceenhancing purposes, as it allows for less control over blood hormone levels.
Those women who absolutely must use the injectable commonly administer 25
mg every 3 or 4 days. Although this compound is weakly androgenic, the risk of
virilization symptoms cannot be completely excluded, even at therapeutic doses.
Availability:
Stanozolol remains widely available as a pharmaceutical product. Its production
has been shifting to less regulated markets (mainly in Asia) in recent years,
however, which likely reflects declining interest in using stanozolol as a
medicinal product in the West, and the continuing high demand for this drug
among athletes and bodybuilders. In reviewing some of the more popular
products and changes on the global pharmaceutical market, we have made the
following observations.
British Dispensary in Thailand makes a stanozolol product. Their trade name for
the drug is Azolol, and it contains 5 mg of steroid in a 400 tablet bottle. The
bottle itself looks very similar to that of Androlic, with dark plastic and a shiny
chrome top. Be sure to look for the company’s holographic sticker when
shopping.
Stanol (Thailand) is now sold as a generic drug under the March
Pharmaceuticals label, though is in the same recognizable white bottle with
green-shaded label. The product contains 5 mg of steroid per tablet, and each
bottles holds 200 tablets. To deter counterfeiting, the bottle now carries a
holographic sticker on the front that bears the company logo.
Acdhon in Thailand makes Stanozodon, which comes in the old industry
standard of 2 mg of steroid per tablet. It is packaged in bottles of 1,000.
Counterfeits are not known to be a problem at this time although the product is
not widely distributed on the black market either.
Unigen markets the product Stanztab in Thailand. It contains 10 mg per tablet,
and is packaged in foil and plastic strips of 10 tablets each (5 strips per box).
Winstrol® tablets and injectable ampules are still produced in Spain, by Desma.
This remains the most popular stanozolol injectable in Europe. All boxes are
protected with a holographic sticker, which carries the company logo embedded
into the image. Note that highly accurate counterfeits are currently in circulation
throught Europe and North America.
The Greek generic by Genepharm is still in production. The product should carry
a Greek drug ID sticker on the box, which will show a hidden mark under UV
light.
Chinfield makes a 50 mg/mL injectable stanozolol in Argentina called Nabolic
Strong. This is the same firm that makes regular Nabolic, a very low dosed (2
mg/mL) version of the same drug. This new product is now much more popular
on the black market than the first, due to the more useable dosage. Note that
Chinfield prints their logo on the inside of the vial carton, which offers
somewhat of a simple security check (obviously one very easy to duplicate).
Anabolico Cimol is an injectable form of stanozolol from Argentina. It comes in
multi-dose vials containing 50 mg/mL of the steroid. This item has not been
subject to widescale counterfeiting, but also bears no security features that would
deter this practice.
Stanozoland from Landerlan in Paraguay is common on the black market,
particularly in South America. It comes in the form of a 10 mg tablets, packaged
in bottles of 100 tablets each. The company also makes a 50 mg/mL injectable.
Also from Paraguay is a generic stanozolol injectable from Indufar. It contains
50 mg/mL of steroid in a 1 mL glass ampule. Three ampules are packaged per
box.
Formula Magistral in Argentina makes generic oral and injectable Estanozolol.
The oral comes in the form of 10 mg tablets, loose in pill bottles, while the
injectable contains 50 mg/mL in multi-dose vials. These products bear a small
square holographic security sticker to deter counterfeiting.
The veterinary compounding pharmacy SMP in Canada makes a generic
injectable in 30 mL multi-dose vials (50 mg/mL). This product is made in
limited quantities, however, and is not highly common on the black market.
ANABOLIC AGENTS (NON-STEROID)
Arachidonic Acid (eicosa-5,8,11,14-enoic acid)
Description:
Arachidonic acid is an omega-6 essential fatty acid that serves as the principle
building block for the synthesis of dienolic prostaglandins (such as PGE2 and
PGF2a). These prostaglandins are integral to protein turnover and muscle
accumulation, and have such important activities as increasing blood flow to the
muscles (pumps), increasing local IGF-1 and insulin sensitivity (corresponding
receptor levels), supporting satellite cell activation, proliferation, and
differentiation, and increasing the overall rate of protein synthesis and muscle
growth. Arachidonic acid release serves as the main thermostat for prostaglandin
turnover in skeletal muscle tissue, and is responsible for initiating many of the
immediate biochemical changes during resistance exercise that will ultimately
produce muscle hypertrophy. As such, it is a highly anabolic nutrient. Among
the large variety of nutrients available to athletes and bodybuilders for
supplementation, next to protein, arachidonic acid is the most integral to muscle
growth, as it sits at the very center of the anabolic response.
Clinical Studies:
In 2005, the Exercise & Sport Nutrition Laboratory at Baylor University
conducted a double-blind placebo-controlled study to determine if 50 days of
resistance training and arachidonic acid (X-Factor™) supplementation would
affect training adaptations in 31 experienced (>1 year) resistance-trained males.
The results were presented at the International Society of Sports Nutrition
conference on June 15, 2006. All subjects ingested a total of four capsules each
day (one 250 mg capsule of AA or placebo every four hours). Subjects taking XFactor added an average of 25lbs to their bench press maximum weight in 50
days, which was an increase of nearly 45% greater than the placebo group. The
X-Factor group outperformed the placebo group on Average Power (225% >
placebo), Peak Anaerobic Power (600% > placebo), and Total Work Capacity
(250% > placebo). No side effects were reported during the investigation.
Pharmacology:
Arachidonic acid begins to display its anabolic activity early during exercise.
This nutrient is released from your muscle fibers as they are damaged during
intense training, triggering a localized inflammatory and anabolic response. This
is part of the same biological process that causes you to be sore a day or two
following a good workout, and reminds us that the old adage “no pain, no gain”
is a fundamentally true one. Arachidonic acid liberation from damaged muscle
fibers is, similarly, the very first anabolic trigger in a long cascade that will
control the rebuilding and strengthening of muscle tissue after exercise.
628 629 630
Among other things, by increasing local IGF-1 and insulin receptor density,
arachidonic acid supports the anabolic actions of these hormones, making the
repair process both faster and more intense. As a crude explanation, arachidonic
acid helps direct the body to where it needs muscle tissue repair by facilitating
the localized actions of anabolic hormones.
The availability of arachidonic acid, and our ability to liberate it during exercise,
is important to the anabolic productivity of our workouts. We also need to be
aware of the fact that regular exercise significantly lowers the content of
arachidonic acid in skeletal muscle tissue.
631 632 633 Since dienolic prostaglandin
synthesis is tied to the amount of available arachidonic acid, lower levels result
in less arachidonic acid being released during exercise, and a less intense
anabolic response. The depletion of arachidonic acid in skeletal muscle tissue is
also one of the key reasons we find it harder to get sore the more regularly we
exercise. With lower levels of arachidonic acid, you need to work more
vigorously to receive the same level of release and anabolic stimulation. On the
same note, when you change up your routine and hit your muscles from new
angles, arachidonic acid is the reason you may find yourself more sore than
usual. You have called upon new muscle fibers, which have higher stores of
arachidonic acid to work with. Dan Duchaine once said,“ The best exercise is the
one you are not doing.” This may have a lot to do with what he was talking
about.
History:
The arachidonic acid supplementation protocols, and the concept of using this
nutrient to improve muscle mass, strength, and performance, were first
developed by William Llewellyn, author of this book series. Llewellyn filed
patent on the technology on November 27, 2002, and released an arachidonic
acid supplement under the X-Factor trademark (Molecular Nutrition) shortly
after. Although the product was initially met with a great deal of skepticism and
criticism by industry peers, it has since been proven effective both in the
marketplace and in clinical trials, and established itself as a powerful supplement
for body recomposition goals. The U.S. Patent & Trademark Office granted
Llewellyn’s patent application for arachidonic acid on January 11, 2005 (U.S.
Patent # 6,841,573), and the product has since been offered for license to other
companies in the industry. The original X-Factor product remains widely
available in the U.S. and abroad, and rapid expansion in the arachidonic acid
category is expected as more companies license the technology. Note that any
officially licensed arachidonic acid product sold in the sports nutrition
marketplace will carry the original X-Factor trademark on its packaging.
Structural Characteristics:
Arachidonic acid (eicosa-5,8,11,14-enoic acid) is an essential polyunsaturated
fatty acid found in animal fats. Supplemental arachidonic acid is commonly
produced in two forms, triglyceride and ethyl ester. As with other fatty acid
supplements such as fish oils, the natural triglyceride form (as present in XFactor and licensed products) offers up to 400% greater absorption than the ethyl
ester, and is the preferred form for supplementation.
How Supplied:
Arachidonic acid is sold under the X-Factor trademark by Molecular Nutrition,
and is supplied in 250 mg capsules. Arachidonic acid may also be found in a
number of licensed products; all will display the patent number (#6,841,573) on
the packaging.
Administration (Short-Term Anabolic):
As a short-term anabolic agent, arachidonic acid is supplemented at a dose of
500 mg to 1,000 mg per day (2-4 250 mg capsules). The full 1,000 mg dose is
most commonly used, regardless of bodyweight. The nutrient is cycled in the
same way steroids commonly are, and is taken for a period of 7-8 weeks
followed by an equal amount of time off. This level is sufficient to notice
measurable increases in lean muscle mass, strength, and anaerobic power.
Depending on dietary and individual metabolic factors, these gains may be
accompanied by a decrease in body fat. Gains of 1-2lbs of lean muscle mass per
week are fairly consistent, with total accrued weight gain often measuring
approximately 10lbs during a cycle. There is also no hormonal disruption with
arachidonic acid supplementation, so the retention of gains after the product is
discontinued is generally high. Note that arachidonic acid also has some effect as
a vasodilator, and may produce increased pumps in response to intense training.
This often occurs within two weeks of initiating supplementation at anabolic
levels.
Administration (Normal Supplementation):
Arachidonic acid may also be an important nutrient to consider in regular
supplemental doses, particularly if you do not consume animal products (red
meat, organ meat, eggs) on a regular basis. Studies have shown that given
somewhat comparable amounts of protein, those who consume animal products
will make more progress with resistance exercise than those that do not
(vegetarians).
634 Arachidonic acid may be the missing component in such diets,
too integral to the anabolic response for lower dietary levels not to be noticed.
There is also empirical evidence suggesting that an arachidonic acid deficiency
exists in many experienced bodybuilders, given that training depletes AA stores.
On a number of cases, tissue tests for the content of phospholipids have revealed
unusually low levels of arachidonic acid in highly trained athletes. For those
who find their intake of animal products inadequate, or feel that they may have
insufficient tissue stores of AA, a single capsule of 250 mg provides about the
equivalent of a day’s supply of arachidonic acid within a normal western diet
with animal products. Taken every day or two, the capsule should provide a
necessary supply of this essential omega-6 fatty acid.
Safety:
In clinical studies involving the supplementation of 1,500-1,700 mg of
arachidonic acid per day, general markers of health were also unaffected with 50
days of continuous use. This includes no notable change in HDL, LDL, or total
cholesterol values, immune system response functioning, or platelet aggregation
values.
635 636 637 Furthermore, the investigation at Baylor University
demonstrated safety on all of the basic markers of health including lipids, blood
pressure, blood cell counts, immune system mediators, and liver enzymes. The
study also produced a strong trend for reduced IL-6 in the X-Factor
supplemented group, which is a principle inflammatory cytokine and stimulus
for the hepatic production of C-reactive protein. High levels of IL-6 are
correlated with poor health and mortality, and are deemed undesirable. The
results suggest that while arachidonic acid may be “proinflammatory” in the
sedentary (inactive) state, when combined with resistance training, a reduction in
systemic inflammation may actually be noticed. It is speculated that an
amplification of some of the health-beneficial aspects of resistance exercise,
namely the improved management of insulin, may be responsible for reducing
this inflammatory marker.
On a more general note, the American Heart Association announced its position
on Omega-6 EFA consumption in early 2010. In reviewing some of the more
current data, they found that diets low in Omega-6 fats were associated with an
increased risk of heart disease compared to diets with higher intakes. The paper
also discusses arachidonic acid, and how this essential fat is normally not
proinflammatory, nor outwardly unhealthy to consume. The American Heart
Association now recommends that 5-10% of your calories each day come from
Omega-6 fats, including ARA. Diets rich in Omega-3’s are, of course, also
healthy, but not at the exclusion of Omega-6’s.
Side Effects:
Arachidonic acid (X-Factor) often produces an amplification of residual postworkout (Delayed Onset) muscle soreness. Often recovery is slightly prolonged
(perhaps an additional day of rest is required), and the user may need to adjust
their schedule accordingly. This is due to an intensification of the normal
physiological response to training, and represents increased intensity of the
anabolic cascade (and rate of muscle growth). Those with existing minor muscle,
connective tissue, or joint injuries may notice more pain, due to the greater
prostaglandin signaling caused by supplementation. While arachidonic acid
should not exacerbate the injury, if greater soreness interferes with one’s ability
to train comfortably, the supplement should be discontinued until the injury is
healed. Arachidonic acid supplementation may also produce a greater incidence
of headaches in a small percentage of users, which may be due to its effect as a
vasodilator. Increasing daily water consumption often alleviates this side effect.
Additionally, arachidonic acid seems to produce a very weak androgenic effect
in some users, often producing minor oily skin. This may be caused by a slight
amplification of testosterone’s effect. It should not be strong enough to concern
females about virilizing side effects.
Contraindications:
Those with an existing medical condition related to inflammation may find that
the added arachidonic acid exacerbates symptoms of their disorder, and should
avoid supplementation. This supplement should only be used after the approval
of a physician if someone is taking medication, has an existing medical
condition, or has a familial predisposition for cardiovascular disease, high blood
pressure, or any other disorder that may require the limiting of dietary
arachidonic acid. Also, as a potent growth-promoting agent, arachidonic acid
joins androgens (testosterone, anabolic steroids), growth hormone, IGF-1,
estrogens,and many other growth factors as potentially supporting the growth
rate of certain cancer cells if you have the disease. Dietary arachidonic acid
intake has been generally eliminated as a causative factor in cancer,
638 639
just as
testosterone level has been eliminated as predictive of prostate cancer risk,
however these types of growth-promoting agents should be avoided in such
diseased states unless approved by a physician. If you have prostate cancer, for
example, the last thing you want to start taking is a growth promoter like
testosterone. The same goes for arachidonic acid. The bottom line is that if you
are in poor health, you should probably not be taking this supplement. If you are
healthy, you should be able to use it with great safety.
During the clinical study, subjects taking X-Factor added an average of
25lbs to their bench press maximum weight in 50 days.This increase was
nearly 45% greater than that noted in the exercise-only (placebo) group.
Some subjects gained more than 50 lbs on their bench press 1-rep max over
the 50-day period.
Using the standard Wingate cycle ergometer test to measure relative peak
anaerobic power, subjects taking X-Factor increased leg power by 1.2
Watts•kg-1.This represents a net increase of more than 600% over the
placebo group (-.2 Watts•kg-1).
In the standard Wingate cycle ergometer test to measure anaerobic power
and performance, the X-Factor group outperformed the placebo group on
Average Power by an amazing 21 watts (AA: 37.9W P: 17.0W).That's a net
increase of nearly 225% compared to placebo.
Total Work, as recorded in the standard energy unit Joules, increased by
1,292J in the group taking X-Factor, while Total Work increased 510J in
the placebo group.This is more than a 250% increase compared to placebo.
Kynoselen®
Description:
Kynoselen is an injectable veterinary drug, currently produced by the
international firm Vetoquinol. It contains a mixture of heptaminol, AMP
(adenosine monophosphate), vitamin B-12, sodium selenite, magnesium
aspartate, and potassium aspartate. This blend makes for a restorative “tonic”
type drug, administered to protect an animal’s muscle mass and overall wellness
after illness, injury, or trauma. It is most often used on horses, and is typically
applied as an anti-catabolic after strenuous activity, or to help get an animal back
on its feet after a debilitating infection/illness. At other times it is simply used to
support the vitality of an animal that is otherwise healthy, but at the moment less
than vigorous in its daily activities. In some cases it is even used for the very
basic purpose of remedying a deficiency in vitamin B-12 or selenium intake.
Bodybuilders are attracted to Kynoselen for its mild anabolic and lipolytic
properties.
The principle active ingredient in Kynoselen is heptaminol, which is classified as
an amino alcohol with myocardial stimulant and vasodilatory properties. It is
also identified as an inotropic compound, which increases contractile strength,
and minimizes fatigue, of skeletal muscles.
640
It has demonstrated a specific
ability to increase the differentiation of satellite muscle cells,
641 a process that
helps generate new muscle tissue (skeletal muscle growth). This same ingredient
is also known to affect the release and uptake of norepinephrine (noradrenalin),
increasing levels of this hormone/neurotransmitter in the blood.
642 Since
noradrenalin is an important regulator of lipolysis in humans, this allows
heptaminol to impart some fat-loss effect. Adenosine triphosphate is also
regarded as a key component of the product, and plays a role in the storage and
release of energy. Overall, both the anabolic and lipolytic properties of
Kynoselen are measurable when used in humans, but not dramatic. It is capable
of imparting some increases in strength, muscle mass, and fat loss, but the results
will not rival those of anabolic steroids. Still, being that this drug is legal in most
jurisdictions, it remains an attractive alternative to anabolic steroids for many
individuals.
History:
Heptaminol, the principle active ingredient in Kynoselen, was first heavily
investigated in clinical medicine during the early 1950s. It was soon developed
into a prescription drug, and has since been sold by a series of drug
manufacturers in many different parts of the world. Currently its most common
therapeutic use is to treat orthostatic hypotension, which is a sudden drop in
blood pressure upon standing. Various preparations containing heptaminol have
been produced over the years, the most notable of which have included
Amidrina (Italy), Cortensor (Belgium and Switzerland), Hept-A-Myl (USA),
Heptamyl (Belgium and Switzerland), and Heptylon (France). Although a
variety of human medications containing heptaminol have been in commerce for
decades, these preparations were rarely of interest to athletes. Years later, under
a far different medical setting, Western athletes were first introduced to the drug.
The French veterinary preparation Kynoselen would be the first heptaminolcontaining drug to grab large-scale international attention, becoming popular
among American bodybuilders and athletes during the latter part of the 1990s.
This was some years subsequent to laws being passed that had increased the
penalties for dealing in anabolic steroids. During this time, availability of the
drugs had shifted, and for some buyers scarce supply and high legal risk made
the drugs less attractive. Many athletes were becoming increasingly resourceful
in finding other non-scheduled performance-enhancing drugs that could be
purchased and used with less legal risk. Kynoselen was already known to
athletes in Europe, and would quickly cross the Atlantic. By the year 2000, a
number of exporters had set up operation to market the drug directly to
American athletes. Today, Kynoselen remains unscheduled and widely available
in the United States and many areas abroad.
How Supplied:
Kynoselen is most commonly supplied in a 100 mL multi-dose vial for injection.
Active ingredients are heptaminol, disodic adenosine monophosphate, vitamin
B12, selenium (sodium selenite), magnesium aspartate, and potassium aspartate.
Structural Characteristics:
Heptaminol (supplied as heptaminol hydrochloride) is an amino alcohol with a
structure of 6-amino-2-methylheptan-2-ol.
Administration:
Kynoselen is not approved for use in humans. Prescribing guidelines are
unavailable. An effective dosage for physique-or performance-enhancing
purposes generally falls in the range of 1 mL weekly for every 25 pounds of
bodyweight. This would mean that a 200lb bodybuilder would use around 8 mL
per week. Due to high injection volume, some opt to take a lower dosage,
injecting at the very least a 2 mL three times per week. At this dose, a single 100
mL vial would last about 16 weeks. At 8-10 mL per week a 100 mL bottle would
last for 10 to 12 weeks. It is generally recommended to use the entire bottle once
it has been opened, or discard any remaining drug that was not used during the
cycle. As with all injectable drugs packaged in multi-dosed vials, contaminants
will be introduced into the solution immediately once the seal is broken for the
first injection.
Because it tends to increase noradrenalin levels, Kynoselen is also a mild
stimulant. It is likely for this specific reason that its use has been banned by
certain horseracing organizations. This means that one can expect certain
stimulant-related side effects, especially when taking this drug in higher dosages.
This includes rapid heartbeat, sweating, jitters, restlessness, increased blood
pressure, or insomnia. A good rule of thumb used by bodybuilders to try and
keep such side effects from becoming a problem is to never inject more than 2
mL per day. They may also want to start with an amount lower than the
recommended dosage (determined by bodyweight), perhaps even half of this.
The dose is then slowly increased, so that the peak level is reached only after
three to four weeks of slow incremental increases.
Warnings:
Individuals with high blood pressure or cardiovascular disease should not use
Kynoselen.
Availability:
Kynoselen usually sells for $75 to $100 per bottle at the retail level. It is not a
controlled substance in the United States, and is likewise pretty easy to obtain
locally or via mail order. Currently no significant fakes are known to exist.
Given its abundance and low cost, counterfeits are not expected to be a
significant problem anytime soon. It is also important to note that legitimate
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Lutalyse® (diniprost tromethamine)
Description:
Dinoprost tromethamine is a pharmaceutical form of the natural prostaglandin
PGF2alpha. Prostaglandins are a series of natural oxygenated unsaturated cyclic
fatty acids, which have a variety of hormone-like actions in the body. Among
other things, PGF2alpha is involved in vasoconstriction, increasing protein
synthesis in skeletal muscle tissue, and reducing adipose tissue mass. This
hormone-like chemical also stimulates smooth muscle contraction, and is
involved in pain, inflammation, fever, ovulation, gastric motility, and fluid
absorption in the gastrointestinal tract. In veterinary medicine dinoprost
tromethamine is most commonly used in estrus synchronization/fertility timing,
for treating chronic endometriosis, and to induce abortion or labor. Dinoprost is
not widely used in human medicine, but is sometimes applied to terminate
pregnancy or induce labor.
Athletes and bodybuilders are attracted to dinoprost tromethamine for its strong
thermogenic and muscle-building properties. The anabolic effect of this drug has
been substantiated by clinical studies, which have shown PGF2a to be a strong
stimulator of protein synthesis, and key to both the immediate and long-term
physiological adaptations to resistance training.
643 644 645 646 Reports from
athletes who have experimented with this agent generally support this compound
being an excellent promoter of localized muscle growth, usually resulting in both
increases in muscle size and definition. Dinoprost is also reported to be a very
fast acting drug, with many claiming it has caused noticeable effect after being
injected in a particular muscle group for only a couple of weeks. Clinical data
also supports it being a substantially potent fat-loss drug, with PGF2a shown in
studies to inhibit the stimulation of lipogenesis in fat cells.
645 Again there is a
great deal of anecdotal support for this property of dinoprost tromethamine
among athletes and bodybuilders, with many claiming they notice a slight
temperature elevation and marked fat loss during therapy.
History:
Dinoprost tromethamine was first introduced into clinical medicine in the early
1970s. The first approved use of the drug in human patients was to stimulate
abortion during the second trimester. It has since remained of use for this
purpose, but is most commonly associated these days with veterinary medicine.
Here, it is widely applied to help farmers regulate the estrous cycle and fertility
of various livestock. Interest in dinoprost tromethamine as an
anabolic/thermogenic drug for athletes and bodybuilders did not appear until the
late 1990s. This likely occurred subsequent to the release of numerous medical
studies linking PGF2alpha to muscle hypertrophy. Early theoretical concepts
stemming from this research evolved into modern application protocols for the
drug, which in spite of a high propensity to generate side effects, have proven to
be highly successful for many athletes and bodybuilders.
Over the years dinoprost tromethamine has appeared as a human medicine under
a wide number of trade names, including such popular drug products as
Amoglandin (Sweden), Prostin (Sweden), Prostin F2 alpha (U.S., Australia,
Israel, Italy, New Zealand, South Africa, and the United Kingdom), Minprostin
F2a (Germany), Enzaprost (Greece, Poland) and Prostarmon (Japan). Prostin F2
is no longer sold in the U.S., however, and there is presently no FDA approved
replacement available for human use. Veterinary versions are more widely
available and tend to provide significantly more active drug for less money than
their human counterpart medicines, and as a result have been the products most
commonly associated with the physique-or performance-enhancing use of
dinoprost tromethamine. Popular veterinary brands have included Lutalyse
(Pharmacia Animal Health), Prostamate (Pfizer), Panacelan (Daiichi
Pharmaceutical Co.) and Dinolytic (Upjohn). Several corporate mergers have
taken place in this segment of the market, and the (now larger) conglomerate
Pharmacia has emerged as the worldwide leader in dinoprost sales. Lutalyse is
consequently the most common form of dinoprost tromethamine of use among
the athletic/bodybuilding community.
How Supplied:
Dinoprost tromethamine is most commonly supplied in a multi-dose vial (5 mL100 mL) in a dose of 5 mg per mL. It is prepared in a sterile solution of water
with benzyl alcohol added as a preservative and sodium hydroxide and/or
hydrochloric acid to adjust pH.
Structural Characteristics:
Dinoprost tromethamine is the tromethamine salt of prosta,5,13-dien-1-oic acid
(PGF2alpha).
Side Effects:
Possible side effects or signs of dinoprost tromethamine overexposure may
include such respiratory effects as bronchoconstriction, wheezing, coughing,
lung irritation, rapid breathing, and anaphylaxis. Asthmatic individuals may be
particularly susceptible to these effects. Dinoprost may also cause
gastrointestinal disturbances such as abdominal cramping, diarrhea, vomiting
and nausea. Other effects may include increased pulse rate, elevated blood
pressure, chills, fever, and anorexia, and in women uterine contractions, vaginal
bleeding, and uterine or urinary infections. Pregnant women should not take or
handle dinoprost. Reports of side effects among athletes using dinoprost for
physique-or performance-enhancing purposes are common, and often extreme.
This includes pronounced soreness at the site of injection; often beginning with a
dull burning almost immediately after the shot is given. Chills and flu-like
feelings are also commonly reported during cycles, as are bouts of shortness of
breath. Injections are also commonly followed by uncontrollable urges to urinate
or defecate, including strong spasmodic contractions of the muscles involved in
the control of these functions. Nausea and vomiting have also been commonly
reported. For many, the cramping, diarrhea, pain, and general feelings of upset
stomach, malaise, and discomfort make dinoprost a drug they experiment with
only briefly. Others, however, continue on with the drug, and often report that
side effects become more tolerable over time.
Administration:
As a human medication, dinoprost tromethamine is most commonly given intraamniotically at a dose of 40 mg for the termination of pregnancy. It is also
sometimes given orally to pregnant women at a dose of 30-100 mg to induce
labor, although this tends to produce more side effects than other, more recently
adopted, medications. When used for physique-or performance-enhancing
purposes, dinoprost tromethamine is generally given by intramuscular injection.
Most noted for its ability to generate localized growth, common sites of injection
include the shoulders, biceps, triceps, calves, chest, back, and legs. The user will
typically inject in only one site per day at the start of therapy, but this may be
increased to 2 or more injections per day as they become more accustomed to the
drug and its side effects. Therapy begins slowly, and is initiated with a low
starting dose of approximately .5 milligram per injection. If the first injection
were given without significant side effects, the next injection would be increased
to 1 milligram. This is slowly increased by .5-1 mg per application until a peak
dose is reached. This might be a maximum of 5 mg per injection site. Injection
sites are also regularly rotated so that several days separate administration in the
same muscle group. Note that for some, the pain after injection is so severe that
training for that specific muscle group must be delayed for at least a few days.
Individual sensitivity to the drug may, therefore, require modifications of their
injection and training schedule to maximize results and comfort.
Availability:
Dinoprost tromethamine is available in the U.S. and many other nations as a
prescription drug product. It is also found infrequently on the black market.
Anti-Estrogens
Arimidex® (anastrozole)
Description:
Anastrozole is an anti-estrogenic drug developed for the treatment of advanced
breast cancer in women. Specifically, this agent is the first in a newer class of
third-generation selective oral aromatase inhibitors.
646
It acts by blocking the
enzyme aromatase, subsequently blocking the production of estrogen in the
body. Since many forms of breast cancer cells are stimulated by estrogen,
reducing levels of this hormone in the body may retard the progression of the
disease. This is also the fundamental use of tamoxifen citrate (Nolvadex®),
except Nolvadex blocks the action of estrogen at the receptor, not its actual
endogenous production. The effects of anastrozole can be very substantial, with
a daily dose of 1 mg (commonly 1 tablet) capable of producing estrogen
suppression greater than 80% in treated patients. With the powerful effect this
drug has on hormone levels, it is usually only prescribed to postmenopausal
women. Side effects like hot flashes and hair thinning can present themselves
during therapy, and would be much more severe in pre-menopausal patients. For
the steroid-using male athlete, anastrozole is applied to minimize the side effects
associated with elevated estrogen levels secondary to anabolic/androgenic
steroid use. In comparison with traditional methods such as Nolvadex and
Proviron, anastrozole is significantly more effective at controlling estrogen.
History:
Anastrozole was developed by Zeneca Pharmaceuticals, and approved for use in
the United States at the end of 1995. The drug was developed as a new adjunct
treatment for operable breast cancer in postmenopausal female patients, an area
of medicine that had a long history of tamoxifen use. Substantial data was
needed to shift prescribing trends away from such an established medication
treatment. Shortly after its release, anastrozole was investigated as part of an
extremely large multicenter double blind trial based out of Rome (ATAC). The
study evaluated the use of anastrozole and tamoxifen, alone or in combination, in
9,366 postmenopausal women following breast cancer surgery. The results
favored anastrozole over tamoxifen at promoting disease regression and
improving overall survival rates. Upon publication of this trial in 2002,
anastrozole emerged as a new contender for the adjunctive treatment of
postmenopausal breast cancer.
647 648 Around this same time the drug was also
gained popularity with male bodybuilders and athletes who began taking notice
of the strong estrogen suppression caused by anastrozole, both in the anecdotal
reports of others and in clinical trials.
How Supplied:
Anastrozole is most commonly supplied in tablets of 1mg.
Structural Characteristics:
Anastrozole is classified as a selective non-steroidal aromatase inhibitor. It has
the chemical designation 1,3-benzenediacetonitrile,a,a,a’,a’-tetramethyl-5-(1H1,2,4-triazol-1-ylmethyl).
Side Effects:
Common side effects associated with the use of an aromatase inhibitor include
hot flashes, joint pain, weakness, fatigue, mood changes, depression, high blood
pressure, swelling of the arms/legs, and headache. Aromatase inhibitors may
also decrease bone mineral density, which may lead to osteoporosis and an
increase in fractures in susceptible patients. Some individuals may also respond
to the medication with gastrointestinal side effects including nausea and
vomiting. Aromatase inhibitors can harm the development of an unborn fetus,
and should never be taken or handled during pregnancy. When taken by men (as
an off-label use) to reduce estrogenicity during prolonged periods of steroid
treatment, aromatase inhibitors may increase cardiovascular disease (CVD) risk
by retarding some beneficial properties of estrogen on cholesterol values.
Studies have demonstrated that when an aromatizable steroid such as
testosterone enanthate is taken in conjunction with an aromatase inhibitor,
suppression of HDL (good) cholesterol levels become significantly more
pronounced. Since the estrogen receptor agonist/antagonist Nolvadex® generally
does not display the same anti-estrogenic (negative) effect on cholesterol values,
it is usually favored over aromatase inhibitors for estrogen maintenance by male
bodybuilders and athletes concerned with cardiovascular health.
Administration:
Anastrozole is FDA approved for adjunctive treatment of postmenopausal
women with hormone receptor-positive early breast cancer, first-line treatment
of postmenopausal women with hormone receptor-positive or receptor unknown
locally advanced metastatic breast cancer, and treatment of advanced breast
cancer in postmenopausal women with disease progression following tamoxifen
therapy. The dosage prescribed in all instances is 1mg per day until disease
progression has halted. When used to mitigate the estrogenic side effects of
anabolic/androgenic steroid use, male athletes and bodybuilders will commonly
take .5 mg to 1 mg of anastrozole per day. In some instances a half of a tablet (.5
mg) taken every other day is sufficient to mitigate the buildup of estrogen. When
used with readily aromatizing androgens such as methandrostenolone or
testosterone, gynecomastia and water retention are often effectively blocked.
Additionally, the use of anastrozole may decrease fat mass, which can also be
tied to estrogen levels. The result can be a harder and much more defined
appearance to the muscles and physique, which makes this agent of interest for
dieting/cutting purposes as well.
It is of note that food does not appear to affect the absorption of anastrozole, so
the drug may be taken with or between meals.
Availability:
Anastrozole is widely available in the U.S. and many other nations as a
prescription drug product. It is also found readily on the black market.
Aromasin® (exemestane)
Description:
Exemestane is a steroidal suicide aromatase inhibitor. It is very similar in
structure and action to formestane, although it is significantly more potent in
comparison. As a class of drugs, aromatase inhibitors offer an anti-estrogenic
effect by blocking the enzyme responsible for synthesizing estrogens.
Exemestane is approved by the FDA for the treatment of breast cancer in
women, specifically in postmenopausal patients whose cancer has progressed
following therapy with tamoxifen. Male bodybuilders and athletes often use the
drug for non-approved purposes, namely to counter the estrogenic side effects
associated with the use of aromatizable anabolic/androgenic steroids. This may
include gynecomastia, fat buildup, and water retention. In some instances
aromatase inhibitors may also assist this group with the loss of body fat and
increases in muscular definition. Exemestane is one of the most potent aromatase
inhibitors presently available. The most commonly cited data (found in the
Aromasin packaging insert) reports a lowering of serum estrogen levels by 85%
on average in clinical studies with women.
History:
Exemestane was developed by Pharmacia & Upjohn (Pharmacia), which gained
FDA approval for sale of the drug in late 1999. They introduced it under the
Aromasin brand name in early 2000. Although the drug proved to be effective in
doses as low as 2.5 mg per day in some patients, the company developed it in a
standard and near universally effective dosage of 25 mg per tablet. The company
has since introduced the drug to many other nations under the same trade name.
Due to various patents and general market dominance, Aromasin is the only
brand name of exemestane one is likely to come across in general commerce at
the present time. It is currently available in over three dozen countries including
Argentina, Australia, Austria, Belgium, Brazil, Canada, Czech Republic, Chile,
Denmark, Finland, France, Germany, Greece, Hong Kong, Hungary, Ireland,
Israel, Italy, Malaysia, Netherlands, Norway, New Zealand, Philippines, Poland,
Portugal, Russia, South Africa, Singapore, Spain, Sweden, Switzerland,
Thailand, Turkey, United Kingdom, United States, and Venezuela.
How Supplied:
Exemestane is most commonly supplied in tablets of 25 mg.
Structural Characteristics:
Exemestane is classified as an irreversible steroidal aromatase inhibitor. It has
the chemical designation 6-methyl-enandrosta-1,4-diene-3,17-dione.
Side Effects:
Common side effects associated with the use of an aromatase inhibitor include
hot flashes, joint pain, weakness, fatigue, mood changes, depression, high blood
pressure, swelling of the arms/legs, and headache. Aromatase inhibitors may
also decrease bone mineral density, which may lead to osteoporosis and an
increase in fractures in susceptible patients. Some individuals may also respond
to the medication with gastrointestinal side effects including nausea and
vomiting. Aromatase inhibitors can harm the development of an unborn fetus,
and should never be taken or handled during pregnancy. When taken by men (as
an off-label use) to reduce estrogenicity during prolonged periods of steroid
treatment, aromatase inhibitors may increase cardiovascular disease (CVD) risk
by retarding some beneficial properties of estrogen on cholesterol values.
Studies have demonstrated that when an aromatizable steroid such as
testosterone enanthate is taken in conjunction with an aromatase inhibitor,
suppression of HDL (good) cholesterol levels become significantly more
pronounced. Since the estrogen receptor agonist/antagonist Nolvadex® generally
does not display the same anti-estrogenic (negative) effect on cholesterol values,
it is usually favored over aromatase inhibitors for estrogen maintenance by male
bodybuilders and athletes concerned with cardiovascular health.
Administration:
Exemestane is FDA approved for adjunctive treatment of postmenopausal
women with estrogen-receptor positive early breast cancer with disease
progression following tamoxifen. Therapy is initiated 2-3 years after tamoxifen
has failed to elicit a desirable response, at which point tamoxifen is discontinued.
Treatment with exemestane is continued for 2-3 additional years, and is
completed after 5 years of cumulative adjunctive drug therapy (tamoxifen and
exemestane treatment combined). The dosage prescribed in all instances is one
25 mg tablet per day, taken after a meal. When used to mitigate the estrogenic
side effects of anabolic/androgenic steroid use or increase muscle definition,
male athletes and bodybuilders will commonly take 12.5 mg to 25 mg of
exemestane per day. In some instances a half of a tablet (12.5 mg) taken every
other day is sufficient to prevent the onset of estrogenic side effects.
Availability:
Exemestane is available in the U.S and in more than three dozen other nations
under the Aromasin brand name (Pharmacia). Aromasin, likewise, dominates the
global market, and is presently the only exemestane product one is likely to
encounter.
Clomid® (clomiphene citrate)
Description:
Clomiphene citrate is an anti-estrogenic drug that is prescribed to women to treat
anovulatory infertility (inability to ovulate). In clinical medicine it is specifically
referred to as a nonsteroidal ovulatory stimulant. The drug works by interacting
with estrogen receptors, often in an antagonistic manner, in various tissues of the
body including the hypothalamus, pituitary, ovary, endometrium, vagina, and
cervix. One main focus is that the drug will oppose the negative feedback of
estrogens on the hypothalamic-pituitary-ovarian axis, enhancing the release of
gonadotropins (LH and FSH). This surge in gonadotropins may cause egg
release (follicular rupture), ideally leading to conception. Clomiphene citrate is
chemically a synthetic estrogen with both agonist/antagonist properties, and in
this regard is very similar in structure and action to Nolvadex®. It is believed
that both the estrogenic and anti-estrogenic properties of clomiphene citrate play
a role in its ability to support female fertility.
In men, clomiphene citrate also acts as a partial anti-estrogen, and may be used
to counter some of the side effects of aromatizable steroid use including
gynecomastia and increased water retention. As an anti-estrogenic drug,
clomiphene citrate may also produce an elevation of follicle stimulating
hormone, and luteinizing hormone levels, which can elevate testosterone
production. This effect is especially beneficial at the conclusion of a steroid
cycle, when endogenous testosterone levels are depressed. Here, clomiphene
citrate is most often applied in combination with hCG and tamoxifen, in an effort
to restore endogenous testosterone production more quickly (see PCT: PostCycle Therapy). If testosterone levels are not brought back to normal in a short
period of time, a significant loss in size and strength may occur. This is due to
the fact that without testosterone (or other anabolic/androgenic steroids) to
impart an ongoing anabolic message, the catabolic hormone cortisol becomes the
dominant force affecting muscle protein synthesis. Often referred to as the poststeroid crash, when not corrected this state of imbalance in the endocrine system
can quickly reduce muscle mass levels, diminishing the long-term return on
anabolic/androgenic steroid therapy.
Note that the triphenylethylene compounds (toremifene citrate, tamoxifen citrate,
clomiphene citrate) tend to be somewhat intrinsically estrogenic in the liver. This
means that while they can block estrogenic activity in some areas of the body,
they can actually act as estrogens in this other key area. Estrogenic action in the
liver is important in the regulation of serum cholesterol (it tends to support HDL
synthesis and LDL reductions). Since steroid-using bodybuilders are already
dealing with the negative cardiovascular effects of these drugs, compounding the
issue with aromatase inhibitors (which will lower total serum estrogen levels)
may not always be the best option. Using a drug that blocks gynecomastia, for
example, while at the same time supporting improved cholesterol values, might
be much more ideal.
History:
Clomiphene citrate is a fertility drug with a substantial history of use in the
United States. It first gained widespread acceptance during the early 1970s, and
has been a drug common to the fertility practice ever since. The drug is now
considered a standard medication for certain forms of fertility therapy, and has
been adopted as such far outside U.S. border. Clomiphene citrate is presently
available in most nations worldwide. The two most popular brand names one is
likely to encounter are Clomid and Serofene, although the drug can be found
under numerous other trade names as well including (but not limited to) Sepafar,
Omifin, Pergotime, Gonaphene, Duinum, Clostil, Ova-Mit, and Clostibegyt.
Clomiphene citrate is generally a very inexpensive medication compared to
stronger anti-estrogens such as the newer selective third-generation aromatase
inhibitors. It, likewise, remains a very popular agent of use among bodybuilders
and athletes.
How Supplied:
Clomiphene citrate is most commonly supplied in tablets of 50 mg.
Structural Characteristics:
Clomiphene citrate is classified as a selective estrogen receptor modulator, with
both agonist and antagonist properties. It has the chemical designation 2-[4-(2-
chloro1,2-diphenylvinyl) phenoxy] triethylamine dihydrogen citrate.
Warnings (Visual Symptoms):
Some patients using clomiphene citrate notice blurring or other visual
disturbances such as spots or flashes. These symptoms occur more frequently at
higher doses or longer durations of therapy, and often disappear within a few
days or weeks of use. Prolonged visual disturbances have been reported after the
discontinuation of clomiphene citrate therapy, however, and in some cases may
be irreversible. Those taking clomiphene citrate should be warned that these
symptoms might make activities like driving a car or operating heavy machinery
more hazardous than usual. While the exact cause of these visual symptoms is
not yet understood, it is advisable to discontinue treatment and have a thorough
medical/opthalmological examination should they occur.
Side Effects:
Clomiphene citrate appears to be well tolerated, with a low incidence of
significant side effects. Common adverse reactions during clinical trails included
ovarian enlargement (13.6%), vasomotor flushes (10.4%), abdominal discomfort
(5.5%), nausea/vomiting (2.2%), breast discomfort (2.1%), visual symptoms
(1.5%), headache (1.3%), and abnormal uterine bleeding (1.3%). Data also
suggests that the prolonged use of clomiphene citrate may increase the chance of
ovarian tumor. Clomiphene citrate is occasionally associated with a serious and
potentially life threatening side effect called ovarian hyperstimulation syndrome
(OHSS). Early warning signs of OHSS include abdominal pain and distention,
nausea, diarrhea, and weight gain.
Administration:
Clomiphene citrate is FDA approved for the treatment of women with ovulatory
dysfunction preventing pregnancy. The recommended dosage is 50 mg daily for
5 days, which is initiated approximately 5 days into the menstrual cycle. If
ovulation does not occur, follow up cycles may use a dosage of 100 mg per day
for 5 days. Many clinicians recommend a limit of 6 courses of therapy. When
used by men (off-label) to mitigate the estrogenic side effects of
anabolic/androgenic steroid use, a daily dosage of 50-100 mg (1-2 tablets) is
usually administered while any offending steroids are taken. Note, however, that
tamoxifen is usually given preference over clomiphene citrate for this purpose.
More commonly, clomiphene citrate is used by men at a dosage of 50-100 mg
per day for 30 days at the conclusion of a steroid cycle, in an effort to bring
natural testosterone production back to normal levels. Here, it is usually deemed
most appropriate to use as part of a multi-component post-cycle recovery
program (see PCT: Post-Cycle Therapy). Female athletes occasionally use
clomiphene citrate for the reduction of estrogenicity near the time of a
bodybuilding contest. In some instances this may aid in increasing fat loss and
muscularity, particularly in female trouble areas such as the hips and thighs. The
drug, however, often produces very troubling side effects in pre-menopausal
women, and is likewise not in very high demand among this group.
Availability:
Clomiphene citrate is widely available on the international market in a variety of
brand names. It generally sells for a reasonable price, and is of low interest to
counterfeiters.
Cytadren® (aminoglutethimide)
Description:
Aminoglutethimide is mainly identified as an inhibitor of adrenocortical steroid
synthesis. Its primary function is to block the conversion of cholesterol to
pregnenolone, which is required for the biosynthesis of adrenal glucocorticoids,
mineralocorticoids, estrogens, and androgens. Aminoglutethimide is a
nonspecific inhibitor, and also blocks several other steps in steroid synthesis
including hydroxylation at C-11, C-18, and C-21, and the aromatization of
androgens to estrogens. The drug may be used clinically to treat estrogen
dependent breast cancer, and to treat Cushing's syndrome, which is a condition
where the body overproduces the hormone cortisol. The effect that
aminogluthethimide can have on cortisol and estrogen production is what makes
this a drug of interest to athletes and bodybuilders.
Cortisol Inhibition: While cortisol is an essential hormone for life, its levels may
also vary greatly within “normal” ranges depending on the individual, their
training and dietary status, and many other personal metabolic factors. It has
been a common pursuit in the sports community to find ways to control (limit)
cortisol production. This is because while androgens give your muscle cells a
message to increase protein synthesis, cortisol (a catabolic hormone) imparts a
message to breakdown and release amino acids. If one can limit this catabolic
message, net protein synthesis should, in theory, be increased.
Aminoglutethimide has been used by a number of athletes and bodybuilders for
this purpose, usually in combination with anabolic/androgenic steroids because it
has a low level of androgen inhibition. Together with even a relatively small
dose, it was thought one could shift the ratio of anabolic to catabolic hormones
in favor of the former, the goal being new muscle growth. The results for this
use have been mixed.
When first looked at in the realm of athletics, however, research was bare as to
the best way to use aminoglutethimide as a cortisol lowering anti-catabolic.
Dubbed the “adrenal escape phenomenon”, it has been noted that after a short
period of regular use your body often reacts to lowered cortisol levels by
increasing the release of another hormone, ACTH (adrenocorticotropic
hormone). Increased ACTH could overcome the activity of aminoglutethimide,
resulting in your body resuming its original levels of cortisol production
(negating the benefits of cortisol inhibition).
649 A moderate amount of
hydrocortisone (20-30 mg daily) is given to patients when this occurs. This can
keep glucocorticoid activity from completely diminishing, preventing the ACTH
response and allowing the drug to retain its effect. For athletes, however,
supplementing glucocorticoids would probably be counterproductive given the
desired goal. A 2-day-on 2-day-off regime of administration was, therefore,
implemented as a way to delay or even avoid the adrenal escape phenomenon.
This strategy is based on theory and experimentation, however, and no clinical
studies have evaluated aminiglutethimide as an anti-catabolic agent.
It is important to note that while many people believe they have used this drug as
an anti-catabolic, few have actually taken the correct dosage. Four tablets per
day, or 1,000 mg, appears necessary to significantly inhibit the demolase enzyme
(the enzyme responsible for converting cholesterol to pregnenolone, and the
target when reduced cortisol is desired). Those who do venture this high
commonly report fatigue and discomfort, stating that the drug is intolerable for
any type of prolonged use. Today, many athletes and bodybuilders are accepting
that the original proposed use of aminogluthethimide as a non-steroidal musclebuilding agent does not seem to be a plausible one. The only instances this
author has really heard of this drug ever being used at such doses consistently
with any type of positive response were competitive bodybuilders partaking in
high-dosed Cytadren shortly before a contest. They claimed the short-term rise
in androgen to corticosteroid ratio greatly aided their abilities to bring out a
show-ready hard and dense physique, and credit the drug as genuinely being a
very effective pre-contest agent. In speaking with the late Paul Borresen he
summed up the pre-contest use of Cytadren by stating, “I have had considerable
experience with the high dose use. It makes athletes sleepy and weak. It seems to
help the last ten days before a show, and this is tried and tested.”
Aromatase Inhibition: Aminoglutethimide is an efficient aromatase inhibitor,
and tends to inhibit the activity of this enzyme at a much lower dosage from that
what is required for inhibition of corticosteroid production.
650 651 While a daily
dosage of 1000 mg is typically needed to inhibit cortisol, maximum suppression
of aromatase and estrogen levels is typically achieved at a dosage between 250
mg and 500 mg, a point where strong adrenal steroid blockage is not noted.
There also seems to be no added benefit by adding cortisol in terms of
survival/response rate among breast cancer patients, pointing to the fact that the
“adrenal escape phenomenon” bears little relation to its abilities as an aromatase
inhibitor. Ultimately, it appears that not only do we need a higher dose (1,000
mg or 4 tablets per day minimum) to really inhibit cortisol production, but also
that there is no need for an athlete to implement a rotating dose schedule if the
drug is being used as an anti-estrogen.
Aminoglutethimide is usually regarded highly among athletes and bodybuilders
as an estrogen maintenance agent. Studies have shown it to be capable of
decreasing aromatase activity by as much as 92% after administration of 250 mg
per day. Patient response rates also show aminoglutethimide to be at least as
effective as tamoxifen therapy in treating estrogen dependent cancer cells, and
more effective under certain conditions. Due to its discussed broad range of
nonspecific activity, however, including the potential inhibition of not only
estrogens, but corticosteroids, aldosterone, and androgens as well, it is not
regarded as highly as newer (second and third generation) aromatase inhibitors
in terms of patient comfort and efficacy, and is not widely used for this purpose
today. Athletes, however, still tend to consider it to be an effective remedy for
estrogenic side effects like gynecomastia, increased water retention, and fat gain.
History:
Aminoglutethimide was FDA approved as an anticonvulsant drug in 1960. Side
effects were common with treatment, however, including drowsiness, dizziness,
and partial loss of motor control. In 1966 reports of adrenal insufficiency
subsequent to aminoglutethimide use were reported. The drug was withdrawn
from the U.S. market as an anticonvulsant that same year due to its recently
understood effects on the adrenal gland. By 1967, however, the drug was
reintroduced for a new purpose, namely inhibition of aromatase activity and the
treatment of breast cancer. It was one of the first aromatase inhibitors sold, and
is identified alongside testolactone as a “first-generation” agent of this type.
Given its novel effects on adrenal steroid production, the U.S. FDA also granted
approval for the use of aminoglutethimide for the treatment of Cushing’s
syndrome.
At one time aminoglutethimide was available under numerous brand names and
in more than 2-dozen countries. Ciba’s Cytadren and Orimeten preparations
were by far the most common, and could be found in such nations as Argentina,
Australia, Austria, Brazil, Canada, Chile, Czech Republic, France, Germany,
Hong Kong, Ireland, Israel, Italy, Malaysia, Netherlands, Norway, New Zealand,
Russia, South Africa, Spain, Sweden, Switzerland, United Kingdom, and the
United States. Additionally, the drug could be found on occasion under other
names including Aminoblastin, Rodazol, and Mamomit. The vast majority of
original aminoglutethimide preparations have since been discontinued, however.
Today, the drug remains available in a very small number of countries, most
notably the United States (Cytadren), Russia (Mamomit), Hong Kong
(Orimetene), and Australia (Cytadren).
How Supplied:
Aminoglutethimide is most commonly supplied in tablets of 250 mg.
Structural Characteristics:
Aminoglutethimide is an analog of glutethimide. It has the chemical designation
2-(4-Aminophenyl)-2-ethylglutarimide;3-(4-Aminophenyl)-3-ethylpiperidine2,6-dione.
Side Effects:
Frequent side effects associated with aminoglutethimide include fatigue,
dizziness, skin rashes, fever, and nausea. Other side effects may include sleep
disorder, apathy, depression, vomiting, stomach upset, thyroid dysfunction,
virilization, jaundice, elevated cholesterol levels, changes in blood cell counts,
and high blood pressure. Additionally, those bodybuilders and athletes taking it
at a dosage high enough to promote cortisol suppression often note that reduced
levels of this hormone bring about more aches and pains in the joints when
trying to lift heavy weights. It seems logical that this might lead to an increased
susceptibility to injury. Users should be careful not to overexert themselves
during the short periods in which this drug is used in high doses. Most of the
listed side effects listed here are most common with higher dosed regimens that
inhibit the adrenal production of cortisol, and are less common with athletes
taking one or two tablets per day as an anti-estrogen. Even in low doses
aminoglutethimide may cause birth defects, and should never be taken during
pregnancy.
Administration:
Aminoglutethimide is medically indicated for the treatment of Cushing’s
syndrome, metastatic breast cancer in postmenopausal women, and palliative
treatment in men with advanced prostate cancer. When used to treat Cushings
syndrome, the dosage used may range from 1,000 mg to 2,000 mg per day, often
in conjunction with 20-30 mg of hydrocortisone to avoid the aforementioned
adrenal escape phenomenon. Athletes and bodybuilders using aminoglutethimide
for cortisol inhibition will commonly take a dosage of 1,000 mg per day, usually
for brief periods of 2-3 weeks or less (10 days of use pre-contest is reported with
some bodybuilders). A schedule of 2-days on, 2-days off may be used in an
attempt to extend the effectiveness of aminoglutethimide for longer periods, but
such use is usually discarded in place of daily short-term administration. The
dosage most commonly used for mitigating the estrogenic side effects of
anabolic/androgenic steroid use ranges from 125 mg to 500 mg per day (1/2 to 2
tablets), with 1 tablet (250 mg) per day appearing to be the most common dosage
selected.
Availability:
Aminoglutethimide is produced in a small number of countries, and is a fairly
expensive pharmaceutical. As such, it may sell for as much as $2 per tablet on
the black market. This, combined with limited availability, has severely limited
its more widespread use.
Evista (raloxifene hydrochloride)
Description:
Raloxifene hydrochloride is a second-generation Selective Estrogen Receptor
Modulator (SERM) of the benzothiophene family. This drug is similar in effect
to tamoxifen, exhibiting estrogen receptor antagonist (blocking) properties in
some tissues while acting as an estrogen receptor agonist (activator) in others.
The main point of variation between these two agents is their tissue selectivity.
While raloxifene hydrochloride is a strong anti-estrogen in breast and uterine
tissues, it appears to be estrogenic in bone. This allows it to protect bone density,
mimicking the beneficial effects of endogenous estradiol. This is quite different
from tamoxifen, which is anti-estrogenic in both breast and bone. In a role that
was novel for an anti-estrogen, raloxifene hydrochloride was approved by the
FDA for the prevention and treatment of osteoporosis in postmenopausal
women. It is also being investigated for several other potential uses, including
the treatment and prevention of cardiovascular disease, breast cancer,
gynecomastia, prostate cancer, acromegaly, and uterine cancer.
As an anti-estrogen, athletes and bodybuilders may use this compound to combat
the estrogenic side effects caused by aromatizable or estrogenic steroids. The
principle among these side effects is gynecomastia, a purpose for which
raloxifene hydrochloride seems better suited than tamoxifen. This was
demonstrated in a July 2004 study in the Journal of Pediatrics, which looked at
how these two agents compared in the treatment of persistent pubertal
gynecomastia.
652 The investigation involved a group of 38 patients, averaging 15
years of age and suffering from gynecomastia for a little over 2 years. Treatment
for 3 to 9 months with either agent had a high success rate for seeing “some
improvement” (91% for raloxifene and 86% for Nolvadex). However, a
significant reduction of gynecomastia was seen in more than twice as many
patients with raloxifene hydrochloride (86% compared to 41%). Given its
relative potency, raloxifene hydrochloride may offer an alternative to surgery for
some cases of gynecomastia.
Typical of an anti-estrogen, raloxifene hydrochloride should also offer some
benefit as a testosterone-stimulating compound. We see this effect demonstrated
in studies on a group of older men (aged 60-70 years), where daily doses of 120
mg were able to increase serum and bioavailable (unbound) testosterone by
20%.
653 Though these figures are not dramatic, they do demonstrate an antiestrogenic effect instead of an estrogenic (negative) one when it comes to
testosterone production. This drug may, therefore, be of some value when
utilized as an adjunct to HCG injections during a post-cycle testosterone
recovery program. This same study above also showed raloxifene hydrochloride
to have at least a partial estrogenic effect on serum lipids, exhibiting a trend
toward decreases in all cholesterol values (total, LDL, and HDL). It is difficult to
discern if there are any real benefits to male bodybuilders when it comes to using
raloxifene hydrochloride to counteract the negative cardiovascular side effects of
steroid use. As discussed in its respective profile, this may be a notable benefit
with the use of Nolvadex, a first-generation SERM agent shown to improve
HDL (good) cholesterol levels in many patients.
There are some negatives to inhibiting the actions of estrogen that should be
addressed. For one, estrogen is a beneficial hormone when it comes to IGF-1
levels. In studies with acromegaly patients that suffer from GH hypersecretion,
60 mg of raloxifene hydrochloride twice daily was able to reliably suppress IGF1 levels by an average of 16%.
654 Estrogen is also understood to exert positive
anabolic effects in regards to increasing androgen receptor concentrations in
certain tissues, and enhancing enzymes involved in the utilization of glucose for
tissue growth and repair. This is further support for the belief that anti-estrogens
should not be used unless there is a defined reason for doing so. When used for
simple side-effect prevention (without visible side effects occurring), the drug
may inadvertently lessen the total anabolic potency of steroid therapy.
History:
Raloxifene hydrochloride was developed by Eli Lilly & Company, and FDA
approved for U.S. sale in 1997. Its first indicated use was as that of an
osteoporosis treatment, owing to its ability to increase bone density. In 2007, the
FDA expanded the indicated uses for the drug to include reducing the risk of
invasive breast cancer in two populations: postmenopausal women with
osteoporosis and postmenopausal women at high risk for invasive breast cancer.
Today, raloxifene hydrochloride is a fairly popular drug in clinical medicine, and
is approved for sale in over 50 countries. The Evista brand from Eli Lilly &
Company dominates the global market, although a small number of other brands
can be found including Ketidin, Oseofem, and Raxeto (Argentina), Bonmax,
Estroact, and Ralista (India), and Optruma (Spain, France, Italy).
How Supplied:
Raloxifene hydrochloride is most commonly supplied in tablets of 60 mg.
Structural Characteristics:
Raloxifene hydrochloride is classified a selective estrogen receptor modulator,
with both agonist and antagonist properties. It has the chemical designation 6-
Hydroxy-2- ( p - hyd roxypheny l ) benzo [ b ] thien - 3 - yl - p - ( 2 -
piperidinoethoxy)phenyl ketone hydrochloride.
Warnings (Stroke):
The FDA mandates that the following warning be present on the prescribing
information for Evista (raloxifene hydrochloride): “WARNING: INCREASED
RISK OF VENOUS THROMBOEMBOLISM AND DEATH FROM STROKE.
Increased risk of deep vein thrombosis and pulmonary embolism have been
reported with Evista. Women with active or past history of venous
thromboembolism should not take Evista. Increased risk of death due to stroke
occurred in a trial in postmenopausal women with documented coronary heart
disease or at increased risk for major coronary events. Consider risk-benefit
balance in women at risk for stroke.”
Side Effects:
Common side effects associated with the use of raloxifene hydrochloride include
hot flashes/flushing, headache, malaise, weakness, cramping, edema, sweating,
depression, weight gain, and gastrointestinal disturbances such as nausea,
vomiting, indigestion, and diarrhea. Less common side effects include breast
pain, vaginal bleeding, thrombophlebitis (inflammation of vein associated with
blood clot), and visual disturbances. In rare cases raloxifene hydrochloride use
has been associated with stroke, narrowing of the arteries (transient ischaemic
attack), pulmonary embolus, deep-vein thrombosis, low white blood cell or
platelet count, upper gastrointestinal hemorrhage, or ulcer. anti-estrogens may
harm the developing fetus, and should never be used during pregnancy.
Administration:
Raloxifene hydrochloride is FDA approved for the treatment and prevention of
osteoporosis in postmenopausal women, reducing the risk of invasive breast
cancer in postmenopausal women with osteoporosis, and reducing the risk of
invasive breast cancer in postmenopausal women at high risk for invasive breast
cancer. The recommended dose is one 60 mg tablet administered once per day,
without regard to meals. When used (off-label) to mitigate the estrogenic side
effects of anabolic/androgenic steroid use, male athletes and bodybuilders often
take 30 mg to 60 mg per day.
Availability:
Raloxifene hydrochloride is available in over 50 countries. Aside from a small
number of other brands, the Evista product from Eli Lilly & Company is most
likely to be encountered. Price is often a concern, as raloxifene hydrochloride is
considerably more expensive than some of the anti-estrogens bodybuilders and
athletes are already accustomed to such as Nolvadex and Clomid. The price per
individual daily dose of raloxifene hydrochloride (1 tablet) can exceed $2. That
would add up to $200 or more per 100 doses. A hundred tablets of generic
tamoxifen (20 mg) often sell for approximately $50. This is about 50 cents per
dose, or 1/4th the price of raloxifene hydrochloride. Thus far, price, not
availability, seem to be preventing the more widespread diversion of raloxifene
hydrochloride for black market sale.
Fareston® (toremifene citrate)
Description:
Toremifene citrate is an anti-estrogenic drug, specifically classified as a
Selective Estrogen-Receptor Modulator (SERM) with mixed agonist and
antagonist properties. It is a non-steroidal triphenylethylene derivative, similar in
structure and action to both Nolvadex (tamoxifen citrate) and Clomid
(clomiphene citrate). Toremifene citrate is used for the treatment of breast cancer
in postmenopausal women with estrogen-receptor positive or estrogen-receptor
unknown (unsure if the cancer is estrogen responsive) tumors. It works by
attaching to the estrogen receptor in various tissues in a competitive manner,
blocking endogenous estrogen from exerting biological activity. As an antiestrogen in many tissues, male bodybuilders and athletes may use toremifene
citrate to counter some of the side effects associated with the use of aromatizable
or estrogenic anabolic/androgenic steroids. This may include gynecomastia,
body fat gain, and increased water retention.
The triphenylethylene compounds (toremifene citrate, tamoxifen citrate,
clomiphene citrate) tend to be somewhat intrinsically estrogenic in the liver. This
means that while they can block estrogenic activity in some areas of the body,
they can actually act as estrogens in this other key area. Estrogenic action in the
liver is important in the regulation of serum cholesterol (it tends to support HDL
synthesis and LDL reductions). Since steroid-using bodybuilders are already
dealing with the negative cardiovascular effects of these drugs, compounding the
issue with aromatase inhibitors (which will lower total serum estrogen levels)
may not always be the best option. Using a drug that blocks gynecomastia, for
example, while at the same time supporting improved cholesterol values, might
be much more ideal. In terms of which triphenylethylene agent is most effective
in this regard, evidence suggests that the positive lipid altering benefits of
toremifene are significantly stronger than those of tamoxifen, a drug normally
favored for this purpose. Toremifene citrate may, therefore, be the preferred antiestrogen among those concerned about their lipid profiles.
History:
Toremifene citrate was approved by the FDA as a prescription drug in 1997. It is
sold in the U.S. under the Fareston brand name, which is made by GTx, Inc.
Fareston is also available in over two dozen other countries including Australia,
Austria, Belgium, Czech Republic, Finland, France, Germany, Greece, Hungary,
Ireland, Italy, Mexico, Netherlands, New Zealand, Portugal, Russia, South
Africa, Spain, Sweden, Switzerland,Thailand,Turkey, and the United Kingdom.
How Supplied:
Toremifene citrate is most commonly supplied in tablets of 88.4 mg, which are
labeled as (and equate to) 60 mg of toremifene base.
Structural Characteristics:
Toremifene citrate is classified as a selective estrogen receptor modulator, with
both agonist and antagonist properties. It has the chemical designation 2-{p-
[(Z)-4-chloro-1,2-diphenyl-1-butenyl]phenoxy}-N,Ndimethylethylamine citrate
(1:1).
Side Effects:
Toremifene citrate appears to be well tolerated, with a low incidence of serious
side effects. In clinical trials, common side effects associated with its use
included hot flashes (35%), sweating (20%), elevated liver enzymes (19%),
nausea (14%), vaginal discharge (13%), dizziness (95%), edema (5%), vomiting
(4%), and vaginal bleeding (2%). Other observed rare adverse events that may or
may not be linked to toremifene citrate administration include low white blood
cell and platelet counts, skin discoloration or dermatitis, constipation, difficulty
breathing, partial motor paralysis, tremor, vertigo, itching, anorexia, visual
disturbances, loss of strength, hair loss, depression, jaundice, and rigors
(stiffening of the muscles). Anti-estrogens may harm the developing fetus and
should never be used during pregnancy.
Administration:
Toremifene citrate is FDA approved for the treatment of metastatic breast cancer
in postmenopausal women with estrogen-receptor positive or unknown tumors.
The recommended dose is one 60 mg tablet administered once per day. When
used (off-label) to mitigate the estrogenic side effects of anabolic/androgenic
steroid use, male athletes and bodybuilders may use 30 mg to 60 mg per day
during steroid treatment.
Availability:
Toremifene citrate is widely available under the Fareston brand name. It is not
commonly sold on the black market, nor is it a high profile item for
counterfeiters.
Faslodex® (fulvestrant)
Description
Fulvestrant is a highly selective estrogen receptor antagonist (also classified as
an estrogen receptor downregulator). It exerts its action in the body not by
targeting the production of estrogen, but by preventing it from exerting activity
in the body. It does this by binding available estrogen receptors in a competitive
manner, making them unavailable for circulating estrogens. This mode of action
is very similar to Nolvadex (tamoxifen citrate) and Clomid (clomiphene citrate),
although unlike these two agents fulvestrant does not have mixed
agonist/antagonist properties. It is a pure estrogen receptor antagonist. This agent
also stands out as the first injectable estrogen antagonist to catch the attention of
the athletic/bodybuilding world. Although not widely used here, when applied it
may be an effective drug for mitigating the side effects of excess estrogen
caused by anabolic/androgenic steroid use such as gynecomastia, fat buildup,
and increased water retention.
Fulvestrant is very potent as an anti-estrogen, significantly more so than earlier
medications like Nolvadex and Clomid. Although it targets estrogen at its
receptor and not its production, it can still produce an environment of low
estrogenicity on par with strong aromatase inhibition. One study, for example,
shows fulvestrant to be as effective in Arimidex in treating breast cancer patients
who have already failed with first line endocrine treatments.
655 Another shows
the drug prevents tumor cell turnover and growth significantly more effectively
than tamoxifen citrate.
656 Studies investigating the physiological response to
fulvestrant note that the drug actually downregulates estrogen receptor
concentrations. Furthermore, it also tends to downregulate progesterone receptor
concentrations.
657 Fulvestrant does not cross the blood brain barrier, and for this
reason is believed to produce fewer neurological side effects related to estrogen
antagonism such as hot flashes, mood alterations, and low energy.
History:
Fulvestrant was developed by AstraZeneca. It was approved as a prescription
drug in the U.S. in 2002, and is sold under the Faslodex brand name. The drug is
indicated for the treatment of estrogen receptor positive breast cancer with
disease progression following traditional anti-estrogen therapy (such as
tamoxifen). AstraZeneca has since expanded the market for Faslodex to include
over one dozen countries, including Argentina, Belgium, Brazil, Denmark,
Finland, France, Germany, Greece, Ireland, Israel, Italy, Netherlands, Norway,
Poland, Portugal, Spain, Sweden, Switzerland, United Kingdom, and Venezuela.
How supplied:
Faslodex (fulvestrant) is supplied in pre-filled syringes containing 50-mg/mL
fulvestrant, either as a single 5 mL or two 2.5 mL injections.The product must be
refrigerated for storage.
Structural Characteristics:
Fulvestrant is an estrogen receptor antagonist. It has the chemical designation 7-
alpha-[9-(4,4,5,5,5-penta fluoropentylsulphinyl)nonyl]estra-1,3,5-(10)- triene3,17-beta-diol.
Side Effects:
The most common side effects associated with fulvestrant include
gastrointestinal disturbances such as nausea, vomiting, constipation, abdominal
pain, and diarrhea. Other common adverse effects include headache, back pain,
hot flashes, and sore throat. Less common side effects include rash, loss of
strength, urinary-tract infections, venous thromboembolism, liver enzyme
elevations, vaginal bleeding, muscle pain, and low white blood cell count.
Injection side reactions may also occur. Anti-estrogens can harm the
development of an unborn fetus, and should never be taken during pregnancy.
When taken by men (as an off-label use) to reduce estrogenicity during
prolonged periods of steroid treatment, a pure estrogen antagonist may increase
cardiovascular disease (CVD) risk by retarding some beneficial properties of
estrogen on cholesterol values. This may include a suppression of HDL (good)
cholesterol values greater than that induced by steroid therapy alone.
Administration:
Fulvestrant is FDA approved for the treatment of hormone receptor positive
metastatic breast cancer in postmenopausal women with disease progression
following anti-estrogen therapy. The recommended dose is 250 mg administered
intramuscularly (buttock) per month, as either a single 5 mL injection or two 2.5
mL injections. When used (off-label) to mitigate the estrogenic side effects of
anabolic/androgenic steroid use, male athletes and bodybuilders may find a
similar dose to be beneficial.
Availability:
Fulvestrant is available in more than one dozen countries. At the present time, all
fulvestrant in circulation is likely to be of the Faslodex brand name. The drug
itself is exceedingly expensive, and as a result is not widely traded on the black
market.
Femara® (letrozole)
Description:
Letrozole is a non-steroidal selective third generation aromatase inhibitor. The
structure and activity of this compound are very similar to that of Arimidex
(anastrozole), and it is prescribed for similar medical purposes. More
specifically, U.S. prescribing guidelines for letrozole recommend it be used for
the treatment of postmenopausal women with estrogen receptor-positive or
estrogen receptor-unknown (unsure if the cancer is responsive to estrogen) breast
cancer. It is typically used as a second line of treatment after an estrogenreceptor antagonist like tamoxifen has failed to elicit a desirable response,
although it is sometimes initiated as the first course of therapy depending on the
circumstances. Male bodybuilders and athletes find value in letrozole for its
ability to mitigate the estrogenic side effects associated with the use of
aromatizable anabolic/androgenic steroids, such as gynecomastia, fat buildup,
and visible water retention.
Letrozole represents one of the newer achievements in a long line of drugs
targeting aromatase inhibition. It is among the most potent estrogen-lowering
drugs developed to date, and has an effect significantly stronger than nonselective first generation aromatase inhibitors like Teslac and Cytadren. The
dosage of each tablet of Femara is 2.5 milligrams, which according to product
information was sufficient to lower estrogen levels by an average of 78% during
clinical trails. The drug, however, appears to often remain quite effective in
lower doses. The package insert for the product itself comments that during
clinical studies doses as low as .1 and .5 milligrams produced 75 and 78%
estrogen inhibition, respectively in many patients. The recommended dose,
likewise, reflects a level that seems to elicit a desired level of inhibition in nearly
all patients. A large number of people may, therefore, respond well to lower
doses of the drug.
History:
The U.S. Food & Drug Administration approved letrozole for prescription sale
in 1997, where it is sold by Novartis under the Femara trade name. Novartis also
extensively markets the drug in other nations, and more than 70 nations now
carry letrozole as an approved drug. The Femara brand is by far the dominant
preparation worldwide, and is found in such nations as Argentina, Australia,
Belgium, Brazil, Canada, Chile, Czech Republic, France, Germany, Greece,
Hong Kong, India, Netherlands, New Zealand, Italy, South Africa, Switzerland,
and Russia. Novartis also markets the drug under the Femar trade name in some
other nations including Finland, Denmark, Norway, and Sweden. Additionally,
letrozole products can also be found under such other brand names as Fempro
(India), Oncolet (India), Trozet (India), Insegar (Spain), Aromek (Poland),
Lametta (Poland), Cendalon (Argentina), Fecinole (Argentina), and Kebirzol
(Argentina). Given its high level of efficacy and strong marketing support,
Femara, and Femar, remain the most popular letrozole product currently
available.
How Supplied:
Letrozole is most commonly supplied in tablets of 2.5 mg.
Structural Characteristics:
Letrozole is classified as a non-steroidal selective third generation aromatase
inhibitor. It has the chemical designation 4,4’(1H-1,2,4-Triazol-1-
ylmethylene)dibenzonitrile.
Side Effects:
Common side effects associated with the use of an aromatase inhibitor include
hot flashes, joint pain, weakness, fatigue, mood changes, depression, high blood
pressure, swelling of the arms/legs, and headache. Aromatase inhibitors may
also decrease bone mineral density, which may lead to osteoporosis and an
increase in fractures in susceptible patients. Some individuals may also respond
to the medication with gastrointestinal side effects including nausea and
vomiting. Aromatase inhibitors can harm the development of an unborn fetus,
and should never be taken or handled during pregnancy. When taken by men (as
an off-label use) to reduce estrogenicity during prolonged periods of steroid
treatment, aromatase inhibitors may increase cardiovascular disease (CVD) risk
by retarding some beneficial properties of estrogen on cholesterol values.
Studies have demonstrated that when an aromatizable steroid such as
testosterone enanthate is taken in conjunction with an aromatase inhibitor,
suppression of HDL (good) cholesterol levels become significantly more
pronounced. Since the estrogen receptor agonist/antagonist Nolvadex® generally
does not display the same anti-estrogenic (negative) effect on cholesterol values,
it is usually favored over aromatase inhibitors for estrogen maintenance by male
bodybuilders and athletes concerned with cardiovascular health.
Administration:
Letrozole is FDA approved for 1) adjuvant treatment of postmenopausal women
with hormone receptor positive early breast cancer; 2) the extended adjuvant
treatment of early breast cancer in postmenopausal women who have received 5
years of adjuvant tamoxifen therapy; 3) first-line treatment of postmenopausal
women with hormone receptor positive or hormone receptor unknown locally
advanced or metastatic breast cancer; and 4) the treatment of advanced breast
cancer in postmenopausal women with disease progression following antiestrogen therapy. The recommended dose of letrozole is one 2.5 mg tablet
administered once per day, without regard to meals. When used (off-label) to
mitigate the estrogenic side effects of anabolic/androgenic steroid use or increase
muscle definition, male athletes and bodybuilders often take 1.25 mg to 2.5 mg
per day. In some cases a dosage of a half of a tablet (1.25 mg) taken every other
day is sufficient to prevent the onset of estrogenic side effects.
Availability:
Letrozole is most commonly sold under the brand name Femara by the
international drug-manufacturing firm Novartis. It is widely available at the
present time.
Fertodur® (cyclofenil)
Description:
Cyclofenil is a non-steroidal anti-estrogen that is used in the treatment of
menstrual disturbances and anovualtory infertility (an inability to ovulate). It is
very similar in structure to Clomid® and Nolvadex®, and also works in the body
as a mixed estrogen agonist/antagonist. This drug is commonly used for off-label
purposes by male bodybuilders and athletes, typically at the conclusion of a
steroid cycle for the purpose of increasing endogenous testosterone levels. This
is in an attempt to minimize the negative impact that a period of low androgen
levels may have on the physique, which can include significant muscle loss. The
drug HCG is also commonly used for this purpose, but it works by mimicking
the action of luteinizing hormone, not as an anti-estrogen. HCG is typically
looked at as a rapid acting drug, used in the first couple of weeks after the
steroids are withdrawn. Anti-estrogens like cyclofenil, Clomid® and/or
Nolvadex® are often used in conjunction with HCG, but may be continued for
several weeks after the HCG has been removed (see PCT: Post Cycle Therapy).
Cyclofenil stimulates the release of testosterone via its anti-estrogenic action.
The hypothalamus is one target site of this. By interfering with the binding of
estrogen to its receptor in this area of the body, cyclofenil blocks the negative
feedback inhibition brought fourth by this sex hormone. The enhanced release of
gonadotropin releasing hormone (GnRH) may result, which in turn would
stimulate the pituitary to heighten the release of luteinizing hormone. LH is the
primary signal for the testes to increase the production of testosterone, so its
increased release (provided the testes are properly sensitive to LH) leads to an
elevation in the androgen level. The anti-estrogenic effect of this drug in breast
tissue has also led to its use during a steroid cycle to prevent gynecomastia,
similar to how Nolvadex® might be used. Cyclofenil, however, is reported to be
somewhat weaker than Nolvadex®, which is usually preferred as an estrogen
maintenance drug. Women do occasionally find a use for anti-estrogens, most
often around contest time when the management of endogenous estrogens can
help increase fat loss and definition. The side effects that can be brought about
by a lowering of estrogen activity in the female body are usually strong and
uncomfortable, however, making this approach less than ideal.
History:
Cyclofenil was developed during the early 1960s, a time when other agents of
the same class (such as tamoxifen and clomiphene) were being thoroughly
investigated.
Cyclofenil was soon released as a prescription drug agent, sold mainly to
increase the chance of conception and to counter certain menopausal symptoms.
Although the drug seemed to offer a good clinical effect without significant
health concerns, it did not see extensive success on the global market. Instead,
Nolvadex and Clomid dominated this drug category for many decades. Still,
cyclofenil did not completely disappear, and remained available in certain
nations. The most popular brand was Fertodur, produced by Schering. It was
sold in a few countries, including Brazil, Germany, Italy, Mexico, Switzerland,
and Turkey. Other popular brands have included Rehibin (U.K.), Menopax
(Brazil), Neoclym (Italy), Sexovid (Japan), and Ondogyne (France). Today,
although most original cyclofenil products have been discontinued, the drug can
still be found in some areas including Turkey, Italy, and Brazil.
How Supplied:
Cyclofenil is most commonly supplied in tablets of 200 mg.
Structural Characteristics:
Cyclofenil is classified as a selective estrogen receptor modulator, with both
agonist and antagonist properties. It has the chemical designation
4,4’(Cyclohexylidenemethylene)bis(phenyl acetate).
Side Effects:
Cyclofenil appears to be well tolerated, with a low incidence of significant side
effects. Common adverse reactions include liver enzyme elevations, vasomotor
flushes (hot flashes), abdominal discomfort, nausea/vomiting, breast discomfort,
headache, and abnormal uterine bleeding. Premenopausal women may be more
susceptible to hot flashes due to the stronger effect estrogenic disruption can
have on this population. In males, the testosterone boosting properties of
cyclofenil may result in some androgenic side effects including oily skin, acne,
and increased libido.
Administration:
Cyclofenil is most commonly used (medically) to treat anovulatory infertility.
Therapeutic protocols recommend a dose of 200 mg three times per day for 5
days, which is initiated near the start of the menstrual cycle. If pregnancy is not
achieved with the first cycle, it may be used for 3 or 4 cycles in total. In some
instances the drug is also given in lower doses to treat menopausal symptoms.
When used after steroid administration (off-label) to increase natural
testosterone production, a dosage 400-600 mg per day is the most common. It is
often used for a period of 4 to 5 weeks as part of a comprehensive post-cycle
recovery program in place of Clomid (see PCT: Post Cycle Therapy). Similar
doses are used for estrogen maintenance purposes while on-cycle, although
Nolvadex is usually given preference for this purpose. Some athletes have
experimented with using cyclofenil as a standalone anabolic, finding its ability to
increase testosterone levels beneficial. The dosage used for this purpose is
typically 400-600 mg per day for 6-8 weeks. While some have reported this
approach to be effective, many others find the drug too mild, especially in light
of the effects of exogenous testosterone.
Availability:
Cyclofenil is not widely produced. Availability is presently low on the
international market. When located in the U.S., the drug is usually found in the
form of Fertodur, made by Schering in Turkey. Counterfeits of cyclofenil drugs
have not been a significant problem.
Lentaron® (formestane)
Description:
Formestane is classified as a selective irreversible steroidal aromatase inhibitor.
This agent is structurally a derivative of androstenedione, differing from this
well known prohormone only by the addition of a 4-hydroxyl group. This group,
however, is responsible for causing an irreversible attachment between
formestane and aromatase when the two come into contact with each other. This
means that formestane will bond with the enzyme and never let it go,
permanently deactivating it as a result. The enzyme will need to be replaced,
through normal attrition, before the body will recover its lost estrogen
synthesizing capacity. This may take several days or more following cessation of
therapy. Given this mode of action, formestane is also referred to as a “suicide”
aromatase inhibitor, as the drug essentially sacrifices itself in the process of
blocking estrogen conversion. As a class of drugs, aromatase inhibitors are used
(off-label) by male bodybuilders and athletes to prevent the estrogenic side
effects of certain anabolic/androgenic steroids, and to increase fat loss and
muscle definition while dieting.
Because of its potent estrogen-suppressing action, formestane has been used
clinically to treat breast cancer patients in a number of countries including
England, Germany, Switzerland, Spain, Australia, New Zealand, Italy, and
Malaysia. It has been shown to be an effective option as a second line of defense
after tamoxifen, an estrogen receptor antagonist, has failed to elicit a positive
response with patients, and produces an overall response statistically similar to
tamoxifen when administered as the first-line therapy. In terms of overall
potency, formestane is not as strong as the selective third generation inhibitors
like Arimidex (anastrozole) or Femara (letrozole). One study, for example, notes
a 79% level of suppression of estrogen levels with 4 weeks use of Arimidex 1
mg daily (on par with levels noted with Femara use), but only a 58% level of
suppression with intramuscular formestane injections (250 mg every two weeks).
But next to estrogen receptor antagonists like Clomid (clomiphene citrate) and
Nolvadex (tamoxifen citrate), formestane is significantly more effective at
blocking the effects of estrogen in the body.
History:
Formestane was the first selective aromatase inhibitor to be developed as a
prescription drug, first appearing in Europe during the mid-1990s under the
Lentaron Depot brand name. It was sold by Novartis, which marketed Lentaron
Depot in two-dozen countries including Argentina, Austria, Belgium, Brazil,
Canada, Chile, Czech Republic, Denmark, France, Germany, Greece, Hong
Kong, Ireland, Israel, Italy, Malaysia, Netherlands, Portugal, South Africa,
Spain, Switzerland, Turkey, and the United Kingdom. With the emergence of
newer and more effective aromatase inhibitors, however, formestane soon lost
market presence at a rapid rate. Most of the initial Lentaron Depot preparations
have since been discontinued. The drug remains available today, but only in a
small number of nations. This includes Austria, Brazil, Czech Republic, Hong
Kong, and Turkey.
How Supplied:
Formestane is most commonly supplied in a sterile solution containing 125
mg/mL of drug in a 2 mL ampule.
Structural Characteristics:
Formestane is classified a steroidal selective irreversible aromatase inhibitor. It
has the chemical designation 4-Hydroxyandrost-4-ene-3,17-dione.
Side Effects:
Common side effects associated with the use of an aromatase inhibitor include
hot flashes, joint pain, weakness, fatigue, mood changes, depression, high blood
pressure, swelling of the arms/legs, and headache. Aromatase inhibitors may
also decrease bone mineral density, which may lead to osteoporosis and an
increase in fractures in susceptible patients. Some individuals may also respond
to the medication with gastrointestinal side effects including nausea and
vomiting. Aromatase inhibitors can harm the development of an unborn fetus,
and should never be taken or handled during pregnancy. When taken by men (as
an off-label use) to reduce estrogenicity during prolonged periods of steroid
treatment, aromatase inhibitors may increase cardiovascular disease (CVD) risk
by retarding some beneficial properties of estrogen on cholesterol values.
Studies have demonstrated that when an aromatizable steroid such as
testosterone enanthate is taken in conjunction with an aromatase inhibitor,
suppression of HDL (good) cholesterol levels becomes significantly more
pronounced. Since the estrogen receptor agonist/antagonist Nolvadex® generally
does not display the same anti-estrogenic (negative) effect on cholesterol values,
it is usually favored over aromatase inhibitors for estrogen maintenance by male
bodybuilders and athletes concerned with cardiovascular health.
Administration:
Formestane is indicated for the treatment of advanced breast cancer in
postmenopausal women. The recommended dosage is 250 mg by intramuscular
injection (buttock) every two weeks. Although not a medically approved form of
the drug, studies have demonstrated that a similar level of estrogen suppression
can also be achieved with oral use of formestane. Due to poor bioavailability,
however, the dose needed is around 250 mg per day . When used (off-label) to
mitigate the estrogenic side effects of anabolic/androgenic steroid use or increase
muscle definition, male athletes and bodybuilders often take 250 mg every two
weeks by injection, or 250 mg per day orally.
Availability:
Formestane is not widely available as a prescription drug, and consequently is
rarely circulated in the athletic community.
Nolvadex® (tamoxifen citrate)
Description:
Tamoxifen citrate is a non-steroidal anti-estrogenic drug, used widely in clinical
medicine. It is specifically a Selective Estrogen-Receptor Modulator (SERM) of
the triphenylethylene family, and possesses both estrogen agonist and antagonist
properties. As such, it may act as an estrogen in some tissues while blocking the
action of estrogen in others. In breast tissue tamoxifen citrate is a strong antiestrogen, and as a result it is commonly used in the treatment of hormoneresponsive breast cancer in women. In some cases it is even utilized as a
preventative measure, taken by women with an extremely high familial tendency
for breast cancer. In male bodybuilders and athletes, tamoxifen citrate is
commonly used (off-label) to counter the side effects caused by elevated
estrogens subsequent to the use of certain anabolic/androgenic steroids.
The primary worry among the athletic/bodybuilding population is gynecomastia,
or the very unsightly development of female breast tissue in men. This can be
first noticed by the appearance of swelling or a small lump under the nipple. If
left to progress, this can develop into a large hard-tissue gynecomastia that may
be an irreversible occurrence without surgery. The estrogen can also lead to an
increase in the level of water retained in the body, resulting in a notable loss of
definition as the muscles begin to look smooth (even bloated) due to the
retention of subcutaneous fluid. Fat storage may also be increased as estrogen
levels rise in men. In fact, differences in the estrogen/androgen ratio are one of
the reasons women have a higher body fat percentage, and different fat
distribution (hips/thighs), than men.
Tamoxifen citrate also possesses the ability to increase production of FSH
(follicle stimulating hormone) and LH (luteinizing hormone). This is
accomplished by blocking negative feedback inhibition caused by estrogen at the
hypothalamus, which (via the actions of GnRH) fosters the release of the
mentioned pituitary hormones. This is very similar to the function of Clomid®
and cyclofenil. Since a higher release of LH can stimulate the Leydig’s cells in
the testes (men) to produce more testosterone, tamoxifen citrate can have a
positive impact on one’s serum testosterone level. This “testosterone
stimulating” effect is an added benefit when preparing to conclude a steroid
cycle. Since anabolic/androgenic steroids tend to suppress endogenous
testosterone production, tamoxifen citrate can help restore a balance in hormone
levels. It is most commonly used as part of a comprehensive post cycle recovery
program (see PCT: Post-Cycle Recovery).
Note that like some other triphenylethylene compounds, tamoxifen citrate can
act as an estrogen in the liver . Estrogenic action in the liver is important in the
regulation of serum cholesterol, and tends to support HDL (good) cholesterol
synthesis and LDL (bad) cholesterol reductions. Since steroid-using
bodybuilders are already dealing with the negative cardiovascular effects of
these drugs, compounding the issue with aromatase inhibitors (which will lower
total serum estrogen levels) may not always be the best option. Using a drug that
blocks gynecomastia, for example, while at the same time supporting improved
cholesterol values, might be much more ideal. It is important to note that
tamoxifen citrate is not sufficient to stabilize serum cholesterol at healthy levels
with the use of c-17alpha alkylated orals or high doses of steroids in general.
The effect it would have on cholesterol values would likely be one of degrees,
and cannot be relied upon to eliminate cardiovascular disease risk from
anabolic/androgenic steroid use.
History:
Tamoxifen citrate was first synthesized in 1962 by ICI . It was made
commercially available in the U.S. not long after, but was initially used to treat
certain forms of female infertility, a purpose for which tamoxifen citrate does
not seemed ideally suited. In 1971, the first clinical trials evaluating the
effectiveness of tamoxifen citrate in breast cancer patients were undertaken .
Two years later, noting the link between estrogen and breast cancer and the
success of early trials, ICI pursued marketing the drug in the U.S. to treat breast
cancer. It was not until 1977 that FDA approval for this use would finally be
granted. Tamoxifen citrate was sold by ICI in a wide number of countries under
the Nolvadex brand name (the company would later become known as
AstraZeneca). A number of generics and other brands followed, presently too
numerous to list. In 1998, the FDA approved expanding the indicated uses of
tamoxifen citrate to include breast cancer prevention for women at high risk for
developing the disease. In spite of continued clinical success with the drug for
both cancer treatment and prevention, in June 2006 AstraZenica finally
discontinued the sale of Nolvadex in the U.S. A number of generic versions are
still available in this country, however, ensuring easy patient access to the drug.
Tamoxifen citrate is presently the most popular anti-estrogen used by athletes
and bodybuilders.
How Supplied:
Tamoxifen citrate is most commonly supplied in tablets of 10 mg or 20 mg.
Structural Characteristics:
Tamoxifen citrate is classified as a selective estrogen receptor modulator, with
both agonist and antagonist properties (also known as an estrogen
agonist/angagonist). It has the chemical designation (Z)2- [4-(1,2-diphenyl-1-
butenyl) phenoxy]-N, Ndimethylethanamine 2-hydorxy-1,2,3-
propanetricarboxylate (1:1).
Side Effects:
Common side effects associated with the administration of tamoxifen citrate
include hot flashes, vaginal bleeding, vaginal discharge, vaginal itching, upset
stomach, headache, light-headedness, edema, and hair loss. Other listed adverse
reactions include skin rash, reduced platelet or white blood cell count, visual
disturbances, uterine fibroids, endometriosis and other endometrial changes,
deep vein thrombosis and pulmonary embolism, changes in liver enzyme levels,
and increased triglyceride levels. An increased incidence of endometrial cancer
and uterine sarcoma has been reported in association with tamoxifen citrate.
Tamoxifen citrate may cause birth defects and should not be taken during
pregnancy.
Administration:
Tamoxifen citrate is indicated for 1) the treatment of metastatic breast cancer in
women and men; 2) adjuvant treatment of node-negative breast cancer following
breast surgery and radiation; 3) adjuvant treatment of node-positive breast cancer
in postmenopausal women following breast surgery and radiation; 4) reduction
in incidence of contralateral breast cancer (in the other breast) in the adjuvant
setting; 5) reduction in incidence of invasive breast cancer in women with DCIS
(Ductal Carcinoma in Situ) following breast surgery and radiation; and 6)
reduction in incidence of breast cancer in women at high risk for breast cancer.
In women and men with metastatic breast cancer, a dose of 10-20 mg is
administered twice a day (morning and evening). When used by men (off-label)
to mitigate the estrogenic effects of anabolic/androgenic steroid use, a daily
dosage of 10-30 mg (1-3 tablets) is usually administered while any offending
steroids are taken, or as part of a comprehensive post-cycle hormone recovery
program.
It is important to note that anti-estrogen use may slightly reduce gains made
during a steroid cycle, as many androgenic/anabolic steroids seem to exhibit
their most powerful anabolic effects when accompanied by a sufficient level of
estrogen (See: Estrogen Aromatization). This may be one reason why gains
made with a strong aromatizable androgen like testosterone are usually more
pronounced than those achieved with anabolic steroids that aromatizes to a lower
(or no) degree. Therefore, it is usually advised to identify a specific need for
tamoxifen citrate before committing to its use during a cycle. Many people, in
fact, find the use of an anti-estrogen unnecessary, even when utilizing
problematic compounds such as testosterone or methandrostenolone. Others,
however, find they are troubled by water retention and gynecomastia even with
milder (less estrogenic) drugs like Deca-Durabolin® and Equipoise®. The
estrogenic response to steroid use is very individual, and may be influenced by
factors such as age and body fat percentage (adipose tissue is a primary site of
aromatization).
Availability:
Tamoxifen citrate is widely manufactured, and can be found in virtually every
developed nation of the world. The drug is also commonly circulated on the
black market. Given its relatively low price and high availability, counterfeit
product do not appear to be a large issue.
Teslac® (testolactone)
Description:
Testolactone is a first generation non-selective steroidal aromatase inhibitor,
used clinically to treat estrogen-dependent breast cancer. Its exact mode of
action is unknown, but it is believed to inhibit the aromatase enzyme in a
noncompetitive and irreversible manner. If so, this would be an activity that is
very similar to that of Lentaron (formestane). This might also explain why
cessation of the drug does not provide an immediate restoration of normal
estrogen production. Like formestane, it takes several days after ceasing use for
the body to recover its normal estrogen synthesizing capacity, which is the time
required by the body to replenish its enzyme levels. It seems logical based on
structure and action that the same thing occurs with testolactone.
Although testolactone is technically steroidal in structure, it offers no anabolic or
androgenic effect to its user. This is because it does not possess the traits
necessary to bind and activate the androgen receptor, namely an active 17-betahydroxyl group. In fact, its D ring is an unusual sixmembered lactone ring, and
not the normal five membered carboxylic ring that testosterone and its
derivatives normally possess. This is likely where testolactone got its name,
which may be short for testosterone-lactone. Studies actually suggest this
steroidal drug possesses some level of anti-androgenic action, which likely
occurs via competitive inhibition of the cellular androgen receptor . Regardless
of this, testolactone has been included in the U.S. controlled substance list as an
anabolic/androgenic steroid. For the purposes of this reference book it will
remain classified as an anti-estrogenic drug. Likewise, testolactone is used by
athletes and bodybuilders not to increase muscle mass and performance, but to
mitigate the estrogenic side effects caused by certain anabolic/androgenic
steroids.
Note that the level of aromatase inhibition produced with testolactone is
significantly lower than that produced by the newer selective third generation
inhibitors such as anastrozole, letrozole, and exemestane. For example, one
study conducted in 1985 showed that 1,000 mg of testolactone per day given to
nine normal men for a period of ten days suppressed serum estradiol levels by
25% . Another using the same 1,000 mg dose noted a 50% reduction after six
days of use . These numbers are lower than what would be expected of the newer
third-generation agents given the substantial estrogen suppression figures they
have produced during clinical trials with women.
History:
Testolactone was first approved as a prescription drug by the FDA back in 1970.
It was an early anti-estrogenic drug, exhibiting a moderately pronounced effect
but failing to reach levels of high clinical success. As other more effective
medications began to surface for the treatment of breast cancer, testolactone
would not see the success its developers likely planned for it. It would see
production in a small number of countries outside the U.S., most notably Brazil,
Germany, and Chile. It has since been discontinued in all countries but the U.S.,
where the Teslac brand is still available.
How Supplied:
Testolactone is most commonly supplied in tablets of 50 mg.
Structural Characteristics:
Testolactone is classified as a steroidal noncompetitive irreversible steroidal
aromatase inhibitor. It has the chemical designation 13-hydroxy-3-oxo-13,17-
secoandrosta-1,4-dien-17-oic acid [dgr ]-lactone.
Side Effects:
Common side effects associated with the use of an aromatase inhibitor include
hot flashes, joint pain, weakness, fatigue, mood changes, depression, high blood
pressure, swelling of the arms/legs, and headache. In 1999, the FDA officially
added malaise to the list of possible side effects from this drug, reflecting
something bodybuilders had noticed for some time: low estrogen levels can lead
to lethargy, as this sex hormone plays an important role in the functioning of the
central nervous system. Aromatase inhibitors may also decrease bone mineral
density, which may lead to osteoporosis and an increase in fractures in
susceptible patients. Some individuals may also respond to the medication with
gastrointestinal side effects including nausea and vomiting. Aromatase inhibitors
can harm the development of an unborn fetus, and should never be taken or
handled during pregnancy. When taken by men (as an off-label use) to reduce
estrogenicity during prolonged periods of steroid treatment, aromatase inhibitors
may increase cardiovascular disease (CVD) risk by retarding some beneficial
properties of estrogen on cholesterol values. Studies have demonstrated that
when an aromatizable steroid such as testosterone enanthate is taken in
conjunction with testolactone, suppression of HDL (good) cholesterol levels
becomes significantly more pronounced. Since the estrogen receptor
agonist/antagonist Nolvadex® generally does not display the same antiestrogenic (negative) effect on cholesterol values, it is usually favored over
aromatase inhibitors for estrogen maintenance by male bodybuilders and athletes
concerned with cardiovascular health.
Administration:
Testolactone is FDA approved as adjunctive therapy in the palliative treatment
of advanced or disseminated breast cancer in postmenopausal women when
hormonal therapy is indicated. It may also be used in women who were
diagnosed as having had disseminated breast carcinoma when premenopausal, in
whom ovarian function has been subsequently terminated. The recommended
dosage is 250 mg taken 4 times per day. When used (off-label) for estrogen
suppression in male steroid users, a dosage of 250 mg (five tablets) is usually
taken per day.
Availability:
Testolactone is no longer commonly used in clinical medicine, and consequently
is not manufactured on a large sale globally. Presently a small number of
testolactone preparations still exist, but are not commonly diverted for sale on
the black market given the very low demand for the drug in this population.
Anti-Prolactin
Dostinex (cabergoline)
Description:
Cabergoline is a selective dopamine receptor agonist. This agent is highly
specific in its actions, with a strong affinity for the dopamine D2 receptor, and a
low affinity for serotonin, and 5-HT2-serotonin receptors. Its main clinical use is
for the treatment of hyperprolactinemia, or the hypersecretion of prolactin from
lactotropes in the anterior pituitary (pituitary tumor is a common cause of this
disorder). It is also applied in the management of Parkinson’s disease.
Cabergoline effectively inhibits prolactin secretion, which it does by mimicking
the actions of dopamine on the D2 receptor (dopamine normally serves as
negative feedback for prolactin release). As a targeted agonist of the dopamine
D2 receptor, cabergoline should not affect other pituitary hormones like growth
hormone (GH), luteinizing hormone (LH), corticotrophin (ACTH), or thyroid
stimulating hormone (TSH).
Prolactin is a somatotropic hormone, in the same family as human growth
hormone (somatropin). It is a single peptide hormone, containing a chain of 199
amino acids. This makes it similar to (though slightly larger than) growth
hormone, which is made of 192 amino acids. Any similarity between these two
hormones, however, ends at structure. Prolactin is not an anabolic agent (at least
not to skeletal muscle) but a lactation hormone. Most of its physiological value
is in women, and becomes apparent during pregnancy when it aids in milk
production. Cabergoline, likewise, is sometimes used to suppress lactation
postpartum if there is a particular medical need for it. In men, prolactin has no
known therapeutic value, and high levels are associated with impotence,
infertility, and sometimes even gynecomastia (whether or not it has a causative
role here remains the subject of much debate).
Although this is almost never associated with males, high levels of prolactin
have actually been related to lactating gynecomastia in a very small percentage
of steroid-using athletes. This disorder is often characterized by small fluid
discharge that becomes noticeable with the squeezing of one’s gynecomastic
nipple. Although the situation can become worse, the first sign of this is often
enough to scare the individual away from their current regimen of steroids.
Gynecomastia is not automatically (or even normally) associated with lactation,
so this is a somewhat rare phenomenon. It is probably caused by an unusual
imbalance of hormones (androgens, estrogens, and progestins can all be involved
and play varying roles), and/or a particular personal sensitivity to the disorder.
When it does occur, however, cabergoline has been looked at as a remedy for the
potentially embarrassing situation.
High prolactin levels (as would be associated with the need for cabergoline) are
not regularly documented in steroid-using athletes, further underscoring the
relative uncommon nature of this disorder. We do know that estrogen plays a
stimulatory role here, and likely is the key to increasing prolactin secretion in
males.
658 659 660 Other studies, however, show suppressive actions toward
prolactin from other hormones including androgens.
661 This is perhaps why an
actual hormonal imbalance, and not necessarily high estrogen, may be the cause
of lactating gynecomastia. Scanning the medical books, there are few studies
even looking at prolactin levels and steroid use, and those few are relatively
inconclusive. One study analyzed the effects of testosterone enanthate and
propionate in men and noted a significant prolactin increase 4 days after
injection.
662 Yet another noted a 7-fold increase in estrogen (to values typical for
women) in 5 power athletes self-administering testosterone and other steroids,
yet no consistent effect on prolactin secretion.
663 A third self-administration
study with athletes,
664 and a fourth clinical with nandrolone,
665
failed to show an
increase in prolactin levels.
History:
Cabergoline was developed during the 1980s. The most popular trade name for
this agent is Dostinex, which is produced in the U.S. and many other countries
by the giant pharmaceutical conglomerate Pharmacia. Dostinex retained market
exclusivity on cabergoline in the U.S. for many years, but between 2005 and
2007 several generic versions were approved for sale by the FDA. This includes
products from Barr, Ivax, and Par Pharm. Cabergoline is widely available
internationally, and can be found in more than 3-dozen different countries.
Outside the U.S. the Dostinex trade name still dominates most markets, and can
be found in Argentina, Australia, Austria, Belgium, Brazil, Canada, Chile, Czech
Republic, Denmark, Finland, France, Germany, Greece, Hong Kong, Ireland,
Israel, Italy, Malaysia, Mexico, Netherlands, Norway, New Zealand, Poland,
Portugal, Russia, South Africa, Singapore, Spain, Sweden, Switzerland, Turkey,
United Kingdom, and Venezuela. In addition to Dostinex, cabergoline is
marketed under at least 1-dozen other trade names.
How Supplied:
Cabergoline is most commonly supplied in tablets of 500mcg.
Structural Characteristics:
Cabergoline is an ergot derivative with the chemical designation 1-[(6-
allylergolin-8beta-yl)carbonyl]-1-[3- (dimethylamino)propyl]-3-ethylurea.
Side Effects:
The most common side effects reported with cabergoline use include headache,
nausea, and vomiting, which occurred in 26, 27, and 2% of patients
(respectively) receiving the medication during one clinical trial.
666 Other
potential side effects include (but are not limited to) constipation, dry mouth,
abdominal pain, diarrhea, dizziness, vertigo, fatigue, anxiety, anorexia, malaise,
depression, insomnia, hot flashes, heart palpitations, hypotension, breast pain,
and acne, however nausea and headache were the most prominent side effects.
Many side effects are dose related, further reason for starting off with the lowest
possible therapeutic dose and working up. The prescribing information does not
mention death as a clear consequence of an overdose, but it does list
hallucinations, low blood pressure, and nasal congestion. Note that overdose
patients may need supportive measures to raise blood pressure.
Administration:
When used medically to inhibit prolactin secretion, cabergoline is given in an
initial dosage of 500 mcg per week.This may be taken in one single dose or
divided into 2 or more doses on separate days. The dose may be increased by
500 mcg per week at monthly intervals until a desired physiological response is
achieved. Dosage is most commonly maintained at 1mg per week, although
doses up to 4.5 mg may be used in some cases.When used by
athletes/bodybuilders to inhibit prolactin secretion (as with lactating
gynecomastia), doses on the lower end of the therapeutic range are most
commonly used. The user typically starts with a dosage of 250mcg per
application (a half tablet) twice per week. This is used for four weeks, at which
point the dosage might be adjusted upwards to a full tablet if needed (1 mg per
week).In clinical medicine this drug may be taken for 6 months or longer,
although athletes/bodybuilders usually find a 4-6 week course of therapy
(combined with an intelligent rearrangement of the offending drugs) most
appropriate.
Availability:
Cabergoline is not widely used by bodybuilders and athletes, and consequently is
not commonly traded in black market commerce. The drug itself is widely
available in legitimate medical commerce.
Parlodel® (bromocriptine mesylate)
Description:
Bromocriptine mesylate is a dopaminomimetic ergot derivative with D2
dopamine receptor agonist and D1 dopamine receptor antagonist activities. It is
used most commonly as a prolactin inhibitor in cases of hyperprolactinemia, a
growth hormone suppressant in acromegaly (high doses are required), and as an
adjunctive medication to levodopa in the management of Parkinson's disease.
The structure and activity of this drug are very similar to that of cabergoline
(Dostinex). In the athletic/bodybuilding communities, bromocriptine is
sometimes used to induce fat loss or combat elevated prolactin levels subsequent
to anabolic/androgenic steroid use (a rare occurrence, sometimes marked by
lactating gynecomastia).
The most vocal proponent of bromocriptine use for fat loss is probably Lyle
McDonald, author of the online e-Book Bromocriptine: An Old Drug With New
Uses. In this book McDonald describes how the drug can be used to normalize
the metabolism, such that some of the normal physiological responses to dieting
(which begin to slow the loss of body fat as the duration of dieting increases) are
hindered. A lot of this focuses on leptin, a hormone looked at as sort of a fat
thermostat, telling your brain how much adipose tissue you have on your body
and how many calories you are regularly consuming (an “anti-starvation”
hormone). Dieting tends to lower leptin levels significantly, which causes your
body to respond in an appropriate way for survival (it tries to hold on to its
nutrient stores as much as possible). Maintaining normal leptin stimulation could
be key to keeping any diet productive, and bromocriptine may indeed allow us to
do that.
The human medical data concerning the potential role this drug might play in
supporting ongoing fat loss is encouraging. In cases where it was given while
dieting, bromocriptine was capable of increasing total fat loss by a statistically
significant degree, and seemed to extend the duration in which the diet was most
effective. In one case, both placebo and treatment groups were noticing a
measurable fat loss during the first 6 weeks of calorie restriction. Only the
bromocriptine group, however, continued to lose significant amounts of weight
for the remaining 12 weeks of intervention. Dieting plateau, or a point in which
continued fat loss drastically slows or stops, is a common issue among those
undertaking a calorie-restricted diet for the purpose of reducing body fat mass. A
drug that can prevent or delay this plateau may logically be able to increase the
overall effectiveness of dieting for many individuals.
History:
Bromocriptine has been used widely in clinical medicine for its indicated used
since the 1970s. It is also much more widely distributed than its counterpart
medication cabergoline, which is used for a similar set of clinical indications. In
the U.S., the most common brand name is Parlodel, which is sold by Novartis.
The drug is available in dozens of countries, and is sold under a similarly large
number of different trade names including (but not limited to) Bromed, Criten,
Grifocriptina, Bromo-Kin, Pavidel, and Gynodel. Bromocriptine remains a
common medication today in most developed nations for its intended therapeutic
uses.
How Supplied:
Bromocriptine mesylate is most commonly supplied in tablets of 2.5 mg and 5
mg. The doses are expressed in terms of base bromocriptine, so each 2.5 mg
tablet contains 2.87 mg of bromocriptine mesylate.
Structural Characteristics:
Bromocriptine mesylate is an ergot derivative with the chemical designation
(5’S)-2-bromo-12’-hydroxy-2’-(1-methylethyl)-5’-(2-methylpropyl)-ergotaman3’,6’,18-trione methanesulphonate.
Side Effects:
Bromocriptine can produce a number of unwanted side effects, the most notable
being low blood pressure, dizziness, confusion and nausea. These side effects do
tend to be dose related, with the low recommended doses used in bodybuilding
are not likely to be much trouble for many. Further, initial nausea sometimes
goes away after a couple of applications, once the user becomes accustomed to
the drug. However, the strong incidence of any unwelcome side effects should
warrant discontinuing therapy, especially if blood pressure is becoming
negatively affected (too low a drop). Less common adverse reactions include
anxiety, dry mouth, edema, seizures, fatigue, headache, lethargy, nasal
congestion, rash, elevated liver enzymes, and changes in urinary frequency.
Administration:
When used medically to treat disorders marked by hyperprolactinaemia (hyper
secretion of prolactin), an initial dosage of 1.25 mg to 2.5 mg per day is usually
recommended.This may be increased by 2.5 mg every 2-7 days until an
acceptable therapeutic dosage is established. This may require taking as much as
20-30 mg per day. When used (off-label) to support fat loss, dieting individuals
commonly take between 2.5 mg and 5 mg per day. This is given in a single
morning dose, due to the relatively long half-life of the drug. This may be used
in short dieting cycles, and should not be considered for long-term weight
management. Similar dosing schedules are common when used by athletes and
bodybuilders to counter lactating gynecomastia, although higher doses may be
required in some instances. A 4-6 week course of therapy, combined with a
rearrangement of offending steroids, is usually undertaken.
Availability:
Bromocriptine is produced in most developed countries, including the United
States where it is sold as a generic drug and under the Parlodel brand name.The
brand name product comes in the form of both 2.5 mg tablets and 5 mg capsules,
with 100 doses per bottle. At the pharmacy, 100 5 mg capsules may cost nearly
$400. In some nations, this price may be as low as $50 to 200 ($.50 to $1.00 per
dose) for generic and other brands of bromocriptine. Bromocriptine is not widely
diverted for sale on the black market, but can be found circulating on occasion.
Appetite Stimulants
Periactin (cyproheptadine hydrochloride)
Description:
Cyproheptadine hydrochloride is a first-generation prescription histamine and
serotonin antagonist. This drug is most often given in the U.S. for the treatment
of allergy-related symptoms, including hay fever, runny nose, irritated eyes,
hives, and swelling. It is also FDA approved for the treatment of anaphylactic
reactions caused by allergens, often as an adjunct to injectable epinephrine
(adrenalin). The serotonin inhibiting effect of this drug also gives it a unique
ability to increase appetite. This has led to a considerable amount of off-label use
as a weightgain medication, particularly with patients who are suffering from a
lean tissue wasting associated with AIDS infection, cancer, or other debilitating
diseases. Cyproheptadine hydrochloride is also used on occasion as an adjunct to
growth hormone therapy in children, to foster greater nutrient uptake and
increases in linear growth beyond what is normally achieved with rHGH
alone.
667 Bodybuilders and athletes use the drug on occasion to help increase
caloric intake, usually during periods of bulking training where increased mass is
desired, and often used in conjunction with anabolic/androgenic steroids.
Although this is a controversial use of the drug, references to the appetite
stimulating properties of cyproheptadine hydrochloride are abundant in the
medical literature. One of the more detailed papers compares the appetite
increasing effects of cyproheptadine hydrochloride to megestrol acetate
668
in a
group of 14 men with weight loss associated with HIV infection. The other
agent, megestrol, is a progestin that was approved by the FDA in 1993 for the
treatment of anorexia, cachexia, or weight loss in patients with AIDS. In this
investigation, cyproheptadine hydrochloride was shown to have a similar level
of benefit to FDA approved agent megestrol, with patients consuming about 500
extra calories per day, and gaining a moderate amount of weight with either
medications. While the benefits were similar, the side effects were not. The
investigators reported that more than 50% of the patients taking megestrol
suffered impotence during the investigation, while the cyproheptadine
hydrochloride group had no such side effects. Cyproheptadine hydrochloride
may offer an effective alternative to megestrol therapy for many patients,
especially those prone to negative side effects associated with this type of
hormone manipulation.
History:
Cyproheptadine hydrochloride is an early anti-histamine drug, and has been sold
as a prescription medication in most developed nations for decades. It was
introduced to the U.S. in 1961 under the Periactin® brand name by Merck & Co.
This brand of cyproheptadine hydrochloride was sold for many years in the U.S,
but was voluntarily discontinued by Merck in 2003 (in both the U.S. and
Canada). While Merck & Co. has withdrawn Periactin from a number of other
nations (likely due to low financial interest), the brand is still sold in more than
one dozen countries including Australia, Austria, Belgium, Ireland, Italy,
Netherlands, New Zealand, South Africa, Spain, Sweden, Thailand, and the
United Kingdom. It is also sold under dozens of other brand names around the
world, in both single-and multi-ingredient preparations. A number of generic
products are still sold in both the U.S. and Canada as well. Subsequent to studies
questioning the long-term weight gaining value of cyproheptadine hydrochloride
therapy, in 1994 the World Health Organization warned against using the drug
for this purpose.
669 Regardless of this report, many still support the value of
cyproheptadine hydrochloride as a short-term appetite stimulant.
How Supplied:
Cyproheptadine hydrochloride is most commonly supplied in tablets of 4 mg.
Structural Characteristics:
Cyproheptadine hydrochloride is antihistaminic and antiserotonergic agent with
the chemical designation 4- ( 5H - dibenzo [a,d] cyclohepten - 5 - ylidene) - 1 -
methylpiperidine hydrochloride sesquihydrate.
Side Effects:
As a first-generation anti-histamine, cyproheptadine hydrochloride may be prone
to producing a number of side effects in its users. The most common of which is
sedation or the classic “anti-histamine lethargy”, which is common to these types
of drugs. For some users, the tiredness that cyproheptadine hydrochloride will
produce will outweigh any potential as a weightgaining/performance-enhancing
agent. For most, this side effect of cyproheptadine hydrochloride is not very
noticeable, and perhaps a nuisance (not strong enough to an ingredient.
necessitate discontinuation) at best. Other less common side effects of concern
include, but are not limited to, dizziness, disturbed coordination, muscular
weakness, nausea, vomiting, diarrhea, constipation, dryness of the mouth,
difficulty urinating, vertigo, blurred vision, tightness of the chest, wheezing,
stuffed nose, sweating, early period, headaches, and faintness. Any strong
incidence of unwelcome side effects would immediately warrant discontinuing
the drug, or even seeking immediate medical attention if severe.
Administration:
The dosage required for medical purposes may vary depending on the individual
and their particular needs. The established therapeutic range for cyproheptadine
hydrochloride is 4 mg to 20 mg per day, with most adults requiring 12 mg to 16
mg daily. The total daily dosage is usually divided into three separate
applications. When used (off-label) as an appetite stimulant, a dosage of 4mg is
commonly taken 2-3 times per day (8-12 mg).Above this level, side effects may
become more noticeable (most notably sleepiness), often interfering with the
benefit of the drug. This may be used during a steroid cycle focused on bulking,
with the intake of cyproheptadine hydrochloride usually lasting no more than 4-8
weeks. For those who tolerate this anti-histamine’s side effects (mainly
tiredness), cyproheptadine hydrochloride is often reported to offer significant
value as an appetite stimulant during weight gaining cycles. This is especially so
in individuals that have trouble eating enough food to meet the high
calorie/protein requirements for optimal muscle growth.
Availability:
Cyproheptadine hydrochloride is produced in a wide number of countries.
Although it is not commonly traded on the black market, high supply and the
relatively benign nature of this drug (loose controls) make it easily diverted for
sale when needed. Given its low demand, counterfeiting of cyproheptadine
hydrochloride preparations is not common.
It is interesting to also note that the Dominican steroid product, Anabolex,
actually includes 1.5 mg of cyproheptadine hydrochloride in each 3 mg
methandrostenolone tablet, which was added by its developers to facilitate
increased caloric intake and weight gain during anabolic therapy. The 2:1 ratio
provided is optimal for a daily dose of 24 mg Dianabol (a very common
amount), as it would provide 12 mg of cyproheptadine hydrochloride (the
maximum common daily dose). This is the only common anabolic steroid
product that includes cyproheptadine hydrochloride as an ingredient.
Cardiovascular Support
Lipid StabilTM
Description:
Lipid Stabil is a cholesterol and cardiovascular health support supplement. It was
specifically designed to be a foundation supplement for steroid users, and is
especially useful during on-cycle periods. The formula specifically focuses on
supporting four separate areas of cardiovascular health: 1) reducing LDL (lowdensity lipoprotein) “bad” cholesterol; 2) increasing beneficial HDL (highdensity lipoprotein) cholesterol; 3) reducing serum triglycerides; and 4) reducing
oxidative stress and arterial plaque formation. Antioxidant supplementation is an
important and often overlooked part of managing cardiovascular health during
anabolic/androgenic steroid use, as AAS are known to increase homocysteine
levels and oxidative stress. Although no supplement can completely eliminate
the cardiovascular risks of AAS abuse, a supplement such as Lipid Stabil (or one
with a similar ingredient profile) is highly recommended, as it may help reduce
the lasting negative health impact of these medications.
Lipid Stabil contains a comprehensive blend of nearly one dozen natural
ingredients. Each component in known to play an important role in
cardiovascular health, and many have significant clinical support demonstrating
beneficial effects on key health markers. For example, garlic powder is one of
the backbone ingredients, and has been shown in studies to increase HDL
cholesterol, reduce LDL cholesterol, and improve the antioxidant response.
670
671 Green tea extract (standardized for EGCG and high polyphenol content) is
another backbone ingredient, and like garlic, is also shown to improve
cholesterol and reduce oxidative stress/LDL oxidation.
672 673 Several other
clinically studied ingredients known to improve cholesterol levels, serum
triglycerides, and/or systemic antioxidant capacity round out the Lipid Stabil
formula including resveratrol,
674 phytosterols,
675 policosanol,
676 selenium,
677
and inositol hexanicotinate (no-flush niacin).
678
History:
Lipid Stabil was developed in 2008 by Molecular Nutrition (U.S.). The focus
was specifically on designing a supplement that can help support cardiovascular
health in anabolic/androgenic steroid users. The product can be found through
international distribution, although it may possibly be considered a drug product
in some regions with strict controls on herbal supplement products.
How Supplied:
Each serving of Lipid Stabil is supplied in 3 capsules, and contains a blend of
green tea extract (750 mg), garlic powder (600 mg), inositol hexanicotinate (400
mg), polygonum cuspidatum standardized for resveratrol (200 mg), pantothenic
acid (100 mg), phytosterol complex (100 mg), policosanol (10 mg), and
selenium (200 mcg).
Side Effects:
Lipid Stabil is a natural dietary supplement and is not expected to have notable
side effects.
Administration:
For general cholesterol and lipid support or as an adjunct to anabolic/androgenic
steroid use, Lipid Stabil is generally taken at a dosage of 3 capsules per day.
Note that a natural product such as Lipid Stabil may help reduce cardiovascular
toxicity, but cannot be relied upon to completely eliminate potential
cardiovascular damage from the abuse of anabolic/androgenic steroid drugs.
Care should always be taken to monitor all aspects of health when taking AAS
substances.
Availability:
Lipid Stabil is produced in the U.S. by Molecular Nutrition. It is available for
export, and may be found in Canada, Europe, and other international markets.
Lovaza® (omega-3 ethyl esters)
Description:
Lovaza is a prescription omega-3-acid supplement which contains ethyl esters of
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). It is
fundamentally similar to most over-the-counter fish oil supplements, except that
Lovaza is highly purified to drug quality standards, is made with a high (90%)
concentration of omega-3 acids, and has gone through extensive clinical trials
for a specified therapeutic use. Otherwise, the benefits of EPA/DHA should be
reproducible with any quality mercury-free fish oil supplement. In the U.S.,
Lovaza is approved to lower triglycerides in patients with very high triglyceride
levels (>500 mg/dL). Clinical studies showed triglyceride reductions by as much
as 45% with its use.
679 680
In addition, this prescription supplement has been
shown to increase HDL (good) cholesterol levels, improve lipoprotein particle
size and subclass distribution,
681 and reduce cardiovascular mortality in some
patients by 30%.
682 EPA/DHA supplements are commonly taken by
anabolic/androgenic steroid users in an effort to reduce the negative
cardiovascular effects of AAS.
The mechanism of action of eicosapentaenoic acid (EPA) and docosahexaenoic
acid (DHA) is not fully understood. These omega-3 acids appear to exert their
favorable properties over serum lipids through a number of different but
complimentary pathways. For one, EPA and DHA appear to be effective at
increasing the enzyme hepatic lipoprotein lipase,
683 which can increase the
excretion of LDL cholesterol and triglycerides. These omega-3 acids may also
increase mitochondrial and peroxisomal beta-oxidation, reducing the availability
of fatty acids for lipid synthesis.
684 They may also suppress nuclear SREBP-1,
which reduces hepatic lipogenesis.
685 EPA and DHA also appear to decrease the
activity of the triglyceride-synthesizing enzyme diacylgylcerol acyltranferase.
686
The lipid reducing actions of EPA and DHA, therefore, appear to be several fold,
including reduced substrate availability, reduced lipid synthesis, and increased
lipid breakdown.
History:
The first prescription drug product containing omega-3 acids was approved by
the U.S. Food and Drug Administration in 2004. It was sold in this market under
the Omacor brand name until 2007, when the manufacturer, Reliant
Pharmaceuticals, changed the name of the product to Lovaza. This was done to
eliminate any confusion with the blood clotting medication Amicar
(aminocaproic acid). Lovaza is presently distributed in the U.S. by the
international drug manufacturer GlaxoSmithKline.
How Supplied:
Lovaza is supplied in soft gelatin capsules containing approximately 900 mg of
omega-3-acids each. The doage consists mainly of eicosapentaenoic acid (465
mg) and docosahexaenoic acid (375 mg).
Side Effects:
Lovaza is a natural dietary product and is not expected to have notable side
effects. A small percentage of patients reported mild adverse reactions during
clinical trials, including back pain (2.2%), flu symptoms (3.5%), infection
(4.4%), pain (1.8%), angina pectoris (1.3%), indigestion (4.9%), burping (4.9%),
rash (1.8%), and altered taste (2.7%).
Administration:
Lovaza is prescribed in a dosage of 4 capsules per day for the treatment of very
high triglycerides. Given high cost and limited access, Lovaza is not commonly
taken by AAS users. Instead, most steroid users will administer 4-6 grams per
day of a quality fish oil supplement for general cholesterol and lipid support.
Note that a supplement or prescription drug containing the omega-3-acids EPA
and DHA may help reduce cardiovascular toxicity, but cannot be relied upon to
completely eliminate potential damage from the abuse of anabolic/androgenic
steroid drugs. Care should always be taken to monitor all aspects of health when
taking AAS substances.
Availability:
High concentration omega-3 acid is marketed as a prescription drug product in
the U.S. under the Lovaza brand name. Lovaza is also sold in select European
and Asian markets. High quality fish oil supplements containing EPA and DHA
are widely available over-the-counter in most markets.
Diuretics
Aldactone® (spironolactone)
Description:
Spironolactone is an antagonist of aldosterone and is pharmaceutically classified
as a diuretic. It acts by competitively inhibiting aldosterone binding to receptor
sites, especially in the renal tubes where aldosterone is involved in sodiumpotassium exchange. The drug causes increased amounts of sodium and water to
be excreted and potassium to be retained. This is different from some other
agents of this class, such as a loop diuretic like furosemide, which can
significantly increase the excretion of sodium, water, and potassium. In this
light, spironolactone is commonly referred to as a “potassium sparing” diuretic.
It is used medically for a number of conditions including the treatment of high
blood pressure, edema related to congestive heart failure, hyeraldosteronism (the
over production of aldosterone), and hypokalemia (drop of potassium, often
associated with other medical interventions). Spironolactone is often used (offlabel) by competitive athletes and bodybuilders to make short-term adjustments
in water weight. The primary focus is to bring about increased muscle definition
by shedding subcutaneous water (bodybuilders), or to make category
adjustments during the weigh-in procedure in sports with restricted weight
classes (athletes).
History:
Spironolactone was developed during the late 1950s, and first saw widespread
use in clinical medicine during the early 1960s. The drug filled an important
need for a diuretic that does not deplete potassium, and therefore has a less
dramatic impact on electrolyte balance in the body. In many regards it is looked
at as a “safer” and “milder” diuretic compared to other agents in this general
category, such as loop diuretics or thiazides, allowing this agent room for market
stability and success. Today, spironolactone is widely distributed throughout
most of the developed world. It is available in dozens of brand names, the most
commonly identified is probably Aldactone from Searle. It is also widely sold in
mixed-ingredient preparations alongside other diuretics. This includes
furosemide, as seen in the product Lasilacton, or hydrochlorothiazide, in Searle’s
(also widely distributed) mixed diuretic product Aldactazide.
How Supplied:
Spironolactone is most commonly supplied in tablets of 25 mg.
Structural Characteristics:
Spironolactone is an aldosterone antagonist and diuretic. It has the chemical
designation 17-hydroxy-7alpha-mercapto-3-oxo-17alpha-pregn-4-ene-21-
carboxylic acid y-lactone acetate.
Warnings (Dehydration, Elevated Potassium, Death):
The misuse of diuretic drugs for physique-or performance-enhancing purposes is
characterized as a high-risk practice. Diuretics may produce a life-threatening
level of dehydration and electrolyte imbalance when administered without
proper medical supervision. Many deaths have been associated with the misuse
of these drugs. It is also important to note that the supplementation of potassium,
either through pharmaceuticals or a diet rich in potassium, is generally not
advised while taking a potassium-sparing diuretic like spironolactone. Excessive
potassium intake may cause hyperkalemia, which may lead to cardiac
irregularities and possibly death.
Side Effects:
Adverse reactions associated with spironolactone administration may include
gynecomastia, cramping, diarrhea, drowsiness, lethargy, headache, skin
irritation, rash, mental confusion, fever, impotence, loss of muscle coordination,
menstrual irregularities, virilization, and deepening of the voice. Spironolactone
has also been shown to cause tumors in rats. Breast cancer has been reported in
some patients receiving spironolactone, but no causal relationship has yet been
established. Additionally, this compound may exhibit anti-androgenic properties,
as both a weak inhibitor of androgen/receptor binding and testosterone
biosynthesis.
Administration:
When used medically to treat hypertension, the initial recommended dosage in
adults is 50 mg to 100 mg per day in divided doses. It may take two weeks for a
maximum response to be achieved. The dosage may be adjusted later depending
on the individual needs of the patient. When used (off-label) by male
bodybuilders to increase muscle definition or athletes to reduce weight before a
weigh-in, a dosage of 100 mg per day in a single morning application, is most
common. This may be continued for 3 to 5 days prior to the event, and will often
result in a harder and more defined appearance to the muscles (or substantial
reduction in body weight prior to rehydration).
Women are occasionally attracted to spironolactone for its effect as an antiandrogen. It is sometimes used as a safety net at a point when androgen levels
have become problematic during a cycle, and is used in an effort to reduce the
risk of permanent virilization symptoms. A dosage of 25-75 mg daily for 1 to 2
weeks is often used for this purpose, and may be enough to ward off side effects
while androgen levels decline (the steroid regimen terminated). Since
spironolactone is more effective at lowering endogenous androgen levels than
inhibiting androgen action, it is certainly not to be considered a cure-all remedy
for adventurous steroid-using female athletes.
Since this compound is one of the mildest (prescription) diuretic options, it is a
common starting point for an early competitor. Once familiar with its effects,
many attempt to achieve a stronger level of water loss by mixing spironolactone
with a thiazide or furosemide (Lasix). The goal is to provide strong water
excretion with less calcium/potassium loss than using the stronger diuretics
alone. When mixed with hydrochlorothiazide, for example, the 100 mg
spironolactone dosage is often cut in half, and an equal amount of the thiazide is
taken. The 50 mg/50 mg combination is reported to noticeably increase water
excretion without dramatic side effects. The potassium re-absorption seen with
spironolactone should be balanced out with the thiazide so potassium levels will
not be as greatly affected. On the other hand, Lasix (furosemide) should make an
even stronger addition to spironolactone. In this case, dropping the
spironolactone dosage to 50 mg and adding 20 mg oral Lasix is a popular choice,
and is often said to provide the water-shedding effect that is roughly equivalent
to a 40 mg Lasix tablet. Again, the potassium depleting effect of Lasix may be
offset to some degree by the potassium sparing effect of spironolactone, so
additional potassium supplements are not likely necessary. Many such
combination diuretics are widely available, and appear to be well regarded in
clinical circles.
It is important to note that while Lasix and Hydrodiuril appear to be more
effective at inducing short-term water loss, they also have increased risks as
compared to potassium-sparing diuretics, and should be approached with
caution.
Availability:
Spironolactone is widely manufactured in both single ingredient and multiingredient drug preparations. Low cost and wide scale availability make this a
poor financial target for counterfeiting.
Dyrenium® (triamterene)
Description:
Triamterene is an oral diuretic used medically to treat edema. Edema may occur
without known cause (idiopathic edema), or be associated with liver or kidney
disease, congestive heart failure, corticosteroid/progestin use, or the
overproduction of aldosterone. Triamterene is classified as a potassium sparing
diuretic, increasing the rate of water and sodium excretion but preserving
potassium levels. As the name suggests, this drug produces a pronounced
diuretic effect without the potassium loss associated with thiazides/loop
diuretics. The need for potassium supplementation is, therefore, eliminated with
this agent. The diuretic activity following a single dose of triamterene is usually
evident within 2 to 4 hours, reaching peak effect at approximately 3 hours in
most cases. Its diuretic effect lasts for a total of 7-9 hours following
administration.
Triamterene is utilized (off-label) by bodybuilders and athletes to shed
subcutaneous water prior to a bodybuilding competition, or to make weight class
adjustments in certain competitive sports. Bodybuilders in particular rely heavily
on the increased definition that can result when water retention is reduced. The
highly defined “shredded” physique common to bodybuilding today is nearly
impossible to achieve without the use of diuretics. At the same time, diuretics
are the reason weight class competitors like wrestlers and boxers often appear
much heavier during an event than they do at the weigh-in. A considerable
amount of bodyweight (in the form of water) can be removed with diuretic use,
often resulting in a drop of one or more weight categories. This practice is very
common in sports where the user is not drug tested and has ample time to
rehydrate following a weigh-in, resulting in the athlete competing at a
significantly heavier weight than his or her weight class would dictate.
History:
Triamterene first saw extensive clinical use during the 1960s. It was used largely
as a standalone agent at first, but went on to become a widely used agent in
clinical medicine in combination products with other diuretic drugs. Today this
usually includes other, more potent diuretics like thiazides and loop agents.
Here, the potassium loss of the stronger diuretic is balanced to some degree by
the potassium sparing triamterene, which often results in a reduced or even
eliminated need for potassium supplementation during therapy. Single ingredient
preparations of triamterene are still sold, however, and can be found in several
countries including Belgium (Dytac), United Kingdom (Dytac), and the United
States (Dyrenium).
How Supplied:
Triamterene is most commonly supplied in capsules of 50 mg and 100 mg.
Structural Characteristics:
Triamterene is a potassium-sparing diuretic. It has the chemical designation
2,4,7-triamino-6-phenyl-pteridine.
Warnings (Dehydration, Death):
The misuse of diuretic drug(s) for physique-or performance-enhancing purposes
is characterized as a high-risk practice. Diuretics may produce a life-threatening
level of dehydration and electrolyte imbalance when administered without
proper medical supervision. Many deaths have been associated with the misuse
of these drugs. It is also important to note that the supplementation of potassium,
either through pharmaceuticals or a diet rich in potassium, is generally not
advised while taking a potassium-sparing diuretic like triamterene. Excessive
potassium intake may cause hyperkalemia, which may lead to cardiac
irregularities and possibly death.
Side Effects:
Triamterene use may be associated with electrolyte imbalance, including
elevated or decreased potassium levels. Signs of electrolyte imbalance include
dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pain,
muscle cramping, seizures, reduced urine volume, low blood pressure, and
gastrointestinal disturbances. Other side effects may include nausea, vomiting,
jaundice, blood platelet deficiency, anemia, azotemia (buildup of metabolic
waste products in the blood), renal stones, and other kidney disturbances.
Additionally, some rare side effects characterized as hypersensitivity reactions
have been reported including skin rash, photosensitivity, and anaphylaxis (an
extreme and potentially life threatening allergic reaction).
Administration:
When used medically to treat hypertension, the usual initial dosage in adults is
100 mg twice daily after meals (200 mg per day). This may be increased, but
should never exceed 300 mg per day in total. Among bodybuilders, this drug is
commonly used for only a few days prior to a competition, adjusting the dosage
over the course to elicit the best level of diuretic effect. Since it has a long
lasting action, it is generally administered once per day. One capsule (100 mg) is
usually taken the first thing in the morning with a meal, and the effect judged
over the next several hours. The dosage is usually increased by one capsule per
day for 2-3 days at most, until the user is noticing the proper water loss for
competition. When looking for a stronger diuretic effect, many bodybuilders and
athletes will opt to combine triamterene with another stronger diuretic such as
hydrochlorthiazide or furosemide. The dosage of both agents would be adjusted
downward to compensate for their combined effects. The goal here is usually to
increase short-term diuresis, without causing the extreme potassium loss that can
be associated with the use of thiazides or loop diuretics alone at higher doses.
Availability:
Triamterene is widely sold throughout the developed world. Although singleingredient preparations containing triamterene are available, this drug is most
commonly sold in multi-ingredient preparations targeting edema and/or high
blood pressure. Low cost, modest demand, and high availability make this drug a
low-profit target for counterfeiting.
Hydrodiuril® (hydrochlorthiazide)
Description:
Hydrochlorothiazide is a diuretic from the thiazide family, used medically for
the treatment of edemas and hypertension. This drug acts by reducing the
reabsorption of electrolytes, thereby increasing the excretion of sodium,
potassium, chloride, and consequently water. In comparison to other diuretics,
Hydrodiuril is stronger than the potassium sparing agent Aldactone®
(spironolactone), but weaker then the loop agent Lasix (furosemide). While
potassium excretion is much less pronounced than that seen with Lasix, the use
of a potassium supplement (or a potassium rich diet) may still be necessary with
this product. This is usually dependent on the dose and duration in which the
drug is administered. Calcium excretion may also be pronounced with thiazides,
but again, are weaker in this regard than Lasix.
The use of diuretics has been increasingly popular in a number of athletic
disciplines. For starters, these drugs are very popular among bodybuilders who
use them to shed subcutaneous water before a competition. The ability to have a
winning physique often relies heavily on the definition that can result from
diuretic use. The highly defined, super hard and shredded look common today in
this sport is nearly impossible to achieve without the use of these drugs. Many
athletes competing in sports with weight categories also utilize diuretics.
Wrestlers and boxers, for example, might use diuretics to compete in a heavier
weight class than would be dictated by an earlier weigh-in measurement. Given
that the weight-in is usually done a day (or many hours) before a competition,
the athlete can reduce water weight with diuretics, yet have enough time to
restore fluids and bodyweight before the event. The result can be a shift of one
or more weight categories, which can be a formidable advantage in these types
sports.
History:
Hydrochlorothiazide was developed during the 1950s. Given the widespread
nature of diseases associated with high blood pressure and edema, the drug
found a very large market, and quickly achieved large-scale acceptance and
distribution. Hydrochlorothiazide became a fundamental form of therapy in this
area of medicine, where it remains widely available today. Hydrochlorothiazide
preparations are available in virtually all developed nations, and appear in
literally hundreds of different brand name and generic products. Singleingredient preparations (where hydrochlorothiazide is the only active drug) are
far outnumbered by multi-ingredient preparations, where the drug is often mixed
with other actives that focus on diuresis or blood pressure management.
How Supplied:
Hydrochlorothiazide is most commonly supplied in tablets of 25 mg and 50 mg.
Structural Characteristics:
Spironolactone is an aldosterone antagonist and diuretic. It has the chemical
designation 17-hydroxy-7alphamercapto-3-oxo-17alpha-pregn-4-ene-21-
carboxylic acid y-lactone acetate.
Warnings (Dehydration, Death):
The misuse of diuretic drugs for physique-or performance-enhancing purposes is
characterized as a high-risk practice. Diuretics may produce a life-threatening
level of dehydration and electrolyte imbalance when administered without
proper medical supervision. Many deaths have been associated with the misuse
of these drugs.
Side Effects:
Hydrochlorthiazide use may be associated with electrolyte imbalance. This may
include potassium and sodium deficiency, as well as hypochloremic alkalosis (an
increase in blood bicarbonate due to significant chloride loss). Signs of
electrolyte imbalance include dry mouth, thirst, weakness, lethargy, drowsiness,
restlessness, muscle pain, muscle cramping, seizures, reduced urine volume, low
blood pressure, and gastrointestinal disturbances. Other side effects may include
reduced appetite, nausea, vomiting, constipation, diarrhea, inflammation of
salivary gland(s), headache, dizziness, sensitivity to light, low blood pressure
upon standing, skin irritation, impotence, visual disturbances, jaundice,
pancreatitis, and inflammation of the lung(s). Additionally, some rare side
effects characterized as hypersensitivity reactions have been reported including
skin rash, fever, shock, pulmonary edema, and respiratory distress.
Administration:
When used medically to treat hypertension, the usual initial dose in adults is 25
mg daily given as a single dose. The dose may be increased to 50 mg daily, often
in two doses of 25 mg. Note that daily doses above 50 mg are often associated
with marked reductions in serum potassium. Athletes and bodybuilders typically
use this drug (off-label) for very brief periods (several days) of water
adjustment. A common practice is to administer this drug once per day, after the
morning meal. The athlete will monitor the level of water lost throughout the
day, and adjust the dosage for the following day if necessary. The usual starting
dosage is one 50 mg tablet. The user will adjust the effect by adding a 25 mg or
50 mg tablet each subsequent day. This practice is only followed for three or
four days, until an optimal dosage is calculated. The total daily dosage will
rarely exceed 100-200 mg (doses above 100 mg per day in a clinical setting are
not commonly recommended).
If the application of hydrochlorothiazide is not producing the desired effect,
many bodybuilders/athletes will choose to add another diuretic (mild) before
moving to the stronger loop agents. A combination of a potassium sparing
diuretic like Aldactone® (spironolactone) and Hydrodiuril is regarded as
particularly useful by many, and is believed to slightly balance out the calcium
and potassium loss associated with the use of hydrochlorothiazide. The dosage
of each agent would be reduced considerably, usually starting with a 25 mg/25
mg application and working upwards.
It is important to note that the overuse of diuretics, aside from being potentially
very dangerous, may result in too much water loss. This can lead to flat,
“deflated” looking muscles. A higher diuretic dosage, likewise, does not always
equate to increased definition and muscularity. It is usually regarded as good
advice by those in the athletic community to become familiar with the practice
of using diuretics before using them during competition time. Otherwise, the
user may be left to make frantic dosage adjustments at the last minute, which can
be a dangerous and ineffective practice.
Availability:
Hydrochlorothiazide is widely manufactured in both single ingredient and multiingredient drug preparations. Low cost and wide scale availability make this a
poor financial target for counterfeiting.
Lasix® (furosemide)
Description:
Furosemide belongs to a class of drugs known as loop diuretics, which cause the
body to excrete water as well as potassium, sodium, magnesium, calcium, and
chloride. They are used most commonly to treat edema and high blood pressure.
Like other agents of this type, furosemide works by inhibiting the Na-K-2Cl
symporter in the thick ascending loop of Henle, which is a carrier protein that
pulls sodium, potassium, and chloride inside cells. This mode of action is
independent of any inhibition towards aldosterone. Loop diuretics are among the
strongest diuretics available, and can have an extremely dramatic effect on fluid
and electrolyte levels in the body. Potassium levels need to be closely watched in
particular, and patients may require a prescription potassium supplement. If the
proper levels of potassium and other electrolytes are not maintained, serious
heart complications may develop. Mistakes in potassium dosage have equally
serious consequences; so it is of note that furosemide can be a particularly risky
item to use without proper medical supervision.
Athletes and bodybuilders use diuretics for a couple of specific purposes, and
usually for only brief periods. Competitive athletes in sports with weight class
restrictions may use these drugs to drop water weight, in an effort to make
adjustments in their weight class standings. Since the weigh-in procedure is
often a day or days before a competition, one can drop their bodyweight
considerably with diuretics, and be back to normal within hours after drug
cessation and rehydration. This may provide a strong competitive advantage,
allowing the athlete to compete at a heavier weight than his or her category
would dictate. This advantage is only offset to some degree by the now near
universal nature of some form of “dropping weight” practice in these sports.
Bodybuilders may rely heavily on diuretics when preparing for a contest. Here, a
drug like furosemide can efficiently lower subcutaneous water concentrations,
helping to produce a more defined (“ripped”) look common to competitive
bodybuilding.
History:
Furosemide was developed during the early 1960s. Much of the initial research
on this diuretic was conducted in Europe, mainly Germany and Italy. The drug
proved to be quite successful, however, and within a matter of years gained
worldwide attention and acceptance as a treatment for edema and high blood
pressure. Over the years, furosemide preparations have become among the most
popular medications in their area of medicine. Single-and multi-ingredient
preparations making use of this diuretic can presently be found in virtually all
corners of the world. The most recognized brand name is Lasix, presently sold in
the U.S. and many other nations under the Sanofi Aventis label. The actual
number of different brand and generic forms of furosemide would be difficult to
calculate and list, but would probably measure in the hundreds.
How Supplied:
Furosemide is most commonly supplied in oral tablets of 20 mg, 40 mg, and 80
mg, and injectable solutions containing 10 mg/ml.
Structural Characteristics:
Furosemide is an anthranilic acid derived loop diuretic. It has the chemical
designation 4-chloro-N-furfuryl-5-sulfamoylanthranilic acid.
Warnings (Dehydration, Death):
Furosemide is a highly potent diuretic, which can profoundly increase water
excretion (diuresis) and lead to electrolyte depletion. The misuse of diuretic
drug(s) like furosemide for physique-or performance-enhancing purposes is
characterized as a high-risk practice. Diuretics may produce a life-threatening
level of dehydration and electrolyte imbalance when administered without
proper medical supervision. Many deaths have been associated with the misuse
of these drugs.
Side Effects:
Furosemide use may be associated with electrolyte imbalance. This may include
the depletion of potassium (hypokalemia), sodium (hyponatremia), magnesium
(hypomagnesemia), and calcium (hypocalcemia), as well as hypochloremic
alkalosis, an increase in blood bicarbonate due to significant chloride loss. Signs
of electrolyte imbalance include dry mouth, thirst, weakness, lethargy,
drowsiness, restlessness, muscle pain, muscle cramping, seizures, reduced urine
volume, low blood pressure, and gastrointestinal disturbances. Other side effects
may include pancreatitis, jaundice, anorexia, oral and stomach irritation,
cramping, diarrhea, constipation, nausea, vomiting, hearing loss, numbness or
tingling of the extremities, vertigo, dizziness, headache, blurred vision or other
visual disturbances, anemia, decreased white cell or blood platelet count,
dermatitis, rash, skin itching and sensitivity to light, low blood pressure, high
blood sugar levels (hyperglycemia), muscle spasm, weakness, restlessness,
urinary bladder spasm, fever, blood clot, and excess uric acid in the blood
(hyperuricemia). Additionally, some rare side effects characterized as
hypersensitivity reactions have been reported including inflammation of blood
vessels, kidney inflammation, and inflammation of blood vessels or lymph ducts
(angiitis).
Administration:
When used medically to treat edema, it is often given orally in a dose of 20 mg
to 80 mg per day, which is taken in one single application. For the treatment of
hypertension, it is generally recommended to administer 80 mg per day, which is
given in two separate 40 mg applications spaced 12 hours apart. Athletes and
bodybuilders typically use this drug (off-label) for very brief periods (several
days) of water adjustment. The dosage and method of administration is tailored
to the individual, dependent on the desired goals and condition of the athlete.
Oral tablets are the most common form of administration. The athlete will
usually start with a low dose, and increase the amount slightly on subsequent
days. The main focus is to calculate the optimal dosage, as well as to determine
the best intake schedule, in relation to a show or competition. The initial dosage
is usually 20 mg to 40 mg, and the maximum daily intake rarely exceeds 80 mg.
In order to minimize the side effects associated with this drug, it is generally
used for no longer than 4-5 days.
Note that since furosemide has such a strong effect on electrolyte levels, it is
generally considered much safer to add a potassium sparing agent like
Aldactone® (spironolactone) than it is to keep increasing the amount of
furosemide used. Combination diuretics like this are widely produced as
prescription medicines for this reason. The use of 50 mg Aldactone® and 20 mg
furosemide is a common starting point, and is believed to have a roughly similar
diuretic effect to 40 mg of furosemide, but without the same level of potassium
loss. This dosage may be adjusted on subsequent days in order to determine the
optimal amount and intake schedule, but should rarely exceed 100 mg/40 mg per
day. It is important to remember that these drugs can be active for many hours. It
can become difficult to control the dehydrating effect with an overlapping
schedule, therefore one should be careful not to administer diuretics on multiple
occasions during the same day.
Injectable furosemide solutions are considered to be significantly more powerful
forms of the drug milligram for milligram. Furosemide solutions can be
administered intramuscularly or intravenously, depending on the individual
needs of the patient. The IV method is much more rapid acting, and produces
significantly higher peak blood levels of the drug. Given that the action of
furosemide can be noticed in a matter of seconds or minutes when given by
injection, the effect is actually easier to judge and control with this method of
use, at least under normal conditions. Since the injection is much more powerful
than the oral, however, is important to emphasize that the dosage must be
considerably reduced in comparison. Intramuscular injection is most common
with bodybuilders and athletes, and is usually given at a dosage of 10-20 mg.
Doses in excess of 40 mg per day are rarely used in the bodybuilding/athletic
population.
Availability:
Furosemide is widely available, and is manufactured and sold under many
different brand names, in many countries. No version of Lasix (or any other
diuretic) is currently being counterfeited on any large scale. Although it is
doubtful these will circulate, make sure to never purchase the drug in 500 mg
tablets. These are used only in severe medical conditions, and contain a dosage
that would likely prove fatal to a healthy person.
Endurance/Erythropoietic Drugs
Aranesp® (darbepoetin alfa)
Description:
Darbepoetin alfa is a synthetic derivative of the human erythropoietin protein. It
also has the same pharmacological action as recombinant human erythropoietin
(epoetin alfa). In the body, erythropoietin is normally released by the kidneys in
response to hypoxia (low blood oxygen levels). This in turn triggers bone
marrow to increase red blood cell production. As such, this hormone is vital to
the regulation of normal red blood cell concentrations in humans. With a similar
mode of action to recombinant erythropoietin, darbepoetin alfa can be used to
augment erythropoiesis when the body is not maintaining adequate red blood
cell levels on its own. It is FDA approved for the treatment of anemia (low red
blood cell count) associated with chronic renal failure or chemotherapy.
Darbepoetin alfa differs from recombinant human erythropoietin (epoetin alfa)
mainly in its duration of activity. This new protein maintains its levels in the
blood for approximately three times longer, causing it to have a much longer
therapeutic window. This means that with darbepoetin alfa patients are required
to administer the product much less frequently than they would epoetin alfa.
While epoetin alfa is usually injected on a schedule of three times per week,
darbepoetin alfa requires only one injection in the same time frame. This may
enhance patient comfort considerably, especially when the patient is visiting the
physician for routine drug administration.
Endurance athletes are highly attracted to darbepoetin alfa for the effect it has on
red blood cell production. It is no secret that the practice of blood doping has
been popular with endurance sports. This procedure involves removing,
concentrating, and storing a quantity of red blood cells from your own body to
be transfused later. By adding the stored cells before an event (by then the body
has restored the lost blood volume), the athlete has a much greater concentration
of red blood cells. The blood should, likewise, transport oxygen more efficiently,
and the athlete may be given a significant endurance boost. This procedure can
be quite risky, however, as blood products can be difficult to store and
administer correctly. Darbepoetin alfa is a drug that basically equates to
chemical blood doping, and can achieve the same end result (higher red cell
concentrations) with the use of a simple medication.
History:
Darbeopetin alfa was developed as a prescription drug by Amgen. The U.S.Food
& Drug Administration first approved it for sale in 2001. Amgen is the world’s
largest biotechnologies company, and the same firm that first brought
recombinant erythropoietin (epoetin alfa) to the U.S. market in 1984. The main
focus with darbepoetin alfa appears to have been the development of a much
longer acting erythropoietic protein in comparison to their earlier recombinant
erythropoietin, which is commonly injected on a schedule of three times per
week. The prescribing guidelines for darbepoetin alfa recommend a once per
week schedule, which seems to offer strong comfort advantages to epoetin alfa
for patients that do not like receiving frequent injections. Darbepoetin alfa has
not yet reached the level of market success that has been noted with epoetin alfa
preparations, but has been a strong selling drug for Amgen ever since its release.
How Supplied:
Darbepoetin alfa is most commonly found in single-dose vials and prefilled
syringes containing 25, 40, 60, 100, 150, 200, 300, or 500 mcg of drug.
Structural Characteristics:
Darbepoetin alfa is a 165-amino acid protein that differs from human
erythropoietin by the substitution of amino acids on the erythropoietin peptide
backbone, which allows the addition of two additional N-linked oligosaccharide
chains.
Warnings (Death, Viral Disease):
The misuse of darbepoetin alfa for physique-or performance-enhancing purposes
is characterized as a high-risk practice. Like traditional blood doping methods,
darbepoetin alfa can produce an abnormally high concentration of hemoglobin in
the blood (polycythemia), which may result in heart attack, stroke, seizure, or
death.
Some forms of darbepoetin alfa contain albumin, a purified human blood
product. Although effective donor screening and product manufacturing
procedures are in place, it still carries a risk, though extremely remote, for
transmission of viral disease.
Side Effects:
Side effects associated with the use of darbepoetin alfa may include flu-like
symptoms such as fever, chills, headache, muscle pain, weakness, or dizziness.
Such effects tend to be more pronounced at the initiation of therapy. Other
adverse reactions may include infection, rash, swelling of the skin, nausea,
vomiting, diarrhea, high blood pressure, low blood pressure, cough, bronchitis,
or edema. In some instances darbepoetin alfa has been associated with
thromboembolism, deep-vein thrombosis, pulmonary embolism, heart attack,
and cerebrovascular accidents.
Administration:
Darbepoetin alfa is indicated for the treatment of anemia associated with chronic
renal failure (CRF) and chemotherapy. The recommended starting dose for the
treatment of anemia in adult CRF patients is .45 mcg/kg body weight,
administered once per week as a single IV or SC injection. The dosage is
subsequently adjusted based on changes in hematocrit. Healthy athletes using
darbepoetin alfa for performance-enhancing purposes generally start on the very
low end of the therapeutic spectrum, and adjust according to changes in
hematocrit. This may entail initiating therapy with as little as .05 mcg/kg of body
weight once per week. Note that it is considered very important to monitor blood
cell counts closely during the entire intake of darbepoetin alfa to help ensure
hematocrit is not allowed to increase to an unhealthy level.
Availability:
Darbepoetin alfa is not widely sold on the black market. Yet because of the high
cost for erythropoiesis stimulating agents like darbepoetin alfa, it is a high
profile target for counterfeit drug manufacturing operations. Counterfeit drugs of
this class have even infiltrated legitimate pharmaceutical distribution channels,
suggesting that care should be taken when purchasing this and similar drug
products.
Epogen® (epoetin alfa)
Description:
Erythropoietin is a glycoprotein that is produced in the kidneys, and is
responsible for stimulating red blood cell production. Epoetin alfa is a
pharmaceutical form of erythropoietin, which was manufactured using
recombinant DNA technology. The compound is produced from animal cells
into which the gene coding for human erythropoietin has been inserted. The
biological activity and structure of epoetin alfa are indistinguishable from that of
human erythropoietin. Epoetin alfa is used to treat many forms of anemia,
effectively stimulating and maintaining erythropoiesis in a large percentage of
patients treated. The efficiency of this drug quickly made it a ready replacement
for older (less effective) therapies such as Anadrol 50®.
Endurance athletes are highly attracted to epoetin alfa for the effect it has on red
blood cell production. It is no secret that the practice of blood doping has been
popular with endurance sports. This procedure involves removing,
concentrating, and storing a quantity of red blood cells from your own body to
be transfused later. By adding the stored cells before an event (by then the body
has restored the lost blood volume), the athlete has a much greater concentration
of red blood cells. The blood should, likewise, transport oxygen more efficiently,
and the athlete may be given a significant endurance boost. This procedure can
be quite risky, however, as blood products can be difficult to store and
administer correctly. Epoetin alfa is a drug that basically equates to chemical
blood doping, and can achieve the same end result (higher red cell
concentrations) with the use of a simple medication.
History:
Epoetin alfa was developed by the biotechnologies firm Amgen, and first
introduced to the U.S. market in 1984. The release of the drug is regarded as a
breakthrough in the treatment of anemia, which beforehand was being addressed
mainly with agents that indirectly or nonspecifically targeted red cell production,
such as oxymetholone, which may present a number of unwanted side effects to
the patient. Epoetin alfa marked the development of the first drug that
specifically and effectively stimulated the process of erythropoiesis (red blood
cell production). Its success was rapid and far reaching. Epoetin alfa has since
been introduced to a wide number of different countries. The most popular trade
names include Procrit (distributed by Ortho, manufactured by Amgen), Epogen
(Amgen), and Eprex (Johnson & Johnson). In addition to these, more than one
dozen other trade names are also used to market epoetin alfa.
In 2002 the subcutaneous use of Eprex, which is sold only outside the United
States, was linked to a rare disease called pure red-cell aplasia. This is a
condition where the body loses its ability to produce red blood cells. Those that
suffer from pure red-cell aplasia usually become dependant on continual blood
transfusions for survival. Close to 200 people taking Eprex were identified as
developing this rare condition, far in excess of normal expected numbers.
Internal investigations by Johnson & Johnson linked the high numbers to
changes in the product that were made to satisfy European regulations limiting
the use of albumin. According to a company spokesperson, a chemical reaction
between the new stabilizer that replaced albumin and the rubber stopper allowed
organic compounds to leech into the vials. The company subsequently replaced
its original stoppers with coated rubber to prevent this reaction. The incidence of
pure-red cell anemia in patients receiving erythropoietin seems to have been
reduced as a result, although warnings about this reaction remain on the
prescribing information for all products sold in the U.S.
How Supplied:
Epoetin alfa is supplied as a dry sterile powder that requires reconstitution with
sterile diluent before injection. It is most commonly found in single-and multidose ampules and vials containing 2,000-40,000 Units/ml.
Structural Characteristics:
Epoetin alfa is a single chain polypeptide hormone containing 165 amino acids.
It is identical in structure to the alpha glycoform of human erythropoietin.
Warnings (Death, Viral Disease):
The misuse of epoetin alfa for physique-or performance-enhancing purposes is
characterized as a high-risk practice. Like traditional blood doping methods,
epoetin alfa can produce an abnormally high concentration of hemoglobin in the
blood (polycythemia), which may result in heart attack, stroke, seizure, or death.
Many forms of epoetin alfa contain albumin, a purified human blood product.
Although effective donor screening and product manufacturing procedures are in
place, it still carries an extremely remote risk for transmission of viral disease.
Side Effects:
Side effects associated with the use of epoetin alfa may include flu-like
symptoms such as fever, chills, headache, muscle pain, weakness, or dizziness.
Such effects tend to be more pronounced at the initiation of therapy. Other side
effects include rash, swelling of the skin, nausea, vomiting, diarrhea, high blood
pressure, hyperkalemia (excess potassium in the blood), and irritation at the site
of injection. In some instances epoetin alfa has been associated with
thromboembolism, deep-vein thrombosis, pulmonary embolism, heart attack,
and cerebrovascular accidents.
Administration:
Epoetin alfa injectable solution is given by subcutaneous or intravenous
injection. The two paths of administration have greatly different effects on the
blood level of the drug. When given by IV infusion, peak blood levels of the
drug are reached within 15 minutes, and the elimination half-life ranges from 4
or 13 hours. When administered via the subcutaneous route, peak blood levels
are reached between 5 and 24 hours, and the elimination half-life is
approximately 24 hours. Given an equal dose, the peak plasma concentration of
epoetin alfa will be significantly lower than the intravenous method. When used
medically to treat severe anemia associated with chronic renal failure, the
recommended starting dosage range is 50 to 100 Units/kg of bodyweight, given
3 times per week. The dosage is subsequently adjusted based on changes in
hematocrit. Healthy athletes using epoetin alfa for performance-enhancing
purposes generally start on the very low end of the therapeutic spectrum, and
adjust according to changes in hematocrit. This may entail initiating therapy with
as little as 5 to 10 Units/kg of bodyweight, taken 3 times per week. Note that it is
considered very important to monitor blood cell counts closely during the entire
intake of epoetin alfa to help ensure hematocrit is not allowed to increase to an
unhealthy level.
Availability:
Epoetin alfa is a very expensive compound, and its use is additionally isolated to
certain athletic fields. As such, it is not widely traded on the black market. Given
the high cost of this drug, however, it is a lucrative target for counterfeiters.
Provigil® (modafinil)
Description:
Modafinil, known chemically as benzhydrylsulphinylacetamide, is a central
stimulant (psychostimulant). It is FDA approved for the treatment of narcolepsy
(a disorder characterized by sudden and uncontrollable attacks of deep sleep,
mental fatigue, or excessive sleepiness), sleep apnea, and SWSD (Shift Work
Sleep Disorder). It is being investigated for a number of other uses, including the
treatment of Alzheimer’s disease, depression, and attention deficit disorder.
Modafinil belongs to a group of drugs known as Eugeroics (“good arousal"),
designed to promote a mental state of vigilance and alertness. One of its known
mechanisms is to work as an alpha-1 adrenoceptor agonist, exerting its mood
and energy enhancing effects through the increased release of dopamine in the
CNS. It also results in alterations in local GABA and glutamate levels.
The use of modafinil as a stimulant has been shown in studies to have many
advantages over amphetamines. To begin with, it is believed to have a much
lower potential for abuse due to the fact that it produces a lower sense of
euphoria. It also displays lower peripheral CNS stimulation (less side effects),
has minimal effects on blood pressure, produces no interruptions in normal
sleeping patterns (no hangover or needing “catch-up” sleep), and has an overall
greater safety profile according to clinical trials. This drug is of interest even to
the U.S. military, which is looking at it as an energy enhancer for pilots and
combat soldiers that need to operate for long periods of time without sleep.This
is not as unusual as it may seem at first, as military combat pilots and soldiers
have used Dexedrine (an amphetamine) extensively in the past when sleep was
inconvenient. Soldiers on modafinil often report that they maintain excellent
cognitive functioning for up to 40 hours without sleep, and have fewer side
effects than Dexedrine. Modafinil has been tested in recent combat situations
such as in Afghanistan and Iraq, and seems poised for official acceptance as a
battlefield drug.
Recently, modafinil has become a popular drug among competitive athletes.
They use it not simply to “stay awake” but as a performance enhancing agent
with both stimulant and endurance-increasing properties. This type of use
probably comes as a surprise to those who developed this drug, as early reports
suggested that this was a “mild” alertness drug, without strong stimulant
properties that would improve athletic performance. Recent studies contradict
this determination. A study conducted in Canada shows a very strong athletic
benefit inherent in modafinil.
687 During this double-blind investigation, a dose of
4 mg per kg of bodyweight (this equates to 200 mg for a 220lb man) of
modafinil, or placebo, was given to a group of 15 male volunteers. Three hours
after ingestion, aerobic exercise was conducted on a cycle ergometer at 85%
V02max (maximum aerobic power), and the amount of time until exhaustion
was determined. While taking modafinil, the men were able to exercise for
significantly longer periods of time (~30%), and had greater oxygen intake at
exertion. They also reported lower subjective ratings of perceived exertion
(RPE), which suggests that the increased performance was in part due to a
significantly less pronounced sensation of fatigue during exercise.
History:
Modafinil was developed by Lafon Laboratories in France. It was approved for
sale in the United States by the FDA in 1998, where it was introduced under the
Provigil® brand name. Modafinil is also found internationally under this and
several additional trade names including Modiodal®, Vigil®, Alertec®, and
Modasomil®. Although the drug appears to have a favorable safety record and
profile, it was quickly considered a drug of potential abuse in the U.S. It is
presently classified as a schedule IV controlled substance, which places
modafinil in the same category as Valium and Xanax. This is intended to limit
its diversion for nonmedical purposes by placing considerable legal penalties on
its possession and importation. The medical applications for the drug are fairly
broad, however, including SWSD, which refers to sleep disturbances caused by
changing-or late-shift work. Prescriptions for the drug are, likewise, commonly
granted by physicians in general medical practice.
Modafinil quietly became popular among competitive athletes between 2000 and
2004, before the athletic bodies were aware of the drug. Its use as a
performance-enhancing agent was revealed to the public during the designer
steroid (BALCO) doping scandal of 2004, however, when it was disclosed that
many of the same athletes who tested positive for THG also used modafinil.The
IOC quickly banned its use, and with the help of a number of researchers a
methodology for detecting this chemical in the urine was developed. This test is
now implemented as part of the standard Olympic level drug screening process.
Most of the other international athletic bodies have followed the IOC’s lead in
banning and testing for modafinil. The drug has since lost all appeal as an
“invisible” performance-enhancing agent, although is still being used by many
athletes that are not subject to random urine testing.
How Supplied:
Modafinil is most commonly supplied in tablets of 100 mg and 200 mg each.
Structural Characteristics:
Modafinil is a central nervous system stimulant related to adrafinil. It has the
chemical designation 2- [(diphenylmethyl)sulfinyl]acetamide.
Side Effects:
Side effects associated with modafinil are commonly the result of its central
nervous system stimulating activities, and may include nervousness, insomnia,
shakiness, euphoria, personality changes, and excitation. The drug may also
produce gastrointestinal disturbances such as nausea, vomiting, abdominal pain,
dry mouth, anorexia, and headache. Hypertension, heart palpitations, or
abnormal heart rate may also be noticed. In rare instances allergic rash, increases
in alkaline phosphatase, or impaired voluntary movement have been reported.
Administration:
When used clinically to treat excessive daytime sleepiness associated with
narcolepsy or obstructive sleep apnea, the recommended dose is typically 200 to
400 mg per day. This may be given in a single morning application, or in two
divided doses (morning and at midday). When used to enhance physical
performance, the typical effective dose is in the range of 100-400 mg. This is
often given at least 2-3 hours prior to athletic competition. Note that side effects
can be dose dependant. It is often advised to start using modafinil on the low end
of the effective dosage range, and increase by 50-100 mg per application until an
optimal level is determined.
The arenas in which this drug is applied are vast, and essentially include any
sport focused on aerobic activity or endurance. It may also work well with those
athletes focused on short repeat bursts of strength or speed (anaerobic activities),
such as shot-putting, pole-vaulting, or long-jumping. Modafinil is not a popular
drug among bodybuilders, as it holds little direct value for building muscle or
reducing body fat levels. Some, however, do find it to be an effective preworkout stimulant, especially during periods when fatigue or loss of physical
drive may be noticed subsequent to a busy work or personal schedule.
Availability:
Modafinil is presently available in more than two dozen countries. The drug is
not highly diverted for black market sale, however, and is not a lucrative target
for drug counterfeiting operations.
Fat Loss Agents - Sympathomimetics
Adipex-P® (phentermine hydrochloride)
Description:
Phentermine hydrochloride is a sympathomimetic stimulant of the amphetamine
family. Like other amphetamine derivatives, it is categorized as an anorectic
(appetite suppressing) agent. Phentermine is commonly prescribed as a weight
loss aid in obese patients. It is typically used for short periods of time (less than
12 weeks), and as an adjunct to support an ongoing exercise and dieting
regimen.The main focus is to curb the desire to eat, thereby reducing the total
caloric intake. Although the data seems to vary from trial to trial, much of it
supports at least a modest additional loss of fat mass with the use of phentermine
hydrochloride.
886 Athletes and bodybuilders use phentermine hydrochloride for
the same purpose, typically when weight loss is required for physique
remodeling or competition.
History:
Phentermine hydrochloride was first introduced to the U.S. drug market in the
1970s. Base phentermine was available in the U.S. as far back as 1959.
Phentermine had long been used as an appetite suppressant, although the most
notable attention to it came in the early 1990s, when the drug was successfully
paired with fenfluramine during diet studies. Investigators had shown that this
type of drug combination was actually more effective at promoting weight loss
than diet and exercise, results that quickly catapulted Fen-Phen into top place in
the prescription weight loss drug market. By 1997, however, it had become
apparent that a very high percentage of Fen-Phen users were noticing heart valve
defects as a result of the drugs. Fenfluramine was identified as the principle
cause, and was withdrawn from the U.S. market that same year. Phentermine
remains available in the U.S. and many nations abroad today. Popular trade
names include Adipex, Ionamin, Anoxine, Phentrol, and Obenix. Note that as an
amphetamine derivative, this medication has a tendency to be habit forming. For
this reason it has been added to the U.S. controlled substances list as a schedule
IV medication.
How Supplied:
Phentermine hydrochloride is most commonly supplied in tablets and capsules of
18.75 mg and 37.5 mg each.
Structural Characteristics:
Phentermine hydrochloride is a central stimulant and indirect-acting
sympathomimetic of the amphetamine family. It has the chemical designation 2-
methyl-1-phenylpropan-2-amine (2-methyl-amphetamine).
Side Effects:
Common side effects associated with phentermine hydrochloride include
insomnia, increased blood pressure, irritability, nervousness, and euphoria. Less
common side effects include vision disturbances, reduced libido, confusion,
diarrhea, dizziness, dry mouth, headache, irregular heartbeat, nausea, vomiting,
rash, and tiredness. Phentermine is a CNS stimulant with potential for fatal
overdose. Signs of overdose may include rapid breathing, fever, hallucinations,
blood pressure irregularities, irregular heartbeat, unconsciousness, trembling,
shaking, panic, extreme restlessness, and severe nausea, vomiting, or diarrhea.
Administration:
For optimal effectiveness, phentermine hydrochloride should not be taken with
food. The usual adult dose is one capsule or tablet (37.5 mg) daily, administered
before or 1-2 hours after breakfast. For some patients a half of a tablet (18.75
mg) daily may be adequate, while in other cases it may be advisable to give a
half of a tablet (18.75 mg) twice daily.When taken more than once per day, the
second dose should never be taken within 4-6 hours of sleep. The drug is
typically used for 3-4 weeks at a time, with longer durations of therapy rarely
exceeding 12 weeks. Bodybuilders and athletes typically use the prescribed
amount of drug in a similar short-term fashion,due to the high likelihood of side
effects as the dose escalates beyond the normal therapeutic range.
Availability:
Phentermine hydrochloride is available in a number of different countries. It is
not widely counterfeited. U.S. residents would not be advised to order the drug
from overseas, however, since phentermine is a schedule IV controlled substance
and carries similar legal restrictions as Valium and anabolic steroids. Many U.S.
doctors who specialize in weight loss medications will readily dispense
phentermine for controlled periods of weight loss.
Albuterol (albuterol sulfate)
Description:
Albuterol sulfate is a selective beta-2 adrenergic agonist, very similar in
structure and action to clenbuterol. Unlike clenbuterol, however, albuterol is
readily available as a prescription drug in the United States. It is also sold as
salbutamol in a number of other countries, which is another generic name for the
drug. Albuterol is most commonly found in the form of a rescue inhaler, which
is designed to disperse a measured amount of the drug immediately and directly
to the bronchial tubes in times of crisis (asthma attack). This form provides the
least amount of systemic drug activity possible, which is great for minimizing
unwanted cardiovascular side effects. Albuterol oral tablets are also available,
however, and provide a systemic dose of the drug. These are the subject of
interest in the bodybuilding and athletic communities, and they can provide
significant beta-2 stimulation and measurable fat loss throughout the body given
the right conditions. Note that a more comprehensive discussion of the benefits,
activities, and side effects of beta-2 agonist drugs can be found under the
clenbuterol drug profile.
History:
Albuterol sulfate was introduced to the U.S. drug market in 1980, sold under the
Ventolin brand name. Albuterol sulfate has grown to be one of the most popular
drugs in history for the management of acute asthma attacks. As a result, many
other companies have invested in the market. The Ventrolin brand name is still
available in the U.S., however, the FDA has also approved a variety of other
generic and brand name forms of the drug. Albuterol sulfate is also presently
sold in both inhalation and oral preparations in most developed countries.
Popular trade names include Aerolin, Airomir, Asmasal, Asthalin, Asthavent,
Asmol, Butahale, Buventol, ProAir, Proventil, Salamol, Sultanol, and Volmax.
How Supplied:
Albuterol sulfate is most commonly supplied in oral metered dose inhalers and
tablets of 2 mg, 4 mg, or 8 mg each.
Structural Characteristics:
Albuterol sulfate (salbutamol sulphate) is a short-acting ‚2-adrenergic receptor
agonist. It is a racemic drug with the chemical designation (±) a1-[(tertbutylamino)methyl]-4-hydroxy-m-xylene-a,a1-diol sulfate (2:1)(salt).
Side Effects:
Common side effects associated with albuterol sulfate include headache,
dizziness, lightheadedness, insomnia, tremor, nervousness, sweating, nausea,
vomiting, diarrhea, and dry mouth. Less common but more serious adverse
events include allergic reactions (rash, hives, swelling of the lips, tongue, or
face, or difficulty breathing), chest pain, high blood pressure, and irregular
heartbeat. Albuterol sulfate is a CNS stimulant with potential for fatal overdose.
Signs of overdose may include rapid breathing, blood pressure irregularities,
irregular heartbeat, unconsciousness, trembling, shaking, panic, extreme
restlessness, and severe nausea, vomiting, or diarrhea.
Administration:
The usual starting dosage for adults and children 12 years and older for the
management of asthma is 2-4 mg three or four times per day. When used (offlabel) for fat loss, an effective dose of albuterol usually starts in the range of one
to two 4 mg tablets per day (1 tablet X 1-2 applications). This is often increased
slightly as the user becomes accustomed to the drug, perhaps to 4 mg three to
four times per day. Individuals very sensitive to the stimulant side effects of beta
agonists usually start with the lower-dose 2mg tablets first. The administration
intervals are spread out as evenly as possible, so as to prevent overlap and
sustain active concentrations in the blood for as much of the day as possible.
Athletes and bodybuilders will often use their body temperature as a marker of
drug efficacy. A degree or two elevation in temperature with use of the drug may
indicate that lipolysis (the removal of stored fatty acids in adipose tissue) is
being effectively stimulated.
As is noted with all beta agonists, tolerance to the thermogenic benefits of this
drug tends to develop quickly. This is usually noticed by the body temperature
returning to normal pretreated levels. Due to the potential side effects of these
drugs, it is not advised to continually increase the dosage in order to chase down
a diminishing effect.Instead, the user will usually opt to discontinue the drug for
some time (4 weeks or longer) to let the body restore its normal beta-adrenergic
receptor concentrations. More recently, the antihistamine Zaditen (ketotifen) has
become popular, which is a potent upregulator of beta-adrenergic receptors,
especially beta-2 receptors. This medication may enhance the thermogenic
potency of this beta agonist, but might also increase drug potency and the
incidence of side effects.
Availability:
Albuterol is a widely available and very cheap medicine. Counterfeiting is not a
strong concern with this medication.
Clenasma (clenbuterol hydrochloride)
Description:
Clenbuterol hydrochloride is an anti-asthma medication that belongs to a broad
group of drugs knows as sympathomimetics. These drugs affect that sympathetic
nervous system in a wide number of ways, largely mediated by the distribution
of adrenoceptors. There are actually nine different types of these receptors in the
body, which are classified as either alpha or beta and further subcategorized by
type number. Depending on the specific affinities of these agents for the various
receptors, they can potentially be used in the treatment of conditions such as
asthma, hypertension, cardiovascular shock, arrhythmias, migraine headaches
and anaphylactic shock. The text Goodman and Gillman’s The Pharmacological
Basis of Therapeutics 9th edition does a good job of describing the diverse
nature in which these drugs affect the body:
Most of the actions of catecholamines and sympathomimetic agents can be
classified into seven broad types: (1) peripheral excitatory action on certain
types of smooth muscles such as those in blood vessels supplying the skin,
kidney, and mucous membranes, and on the gland cells, such as those of the
salivary and sweat glands; (2) a peripheral inhibitory action on certain other
types of smooth muscle, such as those in the wall of the gut, in the bronchial
tree, and in blood vessels supplying skeletal muscle; (3) a cardiac excitatory
action, responsible for an increase in heart rate and force of contraction; (4)
metabolic actions, such as an increase in the rate of glycogenolysis in liver and
muscle and liberation of free fatty acids from adipose tissue; (5) endocrine
actions, such as modulation of the secretion of insulin, rennin, and pituitary
hormones; (6) CNS actions, such as respiratory stimulation and, with some of
the drugs, an increase in wakefulness and psychomotor activity and a reduction
in appetite; and (7) presynaptic actions that result in either inhibition or
facilitation of the release of the neurotransmitters such as such as
norepinephrine and acetylcholine.
Clenbuterol hydrochloride is specifically a selective beta-2 sympathomimetic,
primarily affecting only one of the three subsets of beta-receptors. Of particular
interest is the fact that this drug has little beta-1 stimulating activity. Since beta-1
receptors are closely tied to the cardiac effects of these agents, this allows
clenbuterol hydrochloride to reduce reversible airway obstruction (an effect of
beta-2 stimulation) with much less cardiovascular side effects compared to nonselective beta agonists. Clinical studies with this drug show it is extremely
effective as a bronchodilator, with a low level of user complaints and high
patient compliance . Clenbuterol hydrochloride also exhibits an extremely long
half-life in the body, which is measured to be approximately 34 hours long . This
makes steady blood levels easy to achieve, requiring only a single or twice daily
dosing schedule at most . This of course makes it much easier for the patient to
use, and may tie in to its high compliance rate.
In animal studies clenbuterol hydrochloride is shown to exhibit anabolic activity,
obviously an attractive trait to a bodybuilder or athlete. This compound is
additionally a known thermogenic , with beta-2 agonists like clenbuterol
hydrochloride shown to directly stimulate fat cells and accelerate the breakdown
of triglycerides to form free fatty acids. Its efficacy in this area makes
clenbuterol hydrochloride a very popular fat loss drug among the bodybuilding
community. Those interested in this drug are often hoping it will produce a little
of both benefits, promoting the loss of body fat while imparting increases in
strength and muscle mass. But as was well pointed out by a review published in
the August 1995 issue of Medicine and Science in Sports and Exercise, the
possible anabolic results in humans are very questionable, and based only on
animal data using much larger doses than would be required for bronchodilation
. With such reports there has been a lot of debate as to whether or not clenbuterol
hydrochloride is really anabolic in humans at all. Some seem to swear by the fact
that it builds muscle, and use clenbuterol hydrochloride regularly as an offseason or adjunct anabolic. To others, the MSSE report is confirmation that
athletes have wasted valuable time and money on drugs that do not build muscle.
The debate over clenbuterol hydrochloride’s potential anabolic activity continues
today.
History:
Clenbuterol hydrochloride has been available as a bronchodilator for decades
and is widely used in many parts of the world. Although it has a good safety
record and approval in a wide number of other countries, this compound has
never been made available for human use in the United States. The fact that
there are a number of similar effective asthma medications already approved by
the FDA and available may have something to do with this, as a prospective
drug firm would likely not find it a profitable enough product to warrant
undergoing the expense of the new drug approval process. Regardless of this
fact, foreign clenbuterol hydrochloride preparations are popular among U.S.
bodybuilders and athletes, and today are widely available on the black market.
Note that in recent years, clenbuterol overdose/poisoning has been reported in a
number of people, striking up a great deal of controversy about the safety of this
drug and its off-label use for physique-and performance-enhancing purposes.
How Supplied:
Clenbuterol hydrochloride is most commonly supplied in oral tablets of 20mcg
each. It is also supplied in oral syrups, injectable solutions, and for inhalation
use.
Structural Characteristics:
Clenbuterol hydrochloride is a long-acting selective ‚2-adrenergic receptor
agonist. It has the chemical designation 1-(4-amino-3,5-dichloro-phenyl)-2-
(tertbutylamino) ethanol.
Side Effects:
The possible side effects of clenbuterol hydrochloride include those of other
CNS stimulants, and include such occurrences as shaky hands, insomnia,
sweating, increased blood pressure, and nausea. These side effects will generally
subside after a week or so of use, once the user becomes accustomed to the drug.
Clenbuterol hydrochloride is a CNS stimulant with potential for fatal overdose.
Signs of overdose may include rapid breathing, blood pressure irregularities,
irregular heartbeat, unconsciousness, trembling, shaking, panic, extreme
restlessness, and severe nausea, vomiting, or diarrhea.
Administration:
When used for the management of asthma, the most common clinical dose for
adults is 20mcg (1 tablet) twice per day. Some patients require up to 40mcg (2
tablets) twice per day. When using the drug (off-label) for physique-or
performance-enhancing purposes, bodybuilders and athletes generally tailor their
dosage and cycling of this product based on personal sensitivity to its benefits
and side effects. To accomplish this, one often begins a cycle by taking one or
two tablets per day, and gradually increasing the dosage every third day by one
half to 1 tablet until a desired dosage range is established. At peak therapy some
users can tolerate as many as 6-8 tablets per day (120-160mcg). Given the
potency and potential for serious side effects, however, any dosage outside of the
normal therapeutic range should be approached with an even greater level of
caution.
The drug will usually elevate the body temperature shortly after therapy is
initiated. The rise in temperature is commonly .5 to 1 degree, sometimes a little
more. This elevation is due to one’s body burning excess energy (largely from
fat), and is usually not uncomfortable. The number of consecutive days
clenbuterol hydrochloride is now used is usually dependent on the response of
the individual.To be clear, the athletic benefits of this drug will only last for a
limited time and then diminish, largely due to beta-receptor downregulation. By
most accounts clenbuterol hydrochloride seems to work well for approximately 4
to 6 weeks. During this period, users generally monitor their body temperature
on a regular basis. We are given some level of assurance that clenbuterol
hydrochloride is working by the temperature elevation. Once the temperature
drops back to normal, receptor downregulation has probably diminished the
efficacy of the drug. At this point increasing the dosage is usually not regarded
as effective, and instead clenbuterol hydrochloride is discontinued for a period of
no less than 4-6 weeks.
Many bodybuilding competitors enhance the fat burning effect of clenbuterol
hydrochloride with the use of additional substances. Many have commented that
when the drug is combined with thyroid hormones, specifically the powerful
Cytomel®, the thermogenic effect can become extremely dramatic. Such a mix
is often further used during a steroid cycle, helping the individual elicit a much
more toned physique from the drugs. A clenbuterol/thyroid mix is also common
when using growth hormone, which is believed to enhance the thermogenic and
anabolic effect of HGH therapy. Lastly, ketotifen has also been a popular adjunct
to clenbuterol hydrochloride, which is an antihistamine that upregulates beta-2
receptor density. It seems capable of not only increasing the potency of each
dose of clenbuterol hydrochloride (allowing the user to take less clenbuterol),
but also of perhaps even slowing receptor downregulation (see the Ketotifen
profile for a more comprehensive discussion).
Availability:
Clenbuterol hydrochloride is readily available on the international market.
Although it is usually a very cheap drug in common source countries, allowing
black market dealers ample opportunity to obtain legitimate drugs to divert for
sale, clenbuterol hydrochloride has been the subject of low-level counterfeiting.
A few things are important to note:
Clenbuterol hydrochloride is not produced in the U.S., so avoid anything bearing
a U.S. company name.
Clenbuterol hydrochloride should only be trusted when found with a proper
brand name from a foreign drug maker. Spiropent, Novegam and Oxyflux from
Mexico are the most common products in the U.S.
From Europe, the brand names of Spiropent, Broncoterol, Clenasma, Monores,
Contraspasmin and Ventolase are popular.
Bulgarian clenbuterol hydrochloride is also found commonly, but so are
counterfeits. This is a slightly higher risk item.
Ephedrine (ephedrine hydrochloride)
Description:
Ephedrine is a stimulant drug that belongs to the group of medicines known as
sympathomimetics. Specifically, it is both an alpha and beta adrenergic agonist
(you may remember clenbuterol is a selective beta-2 agonist). In addition,
ephedrine enhances the release of norepinephrine, a strong endogenous alpha
agonist. The action of this compound is notably similar to that of the body’s
primary adrenergic hormone epinephrine (adrenaline), which also exhibits action
toward both alpha and beta receptors. When administered, ephedrine will
notably increase the activity of the central nervous system, as well as have a
stimulatory effect on other target cells. This may produce some effects that can
be beneficial to a bodybuilder or athlete. For starters, the user’s body
temperature should rise slightly as more free fatty acids are produced from the
breakdown of triglycerides in adipose tissue (stimulating metabolism). This may
aid in body fat reductions and increased vascularity. It is also believed that the
anabolic effectiveness of steroids might be increased with this substance
(mildly), as an increase in metabolic rate may equate to an increase in fat,
protein and carbohydrate conversion by the body. The stimulant effect of this
drug will also increase the force of skeletal muscle contractions.
History:
Ephedrine is a fairly old medication, and has been used in the United States for a
number of medical applications over the years including that of a stimulant,
appetite suppressant, decongestant, and hypotension treatment associated with
anesthesia.Today, it is approved as an over-the-counter medicine, and sales are
largely found in this sector. Controls over ephedrine in the United States are
growing in recent years, however, due to the fact that it can be used as a primary
base for the manufacture of methamphetamine. With ephedrine available as an
over-the-counter product, underground manufacturers have been able to easily
obtain it. A trend involving large volume retail purchases for OTC ephedrine
products had been developing, and many states have responded with legislation
controlling the sale of precursor materials like ephedrine. In 2006, a federal law
was passed further restricting the record keeping requirements and available sale
channels for ephedrine in the Unites States. With the widespread increase of
methamphetamine addiction (and related crime), some speculate ephedrine may
soon join the list of federally controlled substances. In spite of tighter
regulations, it is still presently available for over-thecounter sale.
How Supplied:
Ephedrine (as ephedrine hydrochloride or ephedrine sulfate) is most commonly
supplied in tablets of 25 mg or 50 mg each.
Structural Characteristics:
Ephedrine is a sympathomimetic amine related in structure to amphetamine and
methamphetamine. It has the chemical designation (1R,2S)-2-(methylamino)-1-
phenylpropan-1-ol.
Side Effects:
Ephedrine can produce a number of unwelcome side effects that the user should
be aware of. For starters, the stimulant effect can produce shaky hands, tremors,
sweating, rapid heartbeat, dizziness, and feelings of inner unrest. Often these
effects subside as the user becomes more accustomed to the effect of this drug,
or perhaps the dosage is lowered. In general, those negatively impacted by
caffeine would probably not like the stronger effects of ephedrine. The mental
and physical state produced by this drug is also quite similar to that seen with
clenbuterol, so those who find little discomfort with that treatment should
(presumably) be fine with this item (and vice versa). While taking this drug one
may also endure a notable loss of appetite, usually a welcome effect when
dieting. Ephedrine is in fact a popular ingredient in combination (prescription)
appetite suppressants. The user may further notice headaches and an increase in
blood pressure with regular use of ephedrine. Those suffering from thyroid
dysfunctions, high blood pressure, or cardiac irregularities should also not be
taking this drug, as it will certainly not mix well with such conditions. Ephedrine
is a CNS stimulant with potential for fatal overdose. Signs of overdose may
include rapid breathing, blood pressure irregularities, irregular heartbeat,
unconsciousness, trembling, shaking, panic, extreme restlessness, and severe
nausea, vomiting or diarrhea.
Administration:
The primary application for ephedrine among bodybuilders and athletes (offlabel) is that of a cutting (fat-loss) agent. Here, the individual will generally take
this drug a few times per day during a dieting phase of training, at a dosage of 25
to 50 mg per application. The widely touted stack of ephedrine (25-50 mg),
caffeine (200 mg), and aspirin (300 mg) (E/C/A) is shown to be extremely potent
for fat loss, and is more commonly applied than ephedrine alone. In this
combination, the ephedrine and caffeine both act as notable thermogenic
stimulants. The added aspirin also helps to inhibit lipogenesis by blocking the
incorporation of acetate into fatty acids. The athlete may use an increase in body
temperature as a marker that the drug combination is working. This is usually a
degree or so (not an uncomfortable raise). This combination is taken 2 to 3 times
daily, for several consecutive weeks. It is discontinued once the user’s body
temperature drops back to normal, a clear sign these drugs are no longer working
as desired. A break of at least 4-6 weeks is usually taken so that this stack may
once again work at an optimal level.
Ephedrine is also used by some competitive athletes (including powerlifters) as a
stimulant before workouts or competitions. The resulting (slight) strength and
energy increase may improve anaerobic performance and weight totals on major
lifts. On this same note, it is also believed by some to provide a mental edge,
making the user more energetic and better able to concentrate on the tasks ahead.
A pre-event dose of 25-50 mg of ephedrine is typically used for this purpose. It
is important to note that this compound is not used continuously as a preworkout or pre-event stimulant, as its effect will diminish as the body becomes
accustomed to the drug. In most instances, the user will take the drug only 2 or 3
times per week, usually on those days personally “important”. The individual
would also be wise to take a break (at least 1 to 2 months) from ephedrine after
several weeks have passed, so as to continue receiving the optimal effect from
this drug.
Availability:
Ephedrine is widely available in the U.S. and in a number of countries abroad. It
is not commonly a target of counterfeiting operations.
Meridia® (sibutramine hydrochloride)
Description:
Sibutramine hydrochloride is a selective serotonin and noradrenalin reuptake
inhibitor used for the medical management of obesity.This pharmaceutical is
intended to be an adjunct to a reduced calorie diet, which will help increase
weight loss compared to that achieved with modifying food intake alone.
Sibutramine hydrochloride is not advertised as a rapid acting drug, but instead
one that fosters slow, safe, and steady losses in fat mass which are maintained
long-term.
Sibutramine hydrochloride exerts a weight-loss effect through two distinct
mechanisms. It has a marked ability to suppress appetite. During some studies,
patients would reduce their daily energy intake by as much as 1,300 calories
while taking this drug.
689
In addition to its effects on caloric intake, sibutramine
also stimulates metabolism and daily caloric expenditure. A single 10 mg dose
has been demonstrated to increase basal metabolic rate by up to 30%, an effect
that is maintained for at least six hours. This thermogenic action is known to
occur via the adrenergic system, mainly through the indirect support of beta 3
receptor activation. With the use of this drug, we are specifically seeing a strong
increase in brown adipose tissue thermogenesis (BAT), which is accompanied
by body temperature increases of .5 – 1 degree Celsius.
690 Elevated body
temperature is a good indicator that thermogenesis is being triggered, which you
may recall as one of the key things we are looking for when taking clenbuterol.
To get a better idea of exactly how well sibutramine hydrochloride works, we
refer to some of the clinical studies on this agent.One investigation was
conducted at the Kansas Foundation for Clinical Pharmacology in 2001. Here, a
group of 322 obese patients were given either 20 mg of sibutramine or placebo
once daily for 24 weeks. By the conclusion of this study, 42% of patients in the
sibutramine group lost 5% or more of their initial body weight, while 12%
noticed a 10% or greater loss in body weight. Sibutramine was also associated
with significant improvements in serum triglyceride and HDL cholesterol levels,
which were displaying poor values at the onset of the study. Another detailed
investigation was completed in China by the Department of Endocrinology for
Rui-jin Hospital this same year, and involved giving only 10 mg per day of
sibutramine to a group of 120 men and women.
691 This investigation also faired
extremely well, with patients losing an average of 15 pounds by the 24th week
of use.
History:
Sibutramine hydrochloride received Food and Drug Administration approval for
sale as a prescription weight-loss agent in 1998. It was developed and marketed
by Abbott Laboratories, which sold the drug on the U.S. market under the brand
name Meridia. The company also sold the drug in many international markets
under the name Reductil. Sibutramine enjoyed only a limited period of sales in
the U.S., as it was removed from the market in October 2010 under FDA
pressure, citing an increased incidence of adverse cardiovascular events. Abbott
has since also withdrawn sibutramine from many markets worldwide. Note that
sibutramine remains classified as a schedule IV controlled substance in the
United States.
How Supplied:
Sibutramine hydrochloride is most commonly supplied in capsules of 5 mg, 10
mg, and 15 mg.
Structural Characteristics:
Sibutramine hydrochloride is a centrally-acting serotonin-norepinephrine
reuptake inhibitor structurally related to amphetamine. It is chemically a racemic
mixture of (+) and (-) enantiomers of 1-(4-chlorophenyl)-N,N-dimethyl-a-(2-
methylpropyl)-cyclobutanemethanamine.
Side Effects:
The most common side effect with sibutramine is an increase in blood pressure,
a trait that contraindicates its use in patents with high blood pressure or other
cardiovascular issues. Other common side effects include dry mouth,
sleeplessness, irritability, back pain, stomach upset, and constipation, all of
which tend to become reduced in magnitude as the user becomes accustomed to
the drug. Sibutramine hydrochloride should be discontinued immediately if any
of the more serious side effects or symptoms of toxicity occur, including
excitement, restlessness, loss of consciousness, confusion, agitation, weakness,
shivering, clumsiness, rapid heartbeat, large pupils, vomiting, difficulty
breathing, chest pains, swelling of feet, ankles or legs, fainting, disorientation,
depression, high fever, eye pain, tremor, or excessive sweating. Note that
increased incidence of cardiovascular events has prompted the removal of this
product from most markets. It is no longer considered a safe product by many
standards.
Administration:
Sibutramine hydrochloride is used for the management of obesity, including
weight loss and maintenance, and should be used in conjunction with a reducedcalorie diet. This drug has been used with patients who have additional weightrelated risk factors including controlled hypertension, diabetes, and dyslipidemia
(high cholesterol). The recommended starting dosage for most patients is 10 mg
once daily, which is to be adjusted upwards to 15 mg after 4 weeks if weight loss
has not been sufficiently initiated. Higher doses are usually not recommended.
Availability:
This drug is subject to limited availability following an FDA supported recall in
the United States, and subsequently its removal from many other international
markets for safety reasons.
Zaditen® (ketotifen fumarate)
Description:
Ketotifen is an antihistamine drug that is used for the treatment of general
allergy symptoms, certain allergic conditions (including conjunctivitis), and the
management of asthma. When used for asthma, the drug is not regarded as
effective for treating an immediate attack (it is not a rapid bronchodilator).
Instead, over time its use is associated with a reduction in the frequency,
duration, and severity of attacks. It is usually prescribed as a way to increase the
efficacy of other asthma medications. Likewise, ketotifen fumarate will usually
supplement an existing asthma medication program, and not replace the
prescribing of immediate rescue devices such as an asthma inhaler or nebuliser.
Ketotifen fumarate alleviates allergy symptoms by blocking histamine H1
receptors, a property that is common to drugs of the antihistamine class. Its
second and very unique mode of action, however, makes it useful in the
treatment asthma. Ketotifen fumarate increases the concentration of betaadrenergic receptors in the body (especially beta-2 receptors). Drugs that
stimulate beta-2 receptors are commonly prescribed as bronchodilators, used to
increase airflow to the lungs and counter the constriction caused by asthma.
While potentially efficacious alone, one key therapeutic effect of ketotifen
fumarate is to increase the sensitivity of the body to drugs of the beta agonist
class.
The beta-2 receptor upregulating properties of ketotifen fumarate make this drug
of interest to the bodybuilding and athletic communities. This is due to the
strong role of the beta-2 receptor in supporting fat loss. Although not a strong fat
loss compound by itself, when taken with a beta-2 agonist thermogenic like
clenbuterol, ketotifen fumarate may increase thermogenic potency and
noticeably extend the window of active lipolysis. Clenbuterol and other beta-2
agonists normally have a limited duration of usefulness here because beta-2-
adrenergic receptors decrease in number with regular stimulation. Within several
weeks of initiating therapy with such a drug, it usually begins to diminish in
effectiveness. Ketotifen may extend this time period considerably.
The ability of ketotifen to potentiate the effects of beta-2 agonist drugs has been
demonstrated in a number of clinical studies. For example, one study published
in 1990 demonstrated that when ketotifen and clenbuterol were taken together,
there was a significant increase in betaa-drenergic receptor density compared to
the use of clenbuterol alone, which again decreases beta adrenoceptor density
fairly quickly.
692 Other studies with salbutamol (also referred to generically as
albuterol) showed that beta adrenoceptor downregulation caused by long-term
use of this beta-adrenergic agent could be rapidly reversed with as little as 2mg
of ketotifen fumarate per day.
693
History:
Ketotifen was globalized as a prescription medication by Novartis. It is presently
prescribed for allergies, allergic conditions, and (most commonly) the
management of asthma in more than three-dozen countries around the world.
The most widely available brand name is Novartis’ Zaditen, which is sold
throughout most parts of Europe and Asia. In addition to generic forms of the
medication, dozens of other brand names can be found in many different markets
as well. Ketotifen fumarate is approved for sale in the United States, but
currently only as an ophthalmic anti-allergy solution (Zaditor), not an oral
allergy/asthma medication. The dosage of ketotifen fumarate in this product is
also too low for it to be considered useful for any other (off label) purpose.
Given the ready availability of ketotifen fumarate in other countries, the drug is
easily diverted for black market sale. As of now, it is not extremely popular with
bodybuilders and athletes.
The UK guidelines on the clinical management of asthma consider ketotifen to
be ineffective for the management of this disease. There is admittedly conflicting
data on the potential usefulness of ketotifen fumarate for this purpose, with some
studies reporting positive results and others showing an insignificant effect. A
thorough review of the data published on the Cochrane Database of systematic
Reviews in 2004 concluded that it appeared to have some usefulness in
controlling asthma and wheezing in many children, but the variability of the
disease and response to the drug meant that these positive results could not be
generalized for all asthma patients.
694
How Supplied:
Ketotifen fumarate is most commonly supplied in tablets of 1mg. This dosage is
usually expressed in terms of the base, so each tablet actually contains 1.38mg of
ketotifen fumarate.
Structural Characteristics:
Ketotifen fumarate is selective histamine H1 antagonist, anti-allergic, and antiasthmatic agent. It has the chemical designation 4-(1-Methyl-4-piperidylidene4Hbenzo [4,5]cyclohepta[1,2-b]thiphene-1-(9H)-one fumarate.
Side Effects:
Common side effects include dry mouth, appetite stimulation, weight gain,
dizziness, CNS stimulation, and drowsiness. These side effects are all commonly
associated with strong antihistamine compounds. In rare cases severe allergic
reaction on the skin or a urinary bladder inflammation called cystitis may occur.
Administration:
When used to reduce the frequency, duration, and severity of asthma attacks,
ketotifen fumarate is usually initiated at a dosage of 1mg twice per day (2mg
total). If necessary, this may be increased to a maximum dosage of 2mg twice
per day (4mg total). Bodybuilders and athletes will commonly use a dosage of
1mg twice per day (2mg total) for the (off-label) use of preventing receptor
downregulation with clenbuterol or other beta-agonists. This may allow an
individual to obtain a strong thermogenic effect from, and run longer cycles
with, beta-2 agonist drugs. Note that given its ability to increase drug
sensitivity,the dosage of beta-2 agonist medications may need to be reduced
upon ketotifen fumarate administration.
Availability:
Ketotifen fumarate is widely available, and is sold under numerous brand names
in many countries. Large scale counterfeiting of this medication is currently not
known to be a problem.
Fat Loss Agents - Thyroid
Cytomel® (liothyronine sodium)
Description:
Liothyronine sodium is a synthetically manufactured prescription thyroid
hormone. It specially consists of the L-isomer of the natural thyroid hormone
triiodothyronine (T3). Thyroid hormones stimulate basal metabolic rate, and are
involved with many cellular functions including protein, fat, and carbohydrate
metabolism. Liothyronine sodium is used medically to treat hypothyroidism, a
condition where the thyroid gland does not produce sufficient levels of thyroid
hormone. Hypothyroidism is usually diagnosed with a serum hormone profile
(T3, T4, & TSH), and may manifest itself with symptoms including loss of
energy, lethargy, weight gain, hair loss, and changes in skin texture. T3 is the
most active thyroid hormone in the body, and consequently liothyronine sodium
is considered to be a more potent thyroid medication than levothyroxine sodium
(T4).
Bodybuilders and athletes are attracted to liothyronine sodium for its ability to
increase metabolism and support the breakdown of body fat. Most often utilized
during contest preparation or periods of “cutting”, the drug is usually said to
significantly aid in the loss of fat, often on higher levels of caloric intake than
would normally be permissive of such fat loss. To this end, the drug is also
commonly used in conjunction with other fat loss agents such as human growth
hormone or beta agonists. Some users also ascribe an ability of thyroid
hormones like liothyronine sodium to increase the anabolic effect of steroids.
While in theory these drugs may support the greater utilization of protein and
carbohydrates for muscle growth, they are not widely proven or accepted for this
purpose.
History:
The first medication that included T3 was technically a thyroid extract, first
given to a patient with myxedema (a skin disorder associated with
hypothyroidism) in 1891.
695 Natural thyroid extracts contained therapeutically
viable levels of the thyroid hormones T3 and T4, and were widely used in
medical practice for more than 60 years. In the 1950s, however, these drugs
slowly start giving way to new synthetic thyroid medications, namely
liothyronine sodium and levothyroxine sodium, which were consistent in dosage
and effect, and more desirable to consumers than prepared animal extracts.
Although liothyronine sodium and levothyroxine sodium are both widely
available in the U.S. and abroad to this day, liothyronine retains a significantly
smaller portion of the global thyroid market. Given its more potent and fast
acting effect, however, liothyronine sodium remains a popular thyroid drug with
bodybuilders and athletes. Cytomel® is the most recognized trade name for the
drug in the U.S, where it is presently sold under the King Pharmaceuticals brand
name.
How Supplied:
Liothyronine sodium is most commonly supplied in oral tablets of 5 mcg, 25
mcg, and 50 mcg.
Structural Characteristics:
Liothyronine sodium is a synthetic form of T3 thyroid hormone. It has the
chemical designation l-tyrosine,o-(4-hydroxy-3-iodophenyl)-3,5-diiodo-
,monosodium salt.
Warnings:
FDA requires the following black box warning accompany prescription
liothyronine sodium products sold in the U.S.: “Drugs with thyroid hormone
activity, alone or together with other therapeutic agents, have been used for the
treatment of obesity. In euthyroid patients, doses within the range of daily
hormonal requirements are ineffective for weight reduction. Larger doses may
produce serious or even life-threatening manifestations of toxicity, particularly
when given in association with sympathomimetic amines such as those used for
their anorectic effects.”
Side Effects:
Side effects are generally associated with overdosage, and may include
headache, irritability, nervousness, sweating, irregular heartbeat, increased
bowel motility, or menstrual irregularities. Overdosage may also induce shock,
and may aggravate or trigger angina or congestive heart failure. Chronic
overexposure to liothyronine sodium will produce symptoms normally
associated with hyperthyroidism or the overproduction of natural thyroid
hormones in the body.The occurrence of overexposure-linked side effects is
normally cause to immediately reduce or discontinue therapy with liothyronine
sodium. Acute massive overdose may be life threatening.
Administration:
When used to treat mild hypothyroidism, the typical recommended starting
dosage is 25 mcg daily. The daily dosage then may be increased by no more than
25 mcg every 1 to 2 weeks. The established maintenance dose is usually 25-75
mcg per day. Once a day administration of the full daily dose is usually
recommended. Although liothyronine sodium is fast acting, its effects may
persist in the body for several days after discontinuance.
The usual protocol among bodybuilders and athletes taking liothyronine sodium
to accelerate fat loss involves initiating its use with a dosage of 25 mcg per day.
This dosage may be increased by 25 mcg every 4 to 7 days, usually reaching a
maximum of no more than 75 mcg per day. As in a medical setting, the intent of
this slow buildup is to help the body become adjust to the increasing thyroid
hormone levels, and avoid sudden changes that may initiate side effects.
Cycles of liothyronine sodium usually last no longer than 6 weeks, and
administration of the drug should not be halted abruptly. Instead, it is
discontinued in the same slow manner in which it was initiated. This usually
entails reducing the dosage by 25 mcg every 4 to 7 days. This tapering is done so
that the body has time to readjust its endogenous hormone production at the
conclusion of therapy, and to avoid the onset of side effects.
Availability:
Liothyronine is an old and widely prescribed medication. It can be found readily
in most areas of the world, and is sold in a variety of different brand and generic
forms. Counterfeiting is not a large-scale problem. It is important to note than
one should never purchase an injectable form of this drug. These are generally
used as emergency room products only, with potentially very dangerous side
effects if misused.
Synthroid® (levothyroxine sodium)
Description:
Levothyroxine sodium is a synthetically manufactured form of the natural
thyroid hormone tetraiodothyronine (T-4). Thyroid hormones are primarily
responsible for regulating the body’s metabolic rate, and play a vital role in the
body’s utilization of protein, fat, and carbohydrates. Levothyroxine sodium is
used medically to treat cases of hypothyroidism, which is characterized by
insufficient natural production of thyroid hormones.This may manifest itself
with a number of symptoms including loss of energy, lethargy, weight gain, hair
loss, and changes in skin texture. Levothyroxine sodium is considered a slowacting medication, and may take up to 4 to 6 weeks before full therapeutic levels
are reached in the blood. It is also the most commonly prescribed thyroid
medication in the world, and is considered to be the standard form of treatment
for most cases of hypothyroidism.
The action of levothyroxine sodium is very similar to that of the popular thyroid
preparation Cytomel® (liothyronine sodium). Cytomel® is slightly different in
structure, however, being a synthetic form of the thyroid hormone
triiodothyronine (T-3). A healthy individual with have sufficient levels of both
T-3 and T-4 thyroid hormones present in their body. T-3 is considered the
primary active form of thyroid hormone, while T4 serves mainly as a reserve for
T3, exerting most of its metabolic activity via conversion to T3 in peripheral
tissues. T3 is regarded as having an effect that is roughly four times stronger
than that of T-4 on a milligram-for-milligram basis. Likewise, Cytomel® is
considered to be a more potent form of thyroid medication, both with regard to
activity and side effect potential.
Levothyroxine sodium is valued by many drug-using athletes and bodybuilders
for its ability to stimulate the metabolic rate and support the breakdown of body
fat stores. It is usually taken during a period of calorie restriction (“cutting”),
when the individual is focused on fat loss or increasing muscle definition. It is
often thought that the use of thyroid drugs can support fat loss at a higher level
of caloric intake than would otherwise be possible without the drugs, adding to
their perceived value among the communities. Anabolic steroids are generally
used in conjunction with these hormones, and many believe that the metabolism
boosting effect of these drugs may produce faster gains in muscle mass. The
drugs, however, have yet to be widely proven or accepted for this purpose.
History:
Levothyroxine sodium was the first synthetic thyroid medication to be sold in
the U.S., and was first introduced to market in 1955 by Flint Laboratories as
Synthroid. The drug has a long history of therapeutic use in the U.S. and
internationally, and for decades has been the most widely prescribed medication
for the treatment of hypothyroid. The Synthroid brand has historically been the
most successful, with figures estimating that it retained 85% of total
levothyroxine sales and $600 million in annual revenues (1990 estimates). In the
bodybuilding and athletic communities, however, the faster acting and more
powerful drug Cytomel (liothyronine sodium) is most popular. Since Synthroid
is weaker and slower acting, athletes need to take the drug for a longer duration
to achieve similar results.
The Synthroid brand itself has a long and at times controversial history.
696 For
many years after its inception by Flint Laboratories, Synthroid enjoyed a virtual
monopoly on the levothyroxine sodium market. Generic medications finally
began taking a large share of levothyroxine sodium sales going in to the 1980s.
In response, Flint Laboratories funded a study at the University of California in
1986 which attempted to demonstrate that Synthroid had a higher therapeutic
value than its generic counterparts. The study was completed in 1990, and, in
fact, proved that the generic drugs had equal efficacy to Synthroid.
697 Flint
exercised a clause in its contract requiring company approval before the
university could publish its study. A legal battle over its publication ensued.Even
after Flint Laboratories was sold to Boots, and thereafter Boots sold to Knoll,
publication of the study was vigorously opposed. It was eventually ordered into
publication in 1997. A class action lawsuit followed, alleging that misconduct
over the publication and marketing claims forced consumers to pay 2 to 3 times
more for a brand name drug than an equivalent generic counterpart. Knoll
eventually settled for $135 million.
How Supplied:
Levothyroxine sodium is most commonly supplied in oral tablets of 25 mcg,50
mcg,75 mcg, 100 mch, 125 mcg, 150 mcg, 200 mcg, and 300 mcg.
Structural Characteristics:
Levothyroxine sodium is a synthetic form of T4 thyroid hormone. It has the
chemical designation L-3,3',5,5'- tetraiodothyronine sodium salt.
Warnings:
FDA requires that the following black box warning accompany prescription
liothyronine sodium products sold in the U.S. “Thyroid hormones, including
levothyroxine sodium, either alone or with other therapeutic agents, should not
be used for the treatment of obesity or for weight loss. In euthyroid patients,
doses within the range of daily hormonal requirements are ineffective for weight
reduction. Larger doses may produce serious or even life threatening
manifestations of toxicity, particularly when given in association with
sympathomimetic amines such as those used for their anorectic effects.”
Side Effects:
Side effects are generally associated with overdosage, and may include
headache, irritability, nervousness, sweating, irregular heartbeat, increased
bowel motility, or menstrual irregularities. Overdosage may also induce shock,
and may aggravate or trigger angina or congestive heart failure. Chronic
overexposure to levothyroxine sodium will produce symptoms normally
associated with hyperthyroidism, or the overproduction of natural thyroid
hormones in the body. The occurrence of over-exposurelinked side effects is
normally cause to immediately reduce or discontinue therapy with levothyroxine
sodium. Acute massive overdose may be life threatening.
Administration:
When used to treat mild to moderate hypothyroidism, the average replacement
dose of levothyroxine sodium is approximately 1.7 mcg/kg/day. This equates to
100-125 mcg/day per day for a 154lb adult. The full therapeutic dose may be
given from the onset of therapy in otherwise healthy adult patients. Note that due
to the long half-life of levothyroxine, the peak therapeutic effect at a given dose
may not be achieved for 4 to 6 weeks.
When used (off-label) to accelerate fat loss by bodybuilders and athletes, the
typical protocol involves slow buildup of the dosage so that the body has ample
time to adjust to the changing thyroid hormone levels. An individual will
generally start with a low dosage of 25-50 mcg, and will slowly increase the
amount 25-50 mcg each day or two. The final dosage will usually be in the range
of 100-150 mcg, and will rarely exceed 250 mcg. It is important to remember
that thyroid drugs are strong medications with significant side effect potential.
Cautious individuals will be sure not to use excessive amounts of levothyroxine
sodium, nor continue treatment for longer than eight weeks. It is also generally
advised to also reduce the Synthroid dosage gradually at the conclusion of each
cycle. This is usually accomplished by dropping the dosage by 25 mcg every
second or third day. The focus here, again, is to help avoid any sudden change in
hormone levels that might otherwise trigger side effects. Note that due to the
slow acting nature of levothyroxine sodium, it may take several weeks or longer
for the active drug to be fully eliminated from the body.
Availability:
Although levothyroxine sodium is a widely manufactured drug, it is not as
common on the black market as the stronger thyroid drug Cytomel®. Large scale
counterfeiting does not appear to be a problem.
Fatloss Agents - Other
DNP (2,4-Dinitrophenol)
Description:
DNP is one of the most controversial drugs in use by bodybuilders. This agent is
not sold for human use anywhere in the world at this time, but is readily
available as an industrial chemical. Among other things, it is used as an
intermediary for the production of certain dyes, for photographic development,
as a fungicide, in wood pressure-treatment to prevent rotting, and as an
insecticide. It is technically classified as a poison. Although quite incongruous
with this list of strong industrial/chemical uses, this chemical was sold during
the era of patent medicine as a diet drug for humans. It is this property of
dinitrophenol that remains of interest to some bodybuilders today.
Dinitrophenol induces weight loss by uncoupling oxidative phosphorylation,
thereby markedly increasing the metabolic rate and body temperature . While
this is an extremely effective way of producing rapid weight loss, there seems to
be no ceiling to DNP’s temperature increasing effect. Herein lies perhaps its
most dangerous trait; it may allow body temperature to rise to level that can be
damaging, even fatal. Writer Carl Malmberg made perhaps one of the earliest
and most famous quotes about this danger back in the 1930s when he told of a
physician who was "literally cooked to death" from using it. This was far from
an isolated case, and deaths associated with DNP have continued over the
decades. For example, a recent highly publicized story concerns a man that died
on Long Island, NY in 2001 after taking DNP for only four days. The dose used
was reported to be 600 mg per day, just three 200 mg capsules.
History:
The fat-loss properties of DNP were reportedly first noticed during World War I,
when overweight men working with DNP in munitions plants started losing
substantial amounts of weight. It did not take very long for this chemical to be
identified as the cause. Soon after, it was packaged as a drug product. By 1935,
more than 100,000 Americans had already used “patent medicine” remedies that
included DNP. In fact, DNP was the first synthetic drug that was ever used for
weight reduction in this country. While it was available, it was being widely
advertised as a new, safe, and effective way to get thin. Popular brand names for
DNP included Dinitriso, Nitromet, Dinitrenal and Alpha Dinitrophenol. At the
peak of DNP’s popularity, the drug could be found in pharmacies all across the
country.
While the drug may have worked for the intended purpose, it was also
introduced at a time before government review and approval of drug safety. In
this regard DNP had some very strong shortcomings, and it didn’t take long for
reports of side effects to began pouring in. One such incident involved a dozen
women in California who were temporarily blinded by the drug. Numerous
reports of DNP-linked cataracts began coming in from as far away as France and
Italy. It was said to be happening with doses as little as 100 mg daily when taken
for long periods. Reports of more serious injury, even death, from DNP use
followed. With such highly unfavorable safety reports, the drug was soon pulled.
By 1938 it was off the market for good. It has never returned as a medicine for
human or animal consumption. Even so, reports of death associated with DNP
use continue to this day.
Author’s Note: I was hesitant to even include a profile of dinitrophenol in this
book, for fear it might entice someone who otherwise may not have known about
it to use it. But ultimately I decided it would be better to include the historical
information about the drug. The true story of DNP is a scary one and needs to be
remembered. Bodybuilders must understand that the reemergence of
underground DNP in the late 1990s was not a revolutionary new achievement in
fat loss, but a scary repitition of one of the biggest mistakes of the patent
medicine era. It is a drug from a time when an unregulated market was allowing
dangerous chemicals like this to harm the public. The Food and Drug
Administration (FDA) exists today to protect the public from such scenarios.
Almost all experts today agree that DNP is a dangerous drug, and is not
recommended for weight loss.
How Supplied:
DNP is not supplied in a form prepared for human or veterinary consumption. It
is available as a research or industrial chemical only.
Structural Characteristics:
DNP (2,4-Dinitrophenol) is a cellular metabolic poison with the chemical
designation 1-hydroxy-2,4-dinitrobenzene.
Side Effects:
There are many potential side effects associated with DNP use including
increased heart rate, increased breathing rate, nausea, elevated body temperature,
insomnia, profuse sweating, rash, skin lesions, decreased white blood cell count,
cataracts, coma, and death.
Administration:
DNP is not approved for use in humans. Prescribing guidelines are unavailable.
A common dose used among bodybuilders is reportedly 2mg per kg of
bodyweight per day. This calculates to a dosage of 200 mg per day for a person
of approximately 220 pounds of bodyweight. Note that this population tends to
retain more lean muscle mass than the average (sedentary) person of the same
bodyweight, which may substantially alter the results and side effects of a given
dosage. Admittedly, fat loss due to DNP use is highly rapid and extreme, with
some people losing as much as .5 to 1 pound of fat weight per day. This can
equate to a drop of 15 or 20 pounds in only a few weeks. Given the high risks
associated with DNP use, however, it is usually taken for only a few weeks at a
time. The strong incidence of side effects is also regarded as an indicator that the
drug should be discontinued immediately. Note that most experts regard DNP as
a drug with inherent dangers that far outweigh its potential benefits.
Availability:
DNP is not available as a human or veterinary medication in any part of the
world. Availability of products intended for human use is entirely in the
underground realm, where products, dosages, and safety are not the subject of
government approval.
Lipostabil N (phosphatidylcholine/sodium
deoxycholate)
Description:
Lipostabil N is an injectable medication that contains phosphatidylcholine
(PPC), a natural phospholipid. Sodium deoxycholate (a bile salt) is also added
(among other ingredients) to solubilize PPC in water. It was originally developed
as an intravenous solution for the improvement of serum lipids, reduction of
arterial plaque, improving liver values, and the prevention or treatment of blood
vessel blockages by fat particles (fat embolism). It is approved as an intravenous
drug in a number of countries, mainly in Europe. Lipostabil has also had a very
popular off-label use over the past several years, namely as a localized fat loss
agent. Clinics in many areas of the world including Brazil, Europe, and the
United States have actually marketed this as a nonsurgical alternative to
liposuction. In recent years, bodybuilders have been paying some attention to
this drug as well, using it as a cutting or finishing agent.
The mechanism behind Lipostabil’s lipolytic (fat loss promoting) effect is
unique. Upon injection, the solution acts as a detergent, causing nonspecific lysis
(breakdown) of cell membranes.
698 The bile salt sodium deoxycholate is actually
believed to play an important role here, and is therefore considered an active
constituent of Lipostabil for the context of this profile (it is normally considered
an inactive ingredient). During this process the fatty acids stored in the cell
membrane are released, which includes arachidonic acid. This will trigger the
inflammatory cascade, benefiting lipolysis (the inflammatory system can be a
powerful remodeler of body composition) but also causing unwelcome pain and
swelling. Phosphatidylcholine itself also triggers the release of lipases used in
the removal of fat.
699 All of this works together to dismantle localized fat stores,
which are removed via the liver in the form of gall acids.
History:
Lipostabil first appeared as a medication during the 1950s. Although not
approved for prescription use in the U.S., it is approved for medical use in a
number of other countries. The most popular brand name is Lipostabil N by
Nattermann, although it is also found as Lipostabil Forte and simply as
Lipostabil.The application of this drug for fat loss is generally viewed as an “offlabel” use of the medication, although it undoubtedly remains a highly popular
factor in its sales. Some doctors do believe that using Lipostabil for cosmetic
purposes is controversial, and advise against using it for cosmetic reasons.When
you look at the available data, however, its safety profile appears to be
admittedly very high. Lipostabil has been widely used as an intravenous drug for
more than 40 years, and has displayed very few clinically significant side effects
during that time. Injecting the same drug subcutaneously is not likely to present
any significant new or serious risks to the patient.
Network Lipolysis (an organization of some 350 doctors worldwide that
supports this use of Lipostabil) reports over 18,000 cosmetic treatments without
unexpected adverse events. Additionally, Dr. Hasengschwandtner, the medical
director of the Austrian clinic Therapy Centre Bad Loefelden, has reported on
bilirubin and gamma glutamyl transferases (markers of liver stress) values after
subcutaneous Lipostabil use,
700
to see if this new method of fat remodeling is
causing liver strain. The results were in line with IV use, showing no abnormal
change in these values. Although we do not have a great deal of data on this offlabel use of Lipostabil, what can be found is generally very positive, and
suggests this drug (or natural drug, if you will) is quite safe. Lipostabil is
presently sold in Germany, Spain, Italy, Czech Republic, Hong Kong, and South
Africa
How Supplied:
Lipostabil is most commonly supplied in injectable ampules containing 5 mL of
solution each.
Structural Characteristics:
The primary active ingredients in Lipostabil are phosphatidylcholine
(phosphatidyl-Nt-rimethylethanolamine) and sodium deoxycholate (cholan-24-
oic acid, 3,12-dihydroxy-, monosodium salt).
Side Effects:
Potential side effects associated with subcutaneous Lipostabil injections include
localized swelling, redness of the skin, burning, pain, tenderness, and bruising.
Systemic side effects are reported in approximately 3% of users and may include
diarrhea, nausea, dizziness, and intermenstrual bleeding.
701
Administration:
The typical practice for using this drug to promote localized fat loss involves a
series of subcutaneous injections. A total dosage of 1250-2500 mg is often used,
which equates to 25-50 mL of injectable solution. This dosage is divided into 20
or more separate smaller injections. These are spaced throughout the problematic
area (quite commonly the abdominals or thighs), and are all given during the
same office visit or application period. The drug is not administered on a daily
basis.
Lipostabil injections usually cause a significant amount of inflammation in the
area, which may take a week or longer to fully subside. When the inflammation
does subside, however, it usually unveils a noticeable amount of fat loss. In a
clinical setting, this procedure is often repeated a few times, so as to sculpt the
area and achieve the desired level of fat reduction. The current guidelines set
forth by Network Lipolysis call for an 8-week break between treatment periods.
When taken outside of a clinical setting, it is usually advised to apply the first
course at a much lower dosage in order to judge individual sensitivity to the
drug. Some find it simply too painful to use, while others seem to tolerate the
whole procedure extremely well.
As for the ultimate question of how well it works, it is difficult to give exact
numbers, as few clinical studies have been conducted on this use of the drug.
The anecdotal feedback is mixed. Many people who try it report positive results,
particularly for the removal of those last stubborn areas of fat interfering with
muscle definition. There do not seem to be many reports of dramatic weight loss,
however, nor does it seem to be the “pharmaceutical liposuction” that some
clinics describe it to be. Regardless, the reports of visible improvements in fat
loss and muscle definition are consistent and compelling enough to be given
credit. For those extremely overweight, this product is not likely to perform well,
but as a finishing touch it may hold value.
Availability:
Lipostabil is not a controlled drug in the U.S. or Europe, and as such is fairly
easy to obtain on the black market or via mail order drug distributors.
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Growth Hormones & Related
Geref® (sermorelin acetate)
Description:
Sermorelin is a synthetic analog of endogenous growth hormone-releasing
hormone (GHRH or GRF). Sermorelin is a portion of this polypeptide hormone,
specifically consisting of the first 29 of its 44 amino acid structure. As its name
states very clearly, the biological activity of GHRH is to stimulate the synthesis
of growth hormone, which occurs in the pituitary gland. Studies have shown,
however, that the GHRH peptide can be partly truncated without sacrificing its
GH stimulating ability.
702 29NH2) was developed based on this research, and
shares the full biological activity of GHRH with regard to increasing the
endogenous production of growth hormone. Based on its structure and action,
sermorelin is classified as a growth hormone releasing factor (GHRF) or GH
secretagogue.
Sermorelin, as an acetate salt, is used in clinical medicine for two primary
applications. The first is to diagnose pituitary deficiency. The procedure involves
measuring the serum growth hormone response over a 1-2 hour window
following a single IV infusion of sermorelin acetate.
703 An intact hypothalamopituitary-growth-hormone axis should yield a predictable increase in the GH
level. The second common medical application is the treatment of growth
hormone deficiency in children. As with recombinant growth hormone
medications (rHGH, somatropin), sermorelin acetate can provide the benefits of
sustained elevations in GH, including enhanced IGF-1 (Insulin-like Growth
Factor) output and increased linear height.
704 Sermorelin is a very specific acting
drug, and has no effect on prolactin, LH, FSH, insulin, cortisol, glucose,
glucagon, or thyroid hormone levels.
705 This also lends to its therapeutic
potential.
Athletes are interested in sermorelin acetate for the same reasons they use
recombinant human growth hormone. Among other things, growth hormone has
anabolic and anti-catabolic properties. An elevated GH level may support new
muscle tissue growth, and also enhance strength, energy levels, and connective
tissues. GH is also a potent modulator of fat loss. The physique-and
performance-enhancing properties of growth hormone are widely accepted by
the bodybuilding and competitive athletic communities, such that rHGH
medications are very popular. Although sermorelin acetate has a much shorter
history of use, it is slowly gaining acceptance among the community as a viable
alternative to low dose growth hormone injections. It is also presently popular in
anti-aging medicine, where again it serves as an alternative to growth hormone
in the treatment of age-related GH deficiency (“somatopause”).
When comparing this drug to recombinant human growth hormone, sermorelin
acetate does appear to be less effective under normal therapeutic conditions.
During clinical studies, fewer patients on average seem to respond favorably to
therapy in contrast to somatropin, and for those that do respond the
improvements are often less pronounced.
706 Still, it would be a mistake to
exclude sermorelin acetate as a viable therapeutic option. For example, studies
have found that sermorelin acetate can result in significant increases in height
velocity in children with GH deficiency.
707 Furthermore, these improvements
seem to be well sustained after one year of therapy.
708 709 Antibodies to GHRH
do develop in some patients during extended therapy, and may impair the
potency of the drug.
710 The full biological relevance of this antibody reaction,
however, remains unclear.
Sermorelin is approved in the United States for the treatment of GH
deficiency in children only. Prolonged studies treating adults with somatopause
are lacking. One investigation looked at the effects of 2 mg sermorelin acetate
per day for 6 weeks in a group of eleven healthy elderly men (aged 64 to 76)
with low circulating IGF-1 levels.
711 Various measures of body composition and
performance were recorded at the beginning and end of the study. As a result of
treatment, there was a significant increase in nocturnal GH output, area under
peak GH release, and GH peak amplitude. This was accompanied by
improvements in certain measures of strength and endurance including upright
row, shoulder press, and abdominal crunch. Many other measures did not reach
statistical significance, however, which may reflect study limitations such as
small population sizes and a short duration of intake.
Another investigation looked at the effects of sermorelin acetate in a group of
HIV+ men with lipodystrophy.
712 HIV lipodystrophy tends to be characterized
by the abnormal distribution of fat cells and suppressed levels of growth
hormone. During this investigation, 31 men aged 18 to 60 years were given 1 mg
of sermorelin acetate or placebo by subcutaneous injection twice daily for 12
weeks. The primary outcome of the study was a significant increase in serum
IGF-1 in the sermorelin acetate group (104 ng/mL vs 6 ng/mL). This was
accompanied by a favorable increase in lean body mass (+.9 kg vs -.3 kg) and
decrease in visceral and subcutaneous fat. Sermorelin acetate was well tolerated,
and did not result in any change in other health markers including blood
pressure, cholesterol, triglycerides, insulin, or hemoglobin. None of the
participants discontinued therapy due to side effects.
Sermorelin acetate could be viewed as offering a therapeutic advantage over
recombinant growth hormone in some cases, in that it is less likely to result in
GH excess.This is due to the fact that it relies on the body’s own hormone
synthesis instead of exogenous supplementation. Thus, normal IGF-1 feedback
inhibition is likely to help set a natural limit to the growth hormone stimulating
effect.
713 As such, hormone levels are more easily controlled with sermorelin
acetate. Under normal conditions, while sermorelin will produce significant
elevations in GH and IGF-1, these levels should not exceed the high end of the
normal range.
714 Given this feature, sermorelin acetate may be a more
comfortable option for some patients. Studies seem to support this notion,
finding many of the same physical and metabolic benefits of GH injections,
without reporting the same issues with insulin resistance, fluid retention, or
muscle pain.
History:
Sermorelin acetate was developed during the early 1980s, and approved for
prescription sale by the U.S. Food and Drug Administration in 1997. It was
introduced to market under the brand name Geref Diagnostic by the international
biotechnologies firm Serono. As the name implies, it was primarily developed as
a diagnostic tool. It was specifically used for evaluating potential pituitary
deficiency in GH production. Given its effect on growth hormone levels,
however, the drug was also approved by the FDA for the treatment of GH
deficiency in children. Geref was never widely prescribed, however, especially
for uses relating to childhood GH deficiency, where it was never able to compete
with somatropin. Serono ultimately discontinued the product in October 2008,
citing supply issues with the active pharmaceutical ingredient.
715 This was the
only company manufacturing sermorelin as a commercial product in the United
States, thus it is no longer available as a stock pharmacy item.The active
material sermorelin acetate is still made by at least one licensed supplier,
however, so the drug remains available here as a compounded medicine.
How Supplied:
Geref Diagnostic was supplied in ampules containing dry lyophilized sermorelin
acetate, equivalent to 50 mcg of sermorelin. This was reconstituted with a sterile
diluent (also supplied) before use. Generic compounded versions of this
medication typically contain between 3.0 and 7.5 mg of dry lyophilized
sermorelin acetate in a multi-dose vial. Reconstitution before use is also
required.
Structural Characteristics:
Sermorelin acetate is the acetate salt of a synthetic 29–amino acid peptide (GRF
1-29 NH 2) that corresponds to the amino-terminal segment of the naturally
occurring human growth hormone-releasing hormone (GHRH) with 44 amino
acid residues.
Warnings:
Sermorelin acetate should be used with care in epileptic patients. Obesity,
uncontrolled hypothyroidism, hyperglycemia, or elevated plasma fatty acids may
impair the effectiveness of sermorelin. Therapy should be discontinued in
patients treated for childhood GH deficiency once the epiphyses have closed.
Side Effects:
The most common side effects to sermorelin acetate therapy are injection site
reactions such as pain, redness, and swelling. During clinical trials, this occurred
in approximately 17% of patients. Less common side effects include difficulty
swallowing, itching, dizziness, flushing, headache, nausea, vomiting, altered
sense of taste, restlessness, and sleepiness.
Administration:
When used medically for the treatment of idiopathic growth hormone deficiency
in prepubertal children with growth failure, sermorelin acetate is administered by
subcutaneous injection at a dosage of 0.03 mg per kg of body weight once a day
at bedtime. Injection sites should be rotated to avoid irritation or the buildup of
scar tissue. When used to evaluate pituitary capacity in adults, a single
intravenous infusion of 1.0 mcg/kg body weight is administered in the morning
after an overnight fast.This is followed by 60-120 minutes of periodic blood
sampling to measure pituitary hormone output.
When used for physique-or performance-enhancing purposes, sermorelin acetate
is given by subcutaneous injection. It is typically administered at a dosage of 0.2
to 0.5 mg per day (200-500 mcg), which is given before sleep. Studies, however,
do suggest that this drug is more effective when given twice daily.
716 Therefore,
it is often preferred to divide the total daily dosage into two applications,one in
the morning and one in the evening. Cycles of sermorelin acetate usually last
between 8 and 12 weeks. Some anti-aging practitioners will prescribe the
medication for much longer periods of time, however, and cycles lasting 24-48
weeks are not uncommon.The hope is that the extended maintenance of youthful
growth hormone levels will yield more significant physiological changes.
Availability Trends:
Given its low financial value on global pharmaceutical markets, sermorelin
acetate is subject to limited availability worldwide. The preparations most
commonly found diverted for bodybuilding use include those made by private
compounding pharmacies in the United States, and those sold by gray market
research chemical supply companies.
Human Growth Hormone (somatropin)
Description:
As its name suggests, human growth hormone is an important mediator of the
human growth process. This hormone is produced endogenously by the anterior
pituitary gland, and exists at especially high levels during childhood. Its growthpromoting effects are broad, and can be separated into three distinct areas: bone,
skeletal muscle, and internal organs. It also supports protein, carbohydrate, lipid,
and mineral metabolism, and can stimulate the growth of connective tissues.
Although vital to early development, human growth hormone is produced
throughout adulthood. Its levels and biological role decline with age, but
continue to support metabolism, muscle tissue growth/maintenance, and the
management (reduction) of adipose tissue throughout life. Somatropin
specifically describes pharmaceutical human growth hormone that was
synthesized with the use of recombinant DNA technology. Somatropin (rhGH) is
biologically equivalent to human growth hormone (hGH) of pituitary origin.
In a medical setting, somatropin is used to help treat a variety of health
conditions. It is most notably prescribed in cases of childhood growth disorders
that are characterized by insufficient growth hormone production. While usually
not fully corrective, somatropin use is often capable of substantially increasing
the linear growth rate and overall height before further growth is halted in
adolescence. This medication is also used to accelerate growth in children that
were born small and failed to catch up by the age of two. Other uses include the
treatment of short bowel syndrome, growth failure due to renal insufficiency,
muscle wasting associated with HIV infection, and adult growth hormone
deficiency.
Somatropin is also sometimes prescribed to healthy men and women who are
aging. Growth hormone levels tend to decline as we get older, and many
physicians believe that its supplementation to more youthful levels can help slow
some of the damage of aging. Given its beneficial metabolic effects on muscle
mass, strength, energy, cell regeneration, and fat loss, there are many supporters
of this use, even if hGH may not specifically retard the aging process. Note that
in order to prescribe hGH for adult hormone deficiency in the U.S., the patient
must have a diagnosed pituitary disease or history of childhood GH deficiency.
It is specifically illegal according to Federal law to prescribe growth hormone
for any off-label use, which includes anti-aging and bodybuilding purposes.
717
Somatropin may be given by either subcutaneous or intramuscular injection.
During clinical studies, the pharmacokinetic properties of somatropin following
both methods of use were determined. When given by subcutaneous injection,
somatropin has a similar but moderately higher level of bioavailability (75% vs.
63%). The rate of drug metabolism following both routes was also very similar,
with somatropin displaying a half-life of approximately 3.8 hours and 4.9 hours
after subcutaneous and intramuscular injection, respectively. Baseline hormone
levels are usually reached between 12 hours and 18 hours following injection,
with the slower times seen with intramuscular use. Given the delayed rise in
IGF-1 levels, however, which can remain elevated 24 hours after hGH injection,
the metabolic activity of human growth hormone will outlast its actual levels in
the body. Although drug absorption is acceptable by both methods of use, daily
subcutaneous administration is generally regarded as the preferred method of
using somatropin.
A specific analysis of somatropin activity shows a hormone with a diverse set of
effects. It is anabolic to skeletal muscle, shown to increase both the size and
number of cells (processes referred to as hypertrophy and hyperplasia,
respectively). The hormone also seems to have growth-promoting effects on all
organs of the body excluding the eyes and brain. Somatropin has a diabetogenic
effect on carbohydrate metabolism, which means that it causes blood sugar
levels to rise (a process normally associated with diabetes). Excessive
administration of somatropin over time may induce a state of type-2 (insulin
resistant) diabetes. This hormone also supports triglyceride hydrolysis in adipose
tissue, and may reduce body fat stores. Coinciding with this tends to be a
reduction in serum cholesterol. The drug also tends to reduce levels of
potassium, phosphorous, and sodium, and may cause a decrease in levels of the
thyroid hormone triiodothyronine (T3). The latter effect marks a reduction in
thyroid-supported metabolism, and can interfere with the effectiveness of
extended therapy with somatropin.
Growth hormone has both direct and indirect effects. On the direct side, the hGH
protein attaches to receptors in muscle, bone, and adipose tissues, sending
messages to support anabolism and lipolysis (fat loss). Growth hormone also
directly increases glucose synthesis (gluconeogenesis) in the liver, and induces
insulin resistance by blocking its activity in target cells. The indirect effects of
growth hormone are largely mediated by IGF-1 (insulin-like growth factor),
which is produced in the liver and virtually all other tissues in response to
growth hormone. IGF-1 is also anabolic to both muscle and bone, augmenting
growth hormone’s activity. IGF-1, however, also has effects that are strongly
antagonistic to growth hormone. This includes increased lipogenesis (fat
retention), increased glucose consumption, and decreased gluconeogenesis. The
synergistic and antagonists effects of these two hormones combine to form the
character of hGH. Likewise, they also dictate the effects of somatropin
administration, which include the support lipolysis, increased serum glucose
levels, and reduced insulin sensitivity.
Somatropin is considered to be a controversial anabolic and performanceenhancing drug in the realm of bodybuilding and athletics. The main issue of
debate is the exact level of potential benefit this substance carries. While studies
with HIV+ patients in a wasting state tend to support potentially strong anabolic
and anticatabolic properties, studies demonstrating these same effects in healthy
adults and athletes are lacking. During the 1980s, a large body of myth
surrounded discussions of hGH in bodybuilding circles, which may have been
fueled by the high cost of the drug and its very name (“growth hormone”). It was
once thought to be the most powerful anabolic substance you could buy. Today,
recombinant human growth hormone is much more affordable and readily
obtained. Most experienced individuals now tend to agree that it is the fat-losspromoting properties of somatropin that are most obvious. The drug can support
muscle growth, strength gains, and increased athletic performance, but its effects
are generally milder than those of anabolic/androgenic steroids. For a highly
advanced athlete or bodybuilder, however, somatropin can help push body and
performance further than might have been possible with steroids alone.
History:
The first human growth hormone preparations to be used in medicine were made
from pituitary extracts of human origin. These are now commonly referred to as
cadaver growth hormone preparations. Approximately 1 mg of hGH (a 1 day
dose) could be obtained from each cadaver. The first successful treatment with
human cadaver GH was reported in 1958.
718 Soon after these medicines were
introduced to market, and were sold in the U.S. until 1985. The Food and Drug
Administration banned them that year after they had been linked to the
development of Creutzfeldt-Jakob’s disease (CJD), a highly degenerative and
ultimately fatal brain disorder, in a number of patients. The disease can be
transmitted from one person to another under exceptional circumstances (usually
blood transfusion or organ implantation are involved), and was likely caused by
the extraction of hGH from infected cadavers. CJD has a very slow incubation
period, and has been diagnosed anywhere from 4 to 30 years after therapy with
growth hormone of cadaver origin. As of 2004 estimates, at least 26 patients that
received cadaver GH drugs in the United States have been diagnosed with the
disease.
719 The overall incidence of this disease is less than 1%, as
approximately 6,000 patients are documented to have received the medication.
The FDA approved the first synthetic human growth hormone drug in 1985.
Synthesis produced a pure hormone without biological contamination,
eliminating the possibility of CJD transmission. The drug approved was called
somatrem (Protropin), and was based on a manufacturing technology developed
by Genentech in 1979.
720 Somatrem came at an important time given the
removal of cadaver GH by the FDA that same year. This hormone is actually a
slight variant of the hGH protein, but displays the same biological properties of
the natural hormone. Protropin was initially very successful being it was the first
synthetic GH product. By 1987, however, Kabi Vitrum (Sweden) had published
methods for the production of pure synthetic somatropin with the exact amino
acid sequence of endogenous growth hormone.
721
It was also discovered that the
unnatural structure of somatrem causes a much higher incidence of antibody
reactions in patients, which can reduce drug efficacy.
722 Somatropin would come
to be viewed as a more reliable drug, and would dominate the global market
within several years. Today, although somatrem products are still sold,
somatropin retains the vast majority of hGH sales worldwide.
How Supplied:
Somatropin is most commonly supplied in multi-dose vials containing a white
lyophilized powder that requires reconstitution with sterile or bacteriostatic
water before use. Dosage may vary widely from 1mg to 24mg or more per vial.
Somatropin is also available as a stabile pre-mixed solution (Nutropin AQ) that
is biologically equivalent to reconstituted somatropin.
Structural Characteristics:
Somatropin is human growth hormone protein manufactured by recombinant
DNA technology. It has 191 amino acid residues and a molecular weight of
22,125 daltons. It is identical in structure to human growth hormone of pituitary
origin.
Storage:
Do not freeze. Follow package insert for storage information. Refrigeration (2º
to 8ºC, 35º to 46º F) may be required before and after reconstitution.
Side Effects (General):
The most common adverse reactions to somatropin therapy are joint pain,
headache, flu-like symptoms, peripheral edema (water retention), and back pain.
Less common adverse reactions include inflammation of mucous membranes in
the nose (rhinitis), dizziness, upper respiratory infection, bronchitis, tingling or
numbness on the skin, reduced sensitivity to touch, general edema, nausea, sore
bones, carpal tunnel syndrome, chest pain, depression, gynecomastia,
hypothyroidism, and insomnia. The abuse of somatropin may cause diabetes,
acromegaly (a visible thickening of the bones, most notably the feet, forehead,
hands, jaw, and elbows), and enlargement of the internal organs. Due to the
growth promotion effects of human growth hormone, this drug should not be
used by individuals with active or recurring cancer.
Side Effects (Impaired glucose tolerance):
Somatropin may reduce sensitivity to insulin and raise blood sugar levels. This
may occur in individuals without preexisting diabetes or impaired glucose
tolerance.
Side Effects (Injection site):
The subcutaneous administration of somatropin may cause redness, itching, or
lumps at the site of injection. It may also cause a localized decrease of adipose
tissue, which may be compounded by the repeated administration at the same
site of injection.
Administration:
Somatropin is designed for subcutaneous or intramuscular administration. One
milligram of somatropin is equivalent to approximately 3 International Units (3
IU). When used to treat adult onset growth hormone deficiency, the drug is
commonly applied at a dosage of .005/mg/kg per day to .01mg/kg per day. This
equates to roughly 1 IU to 3 IU per day for person of approximately 180-220 lbs.
A long-term maintenance dosage is established after reviewing the patient’s
IGF-1 levels and clinical response over time.
When used for physique-or performance-enhancing purposes, somatropin is
usually administered at a dosage between 1 IU and 6 IU per day (2-4 IU being
most common). The drug is commonly cycled in a similar manner to
anabolic/androgenic steroids, with the length of intake generally being between
6 weeks and 24 weeks. The anabolic effects of this drug are less apparent than its
lipolytic (fat loss) properties, and generally take longer periods of time and
higher doses to manifest themselves.
Other drugs are commonly used in conjunction with somatropin in order to elicit
a stronger response. Thyroid drugs (usually T3) are particularly common given
the known effects of somatropin on thyroid levels, and may significantly
enhance fat loss during therapy. Insulin is also commonly used with somatropin.
Aside from countering some of the effects somatropin has on glucose tolerance,
insulin can increase receptor sensitivity to IGF-1, and reduce levels of IGF
binding protein-1, allowing for more IGF-1 activity
723
(growth hormone itself
also lowers IGF binding protein levels).
724 Anabolic/androgenic steroids are also
commonly taken with somatropin, in an effort to maximize potential musclebuilding effects. Anabolic steroids may also further increase free IGF-1 levels
via a lowering of IGF binding proteins.
725 Note that the stacking of somatropin
with thyroid drugs and/or insulin is usually approached with great care and
caution, given that these are particularly strong medications with potentially
serious or life threatening acute side effects.
Availability:
Somatropin is produced by many different drug companies, and is distributed in
virtually all developed countries. The most common brand names include
Serostim (Serono), Saizen (Serono), Humatrope (Eli Lilly), Norditropin (novo
nodisk), Omnitrope (Sandoz), and Genotropin (Pharmacia).
Somatropin products are high value targets for drug counterfeiting operations.
Many counterfeits are highly deceptive in nature, and have been found in both
illicit and legitimate drug distribution channels. Some counterfeit growth
hormone products are made by relabeling vials of hCG, which bear a very close
visual resemblance to somatropin. A home pregnancy test is sometimes used to
help determine if hCG has been used to make a counterfeit hGH product. This
test works by detecting hCG in the urine. A few days into a cycle with
somatropin, the individual will take a 3-4 IU injection prior to bed. Upon rising,
the pregnancy test will be used, and a positive result will indicate that an hCG
counterfeit has been used. The powder in the vial of somatropin should also be
in the form of a solid (lyophilized) disc. Do not take any product that contains
loose powder.
Increlex® (mecasermin)
Description:
Mecasermin is human insulin-like growth factor-1 (IGF-1) manufactured by
recombinant DNA technology (rhIGF-1). IGF-1 is the primary mediator of the
growth promoting effects of human growth hormone. As such, mecasermin also
can stimulate the growth of bone, muscle, and internal organs. Its effects on
skeletal muscle are also strongly hyperplasic, meaning it causes an increase in
cell number. Unlike hGH, however, mecasermin has very strong insulin-like
effects. It can support growth by increasing the uptake of amino acids, glucose,
and fatty acids, but lowers blood sugar levels so efficiently that it can induce
severe hypoglycemia if too high a dosage is taken. The increased uptake of fatty
acids also means that mecasermin may promote lipogenesis, or an increase in the
storage of body fat.This agent is of interest to bodybuilders and athletes for its
potential to support the growth of skeletal muscle and connective tissue.
Mecasermin is most commonly prescribed for the treatment of severe primary
IGF-1 deficiency (Primary IGFD). This disease is characterized by a failure to
produce normal levels of IGF-1 due to insufficiencies in the growth hormone /
IGF-1 axis (usually involving GH receptor, signaling pathway, or IGF-1 gene
defects). Such patients typically have normal or even high levels of growth
hormone, but their bodies do not respond to it with the sufficient production of
IGF-1. Mecasermin may also be used for the treatment of patients who have
developed antibodies to growth hormone therapy. In both instances the patient is
not GH deficient, but does not respond properly to growth hormone therapy,
making IGF-1 an effective alternative medication. Given its differing effects on
metabolism, however, mecasermin is not considered to be a medical substitute
for hGH therapy, and retains a narrow field of FDA approved uses.
History:
The U.S. Food and Drug Administration approved Mecasermin in August 2005.
It is sold under the brand name Increlex, manufactured by Tercica Inc. of
Brisbane ,California. Tercica licenses this technology from Genentech, which
was the first company to sell a synthetically manufactured human growth
hormone product in the United States (Protropin). Tercica’s rhIGF-1 is produced
by a similar recombinant DNA technology. The process involves inserting the
gene encoding for the human IGF-1 protein into E. coli bacteria, which then
synthesize the protein. In October 2006, Tercia licensed the European rights to
Increlex to the specialties pharmaceutical firm Ipsen. Ipsen received approval to
market Increlex in the European Union in August 2007.
How Supplied:
Mecasermin (Increlex) is supplied in 4mL multi-dose vials containing 10
mg/mL.
Structural Characteristics:
Mecasermin is human IGF-1 protein manufactured by recombinant DNA
technology. It consists of a string of 70 amino acids and has a molecular weight
of 7,649 daltons. Its amino acid sequence is identical to that of endogenous
human IGF-1.
Storage:
Do not freeze. Refrigeration (2º to 8ºC, 35º to 46º F) required before and after
reconstitution.
Side Effects (Hypoglycemia):
The most common adverse reaction to mecasermin therapy is hypoglycemia,
which occurred on at least one occasion in 42% of patients receiving the drug
during clinical trials. Approximately 7% of patients noticed severe
hypoglycemia, and 5% noticed hypoglycemic seizure or loss of consciousness.
Signs of mild to moderate hypoglycemia include hunger, drowsiness, blurred
vision, depressive mood, dizziness, sweating, palpitation, tremor, restlessness,
tingling in the hands, feet, lips, or tongue, lightheadedness, inability to
concentrate, headache, sleep disturbances, anxiety, slurred speech, irritability,
abnormal behavior, unsteady movement, and personality changes. If any of these
warning signs should occur, one should immediately consume a food or drink
containing simple sugars such as a candy bar or carbohydrate drink. Signs of
severe hypoglycemia include disorientation, seizure, and unconsciousness.
Severe hypoglycemia can lead to death and requires immediate emergency
medical attention. Note that in some cases the symptoms of hypoglycemia can
be mistaken for drunkenness.
Mecasermin should never be taken before sleep or in higher than recommended
doses. A meal or snack must be consumed within 20 minutes (before or after) of
administration.
Side Effects (Injection site):
The subcutaneous administration of mecasermin may cause bruising at the site
of injection. It may also cause a localized increase of adipose tissue, which may
be compounded by the repeated administration at the same site of injection.
Rotation of the injection sites is recommended.
Side Effects (General):
Other potential adverse reactions to mecasermin therapy include joint pain,
growth of the tonsils, snoring, headache, dizziness, convulsions, vomiting, ear
pain, hearing loss, and hypertrophy of the thymus gland. Mild elevations in
serum AST, ALT, and LDH levels were found in a significant number of
patients, but they were not associated with hepatotoxicity. Mecasermin can
stimulate the growth of internal organs. Kidney and spleen hypertrophy was
particularly pronounced in the first years of long-term therapy in clinical trials,
without declining renal function. Elevations in cholesterol and triglycerides were
also observed, but remained within the upper limit of normal values. Evidence of
heart enlargement was observed in a few patients, but this appeared without any
apparent clinical significance. The overall relationship between mecasermin use
and cardiac changes has not yet been fully assessed. Thickening of facial soft
tissues was observed in several patients, and should be monitored during
therapy. The abuse of mecasermin may cause acromegaly, which is
characterized by a visible thickening of the bones, most notably the feet,
forehead, hands, jaw, and elbows. Due to the growth promotion effects of hIGF1, this drug should not be used by individuals with active or recurring cancer.
Administration:
Mecasermin is intended for subcutaneous administration. The initiation of
therapy involves close monitoring of blood glucose levels until a proper
maintenance dose is established. The recommended starting dose is .04 to .08
mg/kg (40 to 80 mcg/kg) twice daily. The dose may be increased by .04 mg/kg
per injection, reaching a maximum of .12 mg/kg twice daily. Doses greater than
.12 mg/kg are not advised due to potential hypoglycemic effects. Mecasermin
should always be administered within 20 minutes (before or after) a meal or
snack.
Mecasermin is not widely used for physique-or performance-enhancing
purposes. Common protocols of administration have not yet been established.
Due to the potential for severe hypoglycemia, maximum doses among
bodybuilders and athletes are not likely to measurably exceed those supplied by
therapeutic guidelines. This drug will most likely by taken in cycles lasting no
longer than 8-12 weeks in an effort to minimize unwanted organ growth or fat
gain.
Availability:
Mecasermin is approved for sale in the United States and Europe under the
Increlex brand name.
Protropin® (somatrem)
Description:
Somatrem is a synthetically manufactured form of human growth hormone
(hGH). It is actually a variant of endogenous hGH protein, containing the same
sequence of 191 amino acids, but with the addition of an extra amino acid,
methionine. For this reason somatrem is commonly described as methionyl
human growth hormone. As an hGH medication, somatrem supports the growth
of bone, skeletal muscle, connective tissues, and internal organs. It also plays a
role in protein, carbohydrate, lipid, and mineral metabolism. In a medical setting,
somatrem is used to treat children with growth failure caused by endogenous
growth hormone deficiency. When administered as a long-term treatment before
linear growth is stopped due to closed epiphyses, the drug may impart a
significant positive effect on linear growth. Somatrem is considered to be
therapeutically equivalent to growth hormone of pituitary origin. As an hGH
drug, somatrem is valued by bodybuilders and athletes for its ability to promote
fat loss and muscle and connective tissue growth.
Although somatrem is considered equivalent to human growth hormone, it is not
a natural protein to the human body. This may increase the chance for
developing antibodies to growth hormone during treatment. The antibodies work
by binding with the growth hormone molecule, interfering with its ability to bind
receptors and exert activity. In one clinical investigation, 2/3rd of the children
treated with somatrem developed antibodies to growth hormone after one
year.
726
In a similarly configured investigation involving the administration of
somatropin for one year, only 1 in 7 patients produced serum antibodies to
growth hormone.
727
It is important to note that in both studies the antibody
reactions were not strong, and did not appear to substantially diminish the ability
of the drugs to be therapeutically effective. Diminishment activity (as
determined by antibody levels) appears in an very small percentage (<1%) of
patients taking somatrem. Still, the correct 191 amino acid configuration of
somatropin is considered more desirable to use.
History:
Somatrem was approved for sale in the U.S. in 1985. It was the first synthetic
growth hormone medication available worldwide, produced via a manufacturing
process called Inclusion Body Technology.
728 The technology involves inserting
the DNA encoding for the hGH protein into escherichia coli (E.coli) bacteria,
which assemble and synthesize the pure protein. Prior to the advent of synthetic
growth hormone, hGH was made into a medication only by extracting the
natural protein from human corpses. Biological or cadaver hGH, as it was called,
was banned in the U.S. in 1985 due to the high prevalence of a rare neurological
disease in patients. Somatrem was approved for sale that same year, giving
Genentech a short monopoly on the growth hormone market. Within several
years, however, other biotechnology companies began selling a form of hGH
that was identical to the endogenous protein, called somatropin. Although
somatrem remains available in a number of markets including the United States,
somatropin is much more widely distributed.
How Supplied:
Somatrem is most commonly supplied in multi-dose vials containing a white
lyophilized powder that requires reconstitution with sterile or bacteriostatic
water before use. Dosage may vary from 1mg to 10 mg per vial.
Structural Characteristics:
Somatrem is a polypeptide (methionyl human growth hormone) manufactured
by recombinant DNA technology. It has 192 amino acid residues and a
molecular weight of 22,256 daltons.
Storage:
Do not freeze. Refrigeration (2º to 8ºC, 35º to 46º F) required before and after
reconstitution.
Side Effects (General):
The most commonly reported adverse reactions to somatrem therapy include
carpal tunnel syndrome, increased growth of nevi (moles and birthmarks),
gynecomastia, and pancreatitis. Note that the side effects of somatrem will
generally mirror those of somatropin therapy. The abuse of somatrem may cause
diabetes, acromegaly (a visible thickening of the bones, most notably the feet,
forehead, hands, jaw, and elbows), and enlargement of the internal organs. Due
to the growth promotion effects of human growth hormone, this drug should not
be used by individuals with active or recurring cancer.
Side Effects (Impaired glucose tolerance):
Somatrem may reduce sensitivity to insulin and raise blood sugar levels. This
may occur in individuals without preexisting diabetes or impaired glucose
tolerance.
Side Effects (Injection site):
The subcutaneous administration of somatrem may cause redness, itching, or
lumps at the site of injection. It may also cause a localized decrease of adipose
tissue, which may be compounded by the repeated administration at the same
site of injection.
Administration:
Somatrem is given by subcutaneous or intramuscular injection. One milligram of
somatrem is equivalent to approximately 3 International Units (3IU). When used
to treat children with growth failure due to growth hormone deficiency, the drug
is applied at a dosage up to .04/mg/kg per day. This equates to a maximum of
roughly 10IU per day for a person of approximately 180 lbs. A long-term
maintenance dosage is established after reviewing the patient’s IGF-1 levels and
clinical response over time, and may be substantially lower than 10IU.
When used for physique-or performance-enhancing purposes, somatrem is
usually administered at a dosage between 1IU and 6 IU per day (2-4 IU being
most common). The drug is commonly cycled in a similar manner to
anabolic/androgenic steroids, with the length of intake generally being between
6 weeks and 24 weeks. The anabolic effects of this drug are less apparent than its
lipolytic (fat loss) properties, and generally take longer periods of time and
higher doses to manifest themselves.
Availability:
Somatrem is available in the United States under the Protropin brand name
which is distributed by Roche. In Europe and most nations the vast majority of
hGH is the correct 191 amino acid sequence somatropin. Somatrem can be found
in some markets, however, most commonly in Asia, where it tends to sells for a
substantially lower price than somatropin.
Hypoglycemics
Glucophage (metformin hydrochloride)
Description:
Metformin hydrochloride is an oral antihyperglycemic medication. It is
prescribed for the management of Type-II diabetes, sometimes also referred to as
mature onset diabetes since it tends to develop later in life. The drug is typically
utilized when dietary management and exercise alone have not been able to
control the progress of the disease, yet injectable insulin is not an appropriate
option. While the main activity of metformin HCL is the increased utilization of
glucose, it does not directly mimic the action of insulin. While its precise mode
of action is unknown, it is understood to reduce the output of glucose by the
liver, decrease the intestinal absorption of glucose, and increase insulin
sensitivity in certain organs and peripheral tissues. Use of this agent will lower
the patient’s blood sugar, though its activity makes it less likely to cause a
dangerous state of hypoglycemia if the dosage is accidentally misjudged (a
concern with injectable insulin).
Insulin manipulation is common in sports due to the biological actions of this
hormone. Insulin is involved in nutrient storage, helping to transport amino
acids, fatty acids, and carbohydrates (glucose) into various cells. In the case of
muscle cells, insulin also facilitates cellular anabolic (protein synthesizing) and
anti-catabolic (protein sparing) actions. This hormone also directs nutrient
storage to adipose cells, however, thus its manipulation has the potential to
increase fat mass. Bodybuilders have found, however, that with intense weight
training, insulin can show a much greater affinity for protein and carbohydrate
storage in muscle cells. By manipulating insulin levels (or insulin sensitivity)
under these conditions, muscle growth with minimal fat gain is possible.
Injectable insulin can be risky however, as a mistake in dosage or carbohydrate
intake has the potential to cause life-threatening hypoglycemia (low blood
sugar). Since this effect is rare with metformin, it is considered by some athletes
to be an introduction to insulin manipulation.
History:
Metformin has a long and fairly complicated history in medicine. This drug was
first synthesized in 1929 along with a series of other biguanides. Although some
of its beneficial properties were elucidated at the time, it was not initially subject
to human trials.
729
It sat idle in the research books for nearly three decades after
its creation. The first clinical study investigating its therapeutic potential as a
glucose lowering medication was finally initiated in 1956.
730These trials were
very successful, and metformin was selected for clinical development. It was
given the trade name Glucophage, which translates to “glucose eater”. This, of
course, refers to its ability to help the body dispose of blood glucose.
Glucophage went on to be the most recognized trade name for metformin HCL.
This trade name is still being used to market the drug today, presently by the
Bristol-Myers Squibb Company.
Metformin was not initially the glucose-lowering agent of choice among
clinicians. During the 1950s, it had been studied alongside phenformin and
buformin, which had also been selected for commercial development. Metformin
was initially pushed aside in favor of these two drugs, both of which had proven
to be significantly more potent at lowering blood sugar levels. These drugs
would remain the dominant biguanides for approximately 20 years. By the
1970s, however, it was being reported that phenformin and buformin were
producing unacceptably high incidences of lactic acidosis, an often-fatal
metabolic disorder characterized by a rapid drop in pH. By the close of the
1970s, most governments had determined that these drugs were too risky to
continue using. Phenformin and buformin were subsequently removed from
most pharmaceutical markets worldwide.
The structural and pharmacological similarity of metformin to phenformin and
buformin held back its clinical potential for many years. Researchers were
widely concerned that this agent would also present unfavorable risks.While
lactic acidosis is a legitimate concern, it occurs much less frequently than with
the other biguanides (approximately 1 in 33,000 patients). Following much
evaluation of its benefit-risk ratio, metformin eventually came to be regarded as
the safest drug of the biguanide class. It was widely pushed back into clinical
medicine during the mid-1990s. It was introduced to the United States in 1995,
where it was an immediate success. In the years to follow, metformin continued
to grab a stronger share of the global diabetes medication market. Today, it is
estimated that metformin HCL is the most widely prescribed medication for the
treatment of type-2 diabetes.
How Supplied:
Metformin hydrochloride is most commonly supplied in oral tablets of 500, 850,
and 1000 mg each.
Structural Characteristics:
Metformin is a synthetic derivative of the natural antidiabetic agent guanide. It is
specifically the 1,1-dimethylated biguanide variant.
Warnings:
In rare cases, the use of metformin HCL is associated with lactic acidosis, an
often-fatal metabolic disorder involving (among other factors) an increase in
lactate levels (lactic) and a pronounced decrease in blood pH (acidosis). This
risk increases with conditions such as sepsis, dehydration, excess alcohol intake,
hepatic insufficiency, renal impairment, and acute congestive heart failure.
Symptoms of lactic acidosis include malaise, muscle pain, respiratory distress,
drowsiness, and abdominal distress. Laboratory abnormalities include low
pH,increased anion, and elevated blood lactate. If lactic acidosis is suspected,
metformin HCL should be discontinued and the individual should seek
immediate medical attention.
Side Effects:
Common side effects of metformin HCL therapy include diarrhea (53.2%),
nausea/vomiting (25.5%), flatulence (12.1%), weakness (9.2%), indigestion
(7.1%), abdominal discomfort (6.4%), and headache (5.7%).
731 Metformin must
be used with caution in patients with renal dysfunction, and impaired creatinine
clearance. A serum creatinine concentration above 1.5 mg/dL (men) or 1.4
mg/dL (women) is considered a contraindication to treatment. Metformin may
also impair the absorption of vitamin B12. Hypoglycemia is uncommon with the
use of metformin, though is sometimes noted when caloric intake is deficient, or
when strenuous exercise is not compensated by caloric supplementation. Minor
side effects often subside over time, or with use of a lower metformin HCL
dosage. Lactic acidosis has been reported in approximately 32% of metformin
HCL overdose cases (see: WARNINGS).
Administration:
The oral absorption rate of metformin HCL is slow, with the body taking
approximately six hours to absorb and distribute each dose. Extended release
(XR) formulations are also made, which further delay the absorption of
metformin HCL. Extended release tablets should be taken whole, and not
crushed. In a clinical setting, the drug is given in divided doses with meals,
except for extended release formulations, which are administered once daily
with the evening meal. There is no set adult clinical dose, and the drug must be
tailored to and the drug must be tailored to the individual needs of the patient. It
is typically initiated at a low daily dosage, and slowly escalated by 500 mg each
week or 850 mg every two weeks until the minimum daily dose required for
adequate glycemic control has been established. The maximum recommended
daily dose for type-2 diabetic patients in 2550 mg per day. Fasting plasma
glucose is used to determine the therapeutic response to metformin HCL, and
glycosylated hemoglobin levels are measured every three months. The goal of
therapy is to decrease fasting plasma glucose and glycosylated hemoglobin
levels to normal or near normal levels using the lowest effective dose of
metformin HCL, either alone or in combination with another antihyperglycemic
drug (sulfonylurea or insulin).
When used for physique or performance-enhancing purposes, the typical
protocol is to take 850 mg once or twice per day. If a single application is
desired, it is typically taken 1-2 hours before exercise, so that the drug can have
its peak effect during the early stages of recovery. It is highly common to utilize
a carbohydrate supplement during the hours metformin is active in the body,
especially during the crucial 2-3 hour “nutrient uptake” window following
intense training. The result of metformin treatment is typically not as dramatic as
insulin, but the drug still does have a notable anabolic effect for many users.
Most bodybuilders/athletes opt to use this drug for a limited duration, with
cycles lasting 6-8 weeks in length. This would be followed by an equally long
break (at a minimum) before metformin, insulin, or any other antihyperglycemic
agent is used for physique or performance-enhancing purposes.
Availability Trends:
Metformin is readily available given its widespread use in clinical medicine. It is
sold under many brand names, as both a standalone and combination medication.
Bodybuilders and athletes tend to limit their use to preparations containing only
metformin.While the drug is not the subject of much interest by steroid
counterfeiting or underground manufacturing operations, it is the target of many
other general drug counterfeits given the ease in which it can be sold. As such, it
should not be assumed that all packaged drug products labeled as metformin are
legitimate. Care should be taken to ensure that all products bearing this
ingredient have been acquired through legitimate pharmaceutical channels.
Insulin (rDNA Origin)
Description:
Insulin is peptide hormone produced in the Islets of Langerhans in the pancreas.
The release of this hormone in the human body is most closely tied to blood
glucose levels, although a number of other factors including pancreatic and
gastrointestinal hormones, amino acids, fatty acids, and ketone bodies are also
involved. The main biological role of insulin is to promote the intracellular
utilization and storage of amino acids, glucose, and fatty acids, while
simultaneously inhibiting the breakdown of glycogen, protein, and fat. It is most
notably identified with the control of blood sugar levels, and insulin medications
are typically prescribed to people with diabetes, a metabolic disorder
characterized by hyperglycemia (high blood sugar).While insulin targets many
different organs in the body, this hormone is both anabolic and anti-catabolic to
skeletal muscle tissue,
732 733 734 a fact that explains the inclusion of
pharmaceutical insulin in the realm of athletics and bodybuilding.
The use of insulin to improve performance and body composition can be a little
tricky because this hormone can also promote nutrient storage in fat cells.This,
however, is an activity of insulin that can be somewhat managed by the user.
Athletes have found that a strict regimen of intense weight training and a diet
without excess caloric and fat intake can enable insulin to show a much higher
affinity for protein and glucose storage in muscle (as opposed to fatty acid
storage in adipose) cells. This is especially true in the post-exercise enhancedabsorptive state, where insulin sensitivity in skeletal muscle has been shown to
increase significantly over baseline (rested) levels.
735 When used during the
post-training window, the hormone is, likewise, capable of producing rapid and
noticeable muscle gains. The muscles often begin to look fuller (and even
sometimes more defined) very soon after initiating insulin therapy, and the
overall results of therapy are often described as dramatic.
The fact that insulin use cannot be detected by urinalysis has ensured it a place
in the drug regimens of many athletes and professional bodybuilders. Note that
there has been some progress in drug detection, especially with the analogs, but
to date regular insulin is still considered a ”safe” drug. Insulin is often used in
combination with other “contest safe” drugs like human growth hormone,
thyroid medications, and low dose testosterone injections, and together can have
a dramatic effect on the user’s physique and performance without fear of a
positive urinalysis result. Those who do not have to worry about drug testing,
however, often find that insulin combined with anabolic/androgenic steroids can
be a very synergistic combination. This is because the two actively support an
anabolic state through different mechanisms. Insulin strongly enhances the
transport of nutrients into muscle cells and inhibits protein breakdown, and the
anabolic steroids (among other things) strongly increase the rate of protein
synthesis.
As mentioned, the usual medical purpose for insulin is to treat different forms of
diabetes. More specifically, the human body may not be producing enough
insulin (Type-I diabetes), or may not recognize insulin well at the cell site
although some level is present in the blood (Type-II diabetes). Type-I diabetics
are, therefore, required to inject insulin on a regular basis, as they are left
without a sufficient level of this hormone. Along with medication, the individual
will need to constantly monitor blood glucose levels and regulate their sugar
intake. Together with lifestyle modifications such as regular exercise and
developing a balanced diet, insulin dependent individuals can live a healthy and
full life. When left untreated, however, diabetes can be a fatal disease.
History:
Insulin first became available as a medicine during the 1920s. Credit for the
discovery is most appropriately given to Canadian physician Fred Banting and
Canadian physiologist Charles Best, who worked together to produce the first
insulin preparations, and the world’s first effective treatment of diabetes. Their
work stemmed from an idea initially proposed by Banting, who as a young
doctor theorized that an active extract could be made from animal pancreases to
regulate blood sugar in human patients. He needed help to try and actualize his
idea, and he sought out world-renowned physiologist J.J.R. Macleod at the
University of Toronto. Macleod, initially less than impressed with the unusual
concept (but likely impressed with Banting’s conviction and tenacity), assigned
a couple of graduate students to assist him in his work. A coin flip determined
who would work with Banting, and he was eventually paired with graduate
student Best. Together they made medical history.
The first insulin preparations they produced were made of crude pancreatic
extracts taken from dogs. At one point the supply of laboratory animals was
exhausted, and desperate to continue their research, the pair actually began
taking stray dogs to supplement their pancreas supply. Shortly after, the two
found that they could work with the pancreases of slaughtered cows and pigs,
making their work much easier (and ethically acceptable). They successfully
treated their first diabetic patient with insulin in January 1922. By August of that
year, they had been successful in treating a group of clinical patients, including
15-year-old Elizabeth Hughes, daughter of former presidential candidate Charles
Evans Hughes. Elizabeth was diagnosed with diabetes in 1918, and her dramatic
fight for life with the disease gained national attention. Elizabeth would be saved
by insulin on the doorstep of starvation, as severe calorie restriction was the only
remedy known to slow the disease at the time. Banting and Macleod swiftly won
the Nobel Prize for their discovery, which was presented to them approximately
a year later in 1923. Shortly after, dispute over credit arose, and ultimately
Banting shared his prize with Best, and Macleod shared his prize with J. B.
Collip, a chemist that assisted in the extraction and purification process.
After initially declining the assistance in the hopes that they could work out
production issues on their own, Banting and his team worked with Eli Lilly &
Co. to develop the first mass-produced insulin medicines using their animal
extraction techniques. Their production success was extreme and rapid, and the
drug became commercially available on a wide scale in 1923, the same year
Banting and Macleod won the Nobel prize.That same year, Nordisk
Insulinlaboratorium was founded by Danish scientist Augusta Krogh, who
desperately wanted to bring back an insulin manufacturing technique to
Denmark to treat his wife, who was ill with diabetes.This Denmark firm
eventually became Novo Nordisk, the world’s second leading producer of
insulin next to Eli Lilly & Co.
The early insulin medications were fairly impure by today’s standards. They
typically contained 40 units of animal insulin per milliliter, in contrast to today’s
accepted standard concentration of 100 units. The large doses needed with these
early low-concentration drugs were not very comfortable for patients, and
injection-site reactions were not uncommon. They also contained significant
protein impurities that would sometimes cause allergic reactions in users.
Despite these faults, the drugs saved the lives of countless individuals who
beforehand were faced with a sure death sentence following a diagnosis of
diabetes. Eli Lilly and Novo Nordisk improved the purity of their products in the
coming years, but no major improvements in insulin technology developed until
the mid-1930s, when the first longer-acting insulin preparations began to
surface.
The first longer-acting drug made use of protamine and zinc to delay the action
of insulin in the body, extending the activity curve and reducing the number of
daily injections required for many patients. Dubbed Protamine Zinc Insulin
(PZI), the preparation would have an effect lasting as long as 24-36 hours.
Neutral Protamine Hagedorn (NPH) Insulin, also known as Isophane insulin,
followed, reaching market by 1950. This preparation was very similar to PZI
insulin except that it could be mixed with regular insulin without disturbing the
release curve of the respective insulins. In other words, a regular insulin drug
could be mixed in the same syringe with NPH insulin, providing a biphasic
release pattern characterized by an early peak effect due to the regular insulin,
and an extended action brought on by the NPH.
In 1951 the Lente insulins began to surface, which included semilente, lente, and
ultra-lente preparations. The amount of zinc used in each varied, producing
preparations with distinct and long-acting pharmacokinetics. Unlike previous
Insulins, this was also achieved without the use of protamine. Many physicians
were soon able to successfully switch their patients from NPH insulin over to a
single morning dose of Lente insulin, often heralding the release of the new
drugs as a big advance in insulin medications (though some would still require
an evening dose with a Lente insulin to maintain full control over blood glucose
levels during the 24-hour period). Up to this point the insulin drugs made by the
large pharmaceutical companies worked very well. No substantial step forward
in the development of new insulin delivery technologies would come for another
23 years.
In 1974, chromatographic purification techniques allowed the manufacture of
animal insulin with extremely low impurity levels (less than 1 pmol/l of protein
impurities). Novo was the first to release a drug made with this technology,
which it called monocomponent (MC) Insulin. Eli Lilly also released a version
called “Single Peak” Insulin, likely referring to the single protein peak noticed
upon chemical analysis. This advance, though significant, would be short lived.
In 1975, Ciba-Geigy produced the first synthetic insulin preparation (CGP
12831). And just three years later, scientists at Genentech were able to produce
insulin using modified E. coli bacteria, the first synthetic insulin with an
identical amino acid sequence as human insulin (although the animal insulins
work fine in humans their structures are slightly different). The U.S. Food and
Drug administration approved the first such medicines in 1982, with the
acceptance of Humulin R (Regular) and Humulin NPH from Eli Lilly & Co. The
name Humulin is a contraction of the words “human” and “insulin”, of course.
Novo would follow with semi-synthetic insulins Actrapid HM and Monotard
HM.
The FDA has approved a variety of other insulin drug combinations over the
years, including various biphasic insulin blends that use differing amounts of
rapid and longer-acting insulins. More recently, we have also seen the FDA
approval of Eli Lilly’s rapid-acting insulin analog Humalog. Several other
analogs are also now available including Lantus and Apidra from Aventis, and
Levemir and Novorapid from Novo Nordisk. A number of additional analogs are
also under investigation at this time. With the large variety of different insulin
medications approved and sold in the U.S. and other nations, it is important to
understand that “insulin” represents an extremely broad class of medicines. As a
class, these drugs are likely to continue to expand as new agents are developed
and successfully tested. Today, it is estimated that 55 million people use some
form of injectable insulin on a regular basis to manage their diabetes, making
this an extremely important and lucrative area of human medicine.
How Supplied:
Pharmaceutical insulin comes from one of two basic origins, animal or
synthetic.With animal source insulin, the hormone is extracted from the pancreas
of either pigs or cows (or both) and prepared for medical use. These preparations
are further divided into the categories “standard” and “purified”, dependent on
the level of purity and non-insulin content of the solution. With such products
there is always the slight possibility of pancreatic contaminants making their
way into the prepared drug. Specifically called biosynthetic, synthetic insulin is
produced by a recombinant DNA procedure similar to the process used to
manufacture human growth hormone. The result is a polypeptide hormone
consisting of one 21-amino acid “A-chain” coupled by two disulfide bonds with
one 30-amino acid “B-chain”. The biosynthetic process will produce a drug free
of the pancreatic protein contaminants possible with animal insulin, and that is
structurally and biologically identical to human pancreatic insulin. With the
innate (remote) risk of contamination involved with animal insulin, coupled with
the fact that the structure is (very slightly) different from human insulin,
synthetic human insulin drugs dominate the market today. Biosynthetic human
insulin/insulin analogs are also the most common insulins of use among
athletes,and the main focus of this profile.
There are a variety of synthetic insulins available, with each possessing unique
properties relating to speed of onset, peak and duration of activity, and
concentration of dose. This therapeutic variety may allow physicians to tailor a
treatment program for insulin-dependant diabetics that allows for the least
amount of daily injections and the greatest level of patient comfort. It is
important that one should be aware of the individual activity of any insulin drug
before attempting its use. Due to the differences between preparations, it is also
medically advised that extreme care be taken whenever a physician attempts to
switch an insulin-dependant diabetic patient from one form of insulin medication
to another.
Below is a list showing the distinctions between popular forms of biosynthetic
insulin.
Short-acting Insulins:
Humalog® (Insulin Lispro): Humalog® is a short-acting analog of human
insulin, specifically the Lys(B28) Pro(B29) analog of insulin created when the
amino acids at positions 28 and 29 are reversed. It is considered equipotent to
regular soluble insulin on a unit-to-unit basis, but with more rapid activity.
736
The onset of drug action following subcutaneous administration is
approximately 15 minutes, and its peak effect is reached in 30 to 90 minutes. It
has a total duration of action between 3 and 5 hours. Insulin lispro is usually
used as a supplement to a longer acting insulin product, providing a fast-acting
medication that can be taken before or immediately after meals to mimic the
body’s natural insulin response. Many athletes believe that its short window of
effect makes it an ideal insulin medication for physique-or performanceenhancing purposes, as most of its action can be concentrated in the post-training
enhanced-nutrient-uptake window.
Novolog® (Insulin Aspart): Novolog is a short-acting analog of human insulin
created when the amino acid proline at position B28 is replaced with aspartic
acid. The onset of drug action following subcutaneous administration is
approximately 15 minutes, and its peak effect is reached in 1-3 hours. It has a
total duration of action between 3 and 5 hours. Insulin lispro is usually used as a
supplement to a longer acting insulin product, providing a fast-acting medication
that can be taken before or immediately after meals to mimic the body’s natural
insulin response. Many athletes believe that its short window of effect makes it
an ideal insulin medication for physique-or performance-enhancing purposes, as
most of its action can be concentrated in the post-training enhanced-nutrientuptake window.
Humulin®-R “Regular” (insulin Inj): Identical to human insulin. Also sold as
Humulin-S® (Soluble) in some markets, this product consists of zinc-insulin
crystals dissolved in clear fluid. There is nothing added to slow the release of
this product, so it is generically referred to as soluble human Insulin. This drug
works rapidly and has a short duration of effect.The onset of drug action
following subcutaneous administration is 20-30 minutes, and its peak effect is
reached in 1-3 hours. It has a total duration of action between 5 and 8 hours.
Together with Humalog, these two forms of insulin are the most popular (almost
exclusive) choices among athletes and bodybuilders for physique-or
performance-enhancement purposes.
Intermediate-and Long-acting Insulins:
Humulin®-N, NPH (insulin isophane): A crystalline suspension of insulin with
protamine and zinc to delay its release and extend its action. Insulin isophane is
considered intermediate length insulin. The onset of drug action following
subcutaneous administration is approximately 1-2 hours, and its peak effect is
reached in 4-10 hours. It has a total duration of activity lasting more than 14
hours. This type of insulin is not commonly used for physique-or performanceenhancement purposes.
Humulin®-L, Lente (medium zinc suspension): A crystalline suspension of
insulin with zinc to delay its release and extend its action. Humulin-L is
considered an intermediate length insulin. The onset of drug action following
subcutaneous administration is approximately 1-3 hours, and its peak effect is
reached in 6-14 hours. It has a total duration of activity lasting more than 20
hours. This type of insulin is not commonly used for physique-or performanceenhancement purposes.
Humulin®-U, Ultralente (prolonged zinc suspension): A crystalline suspension
of insulin with zinc to delay its release and extend its action. Humulin-U is
considered a long-acting insulin. The onset of drug action following
subcutaneous administration is approximately 6 hours, and its peak effect is
reached in 14-18 hours. It has a total duration of activity lasting 18-24
hours.This type of insulin is not commonly used for physique-or performanceenhancement purposes.
Lantus (insulin glargine): A long-acting analog of human insulin. Insulin
glargine is created when the amino acid asparagine at position A21 is replaced
by glycine, and two arginines are added to the C-terminus of the insulin B chain.
The onset of drug action following subcutaneous administration is
approximately 1-2 hours, and the drug is considered to have no significant peak
(it is designed to have a very stable release pattern throughout the duration of
activity). Insulin glargine lasts between 20-24 hours in the body following
subcutaneous injection. This type of insulin is not commonly used for physiqueor performance-enhancement purposes.
Biphasic Insulins:
Humulin® Mixtures: These are mixtures of regular soluble insulin for a fast
onset of action, and a long-or intermetiate-acting insulin for a prolonged effect.
These are labeled by the mixture percentage, commonly 10/90, 20/80, 30/70,
40/60, and 50/50. Mixtures using Humalog as the rapid-acting insulin are also
available.
Warning: Concentrated Insulin
The most common forms of insulin come in a concentration of 100 IU of
hormone per milliliter. These are identified as “U-100” preparations in the U.S.
and many other regions. In addition to this, however, there are also concentrated
forms of insulin available for patients that require higher doses and a more
economical or comfortable option to U-100 preparations. In the U.S., products
containing as much as 5 times the normal concentration, or 500 IU per milliliter,
are also sold. These are identified as “U-500” preparations, and are available by
prescription only. It can be extremely dangerous or life threatening to replace a
U-100 insulin product with a U-500 product without making the necessary
dosing adjustments to compensate for the greater drug concentration. Given the
general difficulty in accurately measuring athletic doses (2-15 IU) with a drug of
such high concentration, U-100 preparations are used almost exclusively for
physique-and performance-enhancing purposes.
Side Effects (Hypoglycemia):
Hypoglycemia is the primary danger with the use of insulin. This is a dangerous
condition that occurs when blood glucose levels fall too low. It is a common and
potentially fatal reaction experienced at some time or another by most medical
and nonmedical insulin users, so it needs to be taken seriously. It is, therefore,
critical to understand the warning signs of hypoglycemia. The following is a list
of symptoms that may indicate mild to moderate hypoglycemia: hunger,
drowsiness, blurred vision, depressive mood, dizziness, sweating, palpitation,
tremor, restlessness, tingling in the hands, feet, lips, or tongue, lightheadedness,
inability to concentrate, headache, sleep disturbances, anxiety, slurred speech,
irritability, abnormal behavior, unsteady movement, and personality changes. If
any of these warning signs should occur, one should immediately consume a
food or drink containing simple sugars such as a candy bar or carbohydrate
drink.This will hopefully raise blood glucose levels sufficiently enough to ward
off mild to moderate hypoglycemia. There is always a possibility of severe
hypoglycemia, which is very serious and requires immediate emergency medical
attention. Symptoms of this include disorientation, seizure, unconsciousness, and
death. Note that in some cases the symptoms of hypoglycemia are mistaken for
drunkenness.
It is also very important to note that you may notice a tendency to get sleepy
after injecting insulin. This is an early symptom of hypoglycemia, and a clear
sign the user should be consuming more carbohydrates. One should absolutely
avoid the temptation to go to sleep at this point, as the insulin may take its peak
effect during rest, and blood glucose levels could be left to drop significantly.
Unaware of this condition during sleep, the athlete may be at a high risk for
going into a state of severe hypoglycemia. The serious dangers of such a state
have already been discussed, and unfortunately consuming more carbohydrates
during sleep will not be an option. Those experimenting with insulin would,
therefore, be wise to always stay awake for the duration of the drug’s effect, and
also avoid using insulin in the early evening to ensure the drug will not be
inadvertently active when retiring for the night. It is also important to make sure
others are aware of your use of the drug so that they may inform emergency
medical technicians should you lose consciousness or the ability to inform others
of your condition due to hypoglycemia. This information can spare valuable
(perhaps life saving) time in helping medical professionals establish a diagnosis
and provide supportive treatment.
Side Effects (Lipodystrophy):
The subcutaneous administration of insulin may cause a localized increase in
adipose tissue at the site of injection. This may be compounded by the repeated
administration of insulin at the same site of injection.
Side Effects (Allergy to Insulin):
In a small percentage of users, the administration of insulin may cause a
localized allergy. This may include irritation, swelling, itching, and/or redness at
the site of injection. This often subsides as therapy continues. In some instances
it may be due to an allergy to an ingredient, or in the case of animal insulin, a
protein contaminant. Less common, but potentially more serious, is a systemic
allergic reaction to insulin administration. This may include a rash on the whole
body, wheezing, shortness of breath, fast pulse, sweating, and/or a reduction in
blood pressure. In rare instances this may be life threatening. Any adverse
reaction should be reported to a medical authority.
Administration (General):
Given that there are varying forms of insulin available for medical use with
differing pharmacokinetic patterns, as well as products with different drug
concentrations, it is extremely important that the user be familiar with the dosage
and actions of any specific insulin preparation they intend to use so that peakeffect, total time of effect, total dosage, and carbohydrate intake can be closely
monitored. Rapid-acting insulin preparations (Novolog, Humalog, and HumulinR) are the most popular choices for physique-or performance-enhancing
purposes, and the subject of the dosing information presented in this book. It is
also important to stress that before one considers using insulin they should also
become very familiar with using a glucometer. This is a medical device that can
give you a quick and accurate reading of your blood glucose level. This device
can be indispensable in helping one manage and optimize their
insulin/carbohydrate intake.
Administration (Short-acting Insulin):
Short acting forms of insulin (Novolog, Humalog, Humulin-R) are designed for
subcutaneous injection. Following subcutaneous injection, the injection site
should be left alone and not rubbed, to prevent the drug from releasing into
circulation too quickly. It is also advised to rotate subcutaneous injection sites
regularly to avoid the localized buildup of subcutaneous fat that may develop
due to the lipogenic properties of this hormone (see Adverse Reactions:
Lipodystrophy). The medical dosage will vary depending on the individual
requirements of the patient. Furthermore, changes in such things as diet, activity
level, or work/sleep schedule may affect the required insulin dose. Although not
recommended medically, it is possible to administer some short-acting insulins
via intramuscular injection. This, however, may create more variability (and
potential risk) with regard to drug dissipation and hypoglycemic effect.
Insulin dosages can vary slightly among athletes, and are often dependent upon
factors like body weight, insulin sensitivity, activity level, diet, and the use of
other drugs. Most users choose to administer insulin immediately after a
workout, which is the most opportunistic time of the day to use this drug.
Among bodybuilders, dosages of regular insulin (Humulin-R) used are usually in
the range of 1IU per 15-20 pounds of lean bodyweight; 10IU is perhaps the most
common dosage. This amount may be adjusted downward slightly for users of
the more rapid-acting Humalog and Novolog preparations, which provide a
higher and faster peak effect. First-time cautious users usually ignore
bodyweight guidelines, and instead start at a low dosage with the intention of
gradually working up to a normal dosage. For example, on the first day of
insulin therapy one may begin with a dose as low as 2 IU. Each consecutive
post-workout application this dosage might be increased by 1IU, until the user
determines a comfortable range. Many feel this is safer and much more tailored
to the individual than simply calculating and injecting a dose, as some find they
tolerate slightly more or less insulin than weight guidelines would dictate.
Athletes using growth hormone in particular often have slightly higher insulin
requirements, as HGH therapy is shown to both lower secretion of, and induce
cellular resistance to, insulin.
One must also remember that it is very important to consume carbohydrates for
several hours following insulin use. One should generally follow the rule-ofthumb of ingesting at least 10-15 grams of simple carbohydrates per IU of
insulin injected (with a minimum immediate intake of 100 grams regardless of
dose).This is timed 10 to 30 minutes after subcutaneous injection of Humulin-R,
or immediately after using Novolog or Humalog.The use of a carbohydrate
replacement drink is often used as a fast carbohydrate source. Properly cautious
insulin users will always have a source for simple sugars on-hand in case an
unexpected drop in glucose levels is noticed. Many athletes will also take
creatine monohydrate with their carbohydrate drink, since the insulin may help
force more creatine into the muscles. 30-60 minutes after injecting insulin, one
should also eat a good meal and consume a protein shake. The carbohydrate
drink and meal/protein shake are absolutely necessary, as without them blood
sugar levels may drop dangerously low and the athlete may enter a state of
hypoglycemia (see Adverse Reactions: Hypoglycemia). Carbohydrates and
proteins are continually provided in sufficient amounts to meet glucose
requirements throughout the entire window of insulin effect.
Administration (Intermediate-acting, Long-acting, and Biphasic Insulins):
Intermediate-acting, long-acting, and biphasic insulins are designed for
subcutaneous injection. Intramuscular injection will cause the drug to be
released too rapidly, potentially resulting in hypoglycemia. Following
subcutaneous injection, the injection site should be left alone and not rubbed, to
prevent the drug from releasing into circulation too quickly. It is also advised to
rotate subcutaneous injection sites regularly to avoid the localized buildup of
subcutaneous fat due to the lipogenic properties of this hormone (see Adverse
Reactions: Lipodystrophy). The medical dosage will vary depending on the
individual requirements of the patient. Furthermore,changes in such things as
diet, activity level, or work/sleep schedule may affect the required insulin dose.
Intermediate-acting, long-acting, and biphasic insulins are not widely used for
physique-or performance-enhancing purposes due to their longer acting nature,
which makes them poorly suited for concentrating the nutrient partitioning effect
of insulin during the short post-workout enhanced-nutrient-uptake window.
Availability:
U-100 insulins may be dispensed from pharmacies in the United States without a
prescription. This is so that an insulin-dependent diabetic will have easy access
to this life-saving medication. Concentrated (U-500) insulin is sold by
prescription only. In most regions of the world, high medical use of the drug
leads to easy access and low prices on the black market.
Hypotensives
BP StabilTM
Description:
BP Stabil is a blood pressure management product. It is not pharmaceutical
based, but instead contains natural dietary ingredients that support the
functioning of the circulatory system (it is classified as a dietary supplement). In
addition to several vitamins and minerals necessary for optimal circulatory
health, the formula contains a number of components with substantial clinical
support including hawthorn,
737 quercetin,
738 nattokinase,
739 garlic,
740 green
tea,
741 ginkgo biloba,
742 olive extract,
743 and coq10.
744 BP Stabil is a
bodybuilder/athlete specific product. It is used most often to help maintain blood
pressure levels that are already in the normal healthy range (blood pressure
stabilization), especially during periods of high activity or supplementation.
BP Stabil does not reduce blood pressure simply by increasing water loss
(diuretic). Instead, it takes a multi-level approach to supporting circulatory
health. Most fundamentally, it was designed to help maintain optimal
functioning of the endothelium. The endothelium is a collection of cells that line
the inside of all blood vessels in the body. These cells manage the relative
flexibility of the blood vessels, helping to regulate the flow of blood throughout
the entire circulatory system. If the endothelium is not healthy and reactive, the
system can become rigid or stiff. This would increase blood pressure and
resistance when transporting blood further away from the heart.The loss of
endothelial reactivity can even lead to a state of clinical hypertension, defined by
persistent elevations in blood pressure outside of the normal range.
History:
BP Stabil was released in 2010 by Molecular Nutrition (United States). It is an
expansion of the Health Stabil product line, which contains several products
designed to support the unique needs of bodybuilders and athletes undergoing
aggressive training or supplementation programs. BP Stabil is classified as a
dietary health supplement, and as such is available through many gyms and
health supplement stores. It is prominently available in the United States,
although it can also be found in some international markets including Canada,
Australia, and certain parts of Europe.
How Supplied:
BP Stabil is supplied in capsules containing a blend of hawthorn extract,
quercetin dehydrate, nattokinase, garlic, green tea extract, ginkgo biloba extract,
olive leaf extract, CoQ10, potassium,magnesium, and calcium, and vitamins A,
B3 (niacin), B6 (pyroxidine), C, and D.
Side Effects:
BP Stabil is a natural dietary supplement and is not expected to have notable side
effects. Individuals should monitor their blood pressure closely during use to
make sure normal healthy levels are maintained.
Administration:
For blood pressure support, BP Stabil is taken at a dosage of 3 capsules per day.
A dosage of up to 6 capsules per day may be taken during periods of heightened
activity or supplementation. Note that a natural product such as BP Stabil may
help support healthy blood pressure levels, but cannot be relied upon to replace
the need for prescribed blood pressure medications, especially if a state of
clinical hypertension has developed. Care should be taken to regularly monitor
blood pressure during use.
Availability:
BP Stabil is produced in the United States by Molecular Nutrition. It is available
for export, and may be found in Canada, Europe, Australia, and some other
international markets.
Catapres (clonidine HCL)
Description:
Clonidine is a centrally acting alpha-agonist hypotensive agent. It is most
commonly prepared as a hydrochloride salt for use in tablets and capsules,
although it is also supplied in oral liquids, injectable solutions, and transdermal
patches. Clonidine stimulates alpha-adrenoceptors in the brain, which reduces
sympathetic outflow from the central nervous system. This decreases the heart
rate, and relaxes the blood vessels so that blood is allowed to flow more easily.
Clonidine is widely prescribed for the treatment of hypertension (abnormally
high blood pressure), which can have serious health implications if left
untreated. Bodybuilders typically use this drug for the same purpose, namely to
counter blood pressure elevations caused by anabolic/androgenic steroid use.
Clonidine is also commonly prescribed for off-label purposes including the
treatment of alcohol, opiate, and nicotine addiction, menopause symptoms,
diabetic diarrhea and neuropathy (nerve damage), and ulcerative colitis.
Clinical studies show that clonidine can also produce a significant increase in the
serum growth hormone level. This occurs via stimulation of hypothalamic
GHRH (Growth Hormone Releasing Hormone) release, which in turn supports
the secretion of growth hormone from the pituitary.
745 Given the known anabolic
properties of growth hormone, clonidine is sometimes specifically chosen by
bodybuilders (when a blood pressure medication is needed) because of its
perceived added metabolic benefits. Realistically, however, this drug is rarely
reported to produce performance or body composition improvements. This may
be due to its effects on GH being short lived. Studies suggest that in many
patients, clonidine will not result in sustained increases in GH with continued
daily use.
746 747 The prescribing literature even warns that its GH elevating
properties are acute, and do not result in chronic elevations with long-term use.
Clonidine may be of value for blood pressure management or other off-label
purposes, but at the present time it is not widely accepted as a GH stimulating
drug for bodybuilders.
Oral clonidine is considered a fast acting medication. Its blood pressure lowering
effects are typically noticed within 30 to 60 minutes after ingestion. Peak blood
levels are achieved within 3-5 hours after administration, and the drug is
metabolized with a half-life of approximately 12-16 hours. Given the short
acting nature of the drug, clonidine is usually administered at least twice per day
in order to maintain therapeutically effective blood levels. Food does not appear
to influence the pharmacokinetics of clonidine.
The absorption of clonidine from transdermal patches may be significantly
delayed in comparison to oral tablets, and may take 2-3 days before peak blood
levels are achieved. Tolerance to the blood pressure lowering effects of clonidine
may develop over time. It may be necessary to periodically reevaluate the
dosage during prolonged therapy. Clonidine may be used alone, but is also
commonly combined with a second antihypertensive agent when a stronger
blood-pressure lowering effect is required.
History:
Clonidine first appeared in clinical studies during the late 1960s,
748 and was
approved by the U.S. Food and Drug Administration for prescription sale in
1974.
749 Over the years, its favorable safety profile and level of efficacy have
allowed it to become a somewhat common first-line option for the treatment of
hypertension. The most widely known trade name for clonidine is Catapres, sold
in many different countries by the international pharmaceutical manufacturer
Boehringer-Ingelheim. In the United States, clonidine products are also available
through many generic drug manufacturers including Actavis, Bertek, Global,
Mutual, Mylan, Par, Qualitest, UDL Laboratories, Unichem, and Xanodyne.
How Supplied:
Clonidine hydrochloride is most commonly supplied in oral tablets of 0.1, 0.2,
and 0.3 mg each.
Structural Characteristics:
Clonidine is an alpha-agonist hypotensive agent derived
Clonidine is an alpha-agonist hypotensive agent derived from imidazoline. It
has the chemical designation 2,6-dichloro-N-2-imidazolidinyldenebenzenamine.
Warnings:
Abrupt discontinuation of clonidine may result in side effects including rebound
hypertension, nervousness, agitation, headache, and/or tremor. In rare instances
clonidine withdrawal has been associated with serious cerebrovascular accident
and even death. Patients should not discontinue clonidine treatment without
consulting their physician. When discontinuing clonidine, it is usually advised to
slowly reduce the dosage over a minimum period of 2-4 days to reduce
withdrawal symptoms.
Side Effects:
Common side effects associated with clonidine treatment include dry mouth
(40% of patients during clinical studies), drowsiness (33%), dizziness (16%),
constipation (10%), and sedation (10%). Less frequent adverse reactions include
physical fatigue, fever, increased sensitivity to alcohol, abnormal heart beat,
congestive heart failure, delirium, insomnia, nightmares, paraesthesia (tingling
of the skin), hair loss, rash, abdominal pain, anorexia, hepatitis, vomiting,
decreased libido, erectile dysfunction, frequent waking to urinate during the
night (nocturia), leg cramps, muscle pain, blurred vision, and dryness or burning
of the eyes. Some side effects appear to be dose-dependant. Taking more than
the prescribed amount (overdosage) may result in serious adverse reactions
including hypotension (low blood pressure), respiratory depression, impaired
motor reflexes, weakness, drowsiness, hypothermia, heart irregularities, coma, or
death.
Administration:
When used medically to treat hypertension, the dosage must be tailored to the
individual needs of the patient. The usual initial starting dosage in adults is .1 mg
given twice daily, morning and evening (.2 mg per day). This dosage may be
increased once per week by .1 mg/day until the proper maintenance dosage is
achieved. An effective therapeutic maintenance dosage usually rests between .2
mg and .6 mg per day, although a small percentage of patients require
significantly higher amounts (2.4 mg/day is considered the maximum therapeutic
dosage).When used by bodybuilders to offset elevated blood pressure due to
anabolic/androgenic steroid use, therapeutic use guidelines are usually followed.
Some users will initiate clonidine at sub-therapeutic dosages (.1 mg per day) if
they are unsure of their responsiveness to the drug, or their relative need for a
hypotensive agent. Individuals should be reminded that it is important to monitor
blood pressure closely whenever taking any medications that can have
hypertensive or hypotensive effects.
Availability Trends:
Clonidine is widely sold throughout the developed world. Low demand, low
cost, and high availability make this drug a low-profit target for counterfeiting.
Counterfeits are unlikely to be a significant problem.
Liver Detoxification
Essentiale forte N (Compound N)
Description:
Essentiale forte N is the trade name for a liver-support supplement distributed in
Europe by Aventis Pharma. While this is regarded as a medication in some
regions, it actually contains a selection of natural vitamins and phospholipids.
Likewise, in many areas, including the United States, Essentiale forte N is sold
over the counter. The product specifically contains a complex of B vitamins,
vitamin E, and phospholipid forms of linoleic, linolinec, and oleic acid.
Essentiale forte N is used widely in Europe to treat cases of hepatic dysfunction,
such as those caused by chronic infection, allergy, drug toxicity, or other disease.
Essential forte N is of interest to steroid using bodybuilders and athletes for its
ability to reduce the level of liver strain caused by anabolic/androgenic steroids
(particularly those compounds that are c-17 alpha alkylated).
The main mechanism of action with Essential forte N appears to be focused on
the supply of antioxidants and building blocks necessary for the repair of
damaged cells. This product contains mainly polyunsaturated phospholipids
(mostly phosphatidylcholine), and a complex of B and E vitamins.
Phosphatidylcholine is identified as a membrane lipid, and is a key component
of the Essential forte N formula. This phospholipid is important to the integrity
of cells, adding both flexibility and strength. Phosphatidylcholine has long been
identified as an important supplement for the liver, supporting normal hepatic fat
metabolism and overall liver health. It is also believed to be an important
antioxidant for liver and pancreatic wellness.The additional vitamins in the
Essential forte N formula are likely included to increase the antioxidant and
regenerative properties of the medication.
Essentiale forte N was the first product shown to mitigate the hepatotoxic effects
of anabolic steroid use in a clinical study.
750 The investigation looked at the
effects of steroid abuse (with or without Essential forte N), and compared them
to controls (non-steroid-using subjects). A full panel of liver enzymes was used
to determine the level of relative hepatic strain. As expected, the steroid-only
group noticed a significant elevation in liver enzymes that were well above the
normal range. Liver enzymes were also elevated in the steroid users taking
Essential forte N, however, they were similar to controls and remained within
the normal range.The researchers concluded:“The positive association of the
abuse severity with the increased hepatic enzymes’ levels suggest a relationship
between abused AAS and hepatic cell damage. However, when AAS were taken
with [Essentiale forte N], … the hepatotoxic effect appears to be attenuated.”
While this one study does not assure that steroid liver toxicity can be completely
eliminated, it does lend strong support for the use of Essential forte N with
hepatotoxic anabolic steroids.
History:
Essentiale forte N has been sold in Western and Eastern Europe for many years,
where it is distributed by Aventis (formerly Rhone-Poulenc Rorer). This
compound has been approved for the treatment of hepatic liver steatosis and
other hepatic dysfunction. European bodybuilders have used this medication for
years owing to its understood general value with regard to liver health. It did not
catch the attention of athletes in the United States and Canada until 2008,
however, when the investigation into its effects with steroid abusers was
published in the Clinical Toxicology journal. Since then, this natural medication
has been noting increased popularity with North American consumers.
How Supplied:
Essentiale forte N is supplied in soft gelatin capsules containing vitamin B1
(6mg), vitamin B2 (6mg), vitamin B6 (6mg), vitamin B12 (6mcg), vitamin E (6
mg), niacin (15 mg), and a phospholipid complex [polyene phosphatidylcholine]
(diclyceride esters of choline-phosphoric acid and unsaturated fatty acids
linoleic, linoliec, and oleic acids) (300 mg).
Side Effects:
Essential forte N is a natural vitamin and supplement medication and is not
expected to have notable side effects.
Administration:
When used medically to treat hepatic dysfunction, the most common
recommended dosage is 2 capsules 3 times daily with meals. Bodybuilders and
athletes using this medication to reduce the hepatic stress of oral steroid use will
typically follow the same medical prescribing guidelines, and will taken the
product for as long as the hepatotoxic steroids are administered.
Availability:
Essential forte N is widely available in Western and Eastern Europe. It is a
relatively inexpensive supplement, and is not a high interest target of counterfeit
manufacturing operations.
LIV-52®
Description:
Liv-52 is an herbal medicine used widely in Europe and Asia to support
metabolic and liver health. While in some countries this product is regarded as a
drug, it contains all natural ingredients including capparis spinosa, terminalia
arjuna, cichorium intybus, achillea millefolium, solanum nigrum, tamarix
gallica, and cassia occidentalis. It is specifically used in the prevention or
treatment of hepatitis, alcoholic liver disease, early liver cirrhosis, protein energy
malnutrition, loss of appetite, radiation and chemotherapy-induced liver damage,
as an adjunct to hepatotoxic drugs, and to support metabolism during
convalescence or prolonged illness. As the first three letters of its name would
suggest, overall liver health is the primary focus of this product. Bodybuilders
and athletes use Liv-52 as a way to reduce the level of strain placed on the liver
by hepatotoxic anabolic/androgenic steroids.
Numerous medical studies have been conducted on Liv-52 in recent years, many
of which involve its ability to protect the liver from damage by alcohol or other
toxins.
751 752 753 754 One investigation in particular looked at how the herbal
medication affected the breakdown of alcohol in the body, showing that it
notably increased its excretion, even to the point of being able to reduce next day
hangover symptoms after binge drinking.
755 Another study investigated what
underlying mechanism might be involved in Liv-52’s ability to protect the liver
against alcohol toxicity. It demonstrated that one mechanism involved a specific
ability to slow the rate of glutathione depletion.
756 This may be very important to
the steroid-using athlete, as glutathione depletion is looked at as a direct marker
of liver stress with c-17 alpha alkylated orals. Note that while these studies lend
support for the use of a natural remedy like Liv-52 during hepatotoxic steroid
administration, they do not provide complete assurance that this remedy can
prevent liver damage.
History:
Liv-52 is an herbal product that has its roots in ayurvedic medicine, an age old
form of Hindu science and medicine that centers on the use of natural remedies.
Liv-52 is manufactured by the Himalaya Drug Co. in Bombay, India, and was
first introduced to the global market in 1955. Over the years it came to be a
widely distributed and popular natural product. In 2002, the Swiss government
actually classified Liv-52 as a pharmaceutical product, which is believed to be
the first time an herbal remedy was adopted as a prescription drug in Western
Europe.
757 Liv-52 had already been popular with steroid using bodybuilders and
athletes for many years by this point, and further clinical support only cemented
this position. Liv-52 presently remains the most commonly used form of natural
liver support among the steroid-using community today.
How Supplied:
Liv-52 is supplied in capsules containing a 450 mg of a blend of caper bush
(capparis spinosa), arjuna (terminalia arjuna), wild chicory (cichorium intybus),
yarrow (achillea millefolium), black nightshade (solanum nigrum), tamarisk
(tamarix gallica), and negro coffee (cassia occidentalis).
Side Effects:
Liv-52 is a natural herbal supplement medication and is not expected to have
notable side effects.
Administration:
For general liver support or as an adjunct to hepatotoxic pharmaceuticals, Liv-52
is generally taken at a dosage of 1-2 capsules 2 times per day.
Availability:
Liv-52 is produced exclusively by the Himalaya Drug Company, and is
distributed widely in many areas of the world. In some regions, including the
United States, the product is marketed under the LiverCare® trade name.
Liver StabilTM
Description:
Liver Stabil is a liver support supplement. It contains more than a dozen natural
ingredients designed to help protect and detoxify the liver, and may be
specifically useful during exposure to hepatotoxic substances such as oral
anabolic/androgenic steroids. At the foundation of this formula are several
clinically studied ingredients similar to those found in Liv-52 and Essentiale
forte. For example, cichorium intybus, which was originally an old Turkish folk
medicine, has been the subject of modern studies showing it can protect the liver
from toxic substance damage. It has specifically been shown to lower liver
enzymes (aspartate amino-transferase and alanine amino-transferase) and
bilirubin levels after toxic exposure.
758 Arjuna is also used, and again has been
shown to lower liver enzyme levels and stress markers following hepatotoxic
substance administration.
759 Yarrow (achillea millefolium) was also included,
and may help reduce hepatic inflammation and regulate bile secretion.
760
Phosphatidylcholine (a key constituent of cellular membranes including liver
cells) and a combination of key vitamins round out the Liv-52/Essential fortelike base of the Liver Stabil formula.
Lipid Stapil expands on its foundation with four additional well-studied liver
health ingredients.The most prevalent of these are N-acetyl cysteine and Lglutathione. Both nutrients are important to maintaining ongoing liver health,
and may be especially useful in countering hepatic glutathione depletion,
761 an
effect common with oral AAS toxicity.
762 Next, milk thistle extract standardized
for silymarin content is included. Silymarin contains several key flavonolignans
that protect and detoxify the liver. In fact, this natural remedy is one of the most
extensively studied and proven liver detoxification supplements, and in some
regions is widely prescribed by physicians to treat numerous liver diseases
including alcohol cirrhosis. An extensive review of more than a dozen placebocontrolled studies with the use of silymarin on patients with cirrhosis have
shown it to consistently reduce aspartate amino-transferase levels and even liverrelated mortality.
763 Regardless of the chosen liver support regimen, milk thistle
should be included. Lastly, wasabi japonica is a rich source of 6-
methylsulfinylhexyl isothiocyanate (6-HITC). The nutrient 6-HITC is an
inhibitor of glutathione S-transferase, an enzyme that breaks down hepatic
glutathione.
764
History:
Liver Stabil was developed in 2008 by Molecular Nutrition (United States). The
focus was specifically on designing a supplement that can help support liver
health in users of hepatotoxic substances such as oral anabolic/androgenic
steroids. The formula was intended to target several key areas of steroid-induced
liver toxicity including general liver strain and hepatic enzyme elevations,
glutathione depletion, inflammation, and bile secretion and transport. Liver
Stabil can be found through international distribution, most notably in Canada,
Australia, and certain parts of Europe. Note that in some regions with strict
controls over nutritional supplements Liver Stabil may be considered a natural
drug product, and may be subject to certain rules and regulations concerning its
importation and sale.
How Supplied:
Liver Stabil is supplied in capsules containing a blend of N-acetyl cysteine, milk
thistle extract, wild chicory (cichorium intybus), L-glutathione, wasabi japonica,
arjuna (terminalia arjuna), phosphatidylcholine, yarrow (achillea millefolium),
vitamin B1, vitamin B2, vitamin B6, vitamin B12, vitamin E, and niacin.
Side Effects:
Liver Stabil is a natural dietary supplement and is not expected to have notable
side effects.
Administration:
For general liver support or as an adjunct to hepatotoxic pharmaceuticals, Liver
Stabil is taken at a dosage of 3 capsules per day. A dosage of up to 6 capsules
per day may be taken during periods of heightened hepatic strain. Note that a
natural product such as Liver Stabil may help reduce the level of liver toxicity,
but cannot be relied upon to completely eliminate potential damage from the
abuse of hepatotoxic drugs. Care should always be taken to monitor liver health
when taking liver toxic substances.
Availability:
Liver Stabil is produced in the U.S. by Molecular Nutrition. It is available for
export, and may be found in Canada, Europe, Australia, and some other
international markets.
Reductase Inhibitors
Avodart® (dutasteride)
Description:
Dutasteride is an inhibitor of the 5-alpha reductase enzyme. Reductase inhibitors
are designed to prevent the conversion of testosterone to its more androgenic
counterpart DHT (dihydrotestosterone). DHT is implicated in a number of
disorders in men including male pattern hair loss and benign prostate
enlargement. Dutasteride is specifically approved for the treatment of
symptomatic benign prostate hyperplasia (BPH). While dutasteride is similar in
structure and action to finasteride, it differs from the first generation reductase
inhibitor in its tissue selectivity. Finasteride inhibits the type-2 isozyme of the 5-
alpha reductase enzyme, found prominently in the scalp and prostate.
Dutasteride is non-specific for isotype, and inhibits both type-1 and type-2
reductase. As such, it inhibits DHT conversion in all tissues including the scalp,
liver, prostate, and skin. Because of this it also lowers systemic levels of DHT
much more effectively than finasteride.
The DHT inhibiting effects of dutasteride make this drug of some interest to
bodybuilders and athletes, particularly those concerned with the androgenic
component of testosterone-based steroids. Dutasteride is capable of reducing the
androgenic side effects produced by DHT conversion, changing the profile of
testosterone drugs measurably. Provided moderate doses of testosterone are
being used, the result can be a substantial reduction in the occurrence of oily
skin and acne. For those prone to male pattern hair loss, dutasteride may also
reduce the harsh impact of testosterone on the hairline. Note that as a selective
type-2 inhibitor, finasteride is also effective at lowering DHT levels in the scalp
(and reducing hairline impact of testosterone use), but does not work as well for
reducing oily skin and acne.
In terms of overall potency, a study published in the Journal of Clinical
Endocrinology and Metabolism (May 2004) directly compared dutasteride to its
closest pharmaceutical counterpart, finasteride.
765
In this investigation 399 males
suffering from benign prostatic hypertrophy were assembled and separated into
three general groups, each receiving dutasteride (subdivided by doses of .01, .05,
.5, 2.5, or 5.0 mg daily), finasteride (.5 mg daily) or placebo, for a period of 24
weeks. Over the 24-week period, the dutasteride group noted the strongest level
of DHT inhibition. The beneficial effects of this drug also occurred over a wide
range of dosages. For example, a 5 mg daily amount caused 98.4% inhibition in
DHT levels, while 1/10th of this amount (.5 mg daily, the adopted therapeutic
dose) lowered levels by an average of 94.7%.
This was in great contrast to the 5 mg finasteride group, which noticed only
70.8% inhibition. Researchers also noted that there was significantly more of a
variation in the results of the finasteride group, with some patients noting DHT
suppression in the range of only 50-55%.
Just as there can be benefits to lowering 5-alpha reductase activity by way of less
androgenic side effects, there can also be some drawbacks. For one, a strong
androgen like DHT helps with neuromuscular interaction, fostering strength and
muscle gain. Users of reductase inhibitors often report a drop in their maximum
lifts soon after the drug is initiated. Libido may also decline as DHT
concentrations are lowered. A small percentage of men even find the need to
keep Viagra on hand, as dutasteride renders them otherwise impotent.
Dihydrotestosterone also serves as a potent endogenous anti-estrogen, as this
non-aromatizable steroid competes with other substrates (like testosterone,
which aromatizes) to bind with the aromatase enzyme. Gynecomastia or other
estrogenic side effects may occur when this competition is absent. Gynecomastia
is listed in the warnings for this product, although the frequency of this in testing
was very low (1.1% of users).
History:
Dutasteride was first described in 1997.
766
It was developed by the U.S. based
pharmaceutical company GlaxoSmithKline. It was approved by the FDA in
November 2001, and introduced to market the following year by Glaxo under
the Avodart trade name. GlaxoSmithKline also markets the drug in a number of
other countries in Europe and South America under the same trade name.
How Supplied:
Dutasteride is supplied in soft gelatin capsules containing .5 mg each.
Structural Characteristics:
Dutasteride is a synthetic 4-azasteroid. It has the chemical designation (5·,17‚)-
N-{2,5 bis(trifluoromethyl)phenyl}-3-oxo-4-azaandrost-1-ene-17-carboxamide.
Warnings (Pregnancy):
This drug must never be taken during pregnancy. Be aware that dutasteride can
be absorbed through the skin. Women who are, or might become pregnant,
should never handle dutasteride capsules. The DHT blocking action of
dutasteride can cause severe developmental problems to an unborn male fetus,
even in very small amounts. Unaltered dutasteride can also be recovered in the
semen. It is unknown if the drug can be absorbed during sexual intercourse
enough to harm a developing male fetus. The use of condoms or abstinence is
recommended during therapy.
Side Effects:
The most common adverse reactions to dutasteride therapy are impotence,
reduced libido, and difficulty ejaculating. Gynecomastia was also noted during
clinical trials, but occurred in less than 1% of patients. Some patients have also
developed allergic reactions to the drug, including rash, itching, edema, and
hives.
Administration (General Considerations):
Reductase inhibitors cannot completely protect against androgenic side effects
such as steroid-induced hair loss, oily skin, and acne. Reductase inhibitors lessen
these side effects by reducing, not eliminating, the level of androgenic activity in
the skin and scalp. Androgenic and anabolic effects are both mediated by the
same receptor, and there is presently no way known to completely separate these
two properties. Dihydrotestosterone is also not unique in its ability to facilitate
androgenetic alopecia (male pattern hair loss). DHT inhibition, therefore, does
not offer complete protection against this side effect.
Reductase inhibitors are only applicable with testosterone, methyltestosterone,
and fluoxymesterone. These three drugs are converted to stronger “dihydro”
derivatives by the reductase enzyme. Nandrolone and some of its derivatives
become weaker upon interaction with this enzyme, as their “dihydro”
metabolites bind the androgen receptor very poorly. Reductase inhibition may
intensify their androgenic side effects. Methandrostenolone and boldenone
undergo conversion to stronger 5-alpha reduced metabolites, but at such small
levels that reductase inhibitors have little effect on their androgenicity. Most
other synthetic anabolic steroids are unaffected by the reductase enzyme and
reductase inhibitors.
Administration:
When used medically for the treatment of symptomatic benign prostatic
hyperplasia (BPH), dutasteride is taken in a dosage of .5 mg (1 capsule) per day.
When used by bodybuilders and athletes to reduce the androgenicity of
testosterone, methyltestosterone, or fluoxymesterone, dutasteride is commonly
taken in a dosage of .5 mg (1 capsule) once every 1-2 days. The drug is typically
administered for as long as the offending steroids are also taken.
Availability:
GlaxoSmithKline distributes this drug in the U.S., Europe, and South America
under the Avodart trade name. Additionally, a number of other brands can be
found in different markets including Austria (Avolve, Zyfetor), Greece
(Duagen), India (Duprost), Netherlands (Duagen), Portugal (Duagen), and Spain
(Duagen).
Proscar® (finasteride)
Description:
Finasteride is an inhibitor of 5a-reductase, which is the enzyme responsible for
converting testosterone into DHT (dihydrotestosterone). This drug can
efficiently reduce the serum concentration of DHT, thereby minimizing the
unwanted androgenic effects that result from its presence. The effect of this drug
is quite rapid, suppressing serum DHT concentrations as much as 65% within 24
hours after taking a single 1mg tablet. Medically, this drug is used to treat benign
prostate hyperplasia (prostate enlargement) and androgenetic alopecia (male
pattern hair loss). It is also being investigated as a potential treatment for
hirsutism, which describes male patterned hair growth on the face or body of a
woman. Male athletes and bodybuilders are interested in finasteride for its ability
to reduce the androgenic side effects associated with the use of testosterone and
certain derivatives.
Finasteride is a specific inhibitor of the Type-II 5a reductase enzyme. There are
actually two isozymes of reductase in the human body, labeled as Type-I and
Type-II. Type-I 5a-reductase is predominantly found in the liver and sebaceous
glands of the skin. Type-II 5a-reductase is primarily found in the prostate and
hair follicles. The Type-II enzyme is responsible for about 2/3rd of the
circulating DHT, while the Type-I enzyme produces the remaining 1/3rd. As an
inhibitor of Type-II reductase only, finasteride has a more pronounced effect
with regard to preventing hair loss, but is somewhat less effective at mitigating
oily skin and acne. Since hair loss is the primary worry among most male steroid
users who use reductase inhibitors, finasteride remains a popular ancillary drug
in spite of its inability to block DHT conversion in all tissues.
Finasteride is considered a highly specific drug, as it has little spillover effect on
the other hormones in the body. It has no affinity for the androgen or estrogen
receptors, and therefore does not exhibit any androgenic, antiandrogenic,
estrogenic, or anti-estrogenic properties. It has no appreciable impact on
circulating levels of cortisol, thyroid-stimulating hormone, or thyroxine, nor
does it appear to alter HDL/LDL cholesterol levels. Changes in luteinizing
hormone (LH) or follicle-stimulating hormone (FSH) are also not notable, and it
is not shown to have a significant effect on the hypothalamic-pituitary-testicular
axis. Finasteride has been shown to increase the circulating levels of testosterone
by roughly 15%, however, since a greater amount of the androgen is being left
unaltered by the reductase enzyme.
History:
The first release of finasteride in the U.S. was under the brand name of Proscar®
(Merck), which was approved by the FDA in 1992. It was specifically given
approval for use by patients with benign prostate hyperplasia (prostate
enlargement). In December 1997, the Food and Drug Administration again
approved finasteride, this time for a different purpose, namely the treatment of
male pattern hair loss. Merck released the drug under a different brand name for
this purpose, Propecia®, which contained only 1/5th of the Proscar® dosage.
Today, both Proscar® and Propecia® remain the dominant brands of finasteride
on the global market.
How Supplied:
Finasteride is most commonly supplied in tablets of 1 mg and 5 mg.
Structural Characteristics:
Finasteride is a synthetic 4-azasteroid. It has the chemical designation 4-
azaandrost-1-ene-17-carboxamide,N-(1,1-dimethylethyl)-3-oxo-,(5·,17‚)-.
Warnings (Pregnancy):
This drug must never be taken during pregnancy. Finasteride can be absorbed
through the skin.Women who are, or might become pregnant, should never
handle broken or uncoated finasteride tablets. The DHT blocking action of
finasteride can cause severe developmental problems to an unborn male fetus,
even in very small amounts. Unaltered finasteride can also be recovered in the
semen.It is unknown if enough drug can be absorbed during sexual intercourse
to harm a developing male fetus. The use of condoms or abstinence is
recommended during therapy.
Side Effects:
Adverse reactions commonly associated with the short-term (1 year) use of
finasteride include impotence (8.1%), decreased libido (6.4%), decreased
ejaculate volume located. (3.7%), ejaculation disorder (.8%), gynecomastia
(.5%), breast tenderness (.4%), and rash (.5%).
Administration (General Considerations):
Reductase inhibitors cannot completely protect against androgenic side effects
such as steroid-induced hair loss, oily skin, and acne. Reductase inhibitors lessen
these side effects by reducing, not eliminating, the level of androgenic activity in
the skin and scalp. Androgenic and anabolic effects are both mediated by the
same receptor, and there is no way presently known to completely separate these
two properties. Dihydrotestosterone is also not unique in its ability to facilitate
androgenetic alopecia (male pattern hair loss). DHT inhibition, therefore, does
not offer complete protection against this side effect.
Reductase inhibitors are only applicable with testosterone, methyltestosterone,
and fluoxymesterone. These three drugs are converted to stronger “dihydro”
derivatives by the reductase enzyme. Nandrolone and some of its derivatives
become weaker upon interaction with this enzyme, as their “dihydro”
metabolites bind the androgen receptor very poorly. Reductase inhibition may
intensify their androgenic side effects. Methandrostenolone and boldenone
undergo conversion to stronger 5-alpha reduced metabolites, but at such small
levels that reductase inhibitors have little effect on their androgenicity. Most
other synthetic anabolic steroids are unaffected by the reductase enzyme and
reductase inhibitors.
Administration:
When used medically for the treatment of male pattern hair loss (androgenetic
alopecia) in men, the recommended dosage is 1mg per day. When used for the
treatment of benign prostatic hyperplasia (BPH), 5 mg per day is usually
administered. When used by bodybuilders and athletes to reduce the
androgenicity of testosterone, methyltestosterone, or fluoxymesterone,
finasteride is commonly taken in a dosage of 1mg per day. The drug is typically
administered for as long as the offending steroids are also taken. Since DHT
inhibition can lessen strength and possibly muscle gains during testosterone,
methyltestosterone, or fluoxymesterone therapy (given the positive actions of
androgens on the neuromuscular system), a “use only when necessary” approach
is usually taken with regard to this drug.
Availability:
Finasteride is widely available in most regions of the world.The most prominent
brand names in commerce are Proscar® (5 mg) and Propecia® (1mg), although
a number of other brand and generic forms of the drug can also be located.
Testosterone Stimulating Drugs
hCG (human chorionic gonadotropin)
Description:
Human Chorionic Gonadotropin (hCG) is a prescription medication containing
chorionic gonadotropin obtained from a natural (human) origin. Chorionic
gonadotropin is a polypeptide hormone normally found in the female body
during the early months of pregnancy. It is synthesized in syncytiotrophoblast
cells of the placenta, and is responsible for increasing the production of
progesterone, a pregnancy-sustaining hormone. Chorionic gonadotropin is
present in significant amounts only during pregnancy, and is used as an indicator
of pregnancy by standard over-the-counter pregnancy test kits. Blood levels of
chorionic gonadotropin become noticeable as early as seven days after ovulation,
and rise evenly to a peak at approximately two to three months into gestation.
After this point, the hormone level will drop gradually until the point of birth.
Although it possesses minor FSH-like (Follicle Stimulating Hormone) activity,
the physiological actions of chorionic gonadotropin mainly mimic those of the
gonadotropin luteinizing hormone (LH). As a clinical drug, hCG is used as an
exogenous form of LH. It is typically applied to support ovulation and
pregnancy in women, most specifically those suffering from infertility due to
low concentrations of gonadotropins and an inability to ovulate. Due to the
ability of LH to stimulate the Leydig’s cells in the testes to manufacture
testosterone, hCG is also used with men to treat hypogonadotropic
hypogonadism, a disorder characterized by low testosterone levels and
insufficient LH output. The drug is also used in the treatment of prepubertal
cryptochidism, a condition in which one or both of the testicles have failed to
descend into the scrotum. HCG is used by male athletes for its ability to increase
endogenous testosterone production, generally during, or at the conclusion of, a
steroid cycle, when natural hormone production has been interrupted.
History:
Chorionic gonadotropin was first discovered in 1920,
767 and was identified as a
pregnancy hormone approximately 8 years later.
768 The first drug preparation
containing chorionic gonadotropin came in the form of an animal pituitary
extract, which was developed as a commercial product by Organon. Organon
introduced the extract in 1931, under the trade name Pregnon. A trademark
dispute forced the company to change the name Pregnyl, however, which
reached market in 1932. Pregnyl is still sold by Organon to this day, although it
no longer comes in the form of a pituitary extract. Manufacturing techniques
were introduced in 1940 that allowed the hormone to be obtained by filtering
and purifying the urine of pregnant women, and by the late 1960’s were adopted
by all manufacturers formerly using animal extracts. Over the years the process
and manufacturing protocols have been refined, but hCG is made in essentially
the same way today as it was decades ago. While modern preparations are of
biological origin, the risks of biological contaminants are said to be low
(although cannot be completely excluded).
Early on, the indicated uses for chorionic gonadotropin preparations were much
broader than they are presently. Product literature from the 1950’s and ’60’s
recommended the use of these drugs for, among other things, the treatment of
uterine bleeding and amenorrhea, Froehlich’s syndrome, cryptochidism, female
sterility, obesity, depression, and male impotence. A good example of the wide
uses of chorionic gonadotropin are illustrated in the preparation Glukor, which
was described in 1958 as being, “Three times more effective than testosterone.
For tired young men in male climacteric. For tired old men in male senility.
Beneficial in impotence, angina and coronary heart disease, neuropsychosis,
prostatitis, [and] myocarditis.“ Such recommendations, however, reflect an era
less tightly regulated by government agency and less reliant on proven clinical
trials. Today, FDA-approved indications for hCG are limited to the treatment of
hypogonadotropic hypogonadism and cryptocridism in men, and anovulatory
infertility in women.
HCG has no significant thyroid-stimulating activity. This is specifically pointed
out because hCG was once widely used for the treatment of obesity. The trend
seemed to have become popular in 1954, after a paper was published by Dr.
A.T.W. Simeons claiming that chorionic gonadotropin was an effective adjunct
to dieting. According to the study, patients were able to effectively stave off
hunger with severely low-calorie diets provided they took the hormone
injections. Dubbed the Simeons diet, people all across the country were soon
subjecting themselves to severe calorie restriction (500 calories per day) and
taking hCG injections. Soon after, the hormone itself became the main focus for
fat loss. In fact, by 1957 it was said that hCG was the most commonly prescribed
medication for weight loss. More recent and comprehensive investigations,
however, refute that there is any anorexic or metabolic advantage to the use of
hCG.
769
In 1962, the Journal of the American Medical Association had already
been warning consumers about the hCG-inclusive Simeons diet, stating the more
basic fact that severe calorie restriction, which causes the body to sacrifice
muscle and organ tissue to obtain necessary protein, was more hazardous than
obesity itself. By 1974, the FDA had had enough of the hCG fat loss claims, and
mandated the following statement to be included with all prescribing literature.
“HCG HAS NOT BEEN DEMONSTRATED TO BE EFFECTIVE
ADJUNCTIVE THERAPY IN THE TREATMENT OF OBESITY. THERE IS
NO SUBSTANTIAL EVIDENCE THAT IT INCREASES WEIGHT LOSS
BEYOND THAT RESULTING FROM CALORIC RESTRICTION, THAT IT
CAUSES A MORE ATTRACTIVE OR ’NORMAL’ DISTRIBUTION OF
FAT, OR THAT IT DECREASES THE HUNGER AND DISCOMFORT
ASSOCIATED WITH CALORIERESTRICTED DIETS.” This warning persists
on all product sold in the U.S. today. In spite of this warning and evidence to the
contrary, some clinics still promote the use of hCG for dieting purposes.
Human Chorionic Gonadotropin is a widely popular drug preparation today,
owing to the fact that it remains an indispensable part of ovulation therapy for
many cases of female infertility. Popular preparations in the U.S. presently
include Pregnyl (Organon), Profasi (Serono), and Novarel (Ferring), although
many other trade names have been popular for chorionic gonadotropin
preparations over the years. This drug is also sold widely outside of the United
States, and can be found under many additional trade names, too numerous to
list here. Owing to the fact that this drug is not controlled on a federal level, U.S.
athletes and bodybuilders unable to find a local physician willing to prescribe the
drug to treat steroid-induced hypogonadism often order the product from
international pharmacy sources. Given that this drug is cheap and rarely
counterfeited, most international sources are trusted. Although recombinant
forms of chorionic gonadotropin have been introduced to market in recent years,
the vast supply and low cost of biological hCG continues to make it a staple
product for both labeled and off-label uses.
Structural Characteristics:
Chorionic gonadotropin is an oligosaccharide glycoprotein composed of 244
amino acids. It has an alpha subunit that is 92 amino acids long and identical to
that of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and
thyroid-stimulating hormone (TSH). It has a beta subunit that is unique to hCG.
How Supplied:
Human Chorionic Gonadotropin is widely available in various human and
veterinary drug markets. Composition and dosage may vary by country and
manufacturer, but typically contain 1,000, 1,500, 2,500, 5,000, or 10,000
international units (IU) per dose. All forms are supplied as a lyophilized powder,
requiring reconstitution with sterile diluent (water) before use.
Administration (General):
Human Chorionic Gonadotropin is generally given by intramuscular (IM)
injection. The subcutaneous route is also used, and has been deemed to be
roughly equivalent therapeutically to IM injections.
770 Peak concentrations of
chorionic gonadotropin occur approximately 6 hours after intramuscular
injection, and 16 to 20 hours after subcutaneous injection.
Administration (Men):
When used to treat hypogonadotropin hypogonadism, current FDA-approved
protocols recommend either a short 6-week program, or a long-term program
lasting up to 1 year, depending on the individual needs of the patient. Prescribing
guidelines for short-term use recommend that 500 to 1,000 units to be given 3
times a week for 3 weeks, followed by the same dose twice a week for 3 weeks.
The long-term recommendations call for 4,000 units to be administered 3 times
weekly for 6 to 9 months, after which point the dosage is reduced to 2,000 units
3 times weekly for an additional 3 months. Bodybuilders and athletes use hCG
either on cycle, in an effort to maintain testicular integrity during steroid
administration, or after a cycle, to help restore hormonal homeostasis more
quickly. Both types of use are deemed effective when properly applied.
Post-Cycle:
Human Chorionic gonadotropin is often used with other medications as part of
an in-depth Post Cycle Therapy (PCT) program focused on restoring endogenous
testosterone production more rapidly at the end of a steroid cycle. Restoring
endogenous testosterone production is a special concern at the conclusion of
each cycle, a time when subnormal androgen levels (due to steroid induced
suppression) could be very costly to the physique.The main concern is the action
of cortisol, which in many ways is balanced out by the effect of androgens.
Cortisol sends the opposite message to the muscles than testosterone, or to
breakdown protein in the cell. Left unchecked by a low level of testosterone,
cortisol can quickly strip much of your new muscle mass away. Protocols for the
post-cycle use of hCG generally call for the administration of 2000-3000 Units
every 2nd or 3rd day, taken for no longer than 2 or 3 weeks. If used for too long
or at too high a dose, the drug may actually function to desensitize the Leydig’s
cells to luteinizing hormone, further hindering a return to homeostasis. For a
more comprehensive view of hCG’s role in a proper hormonal-recovery
program, please refer to the Post Cycle Therapy section of this book.
On-Cycle:
Bodybuilders and athletes may also administer Human Chorionic Gonadotropin
throughout a steroid cycle, in an effort to avoid testicular atrophy and the
resulting reduced ability to respond to LH stimulus. In effect, this practice is
used to avoid the problem of testicular atrophy, instead of trying to correct it
later on when the cycle is over. It is important to remember that the dosage needs
to be carefully monitored with this type of use, as high levels of hCG may cause
increased testicular aromatase expression (raising estrogen levels),
771 and also
desensitize the testes to LH.
772 As such, the drug may actually induce primary
hypogonadism when misused, greatly prolonging, not improving, the recovery
window. Current protocols for the use of hCG in this manner involve
administering 250 IU subcutaneously every 3rd or 4th day throughout the length
of the steroid cycle. Higher doses may be necessary for some individuals, but st
no point should exceed 500 IU per injection.
These on-cycle hCG protocols were developed by Dr. John Crisler, a wellknown figure in the anti-aging and hormone-replacement field, for use with his
testosterone replacement therapy (TRT) patients. Although TRT is often
administered on a long-term basis, testicular atrophy is a common cosmetic
complaint of patients irrespective of the maintenance of normal androgen levels.
Dr. Crisler’s hCG program is designed to alleviate this concern in a manner that
is acceptable for longer-term use. For those interested in precisely timing their
hCG shots in relation to a prescribed testosterone replacement program, Dr.
Crisler recommends the following in his paper,“An Update to the Crisler hCG
Protocol,” “…my test cyp TRT patients now take their hCG at 250IU two days
before, as well as the day immediately previous to, their IM shot. All administer
their hCG subcutaneously,and dosage may be adjusted as necessary (I have yet
to see more than 350IU per dose required)… Those TRT patients who prefer a
transdermal testosterone, or even testosterone pellets (although I am not in favor
of same), take their hCG every third day.”
Administration (Women):
When used to induce ovulation and pregnancy in anovulatory infertile woman, a
dose of 5,000 to 10,000 units is administered one day following the last dose of
menotropins.The timing is specific so that the hormone is given precisely at the
right moment in the ovulation cycle. Human Chorionic Gonadotropin is not used
by women for physique-or performance-enhancing purposes.
Availability:
When we find hCG, we see it is always packaged in 2 different vials/ampules
(one with a powder and the other with a sterile solvent). These need to be mixed
before injecting, and any leftover drug should be refrigerated for later use. Make
sure your product matches this description. Human Chorionic Gonadotropin is
widely manufactured, and easily obtained on the black market.To date,
counterfeits have not been much of a concern, although a couple of oddities have
popped up (all in multi-dose vials).
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Glossary
AAS – Anabolic/Androgenic Steroid
Acute – Short duration. An acute effect is one that occurs rapidly, not after longterm administration.
Aerobic – Refers to a process where oxygen is used to generate energy in the
muscles from carbohydrates, fats, and protein, in the form of ATP (adenosine
triphosphate). Long distance running is an example of an aerobic activity.
Adipose – Fat tissue.
Adrenoceptor – A type of receptor in the body involved in the regulation of
heart rate, metabolism, and thermogenesis. Stimulated by endogenous
catecholamines such as epinephrine (adrenaline), norepinephrine
(noradrenaline), and dopamine.
Agonist – A substance that initiates a biological response. An estrogen agonist
acts as an estrogen in the body.
Ampule – A glass container that holds a single dosage unit of a liquid drug
product. An ampule must be broken open before use.
Anabolic – A process that involves the building of tissues such as muscle and
bone. AAS are most valued by bodybuilders and athletes for their anabolic
properties.
Anaerobic – Refers to a process where energy is generated in the muscles from
carbohydrates in the form of ATP (adenosine triphosphate) without the use of
oxygen. Weight lifting is an example of an anaerobic activity.
Androgenic – Refers to the masculinizing properties of a substance. AAS
stimulate male libido, secondary hair growth, acne, and male pattern hair loss via
their androgenic properties.
Antagonist – A substance that inhibits a biological response. An estrogen
antagonist blocks the action of estrogen in the body.
Arrhythmia – An irregular heartbeat. Arrhythmias may be life threatening or
benign in nature.
Atherogenic – Promoting the formation of plaque deposits on the walls of
arteries.
Atherosclerosis – A progressive cardiovascular disease characterized by the
buildup of plaque deposits in the arteries. This may obstruct blood flow, causing
heart attack or stroke.
Bacteriostatic – Inhibits the growth of bacteria. Bacteriostatic water contains
ingredients that prevent bacteria from contaminating the liquid.
Contraindicated – Not advisable for use. A contraindication is a condition that
would prevent someone from using a particular drug product.
Diabetogenic – Increases blood sugar.
Diastolic - The phase of blood circulation where the pumping chambers of the
heart (ventricles) are being filled. Pressure is at its lowest during the diastolic
phase.
Downregulate – To reduce in number. Some cellular receptors downregulate
with high levels of drug stimulation, inducing tolerance. Anabolic/androgenic
steroids generally do not cause a reduction in respective androgen receptor
concentrations. Classic downregulation does not occur.
Edema – The retention of excess water in the circulatory system and/or body
tissues.
Endogenous – Occurring naturally within the body. Testosterone produced by
the testes is an endogenous hormone.
Epiphyses – The growth plates at the end of long bones. The epiphyses plates
regulate increases in linear height during development, and fuse at maturity
preventing further linear growth.
Erythropoiesis – The process in which red blood cells are produced in the body.
Anabolic/androgenic steroids can stimulate erythropoiesis.
Esterified – Refers to a steroid compound that has one or more fatty acids
attached to the molecule, usually to slow its release from an injection site.
Testosterone cypionate is an esterified form of testosterone.
Exogenous – Caused by an agent outside the body.
Glycemic – Relating to blood sugar levels.
Hepatotoxic – Liver toxic. All c-17 alpha alkylated anabolic/androgenic steroids
are considered hepatotoxic.
Homeostasis – A state of equilibrium among physiological processes.
Hyperplasia – Growth that occurs via an increase in cell number.
Hypertrophy – Growth that occurs via increases in existing cell size.
Anabolic/androgenic steroids produce growth through hypertrophy.
Metabolic Syndrome – A poorly defined common metabolic disorder
characterized by abdominal obesity, an atherogenic lipid profile, insulin
resistance, elevated blood pressure, a proinflammatory state, and increased risk
of cardiovascular disease.
Multi-dose Vial – A vial with a rubber stopper on the top, designed to be
pierced repeatedly by a needle (for multiple uses).
Pathological – Involving or caused by physical disease.
Peripheral – Near the surface of the body. Psychoactive drugs are often
regarded as centrally acting (brain/central nervous system), while hormones like
anabolic steroids affect both central and peripheral tissues (such as muscle and
skin).
Prognostic – Serving to predict the likely outcome of a disease.
Pulmonary – Related to the lungs.
Recombinant – Refers to a synthetic manufacturing technology that involves
the splicing of genes or DNA segments and inserting them into a cell culture in
order to replicate a specific protein. Recombinant DNA technology is used to
manufacture many protein-based drug products including human growth
hormone, insulin-like growth factors, and human insulin.
Selective – Describes a drug with a very specific effec, and little spillover into
other biological systems.
Subcutaneous – Located beneath the skin and above the muscle.
Supraphysiological – In excess of normal biological levels. High doses of
testosterone produce supraphysiological levels of hormone in the blood.
Supratherapeutic – In excess of normally defined therapeutic levels.
Systemic – Affecting the entire body through general circulation.
Systolic – The phase of blood circulation where the pumping chambers of the
heart (ventricles) are actively pumping. Pressure is at its highest during the
systolic phase.
Upregulate – To increase in number. Usually relating to cellular receptor
concentrations. Anabolic/androgenic steroids can increase respective androgen
receptor concentrations, possibly increasing sensitivity to androgens.</p>TV REPAIR PARTShttp://www.blogger.com/profile/03272638773780329095noreply@blogger.com0tag:blogger.com,1999:blog-3850502767250139870.post-90486867763448192102024-03-27T07:05:00.000-07:002024-03-27T07:05:05.885-07:00Androgenic-anabolic steroid-induced body changes in strength athletes<p>Androgenic-anabolic steroid-induced body changes in
strength athletes
Citation for published version (APA):
Hartgens, L. M. G., van Marken Lichtenbelt, W. D., Ebbing, S., Vollard, N., Rietjens, G. J. W. M., &
Kuipers, H. (2001). Androgenic-anabolic steroid-induced body changes in strength athletes. Physician and
Sportsmedicine, 29, 49-66. https://doi.org/10.3810/psm.2001.01.316
Document status and date:
Published: 01/01/2001
DOI:
10.3810/psm.2001.01.316
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The Physician and Sportsmedicine
ISSN: 0091-3847 (Print) 2326-3660 (Online) Journal homepage: https://www.tandfonline.com/loi/ipsm20
Androgenic-Anabolic Steroid—Induced Body
Changes in Strength Athletes
Fred Hartgens, Wouter D. Van Marken Lichtenbelt, Spike Ebbing, Niels
Vollaard, Gerard Rietjens & Harm Kuipers
To cite this article: Fred Hartgens, Wouter D. Van Marken Lichtenbelt, Spike Ebbing, Niels
Vollaard, Gerard Rietjens & Harm Kuipers (2001) Androgenic-Anabolic Steroid—Induced Body
Changes in Strength Athletes, The Physician and Sportsmedicine, 29:1, 49-66, DOI: 10.3810/
psm.2001.01.316
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ORIGINAL RESEARCH
Androgenic-Anabolic Steroid-Induced
Body Changes in Strength Athletes
Fred Hartgens, MD; Wouter D. Van Marken Lichtenbelt, PhD; Spike Ebbing, MSc;
Niels Vollaard, MSc; Gerard Rietjens, MSc; Harm Kuipers, MD, PhD
BACKGROUND: Some strength athletes use androgenic-anabolic steroids (AAS) to improve body dimensions,
though the drugs' long- and short-term effects have not been definitively established.
OBJECTIVE: This study sought to investigate the short- and long-term effects of AAS self-administration on body
dimensions and total and regional body composition.
DESIGN: This prospective, unblinded study involved 35 experienced male strength athletes: 19 AAS users (drugs
were self-administered) and 16 non user controls engaged in their usual training regimens. At baseline, 8 weeks,
and 6 weeks after AAS withdrawal (for AAS users) circumferences were measured at 10 sites, and skinfolds
measured at 8 sites. To assess differences in AAS regimens, 9 subjects took AAS for 8 weeks (short-AAS) and
10 athletes took PAS for 12 to 16 weeks (long-AAS). Body composition and anthropometry were assessed at
baseline, at the end of AAS use, and 6 weeks later. Lean body mass (LBM) was calculated from body weight and
percentage fat. Total and regional body composition was measured by dual-energy x-ray absorptiometry.
RESULTS: AAS use increased users' body weight by 4.4 kg and LBM by 4.5 kg, and produced increases in
several circumferences. Percentage of fat decreased (17 .0% to 16.0% ), but fat mass remained unchanged.
Changes persisted 6 weeks after drug withdrawal but were not less than those taken at 8 weeks. Bone-free lean
mass of all regional body parts increased in subjects taking AAS, but fat mass was unaffected. Short- and
long-term AAS users did not differ in any parameter measured at 8 weeks or after drug withdrawal.
CONCLUSION: In AAS users, 8 weeks of self-administered AAS increased body weight, lean body mass, and limb
circumferences, but decreased percentage fat compared with controls. Changes remained 6 weeks after drug
withdrawal, though for some measurements only partially. AAS stimulated the bone-free lean mass of all body
parts, but it did not affect fat mass. Short-term and long-term AAS administration produced comparable effects.
T he use of androgenic-anabolic steroids (MS) in
athletes seems to be widespread. As reported by
laboratories accredited by the International Olympic
Committee,' these drugs have been the most frequently
detected substances in urine samples of athletes. MS
use by elite athletes is of great concern for national and
international sports federations because the drugs give
users an unfair advantage and produce potentially dele
terious health effects.2 • 3 MS use is not limited to elite
For CME, see www.physsportsmed.com/cme.htm
beginning in February 2001
athletes, however, and may be more extensive among
recreational and amateur strength athletes, even though
the media devote less attention to use in these groups.
Strength athletes often progress to self-administra
tion of AAS to increase muscle mass and strength.
Weight lifters and power lifters strive primarily for
strength, whereas bodybuilders train for optimal
muscle mass and body dimensions.' Consequently, in
all strength athletes increased muscle mass is desir
able. Only a few studies have investigated the effects
of MS on muscle mass and body dimensions. Unfor
tunately, data are equivocal, and many questions re
main to be answered.
continued
49
THE PHYSICIAN AND SPORTSMEDICINE e Vol 29 • No. 1 • January 2001
11@@i@j continued
Our study sought answers to three
questions: (1) Which body measure
ments and composition are altered in
strength athletes when they use sev
eral AAS simultaneously? (2) Does
self-administration of AAS exert dis
tinct effects on the separate compo
nents of regional body composition?
and (3) What impact does the dura
tion of AAS use have on anthropome
try and body composition?
Methods
TABLE 1. Baseline Physical and Training Status of Strength Athletes
Characteristic
AAS (n = 19)
Controls (n = 16)
32.8 ± 5.3
177 ± 7
88.5 ± 11.2
19.4 ± 3.6
Age (yr)
Height (cm)
Weight (kg)
Body fat(%)
Training history (yr)
Training regimen (hr/wk)
31.3 ± 7.0
176 ± 9
84.0 ± 9.9
17.0 ± 5.7
10.0 ± 7.3
8.8 ± 2.5
8.8 ± 3.6
8.2 ± 2.3
Values are expressed as the mean± standard deviation; AAS =androgenic-anabolic steroid
Subjects and their AAS use. Strength athletes were
recruited with advertisements at local gyms. Inclusion
criteria were: male, at least 3 years of strength training
experience, and age between 20 and 45 years. Candi
dates excluded were those who smoked or had hyper
tension, diabetes mellitus, liver disease or abnormal liv
er enzyme levels, hereditary hypercholesterolemia,
elevated serum cholesterol levels (>6.5 mrnol/L), or in
fertility. Before participating, all subjects completed a
questionnaire containing questions about medical his
tory, health status, training experience and status, nu
trition, nutritional supplement use, and AAS use.
After the initial screening, each strength athlete under
went a full medical examination by a physician for evalu
ation of health status and to screen for possible missed
exclusion criteria During the examination, we provided
extensive oral and written information about the study to
each subject. All subjects signed an informed consent
form approved by the Ethical Committee of Maastricht
Dr Hartgens is research and science coordinator at The Netherlands' Center
for Doping Affairs in Capelle aan den IJssel, The Netherlands. Or Van Marken
Lichtenbelt is assistant professor in the department of human biology at Maas
tricht University, Mr Ebbing and Mr Vollaard were Masters students at The
Netherlands Center for Doping Affairs in Capelle aan den IJssel. Mr Rietjens is
assistant research and science coordinator at The Netherlands Center for Doping
Affairs in Capelle aan den IJssel and a doctoral candidate in the department of
movement sciences at Maastricht University, Maastricht, The Netherlands. Dr
Kuipers is head of the department of movement sciences at Maastricht University.
Address correspondence to Fred Hartgens, MD, The Netherlands Centre
for Doping Affairs, PO Box 5014, 2900 EA Capelle aan den IJssel, The
Netherlands; e-mail to fred.hartgens@necedo.ni.
University (Maastricht, The Netherlands).
Thirty-five strength athletes participated in this
study. Most athletes (28) performed strength training
mainly for esthetic purposes and characterized their
training regimen as bodybuilding training; only 7 of
these subjects participated in bodybuilding contests.
Seven participants were competitors: 3 engaged in
strength training as a part of their boxing training in
addition to using AAS for esthetic reasons, and 4 ath
letes were principally involved in resistance training
for powerlifting competition.
Among the subjects, 19 had decided to begin using
AAS to supplement their regular strength training regi
men (AAS group). The remaining 16 volunteers who
had not used nor were willing to take AAS served as con
trols (CO group). The physical and training characteris
tics of both groups are presented in table 1.
Assessing AAS status. Before entering the study,
AAS group members were expected not to have used
AAS for at least the previous 3 months. This was veri
fied from information that each subject provided and
was corroborated by urinalysis before the start of the
study. Interviews revealed that AAS subjects had been
drug-free for 8.1 ± 6.4 months (range, 3 to 30 months).
All but l of the AAS group had previously used AAS.
The average participant had started using AAS 4.8
years (range, l to 14 years) before the study, and the
mean number of AAS cycles self-administered was 7.1
(range, l to 30 cycles).
Study disclaimer. Although several subjects had re
ceived a prescription for steroids from a physician,
most AAS users bought the drugs on the black market.
Users devised MS regimens based on information
provided by other strength athletes and on their own
THE PHYSICIAN AND SPORTSMEDICINE e Vol 29 • No. 1 • January 2001
53
(i!Ji@i@j continued
TABLE 2. Subjects and Duration, Route, and Total of Androgenic-Anabolic Steroids Used
ID Number AAS Duration (wk) Drug (route) Total Used*
1. BC101 16
2.SS102 16
3. MB108 8
4. JD111 12
5.ES112 16
stanozolol (im)
nandrolone decanoate (im)
metenolone ~po
l metenolone im
drostanolone (po)
mesterolone (po)
stanozolol (im)
nandrolone decanoate (im)
metenolone f~oj mefenoione 1m
drostanolone (po)
mesterolone (po) --·-·----~------··· --.... -~----~,_
___ ' -·--~ ------·-.. ~--~-~
nandrolone decanoate (im)
trenbolone acetate (im)
methandrostenolone (po)
chorionic gonadotropin (im) ----------------------------------
testosterone enanthate (im)
stanozolol (im)
nandrolone decanoate (im) -· -·-··--··' -------·----~
500 mg
350mg
375 mg
1,400 mg
14 mg
350 mg
500 mg
350 mg
375 mg
1,400 mg
14 mg
350mg
~---~-·~~---~·--·· --~
1,600 mg
228mg
940mg
9,000 IU ------
1,250 mg
700mg
100 mg
stanozolol (im) 750 mg
stanozolol (po) 450 mg
testosterone propionate (im) 375 mg
nandrolone decanoate (im) 875 mg
metenolone (im) 300 mg ----·------·-----·------········· -........................ ______ ..... , ..
_______ .. __
6. JN113 8
7.GS115 16
8.FB121 8
9.RT122 16
methandrostenolone (po)
nandrolone decanoate (im)
drostanolone (im)
~---·-,---~
_,.-..... ··~·-·"-··-----~
.. ---·
clenbuterol (po)
stanozolol (po)
nandrolone decanoate (im)
stanozolol (po)
stanozolol (im)
trenbolone acetate (im)
chorionic gonadotropin (im)
testosterone undecanoate (1m)
tamoxifen (po)
nandrolone decanoate (im)
stanozolol (im)
chorionic gonadotropin (im)
stanozolol (po)
methandrostenolone (po)
testosterone heptilate (im)
AAS = androgenic-anabolic steroid; im = intramuscular; po = oral
960mg
300mg
300 mg
Subject began
stacked use
of these but
did not know
exact doses
Subject said
dosages were
"high" for
each drug ----·-·------·------
2,000 mg
750mg
13,500 IU
1,080 mg
1,240 mg
3,000 mg
I ID Number AAS Duration (wk)
10. GR124 8
11. PW125 8 -·-----------
12. MD139 12
13. CL148 8
~---~---------
14.FL151 12
15. RD161 8
16.HK401 8
17.GT402 16
18.DV403 8
19.EK404 12
insights and beliefs. Table 2 presents the details of MS
use in participants. Readers should note that the inves
tigators did not provide MS, that researchers did not at
tempt to influence which MS was used, and the re
searchers did not have any role in MS administration.
that was divided in three experiments to investigate
the objectives set (figure 1).
Study design. We conducted a nonblinded study
54
Experiment 1: Total body composition and anthro
pometry. Experiment 1 was designed to investigate
changes of body composition and anthropometric
measurements in strength athletes induced by self-ad
Vol 29 • No. 1 • January 2001 e THE PHYSICIAN AND SPORTSMEDICINE
Drug (route)
Total Used*
methandrostenolone (po)
mesterolone (po)
metenolone Jim)
nandrolone ecanoate (im)
testosterone (phenyl-) propionate
isohexanoate (im)
trenbolone acetate (im)
stanozolol (im)
boldenone (im)
stanozolol (po)
mesterolone (po)
metenolone (im)
oxymetholone (po)
nandrolone decanoate (im)
nandrolone decanoate (im)
stanozolol ~po
l
stanozolol im
testosterone enanthate (im)
testosterone cypionate (im)
chorionic gonadotropin (im)
methandrostenolone (po)
testosterone cypionate (im)
trenbolone acetate (im)
chorionic gonadotropin (im)
methandrostenolone (po)
metenolone (po)
mesterolone (po)
560mg
1,400 mg
800mg
400mg
1,750 mg
602 mg
250mg
300mg
420mg
5,600 mg
1,600 mg
3,500 mg
1,625 mg
2,600 mg
1,036 mg
850 mg
3,750 mg
5,000 mg
4,500 IU
980mg
750 mg
880 mg
4,500 IU
1,115 mg
1,850 mg
675mg
stanozolol (po)
oxymetholone (po)
nandrolone decanoate (im)
clenbuterol (po)
testosterone enanthate (im)
testosterone cypionate (im)
drostanolone (im)
tanozolol (im)
stanozolol (im)
testosterone (im)
l
clenbuterol {po
oxymetholone po)
chorionic gonadotropin (im)
tamoxifen (po)
2,170 mg
1,225 mg
4,400 mg
1.68 mg
2,500 mg
1,000 mg
300 mg
1,200 mg
1,150 mg
5,500 mg
1 mg
1,900 mg
1,500 IU
440mg
ministered MS. Body composition and dimensions
were assessed by taking skinfold thicknesses and cir
cumferences, respectively. Measurements were taken
before the start of MS use {baseline) and after 8 weeks
of MS use. In all MS users, measurements were also
tak~n 6 weeks after drug cessation, regardless of the
length of MS self-administration. In controls, the
same measurements were done at the start of the
study and after 8 weeks of strength training.
Experiment 2: Regional alterations of body compo
sition. Eleven strength athletes (6 MS, 5 CO) from ex
periment 1 were randomly selected to participate in
experiment 2. Subjects' body composition was deter
mined with dual-energy x-ray absorptiometry
(DEXA), in addition to the regular body composition
and anthropometric measurements taken in experi
ment 1. In 6 strength athletes, we performed DEXA
measurements at baseline and after 8 weeks of MS
self-administration. In 5 controls, body composition
measurements by DEXA were carried out only at the
start of the study.
Experiment 3: Impact of duration of MS self-admin
istration. Before the start of the study we divided the
MS users from experiment 1 into two subgroups based
on their intended MS course duration. Nine subjects
had decided to take these drugs for 8 weeks (short
MS), while the remaining 10 athletes intended to use
MS for 12 to 16 weeks {long-MS). Anthropometric
measurements and determination of body composi
tion were carried out at baseline, at the end of the drug
administration, and 6 weeks after MS withdrawal.
Measurements. Height was measured with an an
thropometer. Body weight was determined to the
nearest 0.1 kg using a bascule.
Skinfolds were measured with a Holtain caliper at
eight sites: biceps, triceps, subscapular, pectoral,
suprailiac, umbilicus, thigh, and calf. All measurements
were taken twice by an experienced investigator. The
mean of both measurements was recorded. To avoid
interobserver error, a single investigator took measure
Wormersley.4
ments in the same subject throughout the study. The
percentage of fat was estimated from skinfold mea
surements according to the method of Dumin and
Lean body mass and fat mass were calcu
lated using body weight and percentage fat.
Eleven circumference measurements at 10 sites were
taken with a tape measure: neck, thorax, waist, but
tacks, upper arm (relaxed), upper arm (contracted),
forearm, wrist, thigh Uust below the buttocks), thigh
(two-thirds the distance from the major trochanter
and lateral site of the knee joint), and calf. An experi
enced investigator took all measurements twice, and
the mean of both measurements was recorded.
continued
THE PHYSICIAN AND SPORTSMEDICINE e Vol 29 • No. 1 • January 2001
55
@!Ji.jijlltJj continued
Experiment 1: Total body composition and anthropometry.
Subjects: 19 AAS users (9 subjects administered 8 weeks AAS and 10 subjects used for 12-16 weeks) and 16 nonusers.
AAS use for
8 weeks
AAS use for
12-16 weeks
Controls
+
Baseline
+
Baseline
+
Baseline
+
End of AAS use
(= 8 weeks)
//
+
8 weeks
AAS use
+
8 weeks
end of
AAS use
+
6 weeks after withdrawal
(= 14 weeks)
Experiment 2: Regional alterations of body composition (DEXA measurements).
Subjects: 6 AAS users and 5 non users. (DEXA measurements done in controls at baseline only.)
AAS users
+
Baseline
Experiment 3: Impact duration AAS sell-administration.
Subjects were 19 AAS users: 9 short course and 10 long course
Short-AAS
Long-AAS
+
+
6 weeks after
withdrawal
8 weeks AAS use
+
Baseline
+
Baseline
+
End of AAS use
after 8 weeks
+
6 weeks after
withdrawal
+
End of AAS use
after 12-16 weeks
+
6 weeks after
withdrawal
FIGURE 1. Overview of the experiments of AAS use and body changes.
~ = indicates measurement; 11= indicates that the duration of AAS sell-administration varied between subjects from 12 to 16 weeks;
AAS =androgenic-anabolic steroids; DEXA =dual energy x-ray absorptiometry
Total and regional body composition measurements
were performed using DEXA apparatus (DPX-L, Lunar
Carp, Madison, Wisconsin) at a fast scan speed with a
whole-body resolution of 4.8 x 9.6 mm. To determine
the composition of regional body segments and limbs,
DEXA measurements were divided in discrete values
56
for arms, legs, and trunk on the basis of anatomic land
marks. As determined by Mazess et al,S the precision of
these measurements is 1.5% for the arms, 0.8% for the
legs, and 1.1% for the trunk. Total mass, fat mass, and
bone-free lean mass were determined using Lunar
software (version 1.3 z) for each body region (arms,
continued
Vol 29 • No. 1 • January 2001 e THE PHYSICIAN AND SPORTSMEDICINE
@!Ji.jiji@j continued
trunk, and legs).
Monitoring and compli
ance. Information about the
subjects' training and nutri
tional habits was collected
before the start of the study
and in week 8. Subjects' nu
tritional intake was deter
mined with a 3-day diary.
Training data were obtained
by a 1-week log. For long
MS strength athletes, nutri
tional and training data were
also obtained at the end of
the MS administration. In
all MS users, these data were
collected 6 weeks after drug
cessation.
To gauge subjects' compli
ance with drug administra
tion or abstinence before the
start of the study and after
8 weeks, urine samples from
all athletes were obtained for
drug evaluation purposes
(Netherlands Institute for
Drug and Doping Research,
Utrecht, The Netherlands).
For the long-MS group, urine
samples were taken at the
end of the drug-use period.
All MS-using strength ath
letes submitted urine sam
ples 6 weeks after drug with
drawal. From all samples
taken, about one-third were
randomly chosen for analysis.
Statistical analysis. De
scriptive statistics were calcu
lated for all measurements
TABLE 3. Changes in Limb and Trunk Circumferences in AAS and Control Groups
6Wk
Segment
Group
Baseline
Neck
Thorax
Waist
Buttocks
Upper arm (relaxed)
Upper arm (contracted)
Forearm
Wrist
Thigh (upper)
Thigh (lower)
Call
AAS
Control
AAS
Control
AAS
Control
AAS
Control
AAS
Control
AAS
Control
AAS
Control
AAS
Control
AAS
Control
AAS
Control
39.2 ± 1.9
39.6 ± 2.2
95.8 ± 6.5
98.5 ± 7.3
84.8±7.1
86.8 ± 5.4
98.7 ± 5.6
99.3 ± 4.8
36.6 ± 3.0
38.9 ± 3.7
40.1 ± 3.3
42.0 ± 3.6
31.3 ± 1.9
32.8 ± 2.8
18.2 ± 1.0
18.3 ± 0.8
61.5 ± 5.5
63.4 ± 4.6
50.0 ± 3.4
51.8±3.3
8Wk
Postwithdrawal
40.5 ± 2.1 ### 40.2 ± 1.9 * *
39.6 ± 2.2
na
98.4 ± 6.4
99.9 ± 7.2
86.3±7.1
87.1 ± 6.4
100.6 ± 5.5
100.0 ± 4.9
98.1 ± 6.5 * *
na
85.1 ± 7.2
na
100.0±5.5**
na
38.5 ± 3.3 ### 37.8 ± 3.4 **
39.0 ± 3.8
na
41.6±3.1## 41.5 ± 3.5 ***
42.4 ± 3.7
na
32.4 ± 2.1 ### 32.6 ± 2.8 **
32.7 ± 2.2
na
18.5±1.1#
18.3 ± 0.9
63.7 ± 5.1 ##
63.4 ± 4.8
52.2 ± 4.4 ##
51.6 ± 2.9
18.3 ± 1.0
na
62.7 ± 5.1 *
na
50.8 ± 3.6*
na
AAS
Control
38.7 ± 2.2
40.2 ± 2.6
39.6 ± 2.2 ### 39.1 ± 2.2*
40.2 ± 2.7
na
All values are expressed in grams as the mean ±standard deviation. Mann Whitney test for interaction
was used to test interaction, the difference between change in control group and AAS group;#= P<
0.05; ## = P< 0.01; ### = P< 0.001.
Wilcoxon test was used to compare differences between postwithdrawal and baseline; * = P< 0.05; * * =
P< 0.01; *** = P< 0.001.
AAS =androgenic-anabolic steroid; na =data not available
using Stat-View software (Abacus Concepts, Berkeley,
California, 1994). Data are presented as mean plus or
minus standard deviation (SD). The Mann-Whitney
U-test was used to compare differences in the ob
served changes between groups. The Wilcoxon signed
rank test was used for analysis of intragroup changes
after drug withdrawal (experiment 1) and for DEXA
measurements of subjects taking MS (experiment 2).
The level of significance was set at 0.05 for all analyses.
Results
Total body composition and anthropometry. After
8 weeks, the MS group had a significant increase of
approximately 4.5 kg in body weight and lean body
continued
THE PHYSICIAN AND SPORTSMEDICINE e Vol 29 • No. 1 • January 2001
59
(1W@ii(ij continued
TABLE 4. Analysis of the Effects of AAS Use on Regional Body Mass
Region and Segment
Control
AAS Group,
AAS Group, Difference,
Group (g) Baseline (g) 8 Wk (g)
Baseline vs 8 Wk (g)
Arms: Total mass
Fat mass
Bone-free lean mass
10,013
±1 ,993
1,370
±838
8,642
±1 ,296
10,470
±1 ,723
1,721
±1 ,240
8,750
±1 ,066
11,320
± 1,910
1,317
±828
10,004
± 1 '129
0.028
ns
0.03
Legs: Total mass
25,699
24,228
25,390
±4,866
Fat mass
4,649
± 1,755
Bone-free lean mass 21,050
±3,443
±3,390
3,785
±1 ,600
20,443
±2,436
±2,768
3,605
± 1 '1 01
21,785
±2,134
ns
ns
0.03
Trunk: Total mass
Fat mass
35,762
±4,269
6,824
±1,778
Bone-free lean mass 28,938
±3,257
37,798
±4,845
7,073
±3, 119
30,725
±2,602
39,375
±4,372
6,490
±2,670
32,885
±1 ,936
ns
ns
0.046
All values are expressed in grams as the mean ± standard deviation. Paired AAS group data were
analyzed using the Wilcoxon signed rank test at 0.05 significance.
AAS =androgenic-anabolic steroid; ns = not significant
mass, whereas the controls exhibited no significant
change. Mean body weight increased from 84.0 ± 9.9 to
88.4 ± 10.7 kg, and lean body mass rose from 69.6 kg to
7 4.1 kg. The percentage of fat during MS use was sig
nificantly reduced from 17.0% to 16.0%, but this was
not reflected in a loss of fat mass. Gains in body weight
and lean body mass were still partly present 6 weeks
after drug withdrawal (table 3). In both groups, no sig
nificant increase in sk.infold measurements or their
sums were observed during the study.
In the MS group, increases in the circumferences
of neck, upper arm, forearm, wrist, thigh, and lower leg
were significantly larger than in the control group. Cir
cumference changes of the thorax, waist, and buttocks
did not reach significance compared with those of
controls. Although the circumferences were slightly re
duced after drug withdrawal, they were still increased
compared with baseline levels (see table 3).
Regional body composition changes. Baseline
DEXA measurements of body segment composition
were not significantly differ
ent between the MS users
and control athletes. After 8
weeks of AAS use, the
weight of the arm was sig
nificantly increased, but
the weight of the trunk and
legs remained unchanged.
Bone-free lean masses of
the arms, trunk, and legs
were significantly greater
during AAS use than at
baseline (table 4). MS use
did not affect the fat mass of
the arms, legs, and trunk.
Total bone mineral density
and bone mineral content
did not change significantly.
Length of AAS regimen.
No significant differences
were observed in body
weight, percentage of fat,
fat mass, lean body mass,
and circumferences be
tween short-MS and long
MS users. Similarly, these
parameters were not sig
nificantly different between groups 6 weeks after
drug withdrawal .
Training, nutrition, and compliance. Throughout
the entire study, weekly training hours and regimens be
tween groups in the three experiments remained com
parable. The same was true for nutritional intake. Uri
nalysis revealed compliance within the groups: Urine
samples from the MS users contained steroid metabo
lites, and samples of the CO group did not.
Discussion
AAS-induced changes. Experienced strength ath
letes who use a self-composed course of MS for
8 weeks exhibited increased total body weight and to
tal lean body mass compared with those who did
strength training alone; total fat mass remained unaf
fected. Among regional body segments (arms, legs,
and trunk) in these athletes, only arm weight in
creased significantly. However, lean mass was signifi
cantly increased in all regional body parts, and these
60
Vol 29 • No. 1 • January 2001 • THE PHYSICIAN AND SPORTSMEDICINE
em.m•IBJ continued
findings are reflected in the increased arm and leg cir
cumferences. Increases were for the most part still
present 6 weeks after drug cessation. These findings
are relevant because until now scientific data con
cerning AAS effects on anthropometry and body
composition were equivocal.
From cross-sectional studies, one might infer that
AAS-using strength athletes differ in body composition
from nonusing athletes."·' These observations have
been supported by longitudinal studies. The most pro
nounced effects on body weight and lean body mass
were found in athletes who self-administered several
AAS simultaneously in high doses.•·• Such regimens
may increase body weight by an average of about
5.2 kg (ll.4lb). Lean body mass increases may be even
larger, especially after long-term administration."·10
The present study indicates that the use of a single
AAS seems to induce less remarkable effects than mul
tiple-drug regimens."-11-13 This is in line with an observa
tion of Forbes, 1 '
who had previously described a posi
tive relationship between the total dose of AAS used
and the increase oflean body mass. On the other hand,
research9,11Is.Ifi that compared the effects of different
doses of a single AAS indicates that such a relationship
might be less ambiguous than that proposed by Forbes.
Previous methods and DEXA. One factor that may
have contributed to the consistent results is the
method used to determine body composition. No al
terations were seen in studies17-20 that investigated body
composition with underwater weighing. In these stud
ies, the effect of a single drug was analyzed, but,
unfortunately, no reports are available on underwater
weighing assessment of body composition in multiple
drug-using athletes. Although previous studies as
sessed the traditional two-compartment model either
with skinfold measurements or with underwater
weighing, our study employed DEXA to assess a three
compartment model for body composition alterations.
DEXA was designed primarily to estimate bone
mineral content and density in humans.21 Determina
tion of body composition by DEXA is based on the dif
ference in attenuation ofx-rays between soft and bone
tissue as well as the difference in attenuation between
fat and lean tissue. This method provides a three-com
partment model that divides the body into total bone
mineral content, bone-free lean mass, and fat mass.
An advantage of DEXA over hydrodensitometry is that
DEXA appears to be less affected by hydration sta
tus.21.'' This may be an important advantage in esti
mating body composition in athletes since hydration
status may be affected by training.
Assessing regional body changes. Because of the
documented DEXA accuracy for total and regional
body dimension measurement5 · 23 and the AAS poten
tial for inducing regional changes in body composi
tion, strength athletes may have particular interest in
both DEXA and AAS. DEXA measurements in this
study reveal an increase in bone-free lean mass of all
body parts measured in bodybuilders using AAS. One
interesting finding was that the increase in the bone
free mass of the arms was approximately twice that in
the leg or trunk (14% versus about 7%). This finding
could not be attributed to differences in training regi
mens because the training diaries revealed compara
ble regimens in both groups. On the other hand, in an
other study16 the administration a single anabolic
steroid (nandrolone decanoate) induced the largest
gain of bone-free lean mass in the legs and trunk.
Since both studies are complementary, one possibility
might be that different AAS regimens may affect spe
cific areas more than others.
Although evidence has shown that AAS increases
lean body mass,24-26 no one has determined what con
stitutes the change in lean mass. Previous research as
sociated AAS-induced lean body mass alterations with
increments of blood volume and water retention.1w.zs
In a recent study (W Van Marken Lichtenbelt etal,
manuscript submitted for publication), we were able
to investigate the effects of AAS on body composition
with a four-compartment model. That study revealed
that total body water increased from AAS use but that
the ratio between extracellular and intracellular water
remained unaffected. In addition, lean mass hydration
status was not influenced by AAS. Thus, the most likely
explanation for the gain oflean mass can be explained
by muscle increase rather than from water retention.
Dispelling steroid-use myths. Among strength ath
letes, long-term AAS administration is generally be
lieved to produce better results than short-term use.
Additionally, these athletes claim that after long-term
AAS use the gains in body composition parameters
will persist longer than after short-term administra
tion. These beliefs are not supported by the present
study. The effects on body composition and anthropo
continued
THE PHYSICIAN AND SPORTSMEDICINE e Vol 29 • No. 1 • January 2001
61
em.m•IBJ continued
metric variables after short- and long-term MS use
were comparable. The same applied for residual
changes seen after drug withdrawal. Therefore, we
conclude that duration of MS administration in itself
is not the key factor for optimal and longstanding ef
fects on body composition.
Health hazards. From a medical point of view,
long-term MS administration is of great concern.'•
Several investigators•·30• 31 have reported that MS use in
duces an unfavorable lipoprotein profile and thus in
creases the risk for cardiovascular diseases. Recent re
search has demonstrated that duration of MS use has
a strong impact on the lipoprotein profile changes.33
Extended MS administration provokes more dramatic
side effects on the lipoprotein profile compared with
short-term MS use, and the time required for full re
versal of these side effects was prolonged after long
term use (E Hartgens et al, manuscript submitted for
publication). Consequently, long-term users are more
prone to have cardiovascular events.
Most strength athletes are convinced that after drug
abstinence the effects on body composition will persist
for some time. Our results show that 6 weeks after drug
withdrawal the changes of circumferences were still
significantly increased over baseline values, though
slight decreases were seen compared with values at the
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end of MS use. Many MS users take, on average, two
to three courses in l year."~' Their approach is to start a
new MS course when they assume that the side effects
have disappeared but the desired effects on body com
position and strength are still present to some extent.
There are indications that such procedures may be ef
fective," but the effects of such procedures on health
status are unknown and remain of great concern.
Summary
This study has demonstrated that in athletes the
administration of a self-composed, 8-week course of
MS combined with strength training increased body
weight, lean body mass, and limb circumferences
more than did strength training alone. Arm mass, but
not trunk and leg mass, was increased by MS use.
DEXA analysis showed that MS stimulated the bone
free lean mass of all body parts, but the effects on the
arms were the most pronounced. Fat mass was not af
fected by AAS use. The increments in total body
weight, lean body mass, and girths were still largely ev
ident 6 weeks after drug withdrawal. There was no re
lationship between the duration of MS use and the
extent of changes in body composition and anthropo
metric variables. RN
8.
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CASE REPORT
transplant fractures continued from page 40
The level of performance is also affected by the par
ticular kind of grafting. Most kidney and liver trans
plant recipients are able to regain their former physical
condition, but this is not true for heart and lung trans
plant subjects. The latter continue to be affected by
heart denervation and altered lung function, which of
ten keeps them out of competition.
Recommendations
Preventive medical therapy and follow-up measures
as well as sport -specific recommendations are needed
to allow transplant patients safe athletic participation.
Until reliable clinical and epidemiologic studies are
performed, low-impact, recreational, noncontact
sports are recommended, and high-level competition
by transplant patients should be discouraged. AN
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66
Vol 29 • No. 1 • January 2001 e THE PHYSICIAN AND SPORTSMEDICINE </p>TV REPAIR PARTShttp://www.blogger.com/profile/03272638773780329095noreply@blogger.com0tag:blogger.com,1999:blog-3850502767250139870.post-6392845286169657562024-03-27T07:03:00.000-07:002024-03-27T07:03:25.904-07:00Men´s experiences of using anabolic androgenic steroids<p> INTERNATIONAL JOURNAL OF QUALITATIVE STUDIES ON HEALTH AND WELL-BEING
2021, VOL. 16, 1927490
https://doi.org/10.1080/17482631.2021.1927490
Men´s experiences of using anabolic androgenic steroids
Annica Börjesson
a
,
Margaretha Ekebergh
b
,
Marja-Liisa Dahl
a
,
Lena Ekström
a
,
Mikael Lehtihet
and Veronica Vicente
e
a
b
c,d
Department of Laboratory Medicine, Division of Clinical Pharmacology, Karolinska Institutet, Karolinska University Hospital, Stockholm,
Sweden;
Faculty of Caring Science, Worklife and Social Welfare, University of Borås, Borås, Sweden;
Karolinska Institutet, Stockholm, Sweden;
d
Karolinska Institutet and are working at S: t Görans hospital;
c
Department of Medicine,
e
The Ambulance Medical Service
in Stockholm (AISAB), Academic EMS Stockholm and Department of Clinical Science and Education, Södersjukhuset Karolinska
Institutet, Stockholm, Sweden
ABSTRACT
Purpose: Anabolic androgenic steroids (AAS) are used by men for their aesthetic and
performance-enhancing effects and are associated with risk for side effects. Our research
aims to deepen knowledge and understanding of men´s experiences of using AAS.
Method: This phenomenological study is based on the reflective lifeworld research approach.
Lifeworld interviews were conducted with twelve men about their experiences of using AAS.
Results: By using AAS, men strive towards a muscular, strong and athletic ideal. Self-imposed
demands, self-discipline and performance accelerate male physical development. The perfect
male body ideal thus attained is fragile from both an existential and a biological perspective.
The perfect self-image can easily be shattered by adversity. A man’s very existence may be
jeopardized if the use of AAS is revealed to others or if the body is let down by illness.
Conclusions: Men´s use of AAS is a complex phenomenon. It partly concerns a traditional
view of masculinity that is reflected in the community. It requires both broad and deep
knowledge and understanding to be able to meet men using AAS in their problems and
vulnerability; a meeting that is hampered by their low trust in healthcare, and by the fact that
AAS are illegal.
Introduction
Anabolic androgenic steroids (AAS) are considered to
be a health problem because of adverse effects and
their widely spread use in many countries (Eklof et al.,
2003; Kanayama et al., 2018). AAS are used in supra
physiological doses (Ip et al., 2011; Lood et al., 2012)
to attain the anabolic effect (Brower et al., 1994;
Petersson et al., 2010) and are hugely effective
(Bhasin et al., 1996; Rogerson et al., 2007). Most of
the users are males who define themselves as recrea
tional exercisers or bodybuilders (Eklof et al., 2003; Ip
et al., 2011; Kanayama et al., 2020). In many parts of
the world, men experience dissatisfaction with their
bodies (Kelley et al., 2010) which may be a reason for
using AAS (Mitchell et al., 2017; Pope et al., 1997). The
main motives for using AAS are improvement of body
image and appearance or enhancement of perfor
mance (Börjesson et al., 2016; Melia et al., 1996;
Petersson et al., 2010). Further reported motives are
low self-esteem, curiosity, desire for increased brave
ness or criminality (Bonnecaze et al., 2020; Ip et al.,
2011; Nilsson et al., 2001).
ARTICLE HISTORY
Accepted 5 May 2021
KEYWORDS
Anabolic androgenic
steroids; AAS; doping;
phenomenology; reflective
lifeworld research
effects increase with higher doses and longer duration
(Bolding et al., 2002; Evans, 2004). Typical AAS-
induced physical side effects in men include sexual
problems most commonly erectile dysfunction and
decreased libido, acne and gynaecomastia. An asso
ciation has been seen with a variety of psychiatric
complications (Börjesson et al., 2020; Eklof et al.,
2003; Pope & Katz, 1994; Pope et al., 2014). Typical
psychiatric side effects include depression, sleep dis
orders and mood disturbances (Sjoqvist et al., 2008).
AAS use may also increase the risk of cardiovascular
complications such as hypertension, disturbances in
the cholesterol profile (Chang et al., 2018; Gårevik
et al., 2011). Cardiovascular consequences of AAS
have received attention due to case reports of sudden
or unnatural death (Darke et al., 2014). Swedish legis
lation forbids the use of AAS, not only the possession
and distribution of AAS, but also the presence of
exogenously AAS in the body.
Use of AAS can cause side effects, some are mild
while others may be more serious. The risks for side
This is the first interview study with AAS users that
has practised the reflective lifeworld perspective
(Dahlberg et al., 2008) (RLR) with a caring science
perspective (Dahlberg, 2011). In this research, we
turn to the men themselves and to their lifeworld.
The study aims to deepen knowledge and the
CONTACT Annica Börjesson
annica.borjesson@ki.se
Department of Laboratory Medicine Division of Clinical Pharmacology, Karolinska
University Hospital Huddinge SE-14186 Stockholm, Sweden Phone: +46 8 585 811 92
© 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits
unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
A. BÖRJESSON ET AL.
2
understanding of men´s experiences of using AAS and
explore their lived experiences. Through the RLR
approach, we aimed to reach an existential dimension
that is missing in previous research. A deeper knowl
edge is important especially for healthcare profes
sionals since AAS is widespread and may affect an
individual´s health.
Materials and methods
Design
This phenomenological study is based on a reflective
lifeworld research (RLR) approach as described by
Dahlberg et al. (2008). The epistemology of RLR is
based on phenomenology mainly described by the
philosopher Edmund Husserl (1936/1970). RLR is phe
nomenon-orientated throughout the research process
(data collection and analysis) and the phenomenon
being explored and illuminated in this study is men´s
use of AAS. Using a lifeworld perspective helps us to
seek understanding in the lived everyday world. The
lifeworld is our unique existential world as it is experi
enced by each human being, but it is also a common
world that is shared with other people.
In order to understand the phenomenon itself, it is
necessary to be aware of the natural attitude. In our
daily lives, the world is perceived through our natural
attitude, which means that many things are taken for
granted or in other words are not reflected upon. The
researcher therefore needs to keep his/her distance to
the natural attitude, which is achieved through reflec
tion. By reflection, we can raise awareness and con
ceptualize the lifeworld.
Openness, flexibility and bridling are important
methodological principles in RLR. An open mind is
achieved through bridling, i.e., having control of the
whole process of understanding of the phenomenon,
which involves a reflective attitude and flexibility
towards the phenomenon.
Researchers need to be constantly reflective and
critical throughout the research process. To be objec
tive in a phenomenological sense, personal values,
theories and other assumptions may not impede us
from acquiring a new understanding of meaning (van
Wijngaarden et al., 2017).
Participants and study setting
The total number of male participants in this study
was twelve, 20–65 years of age. Half of the partici
pants were ongoing users of AAS, and half were for
mer users. For inclusion, they had to be over 18 years
of age and to understand the Swedish language.
Voluntary informants were recruited in two ways:
either via snowball sampling or by contact with Anti-
Doping Hot-Line. Snowball sampling is a method for
studying social networking structures, originally intro
duced by Goodman (Heckathorn, 2011). This techni
que is a convenient method for hard-to-reach and
hidden populations. Contact with an initial person
can generate new informants. The second way to
recruit was via Anti-Doping Hot-Line which is an
anonymous free telephone counselling service started
in 1993 for people concerned or affected by their
non-medical use of AAS (Eklof et al., 2003). It is man
aged by trained nurses and clinical pharmacologists
and is localized at the Department of Clinical
Pharmacology, Karolinska University Hospital in
Stockholm, Sweden. Half of the informants were
recruited by each method.
Data collection
The lifeworld interviews were conducted by AB and
VV in an undisturbed setting. The interviews lasted
60–90 minutes and began with a presentation of the
study and its purpose. Each interview started with an
opening question (Brinkmann & Kvale, 2014; Dahlberg
et al., 2008) directed to the phenomenon: How is it to
use anabolic androgenic steroids? Follow-up ques
tions were asked aiming to support the informant in
clarifying, deepening and explaining what was meant
and to encourage detailed descriptions of the phe
nomenon (e.g., how do you mean, can you describe
more?)
Data analysis
The phenomenological analysis followed the guide
lines for RLR (Dahlberg et al., 2008), which are open
ness, bridling and flexibility. During the process of
analysis, the researcher must adopt an open attitude.
To promote this, the researcher needs to slow down
the process of understanding and not be too quick to
make definite what is indefinite (Dahlberg & Dahlberg,
2003). The analysis process concentrates on the phe
nomenon and not on the individual. The aim is to
search for meanings in all the experiences collectively.
The analysis process starts with familiarization, an
open-minded repeated reading of the interview
transcripts in their entirety to create a deep feeling
for and understanding of the whole text. Then
a movement between data follows, which means
pendling between the whole (interviews) and the
parts (meanings of the data) and finally reconstruct
ing a new whole (essential meaning) (Dahlberg
et al., 2008). The material is divided into smaller
parts (words, sentences or longer pieces of text) in
the search for meaning. From a phenomenological
perspective and validity, research should be mean
ing-orientated (van Wijngaarden et al., 2017).
Reflective questions are used in order to understand
the meaning of each unit, likewise it is important to
INTERNATIONAL JOURNAL OF QUALITATIVE STUDIES ON HEALTH AND WELL-BEING 3
reflect carefully and not take anything for granted.
Reflection and questioning are repeated until mean
ings that seem to be related to each other can be
clustered together. Once the clusters are estab
lished, the meaning of the phenomenon slowly
begins to emerge and the pattern between the
clusters and the essential meaning of the phenom
enon becomes visible. The analysis process results in
a meaning structure that includes both essential
meanings and the more varied meanings. From the
most abstract essential meanings, that is the essence
to the more concrete and more contextual mean
ings, that is the constituents. All authors have parti
cipated in all steps of the data analysis.
Ethical considerations
Ethical approval was obtained from the Regional
Ethics Committee in Stockholm (nr. 2016/1762-31/5).
The informants received oral and written information
about the purpose of the study before and at the time
of the interview. They were informed that participa
tion was voluntary and that they had the right to
withdraw their participation at any time without
explanation. They also received information about
the confidentiality of the interviews before giving
their written consent. Participants were offered care
and support if they so desired.
Results
The results are first presented through the essential
structure of meanings, followed by the meaning con
stituents: the male body ideal as a model; the perfect
male identity; individual existence may be jeopardized
when demands are too overpowering.
The use of AAS aims to achieve a perfect male
body ideal, which traditionally is muscular, strong,
athletic and healthy. Male physical development is
accelerated through the use of AAS combined with
high self-imposed demands, self-discipline and per
formance. A prerequisite for starting to use AAS is
having achieved training maturity as well as having
self-control and the potential for further physical
development. The body is sculpted by self-centred
effort directed towards the desired body ideal. An
identity is created and shaped, which over time
leads to self-confidence and a positive self-image.
An inseparable new self-identity stimulates respect
by being impressive, prominent and dominant. The
challenge is to maintain the arduous and disciplined
lifestyle. However, both external and internal factors
may limit the body as experienced, thus weakening
the self-image. The perfect self-image is fragile and
can easily be shattered by adversity. The role of the
perfect male ideal is maintained in interaction with
the environment and kept alive through other peo
ple’s confirmation, acceptance and integrity.
The male body ideal as a model
The men in this study strive to create the perfect
physique based on the masculinity norm, i.e., beha
viours and traits that traditionally characterize and are
associated with masculinity. They include physical and
mental strength and self-control as well as being
performance-orientated, invulnerable and confident.
Through hard training and discipline, these men
steer their bodies towards achieving male physical
perfection. They perceive their development as
a reflection of their masculine role model and their
perception changes as their physical development
progresses.
What drives the men in this study is that they do not
want to look thin, they want to get bigger, build muscle
and strengthen their masculinity. One man comments:
I
was extremely fascinated by these masculine men
with big arm muscles and stuff. Today, when I look
back, it’s often associated with what I call authorita
tiveness because I thought that men who were well-
muscled were self-assertive in a certain way.
The men in this study are fascinated by how fast their
bodies can develop with AAS. The effect makes it
easier for them to steer and control their bodies in
the desired direction: “. . .when we used that substance,
we just laughed our way through every single training
session/workout for six weeks.”
They feel satisfied with achieving what they want
but cannot settle for that since they constantly want
to develop even more. There are always areas for
improvement and shortcomings to work with, such
as more defined and better-developed muscles. It is
sometimes difficult to perceive correctly the actual
size of the body. To follow their physical develop
ment and get a reliable picture of their develop
ment, they use scales, photographs and mirrors to
help them. Now and then they experience not look
ing handsome enough, or looking small, which
makes them hide their bodies in large clothes to
avoid attention. However, they sometimes also
become aware that their bodies have actually
become overdeveloped, which feels uncomfortable,
as expressed in the following statement:
I weighed 117 kg for a while, you know. And I’m 1.75
tall, so that´s quite a lot. And then I was too big for
my body like, to put it one way. That’s how I saw it.
Then the thoughts started to come . . . ’hell, should
I
really be doing this?’ Everything was just too tight
everywhere. Yeah, my muscles were tensed and tight
in my skin . . . that way you look a bit more grotesque.
You think you look small even though you’re really as
big as a fucking bull . . . then there’s something that is
very wrong . . .
A. BÖRJESSON ET AL.
4
The body is pressured and challenged to perfection.
These men always give their all in full, making great
demands on themselves and doing nothing light-
heartedly. They are competition-orientated, disci
plined and focused, which however is not always
that easy to maintain, as exemplified: “everyone
wants to be in good shape, but not many have the
discipline” or “some people are just not able to push
themselves that hard.”
There is the explicit idea that everyone should
struggle to be able to reach his goals, and the percep
tion is that everyone should do it the hard way. The
tough and hard bodybuilding culture from the 1970s–
1980s is highlighted as an ideal. The ancient body
ideal with clearly defined muscles and symmetrically
built bodies alongside recognized bodybuilders are
described as role models. Based on this notion of
doing things the hard way, it is not acceptable to
use AAS until full muscular potential has been
reached, i.e., training maturity. Only then may AAS
be used to achieve the desired goal. Training maturity
means that to avoid injuries, the individual must be
physically developed to take on a heavier physical
load, which is important because AAS provide
increased energy and encourage heavier training.
Training maturity also involves being able to achieve
as much as possible the natural way without having
added AAS. Here, however, opinions differ between
the men interviewed. Some are tempted to get on the
fast track and do not see their bodies as “an ongoing
handicraft project” that has to be built up slowly and
laboriously, i.e., if training sessions are missed or if
they have not eaten properly, they increase the dose
of AAS and hope that this will compensate for any lost
results. Some men express that a genuine body
builder should behave exemplary in terms of food
and exercise. Using more AAS than needed is consid
ered as cheating, meaning that they do not get an
honest and fair chance in competitions. They made
comments like: ”they don’t take things that seriously”;
they haven’t understood their natural potential”; and
”your body should be your temple.”
The risks involved in using AAS are justified by the
physical results achieved. The risk of side-effects is
considered small if AAS are taken with caution and
in the right way, but this requires the individual´s
awareness and knowledge. The level of knowledge
differs between individuals; some men are deeply
familiar with the topic while others rely entirely on
the “facts” that their friend has read about AAS: “but
I
didn’t read anything because he had read it all, so
I more or less told him that I trust you”. The choice not
to acquire any knowledge at all may also be
a conscious one, because the individual is afraid of
not daring to try after having read about the side
effects. Despite awareness of the risks of purchasing
AAS substances on the black market, these individuals
are prepared to take that risk. If serious side effects do
not occur, they test several different types of AAS and
to a greater extent, which means that they may
become less careful. They also trust that the side
effects will disappear when they stop their use of
AAS. However, there is also a more cautious approach
to AAS in which winning competitions is not the most
important part. One man describes his intake of AAS
as follows:
Well, if it was only important for me to win, for me to
be the biggest of all like . . . Well, then I’d have to take
much, much more than I do today. I’ve been extre
mely careful for various reasons. On one hand, as
I
said, I do not want to feel unwell. I do not want
any side effects. I do not want to risk my heart and
liver and everything getting damaged. So in that way,
winning is not everything.
To protect their bodies during AAS use, the men
interviewed tried to counteract or prevent side
effects. Dietary supplements and drugs are taken in
their attempts to streamline their bodies’ defence
systems to protect their livers and kidneys. Healthy
food compensates for AAS intake, as one man says:
When you’re on AAS substances, you should think
one step ahead and be even cleaner, even more care
ful, eat extra greens, as well as other nutrients; choose
unsprayed food because the body is more sensitive
which makes the side effects worse; there’s an
increase in harmful blood fats; fatty deposits in the
blood vessels increase, and so on.
It is sometimes difficult to know if the problems and
discomfort perceived are really due to the intake of
AAS or if they have arisen for another reason. When
the realization dawns about the real risks of the sub
stances, it can be extremely upsetting. One man
describes his experience after suffering from
a serious illness:
You see, I’ve been so convinced up to now that this is
not unhealthy, like my blood values, you know –
everything is great. My body hasn’t felt unwell at all,
like when you start having problems with your heart
and therefore I haven’t had any motivation to stop.
Had it turned out that it was bad, then I would defi
nitely have started thinking, but then I would have
thought kind of, well then I’ll stop for a while and
then I can start again. But once I got this, well, it just
suddenly happened one day. So my God, this is
bloody dangerous stuff. It´s not like everyone else
says.
If the men are worried about side effects, they contact
healthcare for help. They believe that their AAS use is
a private matter and that the physician’s task is to
assist people if they do not feel well. Health checks
can prevent injuries and predict when medical mea
sures need to be taken. The men believe that as long
as they endure certain ailments and feel relatively
well, they are justified in continuing to use AAS: ”
INTERNATIONAL JOURNAL OF QUALITATIVE STUDIES ON HEALTH AND WELL-BEING 5
I
experienced that a lot was dose-related, that I could
often create balance by using different doses.”
The perfect male identity
The perfect male identity is acquired through compe
tence in bodybuilding, the physically developed body,
and the masculinity achieved thereby. This identity,
and the successes and the confirmation received on
account of it, lead to satisfaction. The arduous lifestyle
results in a status that needs to be maintained. The
life histories of the men interviewed were influenced
by their bodies’ physical appearance and their fear of
not meeting the male norm. At an early age, they
experience a fascination for muscles and for the func
tional body as strong and good-looking. One man
reports:
It´s just that I want to be big, I want big muscles.
Maybe it´s something genetic, something that has
been inherited, because my dad was also like that
when he was younger, he trained and lifted weights,
Olympic lifting. And my uncle talks about them com
peting against each other to see who could lift the
most and so on.
The intake of AAS sometimes begins through peer
pressure between men. Peer pressure concerns the
fear of falling behind in development and not achiev
ing the same physical success as those who use AAS.
It is described as a form of mutual competition about
performing best, lifting the heaviest weights, achiev
ing the fastest physical development or being the
best-looking and most popular with girls: “that was
the worst thinkable . . . Christ, you couldn’t let your best
mate beat you so totally like . . . so that he was the most
popular.”
The motivation to strive for a bigger body may also
involve not feeling scared or small:
I saw the possibility of never being afraid again in my
whole life. And the bigger you are, the harder you hit.
It’s also the case that nobody dares to attack a guy
who weighs 120 kg, just his muscles alone.
The men interviewed experienced self-affirmation by
taking care of their bodies. This self-experienced
effect is proof that their strategy is working. Their
new larger bodies result in greater self-confidence
and a more positive self-image as the following com
ments show:
When I was walking along the corridor at school,
I
knew that everyone was watching”; and “You feel
good . . . when I feel my muscles, when I see myself.
This greater self-confidence results in satisfaction,
which was variable on different occasions depending
on daily body shape. As one man says:
The mirror is also a kind of method of assessment and
all mirrors are different, as many people know, so
when you are at the gym you see one thing and
when you get home you are completely devastated.
The men compare themselves to men they consider
as having the perfect male body and not to ordinary
normally built men. Getting confirmation and/or
respect for their body development is vital for their
wellbeing: “You kind of wanted to hear that you were
big and looked good.” However, attention and confir
mation sometimes also take too much of their energy,
which they also try to avoid. Who the confirmation
came from was also significant, it being more mean
ingful when it came from someone they look up to or
respect, as one man reports:
When you went to bodybuilding shows, that was
where it mattered. When you went to a stand to
buy PWO or protein or something like that, and
there was a fucking giant there to sell stuff, and you
know, when he pointed out my shoulders for exam
ple, ‘Jesus what fine shoulders’– good shoulders are
something a lot of people have difficulty in getting,
so ‘fine, thanks!’ We have something there. That´s
something. He pointed something out to me and
then I started ‘shit ten years ago, or eight years ago,
I looked like that, you know’, and now I´m here talk
ing to the big guys you know so things are a bit
different. That confirmation is important. But ordinary
people sometimes said, they sometimes said lots of
things, but then I just said ‘uh, look, I´m really small’,
‘no no you are huge’, ‘no I´m really small because I’m
not comparing myself with you, I’m comparing myself
with someone else’ and that’s how it works.
Building one’s body provides the opportunity to
demonstrate skills and value. A role that accompanies
the perfect male identity is the so-called “Guru”. This
is a person whom other people ask for his advice and
knowledge. The role involves status and includes spe
cial knowledge in bodybuilding that gives an indivi
dual the competence to guide others: “He’s the one
you go to for advice on which dietary supplements to
take and which chest exercise to do.”
Men who describe themselves as having a strong
self-esteem, have less need for confirmation.
However, a few positive words are always welcome
and a pat on the shoulder is quite sufficient.
Compliments are not always necessary because the
men are already fully aware of their achievement, as
one man notes:
I´m more of a passive confirmation seeker, I want the
confirmation when I know that I have done some
thing good or when I look good, when I know that
I have fought for my body. Then it´s fun to hear from
others that well you look good, but I do not need to
hear it because I have the confirmation in myself.
In order to develop and maintain an identity, time
needs to be set aside for daily routines. It is crucial
to prioritize and follow one’s busy food and exercise
schedule to achieve set goals. There is an underlying
stress in being disturbed in one’s daily routines, and
A. BÖRJESSON ET AL.
6
what is less important in everyday life has lower
priority: “Stress from not having time to eat, stress
from not having time to exercise. Nothing must come
between.”
A large and muscular body implies that people
around to a larger extent accept and understand the
strict lifestyle. However, this lifestyle is exposed to
both positive and negative comments. The positive
criticism is about bodybuilders’ dedication and fight
ing spirit, while the negative is about the strict diet
they adopt. The social context is limited and only
those who accept the men´s lifestyle are included in
their social circle. It can be both time-consuming and
wearing to respond to all comments. Therefore, they
change their social interaction or protest violently if
their life choices are criticized or questioned. Their
self-confidence is strengthened by the fact that they
live more carefully and take better care of themselves
than other people do:
So I have called people fat when they comment, then
I
have answered but my God I really don’t want to
look like you. Then they shut up.
Another man comments:
I often ate whole cartons of ice cream with tuna and
rice, that was my way of living on Sundays. That´s
what I ate. I remember very well when my sister had
her birthday and that somewhere I thought that
I
should not go to it because it was a birthday and
then there would be cake, but still I took my little
cooler bag and went there with my ice cream cartons
and sat and ate rice and tuna when everyone else was
eating cake. My father had a huge outburst against
me and was very angry and felt offended that I could
do such a thing that day. He had me with my back
against the wall and said how the hell can you do this
today. I answered him, how the hell can you do this,
how the hell can you sit and eat cake, you’re destroy
ing your body, you’ll get fat and get at high
cholesterol.
The existence may be jeopardized when demands
are too overpowering
Existence may be jeopardized if the use of AAS is
revealed to others or if the body is let down by illness.
Society´s attitude is judgemental, which entails a need
to live with lies. Lies may be difficult but necessary to
avoid being treated unfairly by other people. After the
revelation of AAS use, it may be difficult to carry on
one’s life as usual. Dignity may be lost with fear and
anxiety as a result. One man describes his concern
over what he would lose:
Everything. Myself. The lot. I’ll lose myself, or my
whole identity. That was me. My steroids, my training,
that was all I had. That was where I was somebody,
I was myself. I knew what I was doing, I had found my
place.
When demands are made, by close relationships or by
society at large, to return to a normal life, these men´s
freedom is restricted. This overpowering demand
means that their very existence is jeopardized, and it
feels difficult for them to stop using AAS: “I did not
want to quit my steroids, absolutely not. I sat and cried
on my sofa, you have ruined my life.”
It is not certain that these men would choose to
put their families first. One of them describes being
forced to make a choice:
But then it started to get a little unbearable so she
said to me ‘you must choose between me or the
steroids’ and then I said ‘what a stupid question,
I
choose my steroids’. Then she came after a while
and said that ‘either you seek help, or you are not
allowed to see the children’. And that was it, that´s
really the only way to get to me. So her choosing
that, it was a desperate last, last thing she did.
The men are torn between continuing and ending
their use, as one man explains:“best antidepressant
ever, better self-esteem and better self-confidence”.
It is not possible for men who have used AAS to
promise that they will never start again even though
they might have exposed their loved ones to discom
fort, been seriously ill or served a prison sentence: “I’m
completely clean now, but if I will remain clean for the
rest of my life, I cannot say”.
The strong love for AAS despite risks and conse
quences together with positive memories means that
they constantly need to remind themselves of why
they quit. One man says:
I
have to, I have to constantly remind myself. If you
compare with other addicts, you know they can take
out an old photo where they’ve been on drugs for ten
years, you know they look like skeletons and you
know that it’s so ugly that they don’t want to end
up there again. Then all they have to do is to take out
that photo, and that’s nice for them, because then
they think oh no, hell no, don’t want to end up there
again. I don’t have that. I do not have a photo like
that. I look like a god if I go back and look at my
pictures you know. So it´s just like hell, (laughter) so
then I have to go through the negative aspects all the
time in my head, I have to constantly remind myself
that this was not good, it was not good at all. My
children were afraid of me, I threatened my wife, no
I
do not want to end up there again, I do not want
that.
These men need to experience side effects or to be
told straight out that a certain side effect is caused by
AAS before they decide stop using such substances.
Intimidation propaganda is not perceived as an ade
quate deterrent, but they are motivated to stop if it is
possible for them to identify themselves with some
body affected by the side effect in question.
The men experience their authenticity and thus
identity as being called into question if their use of
AAS is revealed. The performances and bodily results
INTERNATIONAL JOURNAL OF QUALITATIVE STUDIES ON HEALTH AND WELL-BEING 7
they have achieved are experienced as being trivialized.
They were given a label that is difficult to get rid of.
The interviewees believe that people outside the
world of doping are convinced that AAS causes users
to become aggressive and violent and thus automa
tically “dangerous”, which in their minds is a wrong
image. All possible events, ill health and behavioural
changes that affect them will be linked to their use of
AAS. The word “doped” is perceived as a negatively
charged word, which for them means a feeling of
being “labelled”. The mass media reinforce this
image and do not take into account the feelings of
those who are vulnerable. Due to this exposure, users
may limit the intake or dosage of AAS, so that the
muscle mass does not increase too fast and arouse
suspicion.
Lying feels difficult, because it may be obvious
when somebody is lying, but at the same time it can
be difficult to tell the truth because then you can be
judged by other people. Living a lie may be tiring and
affects a person’s wellbeing, and people sometimes
feel it would have been easier to be honest. To avoid
being dishonest, the men interviewed tell certain
selected people that they are using AAS. However, it
can be difficult to be honest with those closest to
them. This is partly because they wanted to protect
them from the truth and partly because they do not
want to be exposed to their disapproval. As one man
puts it:
Yes, but our relationship would probably break up.
Either I would probably try to quit, which I was not
prepared to do then, or we would not have any
further contact. At least that’s what I believe, because
my mum, she is quite strict.
Although the men consider it important to contact
a physician when they experience various ailments,
they only make this contact in an emergency. They
then choose not to be completely truthful about their
use of AAS, partly because of their concerns about
consequences since AAS use is illegal and partly
because they experience being treated with
a
condescending and judgemental attitude. This
kind of attitude leads to a low level of trust towards
healthcare personnel. The men feel offended or
experience powerlessness. The lack of respect makes
them prefer to continue their use of AAS.
However, when they meet a “factual”, honest and
non-judgemental physician, they experience strong
sense of trust and security. It is easier to be honest
and open to people who do not judge. They also feel
that in such cases they are more receptive to informa
tion about their AAS use. The men wanted an open
and trusting contact with physicians, since this creates
a more permissive climate regarding the use of AAS.
If the men are suffering from a serious illness, they
feel that support is important. They have good
experiences of support from priests, curators and psy
chologists when needing to end their use of AAS due
to illness. Friends also play an important role when
things feel difficult and daunting. Nowadays they are
happy to tell their stories to process events and to be
available to support others who want to quit or are
having difficulty in quitting. They really want to be
supportive and act as personal contacts.
After quitting the use of AAS, it may be difficult for
former users to start exercising again because the
effect is not as great as with AAS. The desire to
exercise is affected by the lower testosterone levels
that follow a discontinued use. Even though the men
have normal testosterone levels, they no longer feel
vital, instead experiencing depression, decreased sex
ual desire and lack of wellbeing. This means
a suffering for which it is difficult to find help.
Discussion
The participants in our study used AAS because they
had a wish for the perfect male body, they wanted to
get bigger and gain more muscle. The use of AAS
gave them faster muscle development and less body
dissatisfaction. Muscle dysmorphia (MD) is a form of
disorder characterized by a preoccupation with mus
cularity and body image (Phillips et al., 2010). Male
bodybuilders report MD to a greater extent (Mitchell
et al., 2017; Pope et al., 1997) than non-bodybuilders
resistance trainers. It has been known for many years
that men take risks and experiment with different
preparations to create extraordinary bodies (Gaines
& Butler, 1974; Kanayama & Pope, 2012; Klein, 1993).
They focus on a strict diet, extremely heavy weight
training and the use of AAS (Mitchell et al., 2017; Pope
et al., 1997). The men interviewed were aware of the
risks of using AAS, but their concern about side effects
decreased when no serious side effects appeared. In
order not to expose themselves to obvious risks they
tried to protect their bodies by following a healthy
diet, the intake of specific supplements or the use of
lower doses of AAS. Male AAS users have been shown
to neglect the side effects of AAS and short-term
gains generally outweigh long-term risks (Grogan
et al., 2006; Kimergård, 2014). The majority of AAS
users continue their use despite side effects (Ip
et al., 2011) but they are concerned about harmful
effects on health (Börjesson et al., 2020; Parkinson &
Evans, 2006).
The results showed that the men were equipped
with self-control, in other words they were disciplined
and driven by will-power. This is a necessary attribute
to be able to transform and shape the body to such
a great degree. The body is a time-consuming project
and by having self-control they were consciously able
to control their decisions and choices (Egidius, 2008).
The men were constantly self-critical of their bodies’
A. BÖRJESSON ET AL.
8
faults and shortcomings and driven by unhealthy
ideals. Perfectionism has increased in recent decades
which may be due to greater demands, unrealistic
expectations and more competitive environments
(Curran & Hill, 2019). Perfectionistic traits, especially
typical for elite athletes (Lemyre et al., 2008), may
include expectations such as achieving a perfect
body. But if healthy striving gives way to self-
imposed demands, self-critical evaluations of achieve
ments and concerns about negative assessments
(maladaptive perfectionism) it may become unhealthy
(Lundh, 2004).
Large muscles, strength, increased focus, respect
and sexual virility are effects desired by the men in
this study. According to Andreasson and Johansson
(2016), these attributes are linked to manhood and
masculinity. Bodybuilding has been described as
a predominantly masculine subculture (Klein, 1993)
and AAS use involves an anticipated process of trans
formation (Andreasson & Johansson, 2016). Within the
bodybuilding subculture, belonging to the highest
level of the hierarchy is the goal. According to
Raewyn Connell (1995), the male body is an inevitable
ingredient in the construction of masculinity.
Masculinity is built around a hegemony in which
men are divided into categories, so called hegemonic
masculinity. There can be more than one hegemonic
masculinity within a society, and it can pertain within
subgroups where the ideal differs based on context
and environment. Hegemonic masculinity is closely
related to patriarchy and is the ideal that men relate
to and strive for, but very few identify with. The
hegemonic ideal is a leading position, difficult to
achieve, to which men have an ambivalent and com
plicated relation, and which is surrounded by values,
status and power. Reaching the ultimate goal is an
ideal that coincides with hegemonic masculinity
(Connell, 1995). By constantly supporting this ideal,
the men in this study were given the benefits of
hegemonic masculinity.
These men´s feelings of inadequacy indicated that
they had a low self-esteem and self-confidence. The
feeling of being just one of the crowd may have
created the desire to stand out and might be a sign
of why the men in this study felt that they needed to
acquire a perfect body and appearance. Their feelings
of inadequacy might have been influenced by the fact
that positive qualities such as health and success are
often attributed to attractive and good-looking per
sons (Rennels, 2012). The men in this study wanted to
be seen as people who were not frivolous or light-
hearted but who were dedicated, focused, hard-
working and successful.
Performance-based self-esteem (PBSE) is a concept
linked to perfectionism (Hallsten et al., 2005). PBSE is
based on concerns of not being good enough and the
results achieved are an important measure of ability
(Hallsten et al., 2005; Makower, 2018). It is a variant of
low self-esteem based on the individual proving her/his
human value through performance. Individuals with
high PBSE are often ambitious and base their value on
external factors such as success and personal status.
External confirmation becomes a compensation for
their lack of self-esteem (Hallsten et al., 2005).
The men interviewed here received a certain sta
tus within their own group of bodybuilders depend
ing on how well they attained their goals. Their
status was affected by how hard they worked and
that they did not take the easy way of cheating by
using a lot of AAS substances. For some it was
important that the body should be built as an
ongoing handicraft project and for others it was
a matter of quickly achieving a certain result or
goal that would bring respect.
Through the body we have the opportunity to
create and transform our identity and self-image
(Giddens & Sutton, 2013). Identity is what charac
terizes us and makes us unique and we use different
tools to reach our ideal. The physical body becomes
an instrument to work with and the boundaries have
been blurred for what it is realistic to try to achieve.
Individualism places the responsibility on the indivi
dual her-/himself to seek her/his own way and con
struct her/his own identity (Giddens & Sutton, 2013).
International valuation surveys show that individual
ism and self-expression are highly valued in Sweden
(World Value Survey, 2021).
These men´s acquired position as examples of the
perfect male body ideal provided them with a social
role in relation with other people. Goffman’s role
theory (1959) is based on people play different
social roles depending on the situation and the
occasion. The role is a socially defined expectation
that a person with a certain status or social position
tries to live up to. That kind of acquired position is
achieved by the individual her-/himself and the ideal
body may be seen as a result of social processes
(Giddens & Sutton, 2013). The social constructivist
perspective means that we are born into a society
that constantly influences us and we relate to exist
ing norms and conceptual frameworks. How we look
is central and body perception is influenced by the
appearance ideals that exist in society. Goffman says
that the body´s appearance is socialized, shaped and
transformed to fit into the society in which it is
created. The appearance and creation are visible to
the individual and to other people, thereby influen
cing the identity. The roles are presented to an
audience of the same or similar type in which the
body is of great importance because it shows to the
world who you are (Goffman, 1959). The men in this
study strove to fill the role of the perfect male ideal
to display what they had achieved.
INTERNATIONAL JOURNAL OF QUALITATIVE STUDIES ON HEALTH AND WELL-BEING 9
For the men in this study, the acquired perfect
male body included aspects that are essential to exis
tence. According to existential philosophy, a human
being does not choose her/his existence, but by being
aware of her/his choices, he/she can choose how he/
she wants to live and create meaning in her/his life
(Heidegger, 1927/1998; Sartre, 1986). In our study,
bodies were used as instruments to achieve goals
and to receive confirmation. This improved the men
´s self-confidence and raised their self-esteem. The
meaning of self-identity is an entire unite that is
intertwined with meanings of self-confidence, self-
affirmation, self-image. This means that self-identity
is inseparable of all meanings that relate to the “self”.
It creates the person.
Sartre (1986) states that we constantly are on our
way away from being (that which is just now) and
striving for nothingness (our dreams and goals). For
these men to be able to achieve their dreams and
goals and not being judged for their choices, they
needed to lie. They did not want to be exposed to
the feeling of not being genuine and thus jeopardize
the social role they had achieved. According to exis
tentialism, the individual is responsible for the con
scious choices he/she makes and therefore he/she is
able to decide over her/his own life. However, there is
also a constant struggle between different choices
that makes us anxious (Sartre, 1986). Anxiety is con
stant because the choices we make affect others. This
may lead to problems in both work and private life.
The choice of using AAS as men in this study did,
might have led to body failure. The context of mean
ing may change when something with which we
handle the world breaks down, such as a tool, in this
case the body (Heidegger, 1927/1998). Existential free
choices are limited in the event of illness. Pressure
from relatives influenced the men in their choice of
continuing to use AAS. They experienced this as jeo
pardizing their very existence. Having to quit one´s
lifestyle may be experienced as having to leave one´s
body physically, mentally and socially. It may feel like
the end of life. Existence is what frightens us when we
are left to ourselves (Sartre, 1986).
AAS are illegal (Riksdagen, 1992) and therefore AAS
users are a hard-to-reach population. It is easier to
recruit men than women because the use is much
more common in male populations. A total of twelve
interviews were included in this study. We used
a
phenomenological research approach with
a lifeworld perspective, so despite few interviews,
data collection has contributed with meanings (Polit
& Beck, 2017) forming the basis for an analysis and
generating an essential description of the phenom
enon: men´s use of AAS. The results entail
a development of knowledge to be able to under
stand men using AAS.
Descriptions have been based on the men’s lived
experiences and there is of course a risk that the
informants may have chosen their answers taking
the illegality of AAS into account. We, however,
believe that in-depth interviews with support for
reflection have contributed to a truthful material
since substantive meanings have emerged. One weak
ness of the method is that it is time-consuming and
requires knowledge in interview techniques. In order
to gain a deeper understanding, in-depth interviews
as a method have been shown to be a strength.
Conclusions and clinical implications
Men´s use of AAS is a complex phenomenon. It partly
concerns a traditional view of masculinity that is
reflected in society. It also involves an individual driving
force to achieve a body ideal that has winning charac
teristics, not only in competitions. This driving force to
attract attention and to be the best in the group blinds
users to the negative consequences of using AAS,
which do not become visible to these men until illness,
injury or other dysfunction arises. Bodybuilding seems
to be based on low self-esteem and a competitive
instinct among men. However, the built-up body is
fragile from both an existential and a biological per
spective. Self-esteem and self-confidence can quickly
be destroyed in the absence of confirmation from
others and the side effects of the substances may
damage the body in the form of serious physiological
disorders. Therefore, both broad and deep knowledge
and understanding are required to be able to meet
these men in their problems and vulnerability,
a meeting which is hampered by their low trust in
healthcare, and by the fact that the AAS are illegal.
Acknowledgments
We wish to thank all the interviewees for sharing their
experiences and making this study possible.
Disclosure statement
No potential conflict of interest was reported by the
author(s).
Notes on contributors
Annica Börjesson is a nurse and a doctoral student at
Karolinska Institutet, Sweden. She has extensive experience
in providing counselling to individuals who use anabolic
androgenic steroids for non-medical purposes.
Margaretha Ekebergh is a Professor in caring science at
Faculty of Caring Science, Worklife and Social Welfare at
University of Borås. She has extensive methodological
knowledge of life-world research.
A. BÖRJESSON ET AL.
10
Marja-Liisa Dahl is Professor at Karolinska Institutet. She is
a specialist in clinical pharmacology and has over 30 years
of experience in research. She is also the chief physician for
the Anti-Doping Hot-Line.
Lena Ekström is a Lecturer and Associate Professor in
Clinical Pharmacology, at Karolinska Institutet. She has
extensive knowledge and experience of research in the
field of anti-doping and specifically anabolic androgenic
steroids.
Mikael Lehtihet is a physician and Associate Professor at
Karolinska Institutet. He has many years of clinical experi
ence in treatment of individuals using anabolic androgenic
steroids. He has many years of experience in research in the
field of anti-doping.
Veronica Vicente is Associate Professor at Karolinska
Institutet. She is a researcher in emergency medical care
and in caring science. She has a long experience of in-depth
interview technique from a life-world perspective.
Author contribution
AB and VV designed the study. All the authors analyzed the
data. All the authors have read and approved the final
manuscript.
ORCID
Annica Börjesson
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luesurvey.org/WVSContents.jsp?CMSID=Findings</p>TV REPAIR PARTShttp://www.blogger.com/profile/03272638773780329095noreply@blogger.com0tag:blogger.com,1999:blog-3850502767250139870.post-85547260712359818682024-03-27T07:02:00.000-07:002024-03-27T07:02:36.751-07:00The use of post-cycle therapy is associated with reduced withdrawal symptoms from anabolic-androgenic steroid use: a survey of 470 men<p> Grant et al.
Substance Abuse Treatment, Prevention, and Policy
https://doi.org/10.1186/s13011-023-00573-8
RESEARCH
Substance Abuse Treatment,
Prevention, and Policy
Open Access
The use of post-cycle therapy is associated
with reduced withdrawal symptoms
from anabolic-androgenic steroid use: a survey
of 470 men
Bonnie Grant1, Joseph Kean2, Naim Vali3, John Campbell4, Lorraine Maden5, Prun Bijral3, Waljit S. Dhillo1,
James McVeigh6, Richard Quinton7 and Channa N. Jayasena1*
Abstract
Background Anabolic–androgenic steroids (AAS) mimic the effects of testosterone and may include testosterone
itself; they are used for body enhancement within the general population. AAS use has been linked with increased
mortality, cardiovascular disease, mental health disorders, and infertility. AAS-induced hypogonadism can persist
for an uncertain time period despite cessation, during which men may report physical and neuropsychiatric symp
toms. In an attempt to mitigate these symptoms and expedite testicular recovery, many men self-administer post
cycle-therapy (PCT), typically involving human chorionic gonadotrophin (hCG) and selective oestrogen receptor
modulators (SERMs), which are known to potently stimulate testicular function. However, this practice has no objec
tive evidence of effectiveness to lessen the severity or duration of hypogonadal symptoms.
Methods An anonymous survey of four-hundred-and-seventy men using AAS explored the symptoms they expe
rienced when ceasing AAS use; the effect of PCT on relieving their symptoms, and their perceived role for health
service support.
Results The majority of respondents were white, aged 18–30 years old, and working in skilled manual work. 51.7%
(n = 243) reported no issues with AAS use, but 35.3% reported increased aggression. 65.1% (n = 306) of respond
ents had attempted AAS cessation and 95.1% of these experienced at least one symptom upon AAS cessation.
Low mood, tiredness and reduced libido were reported in 72.9%, 58.5% and 57.0% of men stopping AAS use,
respectively, with only 4.9% reporting no symptoms. PCT had been used by 56.5% of respondents with AAS cessa
tion and mitigated cravings to restart AAS use, withdrawal symptoms and suicidal thoughts by 60%, 60% and 50%,
respectively. The effect of stopping AAS on body composition and recovery of testosterone or fertility was a con
cern in 60.5% and 52.4%, respectively. Most respondents felt PCT should be prescribed under medical supervision
in the community.
Conclusions Our survey suggests that the majority of men stopping AAS use are using some form of PCT. Some
self-reported symptoms of AAS-induced hypogonadism such as cravings to restart AAS use reduce by 60% and sui
cidal thoughts reduce by 50%. These individuals are concerned about the negative effect of AAS use and cessation.
*Correspondence:
Channa N. Jayasena
c.jayasena@imperial.ac.uk
Full list of author information is available at the end of the article
© The Author(s) 2023. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which
permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the
original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or
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licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecom
mons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
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Grant et al. Substance Abuse Treatment, Prevention, and Policy
Page 2 of 8
This study provides crucial information for planning future research to evaluate the effects of PCT on symptoms
when men stop AAS use.
Keywords Anabolic–androgenic steroids, Hypogonadism, Image and performance enhancing drugs, Post-cycle
therapy, Testosterone, Withdrawal
Introduction
Anabolic–androgenic steroids (AAS) are synthetic
drugs that mimic the effects of testosterone. They are
misused to promote aesthetic body enhancement,
energy and improved well-being. AAS use was previ
ously confined to improving physical performance in
professional sporting and bodybuilding communities,
but the practice has risen substantially within the gen
eral population [1–3]. Current best estimates predict
that 2% of the U.K male population have used non
medically prescribed androgens, although the true fig
ure may be even higher [4, 5]. AAS use has been linked
with an increased mortality and risks of cardiovascular
disease, transmission of blood-borne viruses, infertility,
and mental health disorders [6–9].
AAS use suppresses endogenous luteinising hormone
(LH)-mediated testosterone production, which may per
sist for many months to years after cessation [7, 10–12].
Men experiencing AAS-induced central hypogonadism
may report physical and neuropsychiatric symptoms,
including weakness, reduced libido, erectile dysfunc
tion, depression, anxiety, and suicidality [10, 11, 13, 14].
Additionally, quality of life scores are found to be lower in
men with all-cause hypogonadism, regardless of underly
ing pathology [15]. Some men resume AAS use to avoid
experiencing these symptoms and thus enter a potentially
dangerous cycle of dependence [16, 17].
Men using AAS may use different strategies to avoid
symptoms of hypogonadism. Some may take a “blast and
cruise” approach whereby large doses of AAS are used
(for instance in preparation for an event) followed by a
longer period of continued lower dose AAS. An alterna
tive is “cycling”, whereby men use AAS for 6–12 weeks
“on-cycle” followed by a period “off-cycle” when they
take post-cycle therapy (PCT) [2, 18]. PCT is a non
medical term used to describe a varied group of self
administered substances, either with the aim to limit
the adverse effects of AAS use between AAS cycles or
to accelerate recovery of endogenous hypothalamic
pituitary–gonadal (HPG) axis function after permanent
AAS cessation [3, 19, 20]. Various PCT regimes have
been reported but typically involve the use of human
chorionic gonadotrophin (hCG) in combination with
selective oestrogen receptor modulators (SERM) and/or
aromatase inhibitors (AI) [18, 19, 21, 22]. hCG directly
stimulates testicular testosterone production within
Leydig cells, while SERMs and AIs indirectly stimu
late LH-mediated testosterone production and follicle
stimulating hormone (FSH)-mediated maintenance of
seminiferous tubule mass by reducing the oestrogenic
negative feedback on the HPG axis. By restoring endog
enous testosterone production quicker than would have
otherwise occurred, men hope to minimise or avert the
symptoms of AAS-induced hypogonadism and thus
avoid some of the negative health effects of AAS use. The
use of PCT to restore HPG function after AAS cessation
is unproven with no randomised controlled trials to sup
port this approach.
T
here is currently minimal evidence describing the
effect of PCT on symptoms of AAS-induced hypog
onadism. We conducted a survey of 470 men using AAS
to investigate their experiences when ceasing AAS use;
the effect of PCT on symptom relief and to establish
whether they perceive a role for health service support.
Methods
An anonymous, self-administered, survey was completed
between December 2021 and February 2023. Participants
either currently or previously used AAS. The survey was
distributed and completed online via Google Forms web
page or paper versions which were subsequently entered
onto Google Forms by the study team. Individuals were
recruited through adverts on websites related to AAS use,
snowball sampling, and via practitioners working within
harm reduction clinics and / or alongside drug treatment
services that provide support for individuals using AAS in
the U.K [23]. This was a survey evaluation as part of patient
and public involvement for a research grant proposal and,
therefore, does not require research ethical approval.
Participation in the survey was voluntary with partici
pation implying informed consent. Information explain
ing the purpose of the study and assurance that all
responses would be kept confidential was stated at the
beginning of the survey. Questions covered demographic
details such as age, ethnic group, location and occupa
tion as defined by the U.K. Office for National Statistics
[24]. Participants were also asked symptoms experienced
when using and stopping AAS and PCT. No identify
ing data was collected. The survey consisted of up to 15
items of multiple-choice questions or Likert scales. Sev
eral questions allowed the respondent to select multiple
applicable responses (Additional file 1).
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Page 3 of 8 Grant et al. Substance Abuse Treatment, Prevention, and Policy
Data analysis
Completed questionnaires were submitted electronically
to Google Forms and then tabulated using Microsoft
Excel. Graphical techniques and analysis were performed
using GraphPad Prism version 9. A total of 470 responses
were received. Where appropriate, data are presented
as median with interquartile range. Chi-squared tests
were used to compare between groups larger than two.
For all statistical testing, a p value of < 0.5 was considered
significant.
Results
Demographics
The survey was completed 470 times by differ
ent individuals. 41.8% (n = 196) and 39.9% (n = 187)
respondents were aged 18–30 years and 31–44 years
respectively. The most common ethnicity was white
(n = 298, 66.1%) and 62.2% (n = 291) lived in Yorkshire.
Most respondents worked in skilled manual occupa
tions (n = 129, 29.5%), followed by supervisory, clerical,
and junior managerial (n = 80, 18.3%) and intermediate
managerial roles (n = 72, 16.4%; Table 1).
Adverse effects of anabolic–androgenic steroid use
Most (n = 227, 51.7%) survey respondents reported
no problems with the use of AAS. 35.3% (n = 155)
reported increased aggression, 8.0% (n = 35) violence
and 1.4% (n = 6) reported imprisonment that they
associated with their AAS use. Respondents were able
to report additional problems experienced with AAS
use as a free text as “other”. Testicular atrophy, acne
and mood swings were the most commonly reported
additional problems (10.0%, 4.3% and 4.1% respec
tively; Table 2).
Anabolic–androgenic steroid cessation and post‑cycle
therapy
An attempt at AAS cessation was reported by 65.1%
(n = 306) of all respondents. 95.1% of respondents who
had attempted AAS cessation reported at least one symp
tom upon AAS cessation. Low mood, tiredness, reduced
sex drive and physical weakness was reported in over
fifty percent of respondents who had attempted AAS
cessation (72.9%, 58.5%, 57.0% and 56.0% respectively;
Fig. 1A). Fourteen respondents (4.9%) reported no symp
toms with AAS cessation.
PCT use when stopping AAS was reported in 56.5%
(n = 160) of respondents. Within our anonymous sur
vey, PCT use was self-reported to reduce cravings to
restart AAS by 60% (IQR 40—80), withdrawal symp
toms by 60% (IQR 50 – 80) and suicidal thoughts by
50% (IQR 30 – 70; Fig. 1B).
58.1% (n = 273) respondents felt it was unlikely, or very
unlikely they would stop AAS use in the next 5 years. The
effects of stopping AAS on body composition or physical
performance and the uncertain recovery of testosterone
or fertility were reported as the biggest concerns in rela
tion to stopping AAS (n = 268; 60.5% and n = 232; 52.4%
respectively). Effectiveness and purity of PCT drugs were
a concern for 41.1% (n = 182), while 24.8% and 24.2% were
concerned about quality and access of NHS advice respec
tively. 31.0% (n = 145) were interested, or very interested
in participating in future trials of PCT. The majority of
respondents (n = 206; 43.8%) felt that the community was
the best place for NHS prescribed PCT, while only 10.0%
(n = 47) preferred NHS specialist clinics (Table 3).
Table 1 Demographics of survey respondents using anabolic
androgenic steroids
Age (Years) Respondents, n = 469 (%)
18–30 196 (41.8)
31–44 187 (39.9)
45–60 81 (17.5)
60 + 4 (0.9)
Ethnicity Respondents, n = 470 (%)
Asian or Asian British 100 (22.2)
Black, African, Caribbean, or Black British 18 (4.0)
Mixed or multiple ethnic groups 52 (11.5)
Other 2 (0.4)
White 298 (66.1)
Location Respondents, n = 468 (%)
England: East 4 (0.9)
England: London and South-East 9 (1.0)
England: Midlands 14 (3.0)
England: North-East 17 (3.6)
England: North-West 14 (3.0)
England: South-West 43 (9.2)
England: Yorkshire 291 (62.2)
Scotland 57 (12.2)
Wales 13 (2.8)
Outside the UK 3 (0.6)
Other 3 (0.6)
Occupation Respondents, n = 438 (%)
High-level managerial, administrative,
or professional
30 (6.8)
Intermediate managerial, administrative,
or professional
72 (16.4)
Supervisory, clerical, and junior manage
rial, administrative, or professional
80 (18.3)
Skilled manual work 129 (29.5)
Semi and unskilled manual work 67 (15.3)
Casual or lowest grade of work, unem
ployed or pension
42 (9.6)
Full-time student 18 (4.1)
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Grant et al. Substance Abuse Treatment, Prevention, and Policy
Page 4 of 8
Table 2 Reported problems with anabolic–androgenic steroid
use by survey respondents
Problems reported with anabolic–androgenic
steroid use
Respondents,
n = 439 (%)
No problems
Becoming more aggressive than usual
Becoming violent
Prison
Other:
Testicular atrophy
Gynaecomastia
Acne
Mood swings
Changes in hair growth
Increased sex drive
227 (51.7)
155 (35.3)
35 (8.0)
6 (1.4)
44 (10.0)
10 (2.3)
19 (4.3)
18 (4.1)
15 (3.4)
9 (2.1)
Association with age
T
he association between age groups and survey
responses are shown in Additional file 2. Older men had
significantly higher rates of attempted steroid cessation
compared with younger men. Increasing age was associ
ated with greater self-reporting low mood (p = 0.0001),
problems sleeping (p = 0.0011) and headache (p = 0.0007)
when stopping AAS use. Younger men were less likely to
report problems with AAS use (p < 0.001) and had fewer
worries about stopping AAS use (p < 0.0001). Younger
men preferred PCT to be available online (p < 0.0001)
whereas older men preferred from general practitioners
(p = 0.0038).
Discussion
Anabolic–androgenic steroid use has risen within the
general population, and many use PCT as an unproven
practice to avoid or minimise the negative health effects
associated with AAS use and cessation. There are cur
rently no clinical guidelines for managing AAS-induced
hypogonadism, and men often seek substances and
advice from internet sources and peers, rarely health
care professionals [2, 25, 26]. This study provides sev
eral novel insights into experiences of AAS cessation
and the role of PCT on symptoms.
T
he demographics within our study are broadly similar
to previously reported [2, 3, 19]. Respondents were com
monly aged 18–44 years old, white ethnicity, and work
ing in skilled manual jobs. They were disproportionately
from Yorkshire, the largest county in Northern Eng
land. The majority of respondents reported no adverse
effects with the use of AAS, contrasting with higher
rates reported in other studies [3, 19, 20, 27]. This may
be due to the limited response options given to our par
ticipants, or a reluctance to divulge this information. A
recent meta-analysis estimated that 73% of AAS found on
Fig. 1 A Percentage (%) of respondents attempting anabolic–androgenic steroid cessation experiencing anabolic–androgenic steroid induced
hypogonadal symptoms. Total n = 284 respondents. B Percentage (%) reported improvement in symptoms with respondents using post-cycle
therapy. Data is shown for cravings/urge to restart anabolic–androgenic steroid use (n = 158), withdrawal symptoms (n = 105) and suicidal thoughts
(n = 27). Data is presented as median, interquartile range, minimum and maximum. Scale is 10 – 100% with 100% being the maximum improvement
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Page 5 of 8 Grant et al. Substance Abuse Treatment, Prevention, and Policy
the black market were counterfeit or of substandard qual
ity; this may explain why half of our respondents did not
report any adverse effects with AAS use [28]. The most
reported symptoms upon cessation in our survey were
low mood, reduced libido, tiredness, and physical weak
ness have been reported previously [10, 11, 14].
Fifty-seven percent of respondents self-reported
reduced libido when stopping AAS use. Two studies
have reported improvements in erectile dysfunction (ED)
symptoms with drugs commonly used as part of PCT.
Firstly, men with a history of non-prescribed andro
gen use were recruited to a single-centre cohort study
to receive treatment with hCG and clomiphene versus
observation, based on patient choice [29]. Following AAS
cessation, there was no statistical significance between
the two groups International Index of Erectile Function
(IIEF) scores. In those who did not receive treatment, a
statistically significant improvement in IIEF scores was
not observed until 12 months after recruitment, whereas
in the treatment group, scores improved from 6 months
onward. A major limitations was that participants were
given the choice of intervention or observation, and
so the conclusions drawn may be due to placebo effect.
Secondly, a cross-sectional observational study by Arm
strong et al. assessed sexual function of 231 men cur
rently, or previously using AAS with the abbreviated
5-item International Index of Erectile Function (IIEF-5)
[30]. They reported higher IIEF-5 scores in those who
concurrently used other substances, such as anti-oestro
gens suggesting this may be a protective factor in main
taining erectile function after AAS use. While these two
studies show higher IIEF scores with hCG and SERM use,
the lack of randomisation or placebo-control limits their
conclusions.
There are currently no studies that quantitatively evalu
ate the effect of PCT on neuropsychiatric symptoms.
In our anonymous survey, the use of self-administered
PCT reduced self-reported craving symptoms and with
drawal symptoms by 60% each and suicidal thoughts by
50%. Griffiths et al.’s thematic analysis reported increased
mood disturbances upon AAS cessation with some
reporting an improvement in symptoms with PCT [31].
Others however reported that the use of PCT worsened
some psychiatric symptoms. Additionally, difficulty
accessing PCT during the COVID-19 pandemic has been
tentatively linked to worsening of mental health disor
ders in men ceasing AAS use, however this was likely
multicausal [32]. While some of the improved symp
toms reported in the survey may be explained by placebo
effect, there may be a role for PCT in managing symp
toms of AAS-induced hypogonadism.
While the majority of respondents felt it was unlikely
or very unlikely they would stop AAS use in the next five
years, this may be explained by worries around the effects
of AAS cessation. Our findings showed the effect of AAS
cessation on body composition or physical performance
and recovery of testosterone levels or fertility was of con
cern to respondents. These findings are corroborated by
Griffiths et al. who reported participants awareness of the
long term health consequences of AAS use, and PCT was
a means used to maintain health or gains, of which fertil
ity risk was a key concern [31]. Participants also reported
challenges in obtaining PCT; in fact, accessing AAS
was deemed much easier, which led some to prolong or
indefinitely continue AAS use. Our findings found that
41.1% of respondents were concerned about the effec
tiveness or purity of PCT. Most PCT is obtained illicitly
through online sources or peers and so the verification
of active hCG or SERM substances within these prod
ucts often cannot be confirmed [28]. Piatkowski et al.
also reported on concerns about the legitimacy of AAS
Table 3 Anabolic–androgenic steroid cessation and post-cycle
therapy
Likelihood of stopping anabolic–andro
genic steroids in next 5 years
Respondents, n = 470 (%)
1 (Very unlikely) 135 (28.7)
2 138 (29.4)
3 96 (20.4)
4 48 (10.2)
5 (Very likely) 53 (11.3)
Worries about stopping anabolic–andro
genic steroids
Respondents, n = 443 (%)
Nothing 82 (18.5)
Recovery of testosterone or fertility 232 (52.4)
Effects on body composition or physical
performance
268 (60.5)
Access to NHS for advice 107 (24.2)
Quality of NHS advice 110 (24.8)
Effectiveness or purity of PCT 182 (41.1)
Other 20 (4.5)
Interest in participating in a research
trial about post‑cycle therapy
Respondents, n = 469 (%)
1 (Not at all interested) 156 (33.3)
2 76 (16.2)
3 92 (19.6)
4 42 (9.0)
5 (Very interested) 103 (22.0)
Where would be best to access National
Health Service (NHS) prescribed post
cycle therapy?
Respondents, n = 470 (%)
Community e.g., harm prevention clinic
or local pharmacy
206 (43.8)
GP surgery 109 (23.2)
NHS Specialist clinic e.g., endocrinology 47 (10.0)
Online service 138 (29.4)
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Grant et al. Substance Abuse Treatment, Prevention, and Policy
Page 6 of 8
or PCT substances used. The men interviewed felt that if
the legitimacy of substances could be confirmed it would
encourage safer practices and reduce potentially danger
ous adverse effects [33]. The concerns highlighted in this
study may be preventing cessation in many men and are
therefore a target for cessation programmes. Importantly,
there was an expression of interest in participating in a
research trial about PCT by some of the respondents and
engagement from within the community is vital for any
future intervention studies. Around a quarter of respond
ents to this survey were concerned about access to NHS
advice or quality of NHS advice. Many physicians have
attempted to manage a patient with AAS-induced hypo
gonadism, but most do not feel confident in treating the
condition [34]. Patients are often advised to wait until
symptoms resolve, with many continuing to experience
unresolved symptoms. Physicians are often rated poorly
by men using AAS regarding their knowledge and exper
tise when compared with coaches, bodybuilding websites
and other men using AAS [3, 26]. In the U.K., men using
AAS may seek support through community harm reduc
tion clinics [23]. The availability, and trust, in this sup
port network may explain why most respondents would
prefer to access prescribed PCT in the community, rather
than via specialist clinics or their general practitioner.
T
he drugs used as PCT are commonly used in the
management of male hypogonadism, however there are
no current controlled trials demonstrating their efficacy
or safety in AAS-induced hypogonadism [35–37]. It is
therefore premature to recommend its use to health
care professionals. If PCT was objectively shown to help
men with AAS-induced hypogonadism, engagement
with healthcare professionals using interviews and focus
groups to scope their attitudes would be important to
translate PCT into practice.
Despite the novel aspects identified in our study there
are several limitations. 60% of respondents were from
the Yorkshire area and our findings may reflect regional
variations in practice, particularly around PCT use. It is
unlikely this has significantly changed our conclusions
however as the proportion of respondents using PCT in
the non-Yorkshire area was similar to the whole group.
As the survey was voluntary and with a focus on PCT,
this exposes selection bias to those using PCT and, as
it required respondents to recall their previous experi
ences, it is necessarily subject to recall bias and uncer
tainty. PCT describes a heterogeneous group of drugs
and differing regimes are often used. A limitation of our
study is that no information was collected about duration
or specific drugs used as PCT, which may have helped
identify specific patterns of usage associated with most
experienced benefit. Details about prior history of AAS
use, dosage and duration were not collected which may
influence reported symptoms. This may have aided with
interpretation of symptoms experienced by respondents
to our survey. Finally, the self-reported improvement in
symptoms may also be attributable to a placebo effect,
and not a direct PCT effect.
In summary, our study provides novel insights into the
experience of AAS cessation and the perceived benefit
of PCT on symptoms of AAS-induced hypogonadism.
Respondents of our anonymous survey self-reported
physical and neuropsychiatric symptoms of hypog
onadism which improved with self-administered PCT
use. The information from this study is critical for firstly
planning future well-designed randomised controlled
studies to compare the effectiveness of cessation versus
hormonal treatment in managing AAS-induced hypog
onadism. Once established, any successful treatment is
likely to require an integrated approach engaging health
care professionals and peer networks to address the
endocrine and neuropsychiatric symptoms experienced
by men motivated to stop AAS use long-term.
Abbreviations
AAS
AI
FSH
hCG
HPG
IIEF
IQR
LH
NHS
PCT
Anabolic–androgenic steroids
Aromatase inhibitors
Follicle-stimulating hormone
Human chorionic gonadotrophin
Hypothalamic-pituitary–gonadal
International Index of Erectile Function
Interquartile range
Luteinising hormone
National Health Service
Post-cycle therapy
SERM Selective oestrogen receptor modulators
Supplementary Information
The online version contains supplementary material available at https://doi.
org/10.1186/s13011-023-00573-8.
Additional file 1: Complete survey administered to participants.
Additional file 2: Supplemental Table 1: Survey responses by age group.
Acknowledgements
We would like to thank all organisations and individuals involved in distribut
ing the survey and to all the respondents for their valuable contribution.
Conflict of interests
Logixx Pharma Ltd (CNJ).
Authors’ contributions
BG, JK, JM and CNJ conceptualised the study. BG, JK, NV, JC, LM, JM and CNJ
collected data. BG and CNJ did data analysis. BG and CNJ drafted the manu
script. JK, NV, JC, LM, PB, WSD, JM and RQ edited the manuscript. All authors
approved the final submitted version.
Funding
The Section of Endocrinology and Investigative Medicine is funded by grants
from the MRC, NIHR and is supported by the NIHR Biomedical Research Centre
Funding Scheme and the NIHR/Imperial Clinical Research Facility. The views
expressed are those of the author(s) and not necessarily those of the NHS, the
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Grant et al. Substance Abuse Treatment, Prevention, and Policy
Page 7 of 8
NIHR or the Department of Health. The following authors are also funded as fol
lows: NIHR Research Professorship (WSD), NIHR Post-Doctoral Fellowship (CNJ).
Availability of data and materials
The datasets used and analysed during the current study are available from
the corresponding author on reasonable request.
Declarations
Ethics approval and consent to participate
This was a survey evaluation as part of patient and public involvement for
a research grant proposal and, therefore, does not require research ethical
approval. Participation in the survey was voluntary with participation implying
informed consent.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Author details
1Section of Investigative Medicine, Commonwealth Building, Imperial College
London, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK. 2 Brad
ford Metropolitan District Council, Britannia House, Hall Ings, Bradford BD1
1HX, UK. 3 Change Grow Live, London, UK. 4 Glasgow Alcohol & Drug Recovery
Services, NHS Greater Glasgow & Clyde, Glasgow, Scotland, UK. 5 We Are
With You, London, UK. 6 Department of Sociology, Manchester Metropolitan
University, 4 Rosamund Street West, Manchester M15 6LL, UK. 7 Department
of Endocrinology, Diabetes & Metabolism, Newcastle-Upon-Tyne Hospitals
NHS Foundation Trust & Translational & Clinical Research Institute, University
of Newcastle-Upon-Tyne, Newcastle, UK.
Received: 18 July 2023 Accepted: 20 October 2023
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onlineservice@springernature.com</p>TV REPAIR PARTShttp://www.blogger.com/profile/03272638773780329095noreply@blogger.com0tag:blogger.com,1999:blog-3850502767250139870.post-74307849046868609712024-03-27T07:00:00.000-07:002024-03-27T07:00:04.960-07:00Anabolic steroids ultimate research guide<p> Anabolic Steroids
Ultimate Research Guide
Vol. 1
DISCLAIMER: Information contained within the Ultimate Research
Guide is for entertainment purposes only. Although medical journals,
textbooks, scientific articles, and information gathered from thousands
of athletes were used to compile this book, we do not advise anyone to
apply this information on themselves or other people. This information
is strictly to show how others have used these drugs and should not be
misinterpreted as medical advice. Neither the authors nor the
publisher assumes any liability for the information presented in this
book. We urge readers to consult with a physician and educate
themselves on the laws of these drugs before using or obtaining them.
Published by:
Anabolic Information, LLC
7 Marina Dr.
Montgomery, TX 77356
www.AnabolicBooks.com
ISBN: 1-59975-100-3
Copyright© 2005 Anabolic Information, LLC
No portion may be reproduced without the express written consent of the author.
Table of Contents
Preface & Dedication 7
Chapter 1 - Why Anabolic Steroids 8
Chapter 2 - How to read this book 10
Chapter 3 - An Introduction to your endocrine system 12
Chapter 4 - How anabolic steroids work 16
Chapter 5 - The game as it’s played 25
Chapter 6 - Injection techniques 31
Chapter 7 - Design your own cycles & Samples 34
Chapter 8 - Remove steroids in 5 days 39
Chapter 9 - Drug profiles 42
Testosterone Derived Steroids 46
Anabolicum vaster 48
Andriol 51
Androderm & Androgel 55
Andropen 275 59
Deposterona 62
Dianabol 64
Drive 68
Equilon 100 70
Equipoise 72
Halotestin 76
Megagrisevit – Mono 80
Methandriol 83
Methyltestosterone 87
Myagen 90
Omnadren 92
Oral Turinabol 96
Spectriol 104
Sten 106
Sustanon 250 109
Test 400 112
Testolent 113
Testosterone Cyclohexylpropionate 115
Testosterone Cypionate 118
Testosterone Enanthate 122
Testosterone Propionate 126
Testosterone Suspension 130
Testoviron 133
19-Nortestosterone Derived Steroids 137
Anabolic DN 138
Anadur 140
Cheque Drops 143
Deca Durabolin 146
Diandrol 151
Durabolan 153
Dynabolan 156
Laurabolan 159
Nandrolone & Methandriol Blend 162
Nilevar 166
Methyltrienolone 170
Orabolin 173
Parabolan 175
Sanabolicum 179
Trenbolone Acetate 182
Trenbolone Enanthate 187
Tri-Trenabol 189
Dihydrotestosterone Derived Steroids 192
Anadrol 193
Anavar 198
Andractim 203
Masteron 205
Masteron Enanthate 209
Miotolan 211
Primobolan 214
Proviron 218
Winstrol 221
Chapter 10 – Ancillary Compounds 224
Arimidex 232
Aromasin 234
Clomid 237
Cialis 239
Cyclofenil 240
EPO 241
Esiclene 243
Falsodex 245
Fareston 246
Femara 247
Finasteride 249
HCG 252
Ketotifen 255
Kynoselen 256
Nolvadex 258
PSGAG 260
Teslac 261
Chapter 11 - Sympathomimetics (Fat Burners) 264
Albuterol 271
Caffine 272
Cimaterol 273
Clenbuterol 275
DNP 282
Ephedrine 287
Yohimbine 288
Chapter 12 - Thyroid Drugs 289
Cytomel 292
Synthroid 295
Triacana 296
Chapter 13 - HGH/IGF/Insulin 300
Human Growth Hormone 301
IGF-1 306
Insulin 310
Chapter 14 – Nutrition 316
Chapter 15 – Legal Interview 326
All Drug Profiles in Alphabetical Order
Albuterol 271
Anabolic DN 138
Anabolicum vaster 48
Anadrol 193
Anadur 140
Anavar 198
Andractim 203
Andriol 51
Androderm & Androgel 55
Andropen 275 59
Arimidex 232
Aromasin 234
Caffine 272
Cheque Drops 143
Cialis 239
Cimaterol 273
Clenbuterol 275
Clomid 237
Cyclofenil 240
Cytomel 292
Deca Durabolin 146
Deposterona 62
Dianabol 64
Diandrol 151
DNP 282
Drive 68
Durabolan 153
Dynabolan 156
Ephedrine 287
EPO 241
Equilon 100 70
Equipoise 72
Esiclene 243
Falsodex 245
Fareston 246
Femara 247
Finasteride 249
Halotestin 76
HCG 252
Human Growth Hormone 301
IGF-1 306
Insulin 310
Ketotifen 255
Kynoselen 256
Laurabolan 159
Masteron 205
Masteron Enanthate 209
Megagrisevit – Mono 80
Methandriol 83
Methyltestosterone 87
Methyltrienolone 170
Miotolan 211
Myagen 90
Nandrolone & Methandriol Blend 162
Nilevar 166
Nolvadex 258
Omnadren 92
Orabolin 173
Oral Turinabol 96
Parabolan 175
Primobolan 214
Proviron 218
PSGAG 260
Sanabolicum 179
Spectriol 104
Sten 106
Sustanon 250 109
Synthroid 295
Teslac 261
Test 400 112
Testolent 113
Testosterone Cyclohexylpropionate 115
Testosterone Cypionate 118
Testosterone Enanthate 122
Testosterone Propionate 126
Testosterone Suspension 130
Testoviron 133
Trenbolone Acetate 182
Trenbolone Enanthate 209
Triacana 296
Tri-Trenabol 189
Winstrol 221
Yohimbine 288
Steroid Listings by Generic Name 336
Steroid Listings by Trade Name 363
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
Preface & Dedication
“If I have seen further than other men, it is because I’ve stood on the
shoulders of giants.”
~Albert Einstein
“Oh no—another steroid book! We don’t need another one of those!” That’s
probably what a lot of people were thinking when this book hit the shelves. It’s what
I was thinking every time another book on Anabolic/Androgenic Steroids hit the
marketplace. And for the most part, I was correct!
So what makes this one different? For starters, it’s not written by a “Guru”; I’m not
trying to sell you on my personality. It’s not written by an “Oracle”; I’m not trying to
give you tons of mystical information, without explanation. I’ve spent a good portion
of my life in pursuit of knowledge…and, to some degree I suppose I have been
successful. I simply wish to share some of that knowledge with you, if you’ll let me.
This book has been a collaborative effort, with writers and researchers from
Steroid.com helping out in many ways. Some of the profiles herein have been
partially researched or written by them, and not entirely by me. All of them have
been exhaustively checked and double-checked in an effort to bring you the highest
standard of work. I have also been greatly helped by the staff and members of
various anabolic steroid discussion boards around the internet, but none more so
than the ones I have cultivated personal and in some cases, intimate, relationships
with the staff. To many of them I owe a debt I can never hope to repay.
I would also be remiss in my duties as an author if I didn’t inform you that much of
the groundwork for this project was predicated by those who came before me in the
field. In particular, I am deeply indebted to Dan Duchaine for his pioneering work in
the field of Anabolics as we know it today, as well as to Karl Hoffman for elevating
the quality of current Anabolic Steroid paradigms to levels heretofore unthinkable.
Both of them will be missed by many, myself especially.
I am of course indebted deeply to Brian Clapp, who believed in me enough to
produce and publish the work you now hold in your hands.
I am going to reserve my final dedication here for something a bit different; I had
originally thought to make a dedication at this point to my family, and friends who
are so dear to me, that I could scarcely imagine completing a project of this
magnitude without their continued love and friendship. That final dedication,
however, I am going to reserve, as disused, and leave unstated. The simple fact of
the matter is that dedicating a book to them would be redundant, as I endeavor each
day to live a life which will make them proud, and in some way justify the friendship
and love they’ve shown me for the past twenty seven years…this book, therefore,
will not be dedicated to those who I have already dedicated my entire life to. At
best, it can be seen as only a small part of a life that is hopefully lived in such a way
as to thank them for being a part of it. It is only as a result of their friendship and
love that, were I given a chance to live my life over again, exactly the same way, I
would gladly take it.
7
Chapter 1
Why Anabolic Steroids?
“There comes a time in a man’s life where, if there are no windows or
doors, he must walk through a wall.”
~Bernard Malamud
If you’re like me, you learned about the Declaration of Independence when you were
in grade school—if not, that’s the thing that says, “All men are created equal.” You
then went out into the schoolyard for recess, and for some reason, maybe you
couldn’t run as fast as some of your classmates. Perhaps you couldn’t jump as high,
or throw a ball as far. All men created equal? Bah! What a load of garbage!
Let’s talk a bit about genetics, ok?
There have been a ton of studies on genetics, and basically, current research from
the Bouchard Labs strongly suggests that up to 50% of the variance in athletic
performance, potential, and adaptation to training is genetic. In other areas such as
height, the genetic contribution to inter-individual variance is around 80%. Basically,
the Bouchards have suggested that athletes are born, and if they aren’t, then they
are certainly born with more potential to react favorably to training. How about
gaining or losing weight? Are you always struggling to gain weight? Are you always
struggling to lose it? Bouchard's work in this area states that there is familial
aggregation of Body-Mass-Index (BM) and other body composition characteristics
such as body fat percentage, metabolism of adipose (fat) tissue, etc. Bouchard’s
work claims that genetic heritability is responsible for between 25 to 40% of these
traits.
Wanna be even more depressed? Check out your fingers and which is longer, the
index finger or the ring finger? The ring finger in males is usually longer than the
index finger; however, the fingers are about the same length in females. This
suggests the role of testosterone in early pre-childhood development (Manning,
2000). The more testosterone you produced as a fetus the longer your ring finger
got, so the smaller the index/ring finger ratio.
Who cares? Men with smaller finger ratios are considerably better athletes. NO! I’m
not kidding. They are more likely to become athletes and to reach much higher
levels in most sports (Manning & Taylor, 2001). Professional football (soccer)
players tend to have lower finger ratios than non-athletes. Starting players have
lower ratios than reserve or youth team players. Footballers who have represented
their country have lower finger ratios than those who haven’t. Men with lower finger
ratios even run faster 800 m and 1500 m races! And that’s all clearly genetics.
Remember that kid in the schoolyard who was taller than you, and was always
picked first for basketball games? Clearly he has the genetics to be taller than you.
But wait, it gets worse: if he has the right genetics, you can train just as hard as
8
him, but he’ll receive a more favorable response from it! Add in some favorable
muscle tie-ins, connective tissues, the right muscle belly length, and some decent
fast twitch fiber recruitment, and that kid will pretty much beat you at any sport.
And those are all simply genetic traits. You can work as hard as him and lose. Even
worse, you can work harder than him and still lose.
Ok, so if you are one of the genetic elite, then that’s all great for you. If you were
the kid who was always picked first for dodgeball in gym class then that’s all well and
good for you. If you are like me, however, one of the genetically average, keep
reading because there may be a solution.
When testing for anabolic steroids wasn’t done in certain elite level track events, (a
brief period in the 80’s) the results for the women’s events began to catch up with
the men’s results. When testing was resumed, it began to fall off and the gap began
to widen once again. Women simply don’t have the same hormones, fast twitch
muscle make up and overall structure that make men more successful in those
events. And, being a woman is certainly genetic (my apologies to Ru Paul). Since
they were all elite level athletes, it can safely be assumed that their training and diet
regimens were optimal. So, how did women begin to bridge that gap? Steroids and
other performance enhancing drugs, it has been speculated, were the “X-Factor” in
helping women track athletes catch up with their male counterparts.
Take away the genetic advantage, and what will you have left to decide who wins
athletic events? You will have training, diet, and most importantly, the will to
succeed. I’d much rather see athletes compete on an even genetic ground (even if it
is “evened up” by performance enhancing drugs); a ground where the deciding factor
will be heart and guts, not genetics. So, this is my effort to level the playing field and
to show you how to “supplement” your genetics. Performance enhancing drugs
won’t win athletic events for someone, but they’ll help to remove the inequality and
accidental nature of a genetic disadvantage. What will be left if we take genetics out
of the picture?
Determination.
Heart.
Guts.
And isn’t that what should decide athletic contests?
9
Chapter 2
How to read this book
I assume you already know how to read (you’re reading right now, right?) and I
want you to consider reading this book in a different way than you would read
something by Dan Brown (the “DaVinci Code” guy) or even by William Llewellyn (The
“Anabolics” guy). I will assume that you have some kind of athletic goals in your
life; they may be related to bodybuilding, athletics, looking good at the beach, or
whatever. I want you to take a sec and consider what they are specifically. Getting
ripped is not a specific goal, but gaining 10lbs of muscle and losing 5lbs of fat is a
goal. Presumably, you’ve bought this book in an effort to learn how to tweak your
body chemistry here or there and to help you achieve your goals.
I’ve written this book with you in mind. All of the information in this book is the
most up to date information I could find in medical libraries, online, and in clinical
studies. Where there is information “missing” on a particular compound, it is
generally unable to be found. Many of the steroids mentioned here in this book (Oral
Turinabol for example) have been totally discontinued by pharmaceutical companies
for decades. As a result, the current Merck Manual doesn’t even list it as existing. It
is, therefore, very difficult to find information on a product that the largest
pharmaceutical companies in the world and every doctor and scientist you speak to
assures you doesn’t exist anymore. For another example, try finding out information
on the Polish company that makes Omnadren without speaking Polish, or knowing
that the original company who made it has changed their name. Try finding
information on Furazabol, which is made exclusively by a Japanese company, without
speaking Japanese. Ever try researching Parabolan (made by the French company
“Negma”) without being able to read or speak that language? Sorry if I’m being
redundant, but I want to assure you, my reader, that I have gone to every possible
length to make this the most complete book on Anabolics available, without learning
another language. I’ve also chosen to include a lot of “redundant” information in
profiles, which you will find in several of them, as well as elsewhere in the book.
Why? Because I want you to be able to read one profile (if you should so choose)
and walk away with a complete understanding of that drug. If that makes parts of
the next profile you read seem redundant, then so be it. You will not find a more
complete steroid book anywhere, even if you should only choose to read bits and
pieces.
As well as the information I have found in medical libraries and such, I’ve also
spoken with literally thousands of bodybuilders and athletes, both in person and
online, via e-mails and anabolic message boards. I have been fortunate enough to
be involved with several very good message boards, the largest being Steroid.com,
which is actually the most visited anabolics website in the world having 3million or so
hits per year. Through that site, I was able to speak with many athletes and
bodybuilders who I otherwise wouldn’t have had access to. They have shared their
stories and experiences with me, and that has all been factored into this book.
This book is made (of course) to be read from start to finish; by doing so you will
gain the most complete understanding of the subject matter at hand. But, if you
10
choose to read only bits and pieces of it, then you will have the most thorough
understanding of those bits and pieces.
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
11
Chapter 3
An Introduction to your Endocrine System
If you’re anything like me, you’ve already read half of the steroid profiles and picked
out a cycle from the sample cycles page. You’ve probably avoided reading this
chapter for as long as possible. In my case, when I bought my first “big” steroid
book, that’s what I did. I put off reading this section for, I dunno, five years?
Well, maybe not that long, but to be honest, this usually isn’t the most interesting
part of your typical steroid book. I will assure you that this isn’t your typical steroid
book, and that this chapter won’t put you to sleep. I’m not trying to give you a
thirty-page explanation of how every little thing in your body works, but rather, a
quick overview of the hormones responsible for muscle growth, and their functions in
your body. This’ll help you understand how anabolic steroids function to assist you
in building muscle and strength.
So, our deal will be that I’ll make it quick, if you promise to read this entire chapter.
I own several really big books on this subject, and I have no desire to bore you with
their entire content or to have to re-read them to do so. Ok, let’s get to it.
Your endocrine system is a system (duh) of cells, tissue, organs, and parts of the
nervous system which all act together within your body to maintain homeostasis (the
status quo). What we’re gonna do is figure out how to tweak this system to grow
some more muscle and gain some more strength.
Hormones: A hormone is simply a substance secreted by a cell that has an effect on
another cell. They can stimulate changes in target cells even when they are only
present in miniscule amounts.
Testosterone: This is the primary male sex hormone. Settle in, this is going to be a
long explanation, but possibly the most important one. Testosterone is
manufactured in the Leydigs cells in the testes, at about 2.5-11mgs/day for the
average male. You know those dudes with full beards in Junior High School? Yeah,
they are probably producing somewhere around the upper limit. The testosterone
molecule floats around in your body eliciting various changes including the building
of muscle, and development of male sexual characteristics. Remember those
receptors I told you about earlier? Yeah, well testosterone “parks” in those spaces
and delivers it’s message (“Build more muscle”), then “unparks” and drives around
the lot looking for another spot to park in and deliver it’s message. In normal males
2% of testosterone is unbound to protein (free), 54% is bound to albumin and other
proteins, and 44% is bound to sex hormone-binding globulin (SHBG).
Prolactin: This is a protein that promotes milk production in the female body, and
even worse, if you screw up, in the male body. Prolactin causes a decrease in
Luteinizing Hormone, and this lowers testosterone (see below).
Follicle Stimulating Hormone: This hormone (commonly referred to as FSH) is a
gonadotropin, which is responsible for egg-cell-containing follicles in the female
ovaries, and it also stimulates follicular cells to secrete estrogen. In males, it helps
12
stimulate the production of sperm cells in the testes during puberty. It also may tell
the testes to secrete testosterone, but certainly influences the number of leydigs
cells, which we secrete testosterone. . Finally, FSH stimulates the production of
Androgen Binding Protein in the Sertoli cells.
Luteinizing Hormone: This stuff (usually called LH, in shorthand) promotes the
secretion of sex hormones. We’re hoping to keep it high (or not let it get too low) so
it keeps telling out testes to secrete testosterone. Both LH as well as testosterone is
secreted in pulses between eight and fourteen times per day, testosterone being
preceded by LH by approximately an hour. Testosterone is, of course, controlled via
a negative feedback loop, thus a higher level of testosterone in your body causes a
decrease in LH.
Estrogen: This is the primary female sexual hormone. Men don’t want much of it
floating around, as it is responsible for some nasty side effects like water retention,
gynocomastia, acne, etc. It also may aid in growth by helping production of IGF and
GH and may even enhance immune function. It can also increase the amount of
androgen receptors in the body. We certainly want some of it around, but not too
much, as it can also lower testosterone levels.
Steroids: These are compounds whose molecules contain fairly complex rings of
Carbon and Hydrogen atoms. Steroid hormones include (but are not limited to)
testosterone and estrogen, and we will be primarily concerned with those two
although we will examine many other hormones. Sometimes we use the term
“steroid” to mean anabolic steroid, which is only one possible type. Steroid hormones
(like testosterone) are soluble in the lipids that make up cell walls. This means they
can get into a cell and mess around with the receptors in the nucleus, which is
exactly what we want.
Receptor: This is a thing in the cell that is basically like a parking spot. When a
steroid hormone comes in, it’s like parking a car in that spot. The steroid hormone
then tells the cell to do something. If the hormone is testosterone, it may tell the
cell to “build more muscle!” If the hormone is estrogen, it may say, “Watch
Desperate Housewives!” Well, not really, but you get the idea.
Androgen Receptor: This is the parking spot “reserved” for steroids like
testosterone and such, in other words, androgens.
Prostaglandins: Some of these regulate cellular responses to hormones and
stimulate the secretion of a variety of hormones.
Negative Feedback System (or loop): This is the system by which your body
recognizes an abundance of a particular hormone and consequently stops producing
it. In simple terms, if you are injecting testosterone, your body will sense this and
stop producing its own.
Pituitary Gland: The anterior lobe of this secretes a variety of hormones such as
growth hormone, thyroid- stimulating hormone, prolactin, follicle-stimulating
hormone, and luteinizing hormone. You want to keep this thing healthy and happy.
Growth Hormone: Growth Hormone (GH) is a protein that stimulates your body’s
cells to undergo more rapid cell division. It enhances the movement of amino acids
through cell membranes and causes an increase in the rate in which they convert
13
molecules to proteins and decrease the rate they use carbohydrates and increase the
rate they use fats. It is secreted in rhythmic pulses, especially while you’re asleep
and has an important anabolic effect on the body.
Growth Hormone-Releasing Hormone: This stuff is the hormone that releases
growth hormone. Clever name, huh? Whenever it’s released, a pulse of GH is also
released.
Insulin: Insulin is a protein secreted by the pancreas that acts on the liver to
stimulate the formation of glycogen from glucose and inhibits the conversion of non
carbohydrates into glucose.
Insulin-Like Growth Factor: Insulin-like growth factor is released from the liver in
response to GH. It has an important anabolic effect on the body.
Glucagon: This is a hormone that is produced in the pancreas and regulates blood
sugar levels. Unlike insulin, glucagon is released when blood sugar levels are low. It
causes the release of glucose from glycogen.
Thryoid Stimulating Hormone: This is a protein bound to a carbohydrate. Yum!
No…just kidding…it is a protein bound to a carbohydrate, but what it does is control
the secretion of hormones from the thyroid gland.
Hypothalamus: This releases gonadotropin- releasing hormone, and also controls
most secretions of the pituitary gland, which leads me to the. ...
Pituitary Gland: This is where the Philosopher Rene’ Descartes thought the soul
lived. Actually, it’s much more important because it controls the secretion of LH and
FSH, and thus, the production of testosterone! It also controls secretion of GH and
thyroid stimulating hormone.
Hypothalamic-Pituitary-Testicular-Axis: This is usually called the HPTA, and as
you can guess, it basically regulates all of the hormones that stimulate the
production of testosterone as well as GH and other goodies. Needless to say,
keeping your HPTA in good working order is very important.
Aromatization: This is the process by which testosterone converts to estrogen, via
the aromatase enzyme. This occurs in various tissues, such as skeletal muscle and
adipose tissues. Also, you’ll experience less of this if you have less adipose tissue
(less fat on a cycle means fewer sides, believe it or not).
Dihydrotestosterone: This stuff, also called DHT, is made from testosterone in
your body via interaction with the enzyme 5-alpha-reductase, which adds 2
hydrogen atoms to testosterone. It has a variety of effects in the human body, and
is responsible for certain unwanted side effects such as hair loss. DHT interacts
strongly with the central nervous system, and has both anabolic as well as
androgenic effects.
14
Ok, so let’s take a look at all of that stuff in action:
That was by no means a comprehensive list of the hormones in your body, or their
functions, and of course it’s not everything that each and every hormone does or can
do under special circumstances. But it’s good enough for our purposes here, and
knowing what those hormones do will help you know what the various steroids we’re
going to discuss will do in your body. That doesn’t mean you can’t read this book
out of order, or read the profiles first. Actually, quite the contrary, I’ve written this
book so that you can read just one anabolic steroid profile (if you want) and walk
away with a complete knowledge of how it works and what it does. Actually, while I
prefer you read the whole book, you can read it out of order, mix and match
chapters, etc. and still walk away with a wealth of knowledge about every single item
you read. But at least now you have a basic understanding (actually, I prefer to call
it a “working understanding”) of the primary hormones we’ll be discussing in this
book. And now that you know whats going on in your body, we can talk about what
steroids are and how they exert their effects.
15
Chapter 4
How Anabolic Steroids Work
Anabolic steroids are drugs that resemble androgenic hormones like testosterone, or
derivations thereof. The defining characteristic, structurally, of all steroids is their
four-ring structure. Your body produces various steroids from Cholesterol (yes, the
icky stuff doctors tell you to avoid), which undergoes modifications and can
eventually become testosterone (if you’re lucky). This chapter will help you
understand what they do in your body, how they exert their effects, and how they
are metabolized.
Ok, so remember that four-ring structure I was talking about? This is called the
Steran Nucleus, and for our purposes there are four rings (A, B, C, and D), and 19
positions on the structure:
C
16
Figure A represents your basic testosterone; Figure B shows you which rings are A,
B, C, D respectively; and Figure C shows you the 19 positions on the rings. Why is
this important? Well, you can add carbon bonds, add beta groups, etc, and that
produces different steroids. Typically, the A-ring and D-ring are modified to produce
different steroids (with different effects). This is because the A and D rings generally
undergo the most drastic metabolation in the body, so modifying them produces
more bang for the buck, generally speaking. The B-Ring metabolism is most
pronounced when A-ring metabolism is in some way hampered. The changes the B
ring typically undergoe are 6b-hydroxylation and 6, 7-dehydrogenation. These
changes are, in fact, not very drastic. C-ring metabolism is even more modest, being
a simple 12-hydroxylation. If you didn’t catch those last few parts, don’t worry,
because they aren’t super-important. Let’s talk about A and D ring metabolism for a
second, ok? These are where we need to focus our energies, because understanding
them is very important, while B and C ring metabolism is generally very limited, and
won’t really be a concern to us at all, in any applicable context. First, A-ring
metabolism…
In the A-ring we see 5alpha and 5beta reduction taking place:
And of course, 5alpha Reduction (5a-Reduction) is what turns testosterone into DHT.
This is the initial step in metabolism of testosterone and many of its analogues, and
basically just reduces the C4, 5 double bond—that’s the little line on the bottom of
the first ring that’s missing in the lower left version of that pic above, where the
hydrogen (“H”) has “appeared”. As you can see, 5beta-reduction is very similar,
though not of prime concern to us here. After this reduction, typically the 3-keto
group is transformed. Stability and instability of the 3-keto group is important to
androgen binding, and the more stable the 3-keto group is, the more avidly a
compound can bind to the Androgen Receptor and/or increase anabolic/androgenic
activity (even doing so, in certain cases, independently of each other). Certain
modifications to steroids can enhance the stability of the 3-keto group, such as 2
methylation or adding a 2-hydroxymethelyne group (the first modification is seen
with Masteron and the second with Anadrol). On the other hand, Ethylestrenol lacks
a 3-keto group totally, and is probably the weakest steroid available. Let’s take a
look at the removal of the 3-keto group:
17
Of course, the above example focused on testosterone, and if you add a double bond
between the one and two carbon atoms of testosterone, you’ve made Boldenone
(Equipoise). As you can see here, Boldenone is metabolized slightly differently since
the 1-2 double bonds slows metabolism (hepatic breakdown, aromatization, etc…)
down:
Add a 17-alpha-methyl group to that Boldenone we just spoke of, and you have
Methandrostenolone (D-bol), which is broken down similarly, although it is orally
active in the body due to the 17a-methly group:
(Boldenone, or Eq-No ester shown)
(Methandrostenolone or Dianabol)
(Note that Dianabol and Equipoise are the same EXACT compound with exception to
the methylation you see at the 17th position for the Dianabol).
18
There are, of course, other actions that happen (or simply can happen) in the A
Ring, but we need not concern ourselves with them here. It is suffice to say that
they are not of interest to us, again, generally speaking.
Now, let’s finally look at D-Ring metabolism…
The D-ring (the weird little one on the end with fewer sides than the other rings) is
metabolized into testosterone’s main metabolites. This occurs by oxidation of 17b
hydroxy groups into 17keto steroids, which are shown less intricately in the first
chart in this chapter. In some cases, they can even be converted back to the
original configuration by the same enzyme (17b-HDS).
Hydroxylation can also occur at other positions, as can epemirization, or oxidation,
within the D-ring. And remember, the D-ring is where we can methylation them to
survive oral ingestion.
All of that was the first phase of anabolic steroid metabolism, which determines the
primary effects they will have in the body. Phase II metabolism has more to do with
metabolites, their degradation, and the eventual elimination of them and the steroid
from the body, and as such is beyond the scope of our discussion here -well…. really,
its just beyond the scope of our interest, more or less, because it’s not going to help
us understand the anabolic actions of steroids any better. The preceding information
should help you later in this book, when I mention that this (or that) steroid has a
particular modification to help it do something (or other). I know that once I started
understanding a little of what I am presenting here to you, I found it a lot easier to
comprehend what was going on when I looked at a steran nucleus or chemical name
for a particular steroid.
19
Synthetic anabolic steroids are based on the principal male hormone testosterone,
modified in one of three ways:
a. Alkylation of the 17-carbon (makes them survive oral ingestion)
b. Esterification of the 17-OH group (alters active life and half life)
c.
Modification of the steroid nucleus (changes their properties)
Pretty simple huh? But despite the number of synthetic AAS that have been
developed by these little modifications here and there, their modes of action are still
poorly understood.
As you know, male hormones, primarily testosterone, are responsible for the
developmental changes that occur in boys during puberty and later in adolescence.
Male hormones have both androgenic and anabolic effects. Androgenic effects are
changes in primary and secondary sexual characteristics, like enlargement of the
penis and testes, voice changes, hair growth on the face, increased nervous system
efficiency, and increased aggressiveness. The anabolic effects of androgens (again,
like testosterone) include increasing and limiting muscle protein synthesis by
increasing transport of amino acid across cell membranes. It is also an anti-catabolic
and inhibits cortisol by competing for receptor sites, as well as reducing cortisol
secretion and the signals, which precede cortisol secretion. In addition to these
anabolic effects, Testosterone increases the secretion of the other anabolic hormones
in the “super family”, such as growth hormone and Insulin-Like Growth Factors from
the liver, and finally, it produces an enhanced rate of erythropoietin synthesis. All of
these effects are, of course beneficial to athletes, and explain how steroids exert
their performance enhancing effects.
These effects are mediated, at least partially by stimulation of receptor molecules in
muscle cells (which we generally call androgen receptors), which activate specific
genes to produce proteins. Binding affinity to the androgen receptor has been used
to explain the differences in potencies and effects of the natural and synthetic
androgens we talk about, but that isn’t the full story. There are, of course, other
effects that steroids exert, and we call those “non-receptor-mediated” effects. These
are effects that happen indirectly, and not as a result of androgen receptor
stimulation. Stimulation of the androgen receptor produces both anabolic and anti
catabolic effects, such as the retention of more nitrogen and the reduction of cortisol,
respectively. Remember, Cortisol causes muscle breakdown.
Sounds great, right? It’s everything we want and more! It’s not all roses, however,
because Anabolic steroid use decreases testosterone secretion. This happens
because your body operates on a negative-feedback-loop in regards to testosterone.
This means we’re going to attempt a balancing act regarding our natural hormones
and the ones we put into our body. If you read this book carefully, you’ll learn how
to use (or simply research) anabolic steroids to produce a heightened state of
athletic ability, strength, speed, and of course, increased muscle mass. Then you’ll
learn how to stop using steroids and not lose everything you’ve gained. Those are,
at least, my humble goals for you.
So let’s get back to the first thing I told you about, which is how steroids are made.
As you saw, simple modifications to the four-ring steran nucleus of testosterone can
produce major changes in the hormone. From those simple changes to testosterone,
scientists have identified the other two major families all anabolic/androgenic
20
steroids are derived from: 19-nor-Testosterone (sometimes called 19-nor’s) and
dihydroTestosterone (called DHT).
19-nor-Testosterone is simply testosterone that lacks a carbon atom in the 19th
position, and Dihydrotestosterone is Testosterone that has had 2 hydrogen atoms
added to it.
Testosterone
Dihydrotestosterone
19-nor-Testosterone
In general, 19-nor derived steroids exhibit a high anabolic effect and a low anabolic
effect with not much aromatization, while DHT-derived steroids usually have a very
nice balance of androgenic and anabolic effects and not much aromatization.
Of course, there are also other things you can do to steroids like methylate them
(this makes them able to survive oral administration) or add an ester to them (this is
a large fatty chain on a steroid that your body needs to work to break down, thus
increasing the active life of the steroid). Adding an ester to a product doesn’t change
its anabolic: androgenic ratio, but methylating it may. Esters do not alter the
anabolic or androgenic properties because an ester is simply a chain composed
primarily of carbon and hydrogen atoms, typically attached to the base steroid
hormone at the 17th carbon position (called the beta position). Attaching an ester to
a base compound slows the release of the base steroid from the site of injection.
Slowing the release of the base steroid is a great benefit to medicine, especially
hormone replacement therapy (HRT) because suspended or free testosterone (or
other steroid hormones) would only remain active in the body for a very short period
of time. This is basically what is seen with testosterone suspension or Winstrol depot.
If you are on HRT, you could take a shot of Testosterone Cypionate (testosterone
with a long ester added) once a week, as opposed to taking testosterone suspension
once or twice a day. Adding an ester also temporarily deactivates the steroid
molecule. With an ester chain blocking the 17th beta position, binding to the
21
androgen receptor is not possible, so the steroid is inactive. Now, in order for the
base compound to become active, the ester must first be removed. This occurs once
the compound has filtered into blood circulation, where your esterase enzymes
cleave off the ester. This restores the necessary hydroxyl (OH) group at the 17th
beta position, which enables the drug to attach to the receptor. Now the steroid is
free to do all the good stuff we want it to do. This is why people often say, “test is
test,” regardless of the ester; regardless of the ester, anabolic and androgenic
properties of the base compound retain their respective integrity.
You may, at this point be asking yourself how these anabolic to androgenic ratio’s
are arrived at. Well, this is kind of weird, but basically, male rats were given a dose
of testosterone, sacrificed (killed to you and me), and then had an untrained muscle
(the levator ani), and a part of the prostate (the ventral prostate) weighed. Those
weights were given a score of 100 each (because 100 is an easy number to work
with). When you want to know the anabolic: androgenic ratio of a new steroid, you
simply administer it to a group of rodents with the same dose of testosterone used in
the original group of rats I just told you about. You then weigh the levator ani and
ventral prostate. The weights that are relative to testosterone (and it’s 100 score)
are the anabolic: androgenic ratio of the new steroid. Of course, that’s not 100%
relevant or applicable to humans.
By tweaking and refining steroids, scientists were able to create some very
interesting compounds that have some profoundly beneficial effects to us as
athletes. And now you know (roughly) how it’s done, and how steroids work.
I think it would be prudent to take a second to show you how they are named so
that you can tie that in with some of the effects we’ve just discussed and to later
(further on in the book) understand the profiles more fully. A lot of what we know
about a steroid, or at least part of that, is "coded" in its name [the part written like
this at the start of my profiles]. If you look in the name of a steroid, and it's
something like this:
2-oxy androstane 17b-ol 2-one
(the chemical name for Anavar)
See the bold part? That means it's a DHT-derivative, with regards to its base carbon
structure.
If it said:
norandrostene 17b-ol 3-one
(Nandrolone)
Then you know the norandrostene part means it's derived from Nandrolone (likewise,
generally, if you see 19-nor or something like that)
And finally, if you see the words testosterone—duh—or androstene in the name of
the structure, then you know it's derived from testosterone.
Therefore, we have a steroid like Boldenone (Eq) again and we can figure out a few
things about it.
Look at the name:
22
BOLDENONE -or-
(17b-ol 1, 4-androstadiene-3-one,) -or-
Equipoise
And what we see is that it starts with "BOL" and the chemical name begins with 17b
ol, hence, "BOL."
See what I'm talking about?
17b-ol 1,4-androstadiene-3-one
Next we see "DEN" (because the word is Bol-Den-One if you break it apart). Looking
in the middle of Boldenone's chemical name we find something similar:
17b-ol 1,4-androstadiene, 3-one
And finally we have "ONE" at the end of Boldenone, and clearly, the chemical name
also has "One" at the very end:
17b-ol 1,4-androstadiene-3-one
So, what does all of this tell us? Well, since it starts with 17b-ol we know that its
got something going on at the 17beta position, which is an "ol" and is a Hydroxy
(oxygen and hydrogen) group. This is where our estrification (added ester) at the
17-beta-position goes. Now, we also have the middle part, androstadiene, which
indicates that this steroid has a double carbon bond on the base of a testosterone's
steran nucleus or a di- bond on androstene. In this particular case, the double
carbon bond at this position slows aromatization. Eq, as we know, aromatizes to a
far lesser degree than testosterone because of this modification. Remember from the
beginning of my explanation on all of this that androstene indicates testosterone as a
base
structure.
Add it all up and we have Boldenone. This is called Equipoise and its name comes
from the Latin root of the word Equine, and as you already know, Equipoise (Eq) was
developed to give to horses.
Now, if we look at Eq (boldenone) and compare it to Dianabol,
(methandrostenolone), we can see how similar they are.
Equipoise:
(17b-ol 1,4-androstadiene-3-one )
And now Dianabol (difference noted in black/bold):
(17a-methyl-17b-ol 1,4-androstadiene-3-one )
As you can see, the only difference between Dianabol and Eq is the 17a-Methyl
group, which is why Dianabol is called a Methylated steroid; it has been 17-alpha
alkylated to survive oral ingestion.
23
And this, my friends, should tell us a few things. We can tell a lot from just the
names I've used in my profiles. When you compare the minor difference in names
with the major differences in effects concerning Dianabol vs. Eq) we discover that
names aren't everything.
Now, let’s talk about the anabolic: androgenic ratio's...
To determine that ratio, testosterone was given to male winstar mice, and then they
were sacrificed, (killed). Their levator ani (a leg muscle which was immobilized
during the 21 days) and their ventral prostate were weighed.
The weight of that untrained muscle is the anabolic rating for testosterone, and the
weight of the ventral prostate is the androgenic rating. Now, other steroids are
administered to these rodents, and the weight of their levator ani and ventral
prostate, relative to the weights of those rodents from the testosterone group, are
that steroid's anabolic: androgenic rating. Testosterone, therefore, has a rating of
100:100, while Trenbolone has a rating of 500:500. This is the same ratio and is
relative to itself, but it is 5 xs as anabolic as testosterone and 5 xs as anabolic.
Again, all of the information in this chapter isn't a perfect way to give us the exact
effects a given compound will have in our bodies. However, its a start and it will
allow you to have an easier time assimilating all of the information contained in the
profiles.
24
Chapter 5
The game as it’s played…
(The state of the Anabolic Steroid Game today)
Let’s have a talk about anabolic steroids as they are bought and sold today. A
couple of decades ago there was a raging debate between Human Grade vs.
Veterinary Grade steroids. Now there is a third contender in the ring, and it’s a free
for all! That third contender is the UnderGround Lab (UGL for short). Let’s talk
about all three of these very worthy contenders and then I’ll give you my thoughts
on each. I will also tell you how I choose to spend my hard earned money, given
these choices.
The easiest of these three to identify is Human Grade gear. Major pharmaceutical
companies like Organon and Upjohn for use by human beings produce these.
Simple, huh?
The second category is veterinary grade steroids. This is a touchy category in recent
years and is increasingly a grey area. See, generally, you would assume
“veterinary” meant for animals, right? And two decades ago, you would have been
correct. If you purchased a bottle of Ganabol, it was certainly intended to end up
being shot into some horse’s butt somewhere or another. Generally, animal steroids
came as low(er) dosed preparations, which was good because, generally, animals
require much lower doses than Mr. Olympia Competitors. Then Ttokkyo came out
with a 300mg/ml 10cc bottle of Nandrolone Decanoate with a huge mastiff (dog) on
the bottle with the slogan “Keep your pets healthy and strong” (wink wink, nudge
nudge). Now there are a lot of “Vet” companies making interesting products which
are clearly intended for human use. The deal is that generally most countries have
much less strict guidelines for vet products as opposed to human grade
pharmaceuticals. As a result, now we have a million “Vet” companies making some
cool stuff for us. Do we consider that veterinary grade? Yeah, for the purposes of
this chapter, if there’s a picture of a dog (or cat, or llama, or whatever) on the box or
bottle we’ll consider it Veterinary Grade, regardless of the intentions of the products
manufacturer.
Now, finally and most interestingly (to me) is the UnderGround Lab. This business is
just booming, and to help keep up with it, and maybe even make some sense of it, I
usually separate them into three categories (three generations, actually).
First generation underground Labs (such as International Pharmaceuticals aka IP)
are the ones who actually buy their raw steroid powders and oils directly from Raw
Pharmaceutical Supply houses. In this category are luminaries such as Dpharm,
(who may or may not be in business anymore) M-Labs, and Stark Labs. Although
British Dragon and British Dispensary are legitimately registered pharmaceutical
companies, I consider them to be in this category as well. Why? Walk into a
hospital anywhere in the world, and you won’t find their products there. The same
25
goes for BodyResearch. They are, for all intents and purposes, just another first
generation UGLab.
Second Generation Underground Labs are ones who don’t obtain their powders
directly from the source. Instead, they go through a middleman, and believe it or
not, that is often simply a first generation Lab. Clearly, they are going to have to
charge considerably more for their products, as compared to first generation Labs.
And of course, there are even third generation UGLabs. As you may have guessed,
these guys are the very bottom of the food chain and often charge a lot for their
products because their raw materials have passed through quite a few hands.
Having been involved in the game for quite some time now, I’ve seen a lot of Labs
come and go. I was involved with the original anabolic steroid message boards, (we
had around 10,000 members almost half a decade ago) and I was there when
powders just started becoming available to the average guy. At that time, Dpharm
was operating under another name and selling human grade anabolics and powders.
He contacted me and gave me some Eq powder (it’s actually an oil at room
temperature) for me to make into an injectable form for myself, and in return, I gave
him some ideas on what a good product line for an emerging underground Lab may
contain. Since then, I know he was looking to get out of the business and may have
done so by the time this book is printed. He was a gentleman in all of my dealings
with him, as were most UGLabs and steroid dealers (called “sources” in current
jargon).
Such is the story of many of the first generation UGLabs who have been around for a
while. The smart ones invest their money and get out of the business.
I also have had the opportunity to watch a very small underground Lab, Stark Labs,
develop from the ground floor to the very well run private Lab it is today. Stark Labs
started out as a member, and later a moderator, on a board I was staffed on. He
then left the staff to pursue his venture as an Underground Lab (this was necessary,
for illegal activities are not tolerated by any Internet discussion boards that I would
be a part of). Anyway, Stark left the staff at that board to pursue this venture, and I
was one of his first customers. I bought and tested many of his products, and they
all came out to contain exactly what they were supposed to and at the proper dose.
Early on, he had some problems with his injectables “crashing” (coming out of
solution) or in the case of his Testosterone Suspension, (made with Propelyne Glycol,
not just an aqueous suspension) it actually became SOLID (!) at room temperature.
Anyway, all that was necessary was to reheat them, but that’s the type of products
you’ll see from a new underground Lab; slightly inconsistent formulas and occasional
problems like this are not uncommon. Stark Labs overcame those issues in later
batches, of course, and produced many fine products.
Unfortunately, I have also been exposed to the dirty side of the Underground Lab
game also. I’ve seen and heard some stories that would make you sick; I don’t need
to repeat all of them here, but I know of a Lab whose products gave one guy an
abscess, while the discussion board that Lab called home (and the staff and owner of
that board) all denied culpability for that Lab’s products being unsafe. I’ve heard of
Labs that threaten people for saying that their products aren’t great, and even some
Labs that give their customers fake or doctored Lab reports on their goods. Others
have tried to pass off one drug (Tren) as being a much more expensive one
(Masteron). At least their customers got something though; some products could
26
contain nothing! But, I still feel your chance of finding a good product (at a good
price) from a reputable Underground Lab is high.
Clearly, there are both good and bad Underground Labs out there, and finding a
good one is all part of the game. You then have to hope that Lab doesn’t get busted
or retire to start a legit business with their drug money!
Remember Dan Duchaine? Well, he used to run a mail order steroid business, and
his old business partner (the co-author of the first Underground Steroid Handbook)
took that money and invested it into a supplement company. That company is now
one of the largest in the world and it was all built from selling amps of Deca and Test
in the 80’s! You’d be surprised (shocked?) at how many supplement companies got
their start from being steroid dealers.
This next part is probably the most shocking thing I’m going to tell you in the entire
book:
I prefer using underground Labs to human grade gear (i.e. I would use Stark Labs
over a major “legit” pharmaceutical company). Why? Several reasons, actually.
There are far fewer counterfeits and/or bootlegs made of them as compared to legit
human grade steroids. It’s much more profitable to counterfeit an amp of Primobolan
and sell it for $12-15 per milliliter than to try to make a fake vial of (say) Stark
Primobolan and sell all ten milliliters for $100. Then economics just aren’t there to
justify faking a UG Product over (say) an Organon one.
In addition, the owners of the first generation Underground Labs have very good
quality control and very sterile conditions to produce their steroids under. You know
why? They use them! Yeah, that’s right, every UGLab owner is basically an AAS
user himself and uses his own products. To my thinking, that’s the best quality
control in the world, and the best endorsement. In addition, you can find some cool
stuff available only from Underground Labs, like long estered Masteron or
Trenbolone. On the next pages, you’ll see the Lab tests I had done on Stark Labs
Trenbolone Enanthate as well as other products. It tested out very well, but as noted
on the Lab report, they had nothing to compare it to, as no Trenbolone Enanthate
existed to get base scores from before underground Labs started producing it. In
addition, with underground Labs, you’ll find some highly concentrated (milligram per
milliliter) gear available, and that brings me to a very interesting point:
You’re going to get better results from taking a more highly concentrated steroid as
opposed to a less concentrated one, even if the milligram amounts are the same.
That’s right, if one guy takes (for example) a 100mg shot of Deca which is 25mgs/ml
(i.e. he takes a 4ml shot equaling 100 total mgs) and another takes that same
milligram amount as one ml (i.e. he takes a 1ml 100mg/ml shot), the second guy is
going to have a higher blood plasma level of Nandrolone (1). Why is this, when they
both took 100mgs total? To be honest, I don’t know why this is, but that’s what the
Minto et. al. study has shown us. This could explain why the 200mg/ml
Drostanolone Enanthate (Masteron Enanthate) I used gave me the better results
than the 100mg/ml Drostanolone Propionate (Masteron) I used, even though the
longer ester prevents a higher peak blood plasma level of a given hormone.*
27
Let’s review those two points:
1. More highly concentrated steroids provide higher blood plasma levels of the
base hormone even when total milligram amounts are the same.
2. Longer esters provide significantly lower blood plasma levels of the base
hormone even when total milligram amounts are the same.
This is another reason why I prefer underground Labs. You can get virtually any
product from them and in any concentration and ester. Clearly, I prefer short esters
and high concentrations when it comes to steroids because they will always,
milligram for milligram provide higher blood plasma levels of the base hormone and
ergo better results.
The trick is finding a reputable underground Lab, and getting on their customer list.
You’re on your own for that one.
However, if you are inclined to buy Human or Vet grade steroids, I have some tips
for you to help spot counterfeits. This is by no means an all-inclusive list, but rather,
some easy to remember tips for your next round of purchases. Here’s what to look
at:
• Uneven levels of liquid- Take a look at two amps from the same manufacturer
side by side. Is the level of oil in them even? If not, at least one is a fake.
• Weird Labels- Does the Label look shoddy on either the box or the vial/bottle
you are buying? Do you think a multimillion (or billion) dollar company would
produce something that looks like a kid with an I-Mac Label maker made it?
If the Label is weird, then the product is probably fake.
• Uneven Labels- Ever see an uneven Label on a legitimate product of any
kind? From a bottle of Jack Daniels to a bottle of Cola, have you ever seen an
uneven Label on one? No, right? Well the same goes for pharmaceuticals.
• Expiration Dates- These should be stamped onto both the box as well as the
product inside, and not printed in the same ink as the rest of the Label. And
they should match, of course.
• Hologram- Look closely…is it a hologram or a silver sticker? If it’s just a silver
sticker, you have yourself a fake.
• Go with your gut instinct- Is there something dodgy about the store you are
buying your products at? Is the source acting shady? Always walk away.
Incidentally, you may notice that we have neglected to include a bunch of glossy
pictures in the back of this book to help you distinguish real steroids from fakes.
Well, this is because at this stage of the game, the fakes are as good as the real
product. A decent graphic designer with any one of a dozen programs can simply
remove a Label from a legit product, scan it, and begin producing his own counterfeit
products. And they’d be perfect. These days, even home computers with the right
printers and programs can generate watermarks, holograms, and perfect forgeries of
virtually any product. A quick trip to the local office supply store can then provide
you with a stamp to put on the date, and you’re in business as a counterfeit steroid
producer.
Finally, you can go to sites like www.Steroid.com, which has a forum where
members post pictures of both real and counterfeit steroids. This way, you can
compare what you’ve been popping into your ass cheeks to a real-time picture of
what’s currently available. This can provide you with some insight as to what is real
and what is fake. You need to be careful, however, as to what discussion boards you
28
frequent. I can tell you that the vast majority (99%) of them produce very little in
the way of worthwhile information, and most have at least one or two UGLabs or
sources on their staff. In most cases, anabolic steroid discussion boards, as well as
the staff on them are very average. If this book is in your hands, there are very few
boards that are going to offer you anything at all over what you are currently
reading. A great many anabolic steroid discussion boards often have a vested
interest, as many of those discussion boards are owned by a dealer or Lab who uses
it to sell their products indiscriminately, or the owner and staff get freebies from a
certain Lab privately and sing that Lab’s praises publicly. This is true of the vast
majority of anabolic steroid discussion boards on the Internet, in one-way or
another. I have been very fortunate to never have been (knowingly at least)
involved with situations like that. If you frequent Internet anabolic steroid discussion
boards, and you ever see a board or staff defend a source tooth and nail, or tell you
a particular Lab is the best thing since Organon…for no reason? The reason is free
product under the table. You can bet on it.
Anyway, if you are still interested in Human/Vet products, and don’t want to buy
fakes, you can also go take a look at the actual sites run by the makers of various
steroids and compare the lot #’s, expiration dates, and pictures to your stash.
Here’s some website addresses to look at:
Bratis:
http://www.bratisLabs.com/
Brovel:
http://www.brovel.com.mx
Denkall:
http://www.ausvetdenkall.com/
ICN:
http://www.icnpharm.com/
Jurox:
http://www.veterinaria.com.mx/
Organon:
http://www.organon.com/
Quality Vet:
http://www.qualityvet.com.mx
Serono:
http://serono.com/
Ttokkyo:
http://www.ttokkyo.com.mx/
Upjohn:
http://www.upjohn.com/
29
Powerline:
www.powerlinemex.com
Animal Power:
http://www.animalpower.com.mx
Tornel:
www.tornel.com
British Dragon:
http://www.britishdragon.com/
Pharmacia El-Ramoz:
http://www.pharmacia-elramoz.com/
Kexing:
http://fitropin.com
Gen-Sci:
http://www.gensci-china.com/green/english/english.htm
Genetech:
http://www.gene.com
That list it by no means exhaustive, but it could save you a few dollars (or Pesos) by
helping you avoid buying fake gear.
Before ending this chapter, I’d like to caution you against going online simply
anywhere to look for pictures of fake vs. real steroids. Most Internet web sites and
bulletin boards allow anyone who registers to post pictures of “real” and “fake”
steroids. Thus, as you can expect, people who sell fake steroids simply register and
post their pictures as “real” steroids, and nobody is the wiser. Caveat Emptor.
Reference:
1. Pharmacokinetics and Pharmacodynamics of Nandrolone Esters in Oil Vehicle: Effects
of Ester, Injection Site and Injection Volume Charles F. Minto, Christopher Howe, Susan
Wishart, Ann J. Conway and David J. Handelsman
30
Chapter 6
Injection Technique
Ok, so you have your bottle(s) of injectable steroid and your needles. Now you’re
ready to give yourself that first shot. I’ll assume you’re like me and you’ve spent
hours staring at the needles and bottles before working up the courage to give
yourself that first shot. When I started out in this game, like many others, I read the
Underground Steroid Handbook and got the advice to do glute shots “high and to the
side” and that’s about it. Well…that was, and still is good advice. If you are a visual
learner (like me), here’s a better idea:
Go grab yourself a porn-mag (no really). Take a look at a pic of someone naked,
facing away from you and standing up straight (you may need to search for that
one…). Now draw a line down one of their ass cheeks, vertically, right down the
middle. That’s your sciatic nerve; stay away from it. Now draw a line across the
middle, this time horizontally, right through the middle of the cheek. See the
upper/outer most past of those 4 parts you just separated the ass cheek into?
That’s where you are aiming when you do an injection in your glute.
If you are nervous, you can practice holding the needle like a dart, and pushing it
into an orange. Apparently the surface tension of the orange makes it very similar
to human skin, so nursing students often use oranges to practice.
So here’s what you want to do for a glute shot (1):
1. Sterilize the area you are going to inject. You can use an alcohol pad, but I
usually just take a shower with anti-bacterial soap, and shoot when I get out.
Remember, your skin also softens up a bit in the shower, and this makes for
an easier shot.
2. If you are using a multi-use vial, clean the top off with an alcohol swab. If you
are using an amp, crack it open.
3. Take the needle out of the package. If you are using oil based steroids, then
you need a 22 or 23 gauge needle. Water based steroids will usually go
through a 25ga. and higher needle depending on the compound. Usually, I
just buy a couple of hundred 23ga.x1” needles with 3cc syringe casings
(that’s the part that holds the liquid). If you are doing deltoids, triceps,
biceps, etc. injections (i.e. small muscles) then you can use anywhere from a
25ga.x5/8th” needle to a 23ga.x1” needle. Glute and quad shots usually
require a 1.5” needle, of the same gauges discussed earlier. As long as the
needle is open enough to let the liquid get through, and long enough to get
past your fat and skin into the muscle, then you’re fine.
4. Pull air into the needle and inject it into the vial. This creates pressure in the
vial, making it easier to draw the steroid out with.
5. Now draw the solution into the syringe by pulling on the stopper while the
needle is facing up.
31
6. Pull the needle out of the vial when you have the desired amount of steroid in
the syringe.
7. Hold the needle upright and tap the sides until the air bubbles are at the top,
and then push them out by tapping the plunger a bit.
8. Now you can either change the needle, or use the same one to inject yourself.
I just use the same one, but if you are drawing from 2-3 vials, then you
might want to replace it at the end before you inject yourself.
9. Stretch the skin on the area of your glute you are going to inject: [with your
thumb and forefinger,]
10. Holding the needle like a dart, push it (in one motion) all the way into your
muscle.
11. Draw back slightly on the plunger, and make sure it doesn’t fill with blood. If
it does, you are in the wrong spot, and you need to start over in another
muscle.
12. Push the plunger in until the syringe is empty.
13. Pull the needle out and put on a Band-Aid. You can massage the area a little
if you want, as this can decrease soreness the next day. Trust me.
If you are shooting elsewhere than the glute, pretty much aim for center mass and
avoid visible veins but follow the same basic procedure that I just shared with you. I
don’t recommend shooting more than 3mls of anything into a given injection at any
given time.
If you are using a particularly thick steroid (and by that I mean the oil is viscous)
then you may want to hold the syringe part horizontal under hot tap water for a
minute. This will heat the oil slightly and let it flow more smoothly. Just remember
to keep the cap on the needle while you run it under water.
Personally, I’ve injected in my glutes, biceps, quadriceps, triceps, traps, and
deltoids. I’ve considered calves, but it seems a bit too awkward, and I’ve considered
pecs, but it seems a bit too “Pulp Fiction”.
I provided information on glute shots because it’s the easiest to explain and because
when you shoot “X”mgs of a given steroid into a large muscle, you will get a higher
blood plasma level than shooting in smaller muscles, even when the amount and
concentration of the steroid is the same (1). The lesson here is that for maximum
results, you will always shoot in the largest muscle possible. But you still can’t shoot
in the same spot more than once per week because you will develop too much scar
tissue. Remember to rotate injection sites if you are doing shots every day or every
other day.
Now, we need to discuss what it’s going to look and feel like if you get an infection.
First of all, you’re going to feel a kind of soreness that’s different from a typical
injection. It’s going to be more of a sharp pain, as opposed to a dull pain. The next
thing is that it’s going to be discolored around the injection area and, will have a
clearly defined border. I’m not talking about a little red area here. It’s more like a
very large blister at first with some kind of fluid inside it. Gross, but wait, it gets
better. During the final stage there is a very viscous fluid inside the border, and a
very dark discoloration. By this time, it will be a very large protruding bulge that
possibly needs to be drained. This final discoloration will be very dark and you’ll
definitely, at this point, know that something has gone terribly wrong.
32
I need to add that you may want to search the Internet for pictures of this, on
medical websites, but you should be forewarned that they typically show pictures of
very easily diagnosed infections and abscesses. What this means is that you’ll be
looking at a very large and absurd picture, which may look quite different from your
own infection/abscess, if that’s actually what you have.
Reference:
1. Pharmacokinetics and Pharmacodynamics of Nandrolone Esters in Oil Vehicle: Effects
of Ester, Injection Site and Injection Volume Charles F. Minto, Christopher Howe, Susan
Wishart, Ann J. Conway and David J. Handelsman
Completely Cleanse Steroids From Your
Body in Just 5 Days!
http://www.SteroidCleanse.com
33
Chapter 7
Designing your own Cycle & Sample Cycles
It is, of course, my hope that you will be able to read this book and design a cycle
for yourself custom tailored to your personal goals. But in this chapter, I’ll give you
my thoughts on bulking and cutting cycles, and how to design them. I will be frank
and say that both of them depend greatly on training and diet, but that bulking
cycles are very dose-dependant and cutting cycles are compound-dependant. What
the hell do I mean? Well, quite simply, steroids follow a dose respondent curve in
terms of muscle gained per mg of steroid. The more you use, the more weight you
gain. Thus, creating a bulking cycle is reasonably simple. In general, I tend to stick
with 2 compounds (test and deca, perhaps) and use moderate to high doses of each.
Cutting cycles are another animal altogether. Instead of simply relying on large
amounts of drugs, you need to remember that when you are in a calorie restricted
state, your sensitivity to exogenous androgens is going to be greater
(Neuroendocrinol 1994; 6: 397-402). Therefore, your selection of compounds needs
to be given greater care than when you are simply trying to gain maximum weight.
Remember, they are going to have a pronounced effect in the absence of libitum
calories. To figure out how to design a cutting cycle, I've been looking around at
various cutting cycles, interviewing athletes and bodybuilders, asking people what
they've gotten their best results from, and keeping track of what compounds and
dosages have been used. My main concern was what type of cycle has been
producing the best results for people, and what similarities do the most prouctive
cutting cycles share. The more I researched, the more I found out that there were
trends within cutting cycles among experienced users. Some will not be surprising to
you, and some will be pretty obvious.
One of the most obvious trends I've noted has been the use of shorter esters in
cutting cycles and longer esters in bulking cycles. Anecdotally, shorter estered drugs
seem to be less likely to cause bloating. This means Testosterone Propionate would
be preferable to Testosterone Enanthate or Cypionate and Nandrolone
PhenylPropionate would be preferable to the standard Deca (Nandrolone Decanoate).
Test Enth or Cyp would of course be fine for a bulking cycle though.
This should come as no surprise to most people.
What I have to say next is probably going to be a major surprise to you.
The most productive cutting cycles I've read about on the 'net ALL followed a simple
structure. Here's the pattern or structure:
Every single highly successful cutting cycle I’ve ever looked at contained
Testosterone. Some also contained another testosterone based compound as well. Eq
is a popular addition here.
Every single one contained a 19-nor-testosterone based compound as well. The
34
Nandrolone branch of the 19-nor family is well known for being very anabolic and not
incredibly androgenic, while the Trenbolone branch is very androgenic. Also, it has
the strongest androgen binding affinity of any commonly used injectable. I feel that
a proper cutting cycle will contain some compounds that bind very strongly to the
Androgen Receptor, and perhaps some others which have several non-receptor
mediated mechanisms of action.
And finally, every really good cutting cycle I looked at contained a DHT based
compound as well. Generally Winstrol and/or Masteron were used.
So, what we have here are all 3 major families of Anabolic/Androgenic Steroids. They
are represented (Testosterone, 19-nor-Testosterone, and DiHydroTestosterone) in
99% of all HIGHLY PRODUCTIVE cutting cycles and are Testosterone 1a-nor
Testosterone, and DiHy6dro Testosterone. Remember, A/A steroids will all fall into
one of the 3 categories I have mentioned.
I can tell you that I'd almost always include Trenbolone with Winstrol in a cutting
cycle. Tren binds very strongly to the anabolic receptor, and Winnie binds rather
poorly...by combining them, we may have some additional synergy.
NPP
(Nandrolone Phenylpropionate) also has a reasonable bind to the AR, so it may be
substituted for Tren. It probably should not used alongside it with any appreciable
synergy. And of course, using either of those without Testosterone would kill your
sex life.
I'm also noticing that most of the magic is easily achieved with doses under 2grams
(total) with regards to cutting cycles. I know that personally, if I were to do a cutting
cycle, I'd run around 400-500mgs or so each of a DHT, 19-nor, and Test based
compound. Price would factor into things, I'm sure, as would availability.
I’ve noticed that cutting cycles require far less milligrams of AAS per kg of
bodyweight. This creates some pretty amazing results but I never really knew why.
Then I was researching androgen efficacy in feed restricted animals (what, you don’t
have hobbies?) and found that feed restriction can encourage enhanced androgen
receptiveness (McManus et. al.). This means the steroids you use will produce
greater results when you are under caloric restriction, and thus, your cutting cycles
will actually be more effective (in a milligrams vs/ results gained) than your bulking
cycles.
Bulking cycles use much higher doses, of course. At the stage in my life, I usually
use testosterone propionate + one other compound for my cycles.
I'm sure many readers want to know about including GH or Clen (or Letrozole) into
this discussion, but it's simply beyond the scope of what I'm doing in this chapter. I
think that those are good compounds and are certainly worth including if you have
access to them and (in the case of GH) the funds but they simply aren't necessary
(unless you need the Letrozole to combat gyno, or simply like to use Clen, which is
now fairly cheap). Perhaps with higher doses, they become more necessary, but I
feel that their inclusion is really on a case by case basis.
There it is, how I would design a cycle for optimal results using optimal compounds
and dosages. As a last word, I'd like to remind everyone that diet and training will be
part of your cycle-puzzle, and that the dugs mentioned above will make things
35
easier. However, keep in mind that they certainly will not make you ripped or huge
on thier own.
Combine those 3 families of steroids and different receptor binding abilities and you
will have a very potent cycle. Use high(ish) doses and you have a very nice bulking
cycle. Now that you have an understanding of how I design my own cycles, I’ll leave
you to design your own. But, I have some sample cycles you may wish to try.
Beginner’s Cycle
This is your basic Beginners Cycle, comprised entirely of testosterone. Not only will
you get more muscular on this cycle, but you will learn how your body reacts to
endogenous amounts of testosterone.
Week
Testosterone (Enanthate or Cypionate)
1 500mgs
2 500mgs
3 500mgs
4 500mgs
5 500mgs
6 500mgs
7 500mgs
8 500mgs
9 500mgs
10 500mgs
11 500mgs
12 500mgs
Beginner’s Cycle (with Kick Start)
This is the same cycle as the one above, but I’ve included Dianabol at a low(ish)
does at the beginning, so you’ll start seeing results almost immediately.
Week
Testosterone (Enan or Cyp)
1 500mgs
Dianabol
20mgs/day
2 500mgs
3 500mgs
20mgs/day
20mgs/day
20mgs/day
4 500mgs
5 500mgs
6 500mgs
7 500mgs
8 500mgs
9 500mgs
10 500mgs
11 500mgs
12 500mgs
36
Intermediate Bulking Cycle
This cycle is for those who have done two previous cycles (hopefully the ones
above). For those looking to add more weight, Deca would be the appropriate choice
here. For those looking to add more lean weight, Eq would be more appropriate.
Week
Testosterone (Enan or Cyp) Deca-Durabolin -or- Equipoise
Dianabol
1 500mgs
400mgs
2 500mgs
20mgs/day
400mgs
3 500mgs
20mgs/day
400mgs
4 500mgs
20mgs/day
400mgs
5 500mgs
20mgs/day
6 500mgs
400mgs
400mgs
7 500mgs
8 500mgs
400mgs
400mgs
9 500mgs
10 500mgs
400mgs
400mgs
11 500mgs
12 500mgs
400mgs
400mgs
13 500mgs
Intermediate Cutting Cycle
This cycle is for those who have a decent amount of mass already, and wish to refine
it.
Weight gains will be minimal, but with a proper diet and training (Cardio and
Weights), single digit body fat levels should be attainable if you are not too sloppy.
Many will disagree with the inclusion of a 17aa like Winstrol for this long, and
certainly you can do ½ of the cycle with Winstrol, and ½ with Tren, or mix and
match. I’ve done it both ways and either works fine.
Week Testosterone Propionate
Winstrol
(injectable) -or- Trenbolone
Acetate
1 100mgs/Every Other Day
(EOD)
Anavar
100mgs/Every
Other Day (EOD)
2 100mgs/EOD
100mgs/EOD
40mgs/day
3 100mgs/EOD
40mgs/day
100mgs/EOD
4 100mgs/EOD
40mgs/day
5 100mgs/EOD
100mgs/EOD
100mgs/EOD
6 100mgs/EOD
7 100mgs/EOD
100mgs/EOD
100mgs/EOD
8 100mgs/EOD
9 100mgs/EOD
100mgs/EOD
100mgs/EOD
10 100mgs/EOD
11 100mgs/EOD
100mgs/EOD
100mgs/EOD
12 100mgs/EOD
100mgs/EOD
37
Advanced Bulking Cycle
Keep some Letrozole or Arimidex on hand for this cycle, if gynocomastia symptoms
develop. This is a very potent bulking cycle, and should be good for a 20lb+ gain
even in advanced users.
Week Testosterone (Cyp or Enan) Deca-Durabolin Anadrol50
1 750mgs 500mgs 50mgs/day
2 750mgs 500mgs 50mgs/day
3 750mgs 500mgs 50mgs/day
4 750mgs 500mgs 50mgs/day
5 750mgs 500mgs 50mgs/day
6 750mgs 500mgs 50mgs/day
7 750mgs 500mgs
8 750mgs 500mgs
9 750mgs 500mgs
10 750mgs 500mgs
11 750mgs 500mgs
12 750mgs 500mgs
Advanced Cutting Cycle
As with the cycle above, keep some Letrozole or Arimidex on hand, and use it if gyno
symptoms begin…this cycle is what I consider to be the “perfect” cutting cycle. If you
start no higher than 15%bodyfat, and you keep your diet and training in check, you
will easily get into single digits.
Week Testosterone
Propionate
Trenbolone Winstrol
(oral)
Clenbuterol
1 75mgs/Every
other Day
75mgs/Every
other Day
25mgs/day 60mcgs/day
2 75mgs/EOD 75mgs/EOD 25mgs/day 60mcgs/day
3 75mgs/EOD 75mgs/EOD 25mgs/day 60mcgs/day
+50mgs of Benadryl
4 75mgs/EOD 75mgs/EOD 25mgs/day 60mcgs/day
5 75mgs/EOD 75mgs/EOD 25mgs/day 60mcgs/day+
50mgs of Benadryl
6 75mgs/EOD 75mgs/EOD - 60mcgs/day
7 75mgs/EOD 75mgs/EOD - 60mcgs/day
8 75mgs/EOD 75mgs/EOD 25mgs/day 60mcgs/day
9 75mgs/EOD 75mgs/EOD 25mgs/day 60mcgs/day+50mgs
of Benadryl
10 75mgs/EOD 75mgs/EOD 25mgs/day 60mcgs/day
11 75mgs/EOD 75mgs/EOD 25mgs/day 60mcgs/day
12 75mgs/EOD 75mgs/EOD 25mgs/day 60mcgs/day+50mgs
of Benadryl
38
Chapter 8
Remove Steroids in 5 Days
*The product discussed below did show to beat steroid drug testing, but we
are not in any way promoting this product to be used to purposely beat
mandatory or random drug testing for sports or work.
This is going to be one of the shortest chapters in the book, but it will also be one of
the most important! Anabolic Steroids can be very toxic to the body and if taken
incorrectly or for a long period of time, they can cause some very serious side
effects. In the past, if you took steroids and decided that you made a terrible
mistake by doing so, or if you just finished up a long cycle and wanted to remove
these drugs, you had to let them run through your system and wait for your body to
cleanse them out naturally. This process can take up to 18 months or longer and
during that time, these steroids can continue to do damage to your body. Well… You
don’t have to wait any more!
We found a product call the “Steroid Cleanse” by Dynamic Sports Nutrition, Inc.
(http://www.SteroidCleanse.com) that claimed to completely remove steroids from
your body in only 5 days! Those were some big claims considering that removing
steroids other than naturally has never proven to work, so we bought a few bottles
to test them out. We took several known steroid users and had them drug tested to
see what exactly they had in their system. It would take a few days to receive the
results back so we had our subjects continue with the cleanse without knowing
exactly what drugs were in their system. After our test subjects gave their urine at a
local licensed drug testing facility, we instructed them to immediately stop taking
any steroids or drugs they were using and to follow the instructions on the “Steroid
Cleanse” bottles to the letter. The cleanse is a 5 day process that requires a clean
diet, water or green tea, exercise, and a toilet within 100 yards at any given time.
Our test subjects reported no signs of negative reactions to this product other than
frequent trips to the bathroom (which is necessary for most cleansing type
products).
After we had received the results back from the first drug test, it was clear that they
were indeed on several types of popular anabolic steroids. The drugs that were
found to be present were:
Nandrolone Decanoate (Deca-Durabolin), Testosterone (they were using
Testosterone Cypionate, Propionate, and Enanthate), Drostanolone (Masteron),
Methandrostenolone (Dianabol), Oxandrolone (Anavar), and Stanolzolol (Winstrol)
were all present.
The steroids listed above are commonly used in many athletes and was a perfect
control group to see if this “Steroid Cleanse” really did work. After our test subjects
completed the 5 day cleanse, they returned back to the licensed drug testing facility
where they gave their last, hopefully cleansed urine samples.
39
Several days after giving the final urine samples, the drug testing facility called us to
let us know the drug tests were in and that we could come pick them up. What we
found out was absolutely amazing! Every single steroid was removed from our
test subjects except for one drug, Nandrolone Decanoate (Deca-Durabolin), which
the company claimed may not be cleansed to begin with. (A small list of drugs that
may not be cleansed can be found at www.steroidcleanse.com)
These tests proved to us that the impossible was now 100% possible. We have found
a product that will actually remove these toxins from your body in only 5 days! That
is shocking in itself, but we are wondering how this will affect the sports industry
now that this product does actually exist? We recommend anyone who wants to
remove steroids and other drugs from your system to use the “Steroid Cleanse”.
To view the exact same test results we saw, please visit the “Steroid Cleanse”
website. We have forwarded our test results to them and have asked them to post
them for everyone to see. Please note the last part of the social security number for
identification purposes, as well as the date of collection on both the before and after
tests.
Completely Cleanse Steroids From Your
Body in Just 5 Days!
http://www.SteroidCleanse.com
40
DRUG
PROFILES
41
Chapter 9
Drug Profiles
This is obviously going to be the longest chapter of the book, and the most
exhaustively researched one. It contains profiles on every major (and minor)
pharmaceutical compound in use for bodybuilding, sports, and athletics today. It
contains literally hundreds of references and works cited, and I believe this to be the
most complete collection of this type of information in the world.
As I said previously, you may, perhaps find some of this information repetitious. If
you read the profile on Equipoise and the profile on Methandriol, then I suspect you
will find the profile on Drive (a rare Australian blend of Equipoise and Methandriol) to
be repetitious. Be that as it may, I have spared no effort to include profiles on drugs
such as Drive, even though the compounds which make it up are addressed
elsewhere. You will not learn what percentage of Drive is made up by Methandriol
land what percentage of it is Equipoise simply by reading the profiles on those two
respective drugs. You will not learn how many milligrams of each per milliliter are in
Drive by simply reading the profiles on the drugs which make it up. And if you want
to have the most complete understanding of steroids and ancillary compounds
possible, then you need to know those things. I want you to walk away from reading
this book with the most complete knowledge possible, and that has required effort
on my part…and now requires effort on yours.
Alot of what we know about a steroid, or at least part of that, is "coded" in it's name
[the part written like this at the start of my profiles]. If you look in the name of a
steroid, and it's something like this:
2-oxy androstane 17b-ol 2-one
(Which is the chemical name for Anavar)
See the bold part? That means it's a DHT-derivative, with regards to it's base carbon
structure.
If it said:
norandrostene 17b-ol 3-one
(Nandrolone)
Then you know the norandrostene part means it's derived from Nandrolone (or if
you generally see 19-nor or something like that)
and finally, if you see:
42
the word testosterone (duh) or androstene in the name of the structure, then you
know it's derived from testosterone.
Therefore, we have a steroid like Boldenone (Eq), we can figure out a few things
about it.
Look at the name:
BOLDENONE -or-
(17b-ol 1,4-androstadiene-3-one, ) -or-
Equipoise
And what we see is that it starts with "BOL" and the chemical name begins with 17b
ol...hence "BOL."
See what I'm talking about:
17b-ol 1,4-androstadiene-3-one
Next we see "DEN" ( because the word is Bol-Den-One if you break it apart).
Looking in the middle of Boldenone's chemical name, we find:
17b-ol1,4-androstadiene, 3-one
And finally we have "ONE" at the end of Boldenone, and clearly, the chemical name
also has "One" at the very end:
17b-ol1,4-androstadiene-3-one
SO what does all of this tell us? Well, since it starts with 17b-ol we know that it's
got something going on at the 17beta position, which is an "ol" which is a Hydroxy
(oxygen and hydrogen) group. This is where our estrification (added ester) at the
17-beta-position goes. Now, we also have the middle part, androstadiene, which
indicates that this steroid has double carbon bond on the base of a testosterone's
steran nucleus or a di- bond on androstene. In this particular case, the double
carbon bond at this position slows aromatization. Eq, as we know, aromatizes to a
far lesser degree than testosterone, because of this modification. Remember that
androstene, from the beginning of my explanation on all of this, indicates
testosterone as a base structure.
Add it all up, and we have Boldenone, which is called Equipoise, from the Latin root
of the word Equine, meaning that it has to do with horses...and as you already knew,
Equipoise (Eq) was developed to give to horses.
Now, if we look at Eq (boldenone) and compare it to Dianabol (methandrostenolone),
we see how similar they are.
43
Equipoise:
(17b-ol 1,4-androstadiene-3-one, )
And now Dianabol (difference noted in black/bold):
(17a-methyl-17b-ol 1,4-androstadiene-3-one, )
As you can see, the only difference between Dianabol and Eq is the 17a-Methyl
group, which is why Dianabol is called a Methylated steroid; it has been 17-alpha
alkylated to survive oral ingestion.
And this, my friends, should tell us a few things, the first being that we can tell alot
from just the names I've used in my profiles...and the second (when you compare
the minor difference in names but the major differences in effects concerning
Dianabol vs. Eq) is that...names aren't everything.
Now, lets talk about the anabolic:androgenic ratio's...
To determine that ratio, testosterone was given to male winstar mice, and then they
were sacrificed (killed), and their levator ani (a leg muscle which was immobilized
during the 21 days) is weighed, as well as their ventral prostate.
The weight of that (untrained) muscle is the anabolic rating for testosterone , and
the weight of the ventral prostate is the androgenic rating. Now other steroids are
administered to these rodents, and the weight of their levator ani and ventral
prostate, relative to the weights of those rodents from the testosterone group, are
that steroid's anabolic:androgenic rating. Testosterone, therefore, has a rating of
100:100, while Trenbolone has a rating of 500:500 (which is the same ratio, relative
to itself, but is 5x as anabolic as testosterone and 5x as anabolic).
Again, this isn't a perfect way to give us the exact effects a given compound will
have in our bodies...but it's a start. Now, start reading profiles!
44
Testosterone
Derived Steroids
45
Testosterone Derived Steroids
As you know, some steroids are derived directly from testosterone, this includes all
of the Testosterones (Methyltestosterone, Testosterone Cypionate, Testosterone
Propionate, etc…) as well as Boldenone, Methandrostenolone, and Fluoxymesterone,
and many more. Below is a partial list of some traits and effects that most, if not all,
Testosterone Derived Steroids have attributed to them
• Excellent Anabolic Properties
• Increased nitrogen retention
• Improved sense of well-being
• Improved Confidence
• Significantly Increased Libido
• Possible improvement of erectile dysfunction
• Conversion to Estrogen (aromatization)
• Possible increased LDL cholesterol
• Possible decreased HDL cholesterol
• Increased aggression
• Increased ability to recover from workouts
• Decreased Cortisol (a catabolic hormone)
• Increased Creatine Phosphate production and utilization
• Increased Lypolysis (fat burning)
• Improved Insulin sensitivity
• Increased Metabolism
• Increased Bone Density
46
• Increased production of red blood cells
• Conversion to DHT
• Increased growth of body hair
• Possible development of male sexual characteristics in women
• Increased acne
• Inhibition of HPTA
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
47
Anabolicum Vister
(Boldenone shown with Undeclynate Ester)
(Qunibolone)
[1,4-androstadiene-3-one,17b-ol (+ ester 17beta-(1-Cyclopenten-1-yloxy) ]
Molecular Formula (of Base): C19H26O2
Molecular Formula (of Ester):N/A
Molecular Weight (of Base): 286.4132
Molecular Weight (of Ester): 352.5156
Melting Point:N/A
Manufacturer: Parke Davis (Discontinued)
Effective Dose(men): 100-200mgs/day
Effective Dose (women): 50-100mgs/day
Active Life: less than 8-12 hours
Detection Time:2-3 months
Anabolic/Androgenic Ratio: 100:50
Unfortunately, Anabolicum Vister (Quinbolone) wasn’t very popular in the United
States, and most of the research on it was written in Italian. Why is that important?
Well, most of the research on it is written in Italian. I’m one of those guys who
doesn’t even like to read the menu out loud at an Italian restaurant I usually have to
point at the item I want to avoid looking too stupid.
Anabolicum Vister is yet another attempt at creating a steroid with the basic idea of
altering the Methandrostenolone/Boldenone structure. As we already know,
Equipoise (Boldenone) is basically a non-17alpha alkylated version of Dianabol, with
an Undeclynate ester added. What we’re looking at in Anabolicum Vister
(Quinbolone) is basically Eq or Boldenone but with a cyclopentenyl ester at the 17
alpha position to increase its lipophillicity, in lieu of the undeclynate ester found in
Eq. It’s yet another attempt at a non-toxic oral anabolic like Andriol, and it used a
similar delivery system. It was sealed in an oil-filled capsule, so that the oil could be
absorbed by the lymphatic system just like it is with Andriol and thus it could by
pass the liver and avoid being broken down that way, which is how most oral
steroids (the 17-alpha-alklyated ones) are. Your lymphatic system is a bunch of
veins and arteries that can only absorb water, the idea behind Anabolicum Vister
takes advantage of this state of affairs.
Anyway, as you may have heard, using the lymphatic system as a delivery vehicle
for steroids is very problematic. Blood levels are all over the place (6)(9), and in
some people it seemed as if most of the time it didn't metabolize properly at all.
Therefore, as with Andriol, effective doses of this steroid are necessarily high.
Originally, each capsule had 10 mg of quinbolone, and you needed to take 10-20caps
48
mg to get any kind of decent anabolic effect (9)(5)(4). Remember, we’re talking
about oral EQ here, so you’re better off with just shooting some nice Stark brand Eq
(or Ganabol, or whatever you happen to like). While you won’t get any benefits with
Anabolicum Vister over regular Eq, it will basically do all of the same things Eq will.
This stuff will help you lose a bit of fat (4)(5), will increase strength and muscle (5),
and also (as Eq is noted for) increase red blood cell production (2). The kicker, for
me, is that this drug was given a new name, Quinbolone, while it’s basically just
boldenone cyclopentenyl. That’s just idiotic.
As we already know from the properties of the Boldenone base, this is a particularly
safe steroid. Anabolicum Vister is not liver toxic (8), and has little or no interaction
with the 5AR enzyme (6), so it doesn't really form much of the more androgenic
metabolite Dihydroboldenone. We also know that it has only half the ability to
interact with aromatase as testosterone, so it won’t convert too much estrogen.
Unlike it’s brother, Methandrostenolone (dbol), it doesn't have the structural
alteration of the 17-alpha-methyl group that makes it form a more potent estrogen
(6).
What we have here (although it has been discontinued) is basically oral Eq, which
requires too many caps per day to be cost effective over injectable Eq, but
nonetheless may be an interesting drug if a underground lab starts producing some.
The original company that made it has, sadly, stopped doing so.
References:
1. [Quinbolone in the therapy of anemia in uremic patients during periodic hemodialytic
treatment]Clin Ter. 1980 Jul 15;94(1):57-65. Italian.
2. [Erythropoietic action of an oral non-17-alkylated anabolic steroid]
Clin Ter. 1979 Nov 15;91(3):267-78. Italian.
3. [Pituitary activity and quinbolone]
Minerva Med. 1977 Jun 30;68(32):2245-8. Italian.
4. [Controlled studies of the comparative effects of an anabolic steroid (quinbolone) and
cobamamide on weight gain, skinfold thickness and secondary sex characters in a group
of children of both sexes. Preliminary note]
Minerva Pediatr. 1972 Jul 14; 24(25):1040-50. Italian.
5. [Human pharmacological study of quinbolone. Clinical and Laboratory investigations
of the effects of anabolic treatment in aged women]
G Gerontol. 1972 Apr; 20(4):361-78. Italian
6. Metabolism of 1-dehydroandrostanes in man. I. Metabolism of 17 -hydroxyandrosta-1,
4-dien-3-one, 17 -cyclopent-1'-enyloxyandrosta-1, 4-dien-3-one (quinbolone) and
androsta-1,4-diene-3,17-dione (1).
Steroids. 1971 Jul; 18(1):39-50.
7. [The action of quinbolone on nitrogen metabolism in humans]
G Clin Med. 1967 Jun;48(6):632-44. Italian.
8. [Considerations on the use of a new non 17-alpha-alkylated anabolic steroid, active
orally: quinbolone. Study of liver function]
Rass Fisiopatol Clin Ter. 1965 May-Jun;37(3):165-77.
49
9. [Clinical study of a new anabolic preparation: Quinbolone]
Gazz Med Ital. 1965 Dec;124(12):360-6. Italian.
Completely Cleanse Steroids From Your
Body in Just 5 Days!
http://www.SteroidCleanse.com
50
Andriol
(Testosterone shown with Undecanoate ester)
(Testosterone + Undecanoate ester)
[Androsta-4-en-3-one, 17b-ol]
Formula: C19 H28 O2
Molecular weight of base: 288.429
Molecular weight of ester: 186.2936
Melting Point: 155
Manufacturer: Organon
Effective dose: 600mgs
Active Life: less than 8-12 hours
Detection Time: 4-5 weeks
Anabolic/Androgenic Ratio: 100:100
Andriol is testosterone with the undecanoate ester attached, and produced in oral
form. It represents the first real attempt to create an oral testosterone since
Methyltestosterone. I can only assume that the scientists responsible for this wanted
to create a viable alternative to both injectable testosterones (which, at least for
Hormone Replacement Therapy, is inconvenient), as well as other oral forms of
testosterone (which have traditionally been very harsh on the liver). What they came
up with has proven to be a very odd steroid in many ways.
To create Andriol, the scientists involved had to come up with a solution to the
problems facing methyltestosterone, namely the fact that it is harsh on the liver and
needs to be taken in very high doses to produce decent results. What they did was
put 40mgs of Testosterone Undecanoate in oleic acid (an oil), and encapsulate it.
Now they use castor oil and propylene glycol laurate instead of oleic acid, but that
only increases the shelf life, and doesn’t do anything else. For some of the aspiring
chemists reading this, you may be asking yourself the obvious question. And the
answer is yes, you can take almost any estrified drug (Nandrolone Decanoate, for
example), and dissolve it in castor oil and propelyne glycol laurate, and create your
own “Deca Caps” or whatever. The problem is that you’d need to be able to make
sealed gel caps, not just the typical 2-part capsules most people throw steroid
powder in. Anyway, I’m digressing; lets get back to Andriol. After you put some
testosterone undecanoate in caster oil and propelyne glycol laurate, you’ll have a
testosterone which is highly fat-soluble due to the (very large) undecanoate ester
51
attached to it, and able to be absorbed through your small intestine via the
lymphatic system. What this means is that it avoids the “first pass” through the liver,
a process which could destroy much of the active steroid, and place an undue
amount of stress on the liver. It also displayed a rapid absorption and turnover in
one study (11), which may account for its ability to not cause unwanted side effects.
It’s not bad for your blood pressure (13), and also has no adverse effects on the
prostate and may even improve blood pressure (12)! Thus, Andriol is remarkably
light on all side effects, especially those related to liver toxicity and estrogenic sides.
In this study, done with women, it even displayed no ability to lower LH and FSH
(Leutenizing Hormone and Follicle Stimulating Hormone, respectively), which are the
hormones that tell your body to make more testosterone (11). I doubt Andriol could
be properly regarded as liver toxic or too damaging to your HPTA (Hypothalamus
Pituitary-Testicular-Axis, the thing that governs your body’s production of
testosterone, among other things), at any kind of reasonable (or even excessive)
dose. Actually, one study noted no adverse reactions or effects at all with the use of
Andriol (10). As for your lipid profile and cholesterol, it has even been shown to have
beneficial effects on them (14)!
So, putting some Testosterone Undecanoate in Gel Caps is what the scientists at
Organon have done with their Andriol product, and it all looks good so far, right? The
active steroid totally bypasses your liver and hence doesn’t get damaged by or
damage your liver, and gets a bunch of Testosterone into your body. Great! But
what happens next? Well, after the lymphatic system has brought the testosterone
undecanoate into circulation in your body, the undecanoate ester begins to be
removed. This would leave you with (roughly) 25mgs of testosterone in your blood
stream, as the decanoate ester takes up a lot of “space” and the cap only contains a
total of 40mgs of testosterone undecanoate (roughly 15mgs of which are ester). The
end results from Andriol would be very similar to the end result of injecting almost
any form of testosterone (4), once your body removes the ester. But remember,
you’d never inject 25mgs of testosterone suspension and call it a day, but that’s
exactly what you are doing when you take only one Andriol cap.
So now you have 25mgs of testosterone floating around in your body. That’s not
much, so if you’re realistically considering using this product, you’ll need to take
quite a few caps of it. And there’s one of the first problems we encounter with this
drug. You see, the method of administration of this drug provides us with a nice
liver-safe product, but this stuff will peak your testosterone levels within around 2
hours after administration, and will only remain (at least slightly) elevated for 10 or
so hours (1). Ideally, you’d be taking a capsule every 2 hours, which is inconvenient
to say the least. Let’s be generous and say you can simply take one every 4 hours.
Problem solved? Not really, because we’re going to need to take at least 2 caps with
each dose if we want to see any sort of anabolic effect, and if we’re taking it every 4
hours (assuming we’re awake for 16hrs every day), then we’ll be taking around 8
caps per day. Now we’ve shifted the problem away from the effort needed to take an
effective does to being a problem with economics. The problem with this type of dose
is going to be cost. Andriol is pretty expensive to be taking in the amount of 8 caps
per day, and I have never seen it made by anyone except for Organon, which means
we won’t find it on any UnderGround Labs product lists. That means we need to pay
whatever price Organon is asking, and they are asking a lot. You can easily run a
cycle with several anabolic compounds for the price of a cycle of just Andriol.
So that’s our major obstacle, the expense of taking Andriol in what would be an
effective dose is prohibitive to most people. One study noted that Andriol therapy,
52
when compared with traditional Testosterone injections is roughly 7-8x more
expensive (5).
Cost notwithstanding; let’s see what kind of results we can expect from Andriol
(besides the catabolic effect it will have on your wallet). Although it has a reputation
for being very mild, you’ll still see some results from Andriol. One study using a very
low dose on adolescent boys still showed a reasonable gain in Fat Free Mass (3) even
though the boys were not training. Another study focusing on the elderly, improved
their quality of life considerably (as androgens often do) (6), and also had beneficial
effects on erectile dysfunction (7). This is certainly promising, but in a world where
first time-ste In fact, it may even be a useful adjunct with Viagra for this purpose
(8). However, in a world where first time steroid users expect upwards of 20lbs per
cycle, I would suspect many will be disappointed with the 5lbs or so a cycle of
Andriol will produce. Granted, that’s a conservative estimate, but I can’t really be
confident predicting much more muscle is to be expected from Andriol. Taking a
large amount of Andriol is actually pretty safe (except for your bank account), and
there was even a 3 month study done in Korea, where a pretty small dose of Andriol
( 160 mg daily for 3 weeks then half that dose for the remainder of the study)
resulted in a very nice rise in testosterone. Serum total testosterone increased from
2.13 +/- 1.20 ng/ml at baseline to 6.04 +/- 3.08 ng/ml (p = 0.005) after 12 weeks.
In addition, free testosterone was (barely) significantly changed from 8.60 +/- 2.25
pg/ml to 11.40 +/- 3.81 pg/ml (p = 0.13) (10). However, there were no significant
changes in liver function tests, red blood cell count or lipid profiles, nor were there
any significant adverse reactions that would have led to the cessation of the
administration of oral testosterone. So the scientists at Organon have succeeded in
making a nice, safe, moderately effective, orally available treatment for low
androgen levels. But can we (athletes and bodybuilders) use it also?
Truthfully, I can’t be confident predicting more than a 5lbs gain with the use of
Andriol, because this product has a very odd property, and that is the widely varying
effects it has on test subjects. In one study I read, four test subjects were each
given Andriol, and one had a huge surge in testosterone levels going up to
60.1nmol/L and the other only had a 11.5nmol/L level (5)! The remaining 2 test
subjects fell in between those levels. I am speculating that the differences
experienced by the test subjects were primarily due to the variances inherent in the
lymphatic system. But to make matters even more inconsistent, there is no evidence
that those variances wouldn’t occur within the same person taking Andriol (i.e. you
get a huge surge in testosterone one day, and a very minor one the next day). This
may be associated with whether this stuff is taken with food or not. Since it operates
via association with your small intestine and lymphatic pathways, taking it with food
greatly enhances its bioavailability (9). This may be a case of “problem solved,” but
I’m hesitant to close the books on andriol’s absorbtion problems so quickly. For now,
we’ll just say you are spending your money much more wisely if you take your
andriol with meals.
Despite all of its problems, if I had the money to run 10-15 caps of Andriol/day and if
I were looking for a stand-alone oral compound to safely run for a full cycle, (of
perhaps 12 weeks) then I have to admit, Andriol would be my #1 choice.
Testosterone undecanoate may also offer a viable alternative for androgen treatment
in women.
53
References:
1. Which Androgen Replacement Therapy for Women? Journal of Clin Endocrinol and
Metab. 83 1998 3920-24
2. A new oral testosterone undecanoate formulation.
World J Urol. 2003 Nov;21(5):311-5. Epub 2003 Oct 25. Review.
3. Effects of oral testosterone undecanoate on growth, body composition, strength and
energy expenditure of adolescent boys.
Clin Endocrinol (Oxf). 1992 Sep;37(3):207-13.
4. Recovery of free androgens in the rat prostate in vivo and in vitro after treatment with
orally active testosterone undecanoate (TU).
Horm Metab Res. 1980 Oct;12(10):541-5
5. Which Testosterone Replacement therapy? Clin Endocrinol (oxf) 21 198497-107
6. Effect of oral testosterone undecanoate on visuospatial cognition, mood and quality of
life in elderly men with low-normal gonadal status.
Maturitas. 2005 Feb 14;50(2):124-33.
7. Effect of 12 month oral testosterone on testosterone deficiency symptoms in
symptomatic elderly males with low-normal gonadal status.
Age Ageing. 2005 Mar;34(2):125-30. Epub 2004 Dec 13.
8. Oral testosterone undecanoate reverses erectile dysfunction associated with diabetes
mellitus in patients failing on sildenafil citrate therapy alone.
Aging Male. 2003 Jun;6(2):94-9.
9. Important effect of food on the bioavailability of oral testosterone undecanoate.
Pharmacotherapy. 2003 Mar;23(3):319-25.
10. Oral testosterone replacement in Korean patients with PADAM.
Aging Male. 2002 Mar;5(1):52-6.
11. Administration of testosterone undecanoate in postmenopausal women: effects on
androgens, estradiol, and gonadotrophins.
Menopause. 2000 Jul-Aug;7(4):251-6.
12. Effects of androgen supplementation therapy on partial androgen deficiency in the
aging male: a preliminary study.
Aging Male. 2002 Mar;5(1):47-51.
13. Effects of androgen supplementation therapy on partial androgen deficiency in the
aging male: a preliminary study.
Aging Male. 2002 Mar;5(1):47-51.
14. Therapeutic effect of andriol on serum lipids and apolipoproteins in elderly male
coronary heart disease patients.
Chin Med Sci J. 1992 Sep;7(3):137-41.
54
Androderm & Androgel
(Transdermal Testosterone)
Transdermal Testosterone has been marketed heavily in the Hormone Replacement
Therapy Market for the last decade. For over 50 years, testosterone therapy has
been used for the treatment of hypogonadism. In recent years, there has been an
increase in the use of testosterone therapy for men with late-onset hypogonadism,
sometimes referred to as andropause. Testosterone therapy in older and
hypogonadic men can significantly improve their sense of well-being, and lead to
increases in muscle and bone mass, upper body strength, virility, and libido (5). Oral
delivery of unmodified testosterone is not really a viable option, due to its rapid first
pass metabolism, possible liver toxicity, and its relatively short half-life. Thus,
injectable testosterone was used for a very long time as an effective hormone
replacement method. Roughly a decade ago, alternatives to injectable and oral
testosterone were developed. Originally, these alternative methods of application for
testosterone meant shaving an area of the skin’s surface (*usually the scrotum, no,
really) and attaching a testosterone patch with low, dry heat like a hairdryer, which
basically hot-glued the testosterone patch to the scrotum. I can’t see, for the life of
me, the logic employed by the doctor who thought this method was preferable to
weekly or twice-monthly injections. Luckily, this painful procedure progressed to the
point where its at now, you can simply apply a self sticking patch or rub some
testosterone gel anywhere on your body, and get the same effect. Recently, the
BALCO scandal featured many references to the gel method. I think, for an adequate
understanding of these types of products, we’re going to have to take a look at both
the drug (testosterone) as well as the method of administration (transdermal
delivery), and see how they work together, and how they compare with testosterone
injections.
When some (nonscrotal) transdermal testosterone preparations were examined, they
showed that the plasma concentration of TS increased very rapidly, and reached the
peak level within 3-6 hours of the application of the experimental patch.(2) This is
comparable with some of the better oral products out there. In my experience, an
athlete would usually swallow a pill rather than have a patch hanging on them for a
day.
Basically, you can expect all of the benefits of injectable testosterone with the
transdermals (if the mg doses were the same…which they are not). What we’re
dealing with here is Androderm, which is a patch containing 12.2mgs of testosterone
and androgel, which gives you about the same (you only get 10% of the total drug
55
contained in the preparation....thus a hundred mgs of test in a gel form, would yield
a 10mg amount in your body).
Here’s a chart comparing a transdermal with an injectable, both using testosterone:
Steady-state pharmacokinetic profiles of T, BT, DHT, and E2 profiles during nightly
applications of TTD systems (n = 27; , left panels) and biweekly IM injections of T
enanthate (n = 29; X, right panels) measured at week 16. Dashed lines denote
upper and lower limits of normal range based on morning serum samples (T, 306
1031 ng/dL; BT, 92–420 ng/dL; DHT, 28–85 ng/dL; E2, 0.9–3.6 ng/dL). Error bars
denote ± SD.(1)
Not so great, huh? A mere 100mg shot of injectable testosterone provides much
higher peak plasma concentrations of testosterone, even though the transdermal
testosterone was more stable, with regards to blood plasma levels. So what are the
advantages of transdermal application? Clearly, it provides a very stable blood level
of the compound administered. I know it seems like I’m killing you with charts, but
take a look at this one:
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Serum T concentrations (mean ± SE) before (day 0) and after transdermal T
applications on days 1, 30, 90, and 180. Time 0 h was 0800 h, when blood sampling
usually began. On day 90, the dose in the subjects applying T gel 50 or 100 was up-
or down-titrated if their preapplication serum T levels were below or above the
normal adult male range, respectively. In this and subsequent figures the dotted
lines denote the adult male normal range, and the dashed lines and open symbols
represent subjects whose T gel dose were adjusted.
So it’s consistent, but who cares? The levels of testosterone it gives us are just
enough to provide a slight boost, at a high (financial) cost. Wouldn’t it be great if we
could get this stuff dosed more highly? Or maybe even with Clen, so we could apply
it directly to fatty areas? Or with Tren? That would be great, huh? It would even
have potential for first time needle-phobic steroid users to use items which were
formerly only available as an injectable! Women could use a Tren product without
leaving needle marks! In fact, with a little creativity, underground Labs could even
make transdermal products which would never get caught by customs (perhaps
disguised as stickers or whatever).
Anyway, I guess that's not in the cards. Let’s move on.
One particularly successful transdermal testosterone delivery method involves the
combination of DuroTak 87-2510 as an adhesive polymer. This is combined with 3%
dodecylamine and 10% span 80. This, combined with testosterone creates a nice
transdermal delivery system (4). Another experimental transdermal testosterone
preparation contains occlusion, octisalate (OS), and propylene glycol (PG), called
Solugel (which is a proprietary hydrogel containing PG 25% w/w) and Tegaderm (a
semipermeable film dressing) on the permeation of TES was assessed. Occlusion had
no effect on the permeation of TES, however, OS increased the flux of TES 2.9-fold.
The concentration of PG which produced optimal TES flux was 20% v/v, and this
concentration resulted in a 1.9-fold increase in TES permeation. By combining OS,
PG, and occlusion, transdermal testosterone permeation through the skin was
increased 8.7-fold, which was a synergistic enhancement, obviously…meaning the
sum of the parts was far more than their individual totals (3). Why did I bother
57
telling you all of the ingredients, which can easily be found at a chemical supply
house, and bought legally? Not so, you could make your own transdermal
preparations of testosterone (or Tren, or clen, or whatever)…that would be illegal.
Even though you now know the ingredients, and could just make a gel with them
and some testosterone (or tren, from Finaplex pellets), and create your own
transdermal drug delivery product. That would be wrong…
References:
1. jcem.endojournals.org/content/vol84/issue10
1. In vitro and in vivo evaluation of a novel nonscrotal matrix-type transdermal delivery
system of testosterone.
Drug Dev Ind Pharm. 2005 Mar;31(3):257-61.
2. Synergistic enhancement of testosterone transdermal delivery.
J Control Release. 2005 Apr 18;103(3):577-85.
3. The current status of therapy for symptomatic late-onset hypogonadism with
transdermal testosterone gel.
Eur Urol. 2005 Feb;47(2):137-46.
4. Effects of androgen substitution on lipid profile in the adult and aging hypogonadal
male.
Eur J Endocrinol. 2004 Oct;151(4):415-24. Review.
5. [Gruenewald, Matsumoto. J Am Geriatr Soc 2003;51:101; Morales. Aging Male 2004;
in press].
58
Andropen 275
(Testosterone shown without esters)
(Testosterone + 5 esters)
[4-androstene-3-one,17beta-ol ]
Formula (base): C19 H28 O2
Formula of Acetate ester: C2 H4 O2
Formula of Propionate ester: C3H6O2
Formula of Phenylpropionate ester:C9 H10 O2
Formula of Cypionate ester: C8 H14 O2
Formula of Decanoate ester: C10 H20 O2
Molecular Weight of base: 288.429
Molecular Weight of Acetate ester: 60.0524
Molecular Weight of Propionate ester: 74.0792
Molecular Weight of Phenylpropionate ester: 150.174
Molecular Weight of Cypionate ester: 132.1184
Molecular Weight of Decanoate ester: 172.2668
Manufacturer: British Dragon
Effective dose (injectable): (Men) 550mgs-1,100mgs+/week
Active Life: 14 days
Detection Time: 3 months (projected)
Anabolic/Androgenic Ratio:100:100
Andropen is a five-ester blend of testosterone produced by British Dragon, and is
clearly an attempt to profit off of the popularity of Sustanon. Actually, if you are
inclined to use blended products such as this (and personally, I’m not anymore),
then I think you’ll find this to be a product far superior to Sustanon.
Andropen contains 20mgs of Testosterone Acetate, 75mgs of Testosterone
Cypionate, 90mgs of Testosterone Decanoate, and 40mgs each of Testosterone
Propionate and Phenylpropionate in a 20ml bottle. I am very impressed with the fact
that this product appears to be designed specifically for bodybuilders and athletes,
and certainly if I wanted to create a long, medium, and short estered testosterone
product, it would be something like this one. Also, due to that fact, I think I’d
recommend shooting it EOD, or E3D or so….giving you a very decent and relatively
stable level of hormone in your body. A few years back, I made a testosterone blend
for my own use out of powders, which was essentially a five estered testosterone
(the same esters as Sust + 100mgs of test with the Cypionate ester per milliliter).
Anyway, now it seems that every Underground Lab is involved with this type of
thing. It’s not uncommon to see a price list with several “custom blends” or “house
blends” of various estered testosterones (or sometimes Trenbolones, or whatever).
59
Testosterone is a relatively cheap drug (the cheapest, actually, in terms of
anabolics), and that’s why it’s not actually a bad choice for blended products. In
terms of “bang for the buck”, it’s a great choice, as it can do just about everything.
It induces changes in both the shape as well as size as muscle fibers (1). It can
change the appearance and the number of muscle fibers (1), which is definitely a
good thing for the cosmetic athlete (read: bodybuilder). Testosterone has the
profound ability to protect your muscle from catabolic (muscle wasting)
glucocorticoid hormones(2), although not as well as Tren or other such (more
expensive) drugs. Glucocorticoid hormones send a message to muscle cells to
release stored protein, while Testosterone sends a message to muscle cells to store
more contractile protein (called actin and myosin). In this way, these two hormones
are at war with each other to cause anabolic vs. catabolic effects. Usually they are at
a stalemate (which is why you don’t gain weight constantly, nor lose it). When you
add in some Testosterone (such as Andropen275), you shift the scales in favor of
anabolism, and away from catabolism. In addition to this, Testosterone has the
ability to increase erythropoiesis (red blood cell production) in your kidneys(3), and a
higher Red Blood Cell (RBC) count is highly sought after by many athletes because it
may improve endurance via better oxygenated blood. More RBCs can also improve
recovery from strenuous physical activity, and seems to give the muscles a more
“full” look when bodyfat levels are reasonably low. Agression levels often rise
dramatically with the use of exogenous testosterone (9), and due to some of the
short esters in Andropen275, I’d expect this effect to become realized within the first
day of injection.
All of these great benefits are to be had with the use of test enth alone, but
realistically, it will be part of a cycle containing one or more other drugs. People who
are bulking will probably choose Deca or Eq (possibly with Dbol as well) and those
who are cutting will probably steer towards Eq and perhaps Trenbolone. Very often
users will shoot this drug once or twice a week, but blood levels are still above
baseline with this drug at around day eight (10).Common wisdom holds that the
testosterone portion of any such cycle should be equal to or greater than any other
injectable drug(s) portion (on a mg basis). I believe that you can get away with less,
but in general, this is a good guideline.
The real advantage to this product, in my opinion, over Sustanon is in it’s
practicality. As you know, I’m not a huge fan of multi-estered products, because it
seems that this gives the manufacturer carte blanche to charge whatever they want.
Well, this product costs roughly $150, for a 20ml, multi use vial. When compared to
buying Sustanon by the amp, you could be paying up to $50 more for the same
amount of testosterone. If you are looking for a product of this nature, this is one
that I would actually recommend.
This product should provide less of the watery “bloated look” that an equal amount
of (for example) testosterone cypionate would give, but more than you’d get with
testosterone propionate. This makes it a possible choice for use in either a bulking or
cutting cycle, or the ever popular “lean mass” cycle we’re seeing lately, on
Steroid.com. Of course, the usual side effects experienced with any testosterone use
would be expected with this product: Acne, water-retention, gyno, etc… And so
would all of the positive effects we use testosterone for: muscle gain, fat loss,
strength gain, etc…
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Really, as I’ve said numerous times, the one principal drawback to using blends of
testosterone tends to be their high cost as compared with single ester tests. If this
product could be had cheaply, I wouldn’t hesitate to recommend it.
References:
1. Anat Histol Embryol. 2003 Apr;32(2):70-9.
2. J Lab Clin Med. 1995 Mar;125(3):326-33.
3. Zhonghua Nan Ke Xue. 2003;9(4):248-51
4. J Clin Endocrinol Metab. 2003 Apr;88(4):1478-85
5. J Clin Endocrinol Metab. 2004 Feb;89(2):718-26.
6. Am J Physiol. 1998 Jun;274(6 Pt 1):C1645-52.
7. Biochim Biophys Acta. 1995 May 11;1244(1):117-20.
8. Am J Physiol Endocrinol Metab. 2001 Dec;281(6):E1172-81.
9. Health Psychol. 1990;9(6):774-91.
10. Fertility and Sterility 33.
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
61
Deposterona
(Testosterone shown without esters)
(Testosterone + 3 esters)
[17b-hydroxy-4-androsten-3-one ]
Formula (base): C27 H40 O3
Formula Esters
Acetate: C2 H4 O2
Valerate; C5 H10 O2
Undecanoate: C11 H22 O2
Molecular Weight(base): 288.429
Molecular Weight Esters
Acetate: 60.0524
Valerate:102.13
Undecanoate: 186.2936
Melting Point (base): 155°C
Manufacturer: Ft. Dodge
Effective Dose (Men): 400-600mgs/week
Active life: 15-16 days
Detection Time: Up to 3 months
Anabolic/Androgenic ratio: 100:100
This is actually a very interesting compound as far as testosterone blends go. It’s
produced by Ft.Dodge, which has a good reputation for quality. I think I’m going to
go against the grain here (shocking, huh?) and say that this is the only testosterone
I would have absolutely no problem recommending to women. A quick look at its
low concentration will show us why:
Testosterone Acetate: 12mgs
Testosterone Valerate: 12mgs
Testosterone Undecanoate: 36mgs
(For a total of 60mgs of testosterone per ml)
So what we basically have here is a blend of short and long esters, in a very low
concentration. I’ll go out on a limb and say that your average athlete won’t be
thrilled with shooting a bottle of this stuff per week. See, it comes packaged as a
10ml vial, in boxes of 12, and you can even buy a case of a “dozen dozen” (a dozen
boxes with a dozen 10ml vials each) aka a gross (144 bottles). This is a great buy,
as you’re getting it for way less than a grand, and its quite a bit of testosterone. The
62
problem is that you need to shoot a bottle per week to get a nice dose of it, but it’s
not too bad if you are using something like Tren A or Masteron with it (and need to
shoot frequently anyway).
A novel use of this may be for a 1x a week (or even every other week) injection for
female athletes daring enough to try testosterone, or even for use in diluting painful
underground gear. I can imagine that using this with Andropen275 or T400 may be
a very viable route for those wishing to ease the pain of those shots and perhaps
create some kind of Frankenstein’s monster blend of testosterone esters within your
syringe.
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63
Dianabol
(Methandrostenolone)
[17a-methyl-17b-hydroxy-1,4-androstadien-3-one]
Formula: C20H28O2
Molecular Weight: 300.44
Melting Point: N/A
Manufacturer: Ciba (originally)
Release Date: 1956
Effective dose: 25-50mgs (as low as 10 and as high as 100 have been reported)
Active Life: 6-8hours
Detection Time: up to 6 weeks
Anabolic/Androgenic Ratio (Range): 90-210:40-60
Dianabol (Methandrostenolone)
This was more or less the second Anabolic Steroid ever produced. The first, as we all
know was Testosterone, which was produced in the early 1900’s and experimented
with by Nazi’s in WW2, in an attempt to produce a better soldier. Russian athletes in
the 1953 World Championships as well as the Olympic games then used testosterone
with great success. After that, John Zeigler, who was a doctor working with the US
Weightlifting Team, began a cooperative project with Ciba to develop an equalizer for
US atheletes. Flash forward to 1956 and enter Dianabol; the original trade name for
Ciba’s Methandrostenolone... but called “Dbol” by athletes. The original package
insert said that 10mgs/day was enough to provide full androgen replacement for a
man, and Dr.Zeigler recommended that athletes take 5-10mgs/day. Incidentally, this
is also the dose that Bodybuilders were reputed to take from then until roughly the
1970’s. Yeah, this was allegedly Arnold’s dose, Zane’s dose, etc. simply stacked with
some testosterone. (For any trivia buffs out there, Dan Duchaine’s mail order steroid
business operated under the name “The John Zeigler Fan Club”).
Enough with the history lesson, lets get into what this stuff is, and what it does.
Well, first off, it’s usually found in pill form, though it can be found as an injectable
also (Under the Trade name: Reforvit-B, which is 25mgs of methandrostenolone
mixed with B-vitamins). It is a 17aa steroid, which means it has been altered at the
17th Carbon position to survive its’ first pass through your liver, and make it into
your blood stream. It’ll raise your blood pressure (4) and is hepatoxic (Liver-Toxic),
so be careful with it. Although I have known people to take up to 100mgs/day of this
stuff and not suffer any ill-effects, one study looked at that exact dose, and the
64
people involved didn’t suffer any intolerable side effects (7). Lets examine this
particular study a bit further, though:
In this study, done in the early 80’s, a very high dose of Dbol (100mgs/day for 6
weeks) decreased plasma testosterone to about 40% of it’s normal value, plasma GH
went up about a third, LH dropped to about 80% of it’s original value, and FSH went
down about a third also (these are all approximate numbers, for the sake of brevity,
but you get the idea). Bodyfat did not go up significantly and Fat Free Mass went up
anywhere between 2-7kgs (3.3kgs average gain). The researchers concluded that
Dbol increases Fat Free Mass as well as strength and performance. I can only agree,
finding this to be the case when I did my first cycle (which was 6 weeks of dbol alone
at 25mgs/day). I gained roughly 25lbs and kept nearly ½ of it. Since then, Dbol has
always had a special place in my heart.
As with many other 17aa steroids, Dbol is also a very weak binder to the Androgen
Receptor, so most of it’s effects are thought to be non-receptor mediated, and are
attributable to other mechanisms (i.e. protein synthesis as inticated by the
production of muscle tissue with very high levels of nitrogen, etc. which was
indicated in the 100mg/day study). In fact, much of its anabolic effect may be from
GH secretion following administration. When Dbol was administered to rats whose
pituitary glands had been removed, it actually demonstrated zero anabolic effects
(6). Therefore, GH secretion must be a large part of its anabolic activity. Also, it has
only had a modest aromatase activity so estrogen doesn’t cause water gain on Dbol,
rather (maybe) GH does. This structure also means it only has a modest aromatase
activity (2).
When Steroid.com members were polled on their results from Dianabol, an
overwhelming majority of them were happy with the result gained from Dianabol and
only 10% were dissatisfied. Dianabol has been, and will continue to be, one the
most popular oral steroids for gaining mass and strength.
How strong is Dbol? Well, on an mg for mg basis, most people agree that it's
stronger than A50. The reason most people don't get the same gains off of Dbol is
that almost nobody takes equivalent doses (I mean, I've heard of people taking
150mgs of A50, but not Dbol, although the Dbol would probably provide more solid
gains and be less toxic, I suspect).
So how do we incorporate this stuff into our AAS regimen? Clearly, the inclusion of
Dbol at any point in a cycle would contribute to gains; however, I’d speculate that
Dbol is most regularly used for 2 reasons:
1. At the start of a cycle to “Kick Start” gains
2. As a “Bridge” between cycles to maintain gains
Let’s examine these two uses.
In order to kick start a cycle, usually what you do is incorporate a fast acting oral like
dianabol (or anadrol) and combine it with long acting injectables (such as Deca or Eq
with some Testosterone). The reasoning here is that the oral (Dbol in this case) will
give almost immediate results, while the injectable takes time to produce results.
The end result is that you start seeing results within the first week of your cycle and
continue up until the end with the injectables. This entails taking anywhere from 25
50mgs of dbol (although as little as 20mgs or as much as 100mgs have been
65
reported) for 3-6 weeks at the start of a cycle (average time for a “Kick Start” is 4
weeks, though) and then ceasing their use as the injectables start to produce
results.
In order to successfully bridge between cycles, (and this means using a low dose of
AAS, in this case dbol) you need to recover your natural hormonal levels to pre-cycle
levels or to within acceptable parameters, and then you start your next cycle. The
idea here is that you won’t lose any gains, but rather a low dose of an AAS will help
you maintain them. Typically, you’d use around 10mgs/day of dbol and combine it
with an aggressive Post-Cycle Therapy (PCT) course of Nolvadex (and/or Clomid)
and HCG. This would give you full androgen replacement from the Dbol and a shot at
recovering your natural hormonal levels via the other stuff you are taking.
Remember, the 100mg/day dose of dbol in the study we looked at earlier did not
suppress Test, LH, or FSH to a degree that would make recovery impossible; And it
certainly can not with 1/10th that dose in conjunction with an aggressive PCT.
All in all, this is a very good drug, and a potent tool for quick gains or retaining gains
when used properly and safely.
Here’s how your body metabolizes Methandrostenolone:
References:
1. 1 Serakovskii S, Mats'koviak I., Effect of methanedienone (methandrostenolone) on
energy processes and carbohydrate metabolism in rat liver cells, Farmakol Toksikol 1981
Mar-Apr;44(2):213-7
2. Brain Res. 1998 May 11;792(2):271-6.
3.Chemfinder. Copyright 2004 CambridgeSoft Corporation. Cambridge, MA, USA.
66
4. Br Med J. 1975 May 31;2(5969):471-3.
5. www.Steroid.com
6. Steinetz BG, Giannina T, Butler M, Popick FEndocrinology 1972 May;90(5):1396-8
7. Clin Sci (Lond). 1981 Apr;60(4):457-61
8. Steroids. 1984 Dec;44(6):485-95.
9. Vrach Delo. 1983 Nov;(11):34-6. Russian
10. Acta Med Acad Sci Hung. 1975;32(1):27-34
11. 4 Nesterin MF, Budik VM, Narodetskaia RV, Solov'eva GI, Stoianova VG., Effect of
methandrostenolone on liver morphology and enzymatic activity, Farmakol Toksikol
1980 Sep-Oct;43(5):597-601
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
67
Drive
(Methandriol and Boldenone shown without esters)
(Methandriol + Boldenone Undeclynate)
(aka Methylandrostenediol)
[17a-Methyl-5-androstene-3B,17B-diol]
Formula: C20 H32 O2
Molecular Weight: 304.4716
Manufacturer: Various
Effective Dose (Men): 30-50mg orally (daily)/ 300-500mg injectable (weekly)
Effective Dose (Women):
Active life: 2-3 days
Detection Time: 6 weeks
Anabolic/Androgenic ratio: 30-60/20-60
Boldenone Undeclynate
(1,4-androstadiene-3-one,17b-ol)
Formula (base):C19 H26 O2
Molecular Weight(base): 286.4132
Molecular Weight (ester): 186.2936
Manufacturer: Various
Effective Dose (Men): 200-600mgs/week
Effective Dose (Women): 50-100mgs/week
Active life: 15 days
Detection Time: Up to 5 months
Anabolic/ Androgenic ratio: 100:50
Drive is a steroid that got a lot of press time about a decade ago when
MuscleMedia2000 printed their now infamous interview with “Bodybuilder X.”
In that article, BodybuilderX referred to Drive as a steroid that increases the
effectiveness of any other steroids used in a cycle. This isn’t really true, and Drive is
simply a combination of Boldenone and Methandriol. Let’s review Equipoise first.
First of all, it slows aromatization, (conversion into estrogen) and the best estimate
is that it does so at roughly half the rate of testosterone. Athletes almost never
report estrogenic side effects with Eq, even when the dose is up to a gram per week.
In women, virilization (development of male sexual characteristics) is not common
and is actually almost never seen with this compound when reasonable doses are
used by female athletes. This is one of the few injectable compounds that could be
68
successfully be used by female athletes and bodybuilders and isn’t often faked.
Primo, Anavar, etc…are usually faked on the black market.
The 5-AR enzyme converts a small amount of Boldenone into Dihydroboldenone
(DHB) which is a very potent androgen. A rare, yet beneficial occurance taook place
because DHB (sold under the name 1-Testosterone for awhile) turned out to be a
very effective anabolic while it was legally available on the market. As I said before,
such a small amount of it is converted that it’s really of no concern or benefit to most
athletes taking Eq.
One of the most pronounced effects in Eq is its ability to raise your RBC’s (red blood
cells). This is very typical of anabolics; however, Eq would appear to do it to a
slightly greater degree than mostIt’s probably the most versatile injectable
compound, next to testosterone.
Athletes taking Eq often report a slow and constant buildup of quality muscle, due to
the very long ester attached to the Boldenone; Undeclynate is a longer ester than
the decanoate ester by one carbon. The accumulation of muscle from Eq to actually
occur at a slightly slower rate than that found with Deca (nandrolone decanoate).
This leads me to advise that if you are considering the use of Eq, you should consider
using it for no less than 12 weeks. Since Eq is the prime muscle builder in this
compound, you are looking at a very large dose of Drive in order to get a sufficient
level of it. There are 25mgs of Boldenone and 30mgs of Methandriol per milligram of
Drive. Can you say “2 bottles per week”?
Methandriol (MAD), as you know from it’s profile, is 5-androstenediol (5AD) that has
had its chemical structure modified by adding a methyl group so the compound can
resist being broken-down by the liver when taken orally. It has an anabolic (muscle
building) effect of 20-60 (compared testosterone which has an anabolic rating of
100), so not much muscle gain can be expected from MAD use. It is also slightly
androgenic, again when compared to testosterone which has an androgenic effect of
100 MAD only rates 30-60. Methandriol low androgenic properties may be a blessing
and a curse, on one hand with its low androgenic effects the drug can be used
without worries by prone individuals who suffer from prostate problems, hair loss
and acne. It may also be used by female bodybuilders who wish to avoid the
virilizing side effects of androgens once they stick to a reasonable dosage and cycle
duration. On the other hand the benefits of using an androgenic steroid are lost,
there is a direct correlation between drugs androgenic levels and strength gains,
highly androgenic steroids also tend to aid in fat loss by binding strongly to the
androgen receptor (A.R). So not much muscle or strength gain from this one. So
what the hell is it good for? Allegedly it is very synergistic with other drugs, notably,
Nandrolone and Boldenone. Is it? Who knows… But Methandriol has been shown to
have an affinity for glucocorticoid-binding sites so this may result in an anti-catabolic
(muscle destroying) effect by inhibiting the muscle wasting effects of glucocorticoid
hormones also the parent hormone of methandriol, 5-androstenediol (5AD) has been
shown to promote favorable immune function . MAD is said to process a unique trait
that no other steroid has, the ability to sensitize the androgen receptor (A.R) to
other hormones or the ability to “unblock” the AR, but that’s highly doubtful.
Due to the very low doses of actual steroid hormone in Drive, its place in a cycle is
very negligible and I can’t really recommend it too highly.
69
Equilon 100
(Boldenone shown without ester)
(Boldenone + 4 esters)
(1, 4-androstadiene-3-one, 17b-ol)
Formula (base): C19H26O2
Formula (esters)
Acetate: C2 H4 O2
Propionate C2H6O2
Cyclopentylpropionate: C8 H14 O2
Undeclynate: C11H20O2
Molecular Weight (base): 286.4132
Molecular Weight (esters):
Acetate: 60.0524
Propionate: 74.0792
Cyclopentylpropionate: 132.1184
Undeclynate: 186.2936
Manufacturer: WDV Pharma
Effective Dose (Men): 200-600mgs/week
Effective Dose (Women): 50-100mgs/week
Active life: 15 days
Detection Time: Up to 5 months
Anabolic/ Androgenic ratio: 100:50
Basically what we’re looking at here is the Equipoise (Boldenone) version of
Sustanon. It’s got 4 esters, 2 of which are long-acting and 2 of which are slow
acting:
Acetate: 10mgs
Propionate: 30mgs
Cyclopentylpropionate (Cypionate) 20mgs
Undeclynate: 40mgs
Now, a multi-estered product (even Eq) is pretty much a forgone conclusion because
a steroid saavy chemist learned of the popularity among athletes of Sustanon, and
figured out that Eq (Boldenone) is a likely candidate for such a multi-estered blend.
The odd thing about this product is the presentation. It comes in 6ml vials! This is
the kind of thing that always leaves me speechless and scratching my head
wondering why someone would do something like this. I mean, 10mls is usually the
industry standard, and it gives us nice round numbers to work with when planning
70
our cycles. The only thing I can think of is that generally, 400-600mgs (and usually
the latter) is the recommended dose for athletes. This product has 600mgs per
bottle, so at the optimal dose a bottle will last an average male athlete or
bodybuilder a week. Now I’m waiting for a 7ml bottle of something with a
propionate ester, specifically made to last a week with everyday injections.
Completely Cleanse Steroids From Your
Body in Just 5 Days!
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71
Equipoise
(Boldenone shown without ester)
Boldenone Undeclynate
(1,4-androstadiene-3-one,17b-ol)
Molecular Weight(base): 286.4132
Molecular Weight (ester): 186.2936
Formula (base): C19H26O2
Manufacturer: Various
Effective Dose (Men): 200-600mgs/week
Effective Dose (Women): 50-100mgs/week
Active life: 15 days
Detection Time: Up to 5 months
Anabolic/ Androgenic ratio: 100:50
This particular compound was actually created while attempting to make a product
which would be be a long acting injectable D-bol (methandrostenolone). What was
actually created was a product that acts nothing like D-bol in the real world, despite
its similarity to it chemically. Think of Equipoise, chemically at least, as being
Dianabol without the 17-alpha-methyl group (that’s the thing which makes D-bol
able to be ingested orally and not be destroyed by your liver). However, having had
first hand experience with both Equipoise (Eq) and D-bol, I can tell you that the
results from each are vastly different.
To make Equipoise, a double bond was added between carbon atoms 1 and 2 of the
Steran Nucleus of Testosterone. What does this mean? Well, first of all, since Eq was
created by one simple modification in the testosterone molecule, you could rightly
suspect that it shares many similarities with it. Eq is just as anabolic as testosterone
(as you can tell by its anabolic rating above) but is only half as androgenic. Those
ratings can be quite deceiving though; I don’t know anyone who would claim that
you can gain as much weight on Eq as you can gain on an equal amount of
testosterone (even though strength gains from the two compounds are very similar).
It’s not very common to compare Eq to testosterone; however, a far more common
comparison is between Eq and Deca. I suspect this because when Dan Duchaine
introduced this compound to the steroid using community, he made an immediate
comparison to Deca, speculating that it would act similarly to Deca, yet be a stronger
version. Eq doesn’t act much like deca at all; Deca is actually a progestin and a 19
nor derived steroid whereas Eq is more closely related to testosterone (being only
one double bond differrent). Duchaine later rescinded his original statement on Eq
72
and said that it was disappointing as a mass builder when compared with Deca, but a
far better drug than for both strength gains and vascularity. Unfortunately, the myth
that Eq’s action is similar to Deca’s has persisted for nearly 2 decades after he
revised his opinion. This is most evident on Internet message boards today, where
many will advise against including both of them in a cycle because “they act the
same way.”
The 1-2 double bonds that Eq has are responsible for many of its characteristics.
First of all, it acts to slow aromatization (conversion into estrogen). The best
estimate is that it does so at roughly half the rate of testosterone (1). This is the
best number I’ve found in studies. Athletes almost never report estrogenic side
effects with Eq, even when the dose is up to one gram per week. Side effects caused
by estrogen include oily skin, acne and gynocomastia. As I have said, those are
usually not found from Eq. Virilization (development of male sexual characteristics in
women) is almost never seen with this compound when reasonable doses are used
by female athletes. This is one of the few injectable compounds that could be
successfully be used by female athletes and bodybuilders and isn’t often faked.
That double bond is also responsible for Eq’s resistance for being changed by the 5-
5-Alpha-reductase enzyme (2)(3). This enzyme converts a small amount of
boldenone into dihydroboldenone, which is a very potent androgen (7 xs as anabolic
as testosterone) (4). As I said though, such a small amount of it is converted that
it’s really of no concern to most athletes taking Eq. This factor, plus its low
aromatisation rate, means that athletes don't need to consider using ancillaries with
Eq.
Athletes taking Eq often report a slow and constant buildup of quality muscle, and
certainly, this has been my experience with the drug. I would speculate that this
slow buildup of muscle is due to the very long ester attached to the boldenone;
Undeclynate is a longer ester than the decanoate ester by one carbon. Thus, we
could expect the accumulation of muscle from Eq to actually occur at a slightly
slower rate than that found with Deca (nandrolone decanoate). This leads me to
advise you that if you are considering the use of Eq, you should consider using it for
no less than 12 weeks. Eq, like Deca, is also detectable in your system for a long
time (although its detection time is substantially less than Deca’s).
Strangely, shorter estered versions of boldenone are available as well. Anecdotally,
many people (and manufacturers) claim that this produces less water retention, but
water retention from Eq is virtually unheard of. Therefore, I consider this to be a
silly idea.
An informal poll I took on Steroid.com (as well as with my friends) seems to put the
ideal dose of Eq at 600mgs/week. Most people I asked about their experience with
Eq seemed to think that using over 600mgs/week produced no additional results, but
the jump from 400mgs/week to 600mgs/week produced noticeable additional gains,
and thus was warranted. I have personally found very nice results from 400mgs
600mgs/week myself.
One of the most pronounced effects in Eq is its ability to raise your RBC’s (red blood
cells). This is very typical of anabolics; however, Eq appears to do it with a slightly
greater degree than most. One of the other effects most Eq users report is an
increased appetite. I can say that this is true for me. Also, this factor makes it
impossible for me to diet on it. Because of its ability to increase appetite, many will
73
include Eq in a mass cycle, and it’s for the quality of muscle gained on it that many
will include it in a cutting cycle. It’s probably the most versatile injectable compound
next to testosterone. People even use a low dosed version of Eq to blend with
irritating injectable drugs such as testosterone suspension or propionate. I'm
thinking of the old Ganabol version that was dosed at 50mgs/ml, here. It's not that
Eq is especially good to cut other steroids with. It was the low dose and cost of
ganabol that made it ideal to cut with when sterile oil wasn't available or desireable.
This low dosed version was also very popular with women who were comfortable
shooting 1cc of this stuff every few days or every week.
Eq will cause a suppression of your hormones, such as endogenous testosterone, so I
would also recommend using injectable testosterone in any cycle containing it.
Failure to do so could result in possible sexual dysfunction and other sides.
Finally, one of the best parts of Eq is its low price and high availability. Eq is
produced by most Underground Labs at very reasonable prices. You shouldn’t be
paying more than $50 for a 10cc bottle dosed at 200mgs/ml, and that price is true of
Mexican veterinary products and underground labs alike.
I’d have to say that due to its incredible versatility, availability, and low price, Eq is
going to be a staple in many cycles for a long time.
Here’s how your body metabolizes boldenone:
References:
1.Endocrinology 71 (1962) 920-25
2. Metabolism of boldenone in man: gas chromatographic/mass spectrometric
identification of urinary excreted metabolites and determination of excretion rates. Biol
Mass Spectrom. 1992 Jan;21(1):3-16.
3. Gas chromatographic/mass spectrometric analysis of boldenone urinary metabolites in
man. Yao Xue Xue Bao. 1991;26(5):362-6. Chinese. Erratum in: Yao Hsueh Hsueh Pao
74
1991;26(9):687.
4.Counsel et al., "Anabolic Agents. Derivatives of 5alpha-Androst-1-ene", J. Org. Chem.,
27 (1962), 248-25
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
75
Halotestin
(Fluoxymesterone)
[9-alpha-fluoro-11-beta-hydroxy-17-alpha-methyl-4-androstene-3-one,17b-ol]
Formula: C20 H29 FO3
Molecular Weight: 336.4457
Melting Point: 240C
Manufacturer: Upjohn, Various
Date Released: 1957
Effective Dose: 10-40mgs/day
Active life: 6-8 hours
Detection Time: 2 months
Anabolic/Androgenic ratio: 1,900/850
Halotestin. This stuff is legendary among powerlifters and strength athletes. The
mere word conjures up images of little mint colored pills that turn Dr. Jeckyl instantly
into Mr.Hyde. Since I’m generally Mr.Hyde 24/7, this isn’t of much concern to me,
but let’s sees what else Ha lotestin can do for us.
If you’re anything like me, the first thing you’ll notice is Ha lotestin’s absurd Anabolic
and Androgenic rating. This stuff is 19 xs as anabolic as testosterone and 8.5 xs as
androgenic! Whoa! I have to admit, those numbers are a bit deceiving, and through
personal experience, I can say that Halotestin will not put anywhere near as much
muscle on you as testosterone. Let’s take a closer look at Halo, see what kind of
realistic effects we can expect from it, and what kind of side-effects we’ll be dealing
with.
Firstly, I have to admit that I love this stuff, and generally its use in athletics and
powerlifting is far more pronounced than it’s use in bodybuilding. Here, it is basically
a one-trick-wonder used in the final weeks before a contest to harden up an already
lean physique and gives the user some added aggression during the final calorie
depleted workouts before a contest. Halo has no estrogenic activity, and thus will not
cause any kind of water retention or most of the bad effects associated with
estrogen. It is, however, hepatoxic (liver toxic) (13) and I recommend keeping doses
at or around 40mgs/day for a maximum of 4-6 weeks. If you are using it for its
pronounced effect on aggression, you can simply use 10mgs prior to a workout. I
personally prefer 10mgs upon rising and 10mgs prior to a workout during the most
intense weeks of a bulking or cutting cycle. This (as you will see later) can be used
with minimum HPTA inhibition.
76
It also has a volumizing effect on the physique, and for those who have a low a
bodyfat percentage, this will immediately cause a more contest ready appearance.
This is due, at least in part, to Halo’s ability to increase mean hematocrit with
hemoglobin levels as well as red cell mass (4)(5)(6). Halo also appears to act
through cells already committed to respond to erythropoietin (11). This is good news
for athletes, of course. As you can see, Halo has quite a profound effect on red blood
cell production. This action is clearly one of the most obvious mechanisms and its
effects increase stremgnth and energy levels. It also points to the possibility of
using it for athletics and sports where a high VO2 max is needed for activities such
as Rugby, Mixed Martial Arts, etc…
It also exerts its effects on strength and fat loss by regulating fatty acid oxidation in
the liver and fast-twitch muscle mitochondria (2). Oddly, for a drug that exerts such
a nice anabolic effect and promotes such good strength gains, it has a pretty low
Androgen Receptor Binding affinity (14). I suppose in this respect, it can be
compared to Winstrol (Stanozolol).
As far as strength and agression goes, Halo is a great drug. It is especially useful on
a cutting or strength cycle. Its use for mass and weight gain have been pretty
disappointing for most users.
Fluoxymesterone administration is (unfortunately) accompanied by a reduction in
thyroid binding globulin which causes associated decreases in T3, while the free T4
index remains totally unaltered, thus, implying that thyroid function was unchanged.
Remember, many anabolic steroids (notably Trenbolone) lower your T3 levels. In
addition, during fluoxymesterone administration there was a reduction in
testosterone, gonadotropins and LH response to LHRH. Basal TSH did not vary, but
there was a reduction in the peak and integrated TSH response to TRH. PRL levels
tend to remain unchanged during fluoxymesterone use (8). Halo is of course
suppressive to your HPTA, but I’ve found that in some studies where measurements
were made of serum FSH, LH, testosterone, up to 20mgs per day of Halo did not
suppress them measurably (9). This could possibly indicate the use of up to
20mgs/day of Ha lotestin without being in any great danger of suppressing
endogenous hormones.
Halo is a testosterone derived steroid, and has an 11-beta group attached to it to
inhibit aromatization. Although it is particularly prone to being 5-alpha-reduced and
may cause DHT related side effects such as acne and hairloss. It is metabolized
primarily by 6 beta-hydroxylation, 4-ene-reduction, 3-keto-reduction, and 11
hydroxy-oxidation. We know this by the indentification of 4 particular metabolites
and the tentative identification of at least 3 other metabolites. Detection of Halo in
urine is possible for at least 5 days after a single 10 mg oral dose to previously
untreated adult males. This occurs by monitoring the presence of 2 metabolites,
since the parent drug is not detectable more than 1 day after the dose (12).
However, the moral-compass of the athletic world, the IOC, has developed a test for
fluoxymesterone metabolites that will detect them for up to 2 months after cessation
of use. This item is not in high demand in bodybuilding except for as a pre-contest
drug and would more likely be found circulating in Athletic and Powerlifting circles
where it is more commonly used in a cycle.
77
Here’s how your body metabolizes Fluoxymesterone:
References:
1. Treatment with anabolic steroids increases the activity of the mitochondrial outer
carnitine palmitoyltransferase in rat liver and fast-twitch muscle.
Biochem Pharmacol. 1991 Mar 1;41(5):833-5.
2. Effects of synthetic androgen fluoxymesterone on triglyceride secretion rates in the
rat.Proc Soc Exp Biol Med. 1975 Jun;149(2):452-4.
3. Metabolism of anabolic steroids in humans: synthesis of 6 beta-hydroxy metabolites of
4-chloro-1,2-dehydro-17 alpha-methyltestosterone, fluoxymesterone, and metandienone.
Steroids. 1995 Apr;60(4):353-66.
4. Influence of fluoxymesterone on in vitro erythropoiesis affected by leukemic cells.Exp
Hematol. 1984 Mar;12(3):171-6.
5. [Erythropoietin in serum and urine in healthy persons and patients with chronic renal
disease upon hypoxic stimulation and hypoxic stimulation after pretreatment with
fluoxymesterone (author's transl)]
6. Fluoxymesterone therapy in anemia of patients on maintenance hemodialysis:
comparison between patients with kidneys and anephric patients.
J Dial. 1977;1(4):357-66
7. Combination hormonal therapy with tamoxifen plus fluoxymesterone versus tamoxifen
alone in postmenopausal women with metastatic breast cancer. An updated
analysis.Cancer. 1991 Feb 15;67(4):886-91.
8. Effect of non aromatizable androgens on LHRH and TRH responses in primary
testicular failure.Horm Metab Res. 1984 Sep;16(9):492-7.
9. The effect of synthetic androgens on the hypothalamic-pituitary-gonadal axis in boys
with constitutionally delayed growth.
J Pediatr. 1979 Apr;94(4):657-62.
10. The effect of synthetic androgens on the hypothalamic-pituitary-gonadal axis in boys
with constitutionally delayed growth.
J Pediatr. 1979 Apr;94(4):657-62.
78
11. Steroids and hematopoiesis. II. The effect of steroids on in vitro erythroid colony
growth: evidence for different target cells for different classes of steroids.
J Cell Physiol. 1976 Jun;88(2):135-43.
12. Testing for fluoxymesterone (Ha lotestin) administration to man: identification of
urinary metabolites by gas chromatography-mass spectrometry.
J Steroid Biochem. 1990 Aug 28;36(6):659-66.
13. Toxic effects of anabolic-androgenic steroids in primary rat hepatic cell cultures.
J Pharmacol Toxicol Methods. 1995 Aug;33(4):187-95.
14. Relative binding affinity of anabolic-androgenic steroids: comparison of the binding
to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone
binding globulin.Endocrinology. 1984 Jun;114(6):2100-6.
15. The relationship of androgen to the thyrotropin and prolactin responses to
thyrotropin-releasinhormonein hypogonadal and normal men.
J Clin Endocrinol Metab. 1981 Feb;52(2):173-6.
Completely Cleanse Steroids From Your
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79
Megagrisevit-Mono
(Clostebol Acetate)
[4-chloro-androst-4-en-3-one, 17b-ol]
Molecular Formula: C21 H29Cl O3
Molecular Weight): 322.8741
Melting Point: N/A
Manufacturer: N/A
Effective Dose: (injectable) 100mgs/day, (oral) 100-200mgs/day
Active Life: (injectable) 2-3 days, (oral) 4-6 hours
Detection Time: 3 months
Anabolic/Androgenic Ratio: 46:25
Clostebol is basically testosterone with an added 4-chloro group in the A-ring. What
does that mean? All it means is that it cannot properly interact with the 5-Alpha
Reductase enzyme to be 5-alpha reduced to dihydrotestosterone. Thus, hair loss and
acne caused by DHT is not possible. Aromatization is also not possible, so estrogenic
side effects aren’t likely either. On paper this looks great and it basically has a
similar anabolic: androgenic ratio to other steroids like Masteron. But I have to say
that since it isn’t DHT-Derived like Masteron is, it’s probably not going to have some
of the cool precontest physique hardening properties of Masteron and other similar
compounds. To be perfectly frank, Clostebol is just a pretty weak testosterone
derived steroid. I wish I could say that it has more to offer, but really, it doesn’t.
Megagrisevit Mono (the brand name for Clostebol Acetate) is presented in a 10 ml
per 1.5 ml vial. This means you’ll need to fill up on many oily injections, which you
are going to have problems finding injection sites for. You know what else? The
short ester found on this stuff will mean that you have to basically load up on tons of
this stuff at least every other day. Women may be able to get by with a bit less,
possibly 1.5mls every other day. There is an oral form of clostebol acetate that is
under the same name of Megagrisevit Mono, but I can’t see that form being
extremely effective either. I think you’ll need to take 100-200mgs of it daily.
Remember, it isn’t 17-alpha-alkylated, so it’ll be destroyed by your liver in pretty
short order. I’ve heard many reports on Steroid.com that a few people have had
access to this drug and liked it, but I’ve not been able to confirm this with anyone
reputable. My advice is that this drug has been discontinued for a good reason and
should be avoided by most serious athletes and bodybuilders.
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As a side note, I’m not really too thrilled with the addition of an Acetate ester to
improve oral absorbtion. When we look at Trenbolone Acetate (oral) vs/ Trenbolone
Acetate (Injectable), on the chart below, we can see that the injectable is around
100 xs as effective for increasing Labc weight, which can be farily accurately used as
a measure of anabolism:
(SC= injection; oral = oral)
That’s a pretty hefty difference in that area, and it is more than enough to get me
wondering about the effects of oral acetate ingestion vs/ intramuscular
administration. I have to say, again, I’m not thrilled with going the oral route, simply
because there’s an acetate ester attached.
One of the most interesting things I found when researching this compound is that
an athlete had tested positive for it by having sex with a woman who had used a
Brazilian compound known as Trofodermin, which is produced by Searle. This
product is indicated for cervicitis, postoperative vaginitis, and ulcerative vaginitis, and
the recommended dose is 5g 1-2x a day. And, of course, it is to be administered
intravaginally. As a result, the athlete who tested positive for Clostebol claimed to
have had sex with a woman who had been using this product. Then tests (all in the
name of science) were performed where two couples had intercourse following the
vaginal application of Trofodermin, and the men were tested via urinalysis for
Clostebol (before and after intercourse). It was then determined that Clostebol can
indeed be absorbed through the penis following vaginal administration of a Clostebol
containing compound. Whoever said that anti-doping research is no fun?
Well, in any case, the subjects involved had fun, although I suppose they weren’t
Olympic athletes. I suppose it would suck to be in the control group for that study,
huh?
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Anyway, here’s how your body metabolizes Clostebol:
References:
1. Clinical Chemistry. 2004;50:456-457. 2004 American Association for Clinical
Chemistry, Inc.
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Methandriol
(Methylandrostenediol)
[17a-Methyl-5-androstene-3B, 17B-diol.]
Formula: C20 H32 O2
Molecular Weight: 304.4716
Molecular Weight:: 304.4716
Molecular Weight (ester): N/A
Formula (base): C20 H32 O2
Formula (ester): N/A
Melting Point (base):
Melting Point (ester): N/A
Manufacturer: Various
Effective Dose (Men):30-50mg orally (daily)/ 300-500mg injectable (weekly)
Effective Dose (Women): ?
Active life: 2-3 days
Detection Time: 3 months
Anabolic/Androgenic ratio: 30-60/20-60
Methandriol is the brand name for the anabolic steroid methylandrostenediol.
Methandriol (or MAD as I like to call it) seems to be one of the more rare and exotic
anabolic steroids. It is actually 5-androstenediol (5AD) that has had its chemical
structure is modified by adding a methyl group so the compound can resist being
broken-down by the liver when taken orally. This results in better utilization by the
body and is called 17-alpha alkylation (17AA). The first aspect that will be addressed
is the one that most interests bodybuilders, the muscle building potential of the
drug. With an anabolic (muscle building) effect of 20-60, (compared testosterone
which has an anabolic rating of 100) not much muscle gain can be expected from
MAD use. It is also slightly androgenic when compared to testosterone which has an
androgenic effect of 100 MAD only rates 30-60. Methandriol low androgenic
properties may be a blessing and a curse. On one-hand with its low androgenic
effects, the drug can be used without worries by individuals who suffer from prostate
problems, hair loss and acne. It may also be used by female bodybuilders who wish
to avoid the masculinizing side effects of androgens once they stick to a reasonable
dosage and cycle duration. On the other hand the benefits of using an androgenic
steroid are lost. There is a direct correlation between a drugs androgenic levels and
strength gains. Highly androgenic steroids also tend to aid in fat loss by binding
strongly to the androgen receptor (A.R). So, there is not much muscle or strength
83
gain from this one. So what the hell is it good for? Glad you asked. Methandriol has
been shown to have an affinity for glucocorticoid-binding sites (2) so this may result
in an anti-catabolic (muscle destroying) effect by inhibiting the muscle wasting
effects of glucocorticoid hormones (3). Also the parent hormone of methandriol, 5
androstenediol (5AD) has been shown to promote favorable immune function (4).
MAD is said to process a unique trait that no other steroid has, the ability to sensitize
the androgen receptor (A.R) to other hormones or the ability to unblock the AR. I do
not know how it started, but this statement is untrue and very misleading. First, the
A.R does not get “clogged up.” In fact, all androgens increase the number of A.R in
muscle tissue (5) so there is no need to use any specific steroid for this purpose. So
far the report on methandriol does not look as good as other anabolic steroids
because there are little muscle and strength gains. However, it may boost immune
function and activate other non-A.R dependant mechanisms of muscle growth.
Adverse androgenic sides are also not a major concern.
Methandriols parent hormone 5AD has been shown to be a steroid with “potent
estrogenic properties” (6). Since methylation makes a hormone more bio-available
and thus “stronger”, I am lead to believe that methandriol’s estrogenic activity is
even more potent than 5AD. This alone is bad news for any Steriod.com members
interested in adding this drug to a cycle. Excessive estrogenic activity can lead to
breast tissue growth in men (gynecomastia), fat gain, water retention, loss of sex
drive, and sluggish natural testosterone production. Worse still is that 5AD itself
activates the estrogen receptor (E.R.) (6). This would make aromatize inhibitors like
letrozole (femera) and anastrozole (arimidex) a bit less effective in combating MAD
estrogenic sides because it does not have to be exposed to the aromatize enzyme to
do any harm. More evidence that supports MAD has direct estrogenic properties is its
use in veterinary injectables. Commonly used for promoting weight gain in animals
(7), studies indicate combining anabolic steroids with female sex hormones
(estrogen, progesterone) promote better weight gain than when alone (8). This is
especially true when female sex hormones are stacked with the non-aromatizing
nandrolone derivative trenbolone (9). MAD estrogenic properties would make it
useful in this regard. This is the REAL reason MAD is added to other anabolic
veterinary preparations, not because it sensitizes the A.R. Most of the profiles on
methandriol says it gives “massive strength gains”; however, looking at the
evidence, it would seem the only “massive strength gains” from MAD could stem
from the increased amount of water retention inside the muscles, which would result
in a rebound effect when the muscles are compressed during the lowering of a
weight similar to the action of a benching shirt. Believe or not estrogen is a muscle
building hormone as well, causing growth by attaching to the estrogen receptor on
muscles (10). These are minor benefits, however, and they are not worth the
potential adverse sides. A common trait from using MAD is elevated blood pressure
(11). This could be from the water retention due to high estrogenic activity or other
actions in the body (11). There is no evidence that methandriol negatively effects
cholesterol, so your cardio vascular heath would be the least of your worries if you
chose to use methandriol.
Now that we know the properties of this drug, we can design cycles to take
advantage of MAD. Doses for MAD range from 30mg to 50mg per day and can be
taken orally or by injection. Being a water based suspension, the active life of the
drug would be measured in hours; thus, methandriol must be injected at least
everyday to keep steady blood levels of the active hormone. If you are to ever come
across this drug in its water based form and did not want to inject it, don’t worry.
Remember, it’s a 17AA compound so, yes, YOU CAN DRINK METHANDRIOL. The
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same thing applies to the drug (oral administration) in tab form, if you were ever to
find it. Being a 17AA steroid, it puts some strain on the liver when orally consumed.
Steroid.com members are advised to limit the drugs intake to several weeks. It is
obvious that MAD is too weak to be used without stacking it with other steroids, and
it is very common to find it included in various exotic steroid preparations. Keep in
mind, MAD itself has an estrogenic action, so the appropriate precautions must be
taken to combat this. Methandriol first must be stacked with testosterone, preferably
a short ester one (see testosterone propionate). Testosterone will combat the libido
lowering effects of MAD, as stated before; estrogenic hormones like MAD seem to
work best when combined with trenbolone, so this would be the second anabolic of
choice. Now you are going to need something to deal with methandriol’s estrogenic
action. Letrozole would be my first choice because it not only block the aromatize
enzyme, but it reduces the concentrations of estrogen receptors as well (12), leaving
MAD with less to bind to. Tamoxifen (novice) would also be a good addition to the
letrozole, binding to what ever estrogen receptors are left. However, ancillary usage
could negate many of methandriol’s benefits because they are seemingly estrogen
dependant!! Now the previously mentioned cycle looks like a cutting cycle. I did not
design it to be one, it’s just that combining MAD with other highly aromatizing
steroids or “bulking” drugs like dianabol, anadrol and long ester testosterones, is
asking for trouble. The level of water retention to follow would surely result in high
blood pressure (not to mention the potential estrogenic side effects). I cannot
recommend MAD be used with other bulking agents. In fact, I do not recommend
that methandriol be used at all!
Methandriol is a rare find in the hands of Steroid.com members. It is an obscure
anabolic that is reported to have special properties it simply does not have. Highly
estrogenic and barely anabolic, it is extremely doubtful this steroid will ever catch on
in the Steroid.com bodybuilding community.
Here’s how your body metabolizes Methandriol:
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References:
1. J Reprod Fertil Suppl. 1982;32:213-8.
2. Endocrinology. 1994 Mar;134(3):1401-8.
3. Endocr Pract. 1999;5(5):277-81.
4. Int J Immunopharmacol. 2000 Jan;22(1):1-14.
5. J Appl. Physiol.94 1153-61 2003
6. J Steroid Biochem Mol Biol. 2003 Sep;86(3-5):423-32.
7. Veterinary Drug List.
8. J Anim Sci. 1999 Dec;77(12):3133-9
9. J Anim Sci. 1997 May;75(5):1256-65.
10. J Anim Sci. 1985 Jan;60(1):294-300.
11. Endocrinology. 1978 Jul;103(1):1-5.
12. Curr Med Res Opin. 2001;16(4):276-84
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
86
Methyltestosterone
(Methyltestosterone)
[17alpha-methyl-4-androstene-3-one,17b-ol]
Formula: C20 H30 O2
Molecular Weight: 302.4558
Melting Point: 162-167
Manufacturer: Most Major Pharmaceutical Companies
Effective dose: (Men)25-100mgs/day; (Women) N/A
Active Life: 6-8 hours
Detection Time: 4-6 weeks
Anabolic/Androgenic Ratio (Range): 94-130/115-150
To understand the history of Methyltestosterone, we need to go back to the 1930’s,
when the structure of the hormones estrone, testosterone, and progesterone were
revealed and understood more completely and their ability to be synthesized from
cholesterol was noted. It was a logical step for researchers to realize that a very
simple chemical modification of the natural hormone would produce an orally active
compound. By the early 1950’s, injectable testosterone, progesterone, and the
subject of this profile, Methyltestosterone, occupied almost 25% of Ciba’s
pharmaceutical turnover (1). Despite the elevations in liver function that oral
testosterone preparations can cause, (and Methyltestosterone is no exception to this)
these drugs still constitute approximately a third of all testosterone prescriptions
filled in the United States (2).
Here, we’re primarily concerned with the use of Methyltestosterone as it applies to
athletes and bodybuilders. As with other Anabolic Androgenic Steroids (AAS), a
quick look at the structure of Methyltestosterone will give us some clues as to how it
will function once in the human body. We can see that it is 17-alpha-methyl altered,
so the hormone can survive its first pass through the liver, and be effective as an
oral agent rather than being destroyed by the liver. Unfortunately, this alteration
also puts stress on the liver and contributes to the hepatoxicity (liver toxicity) of this
compound, which is quite profound with this drug (3). Luckily, it doesn’t have
adverse effects on cholesterol, and can even lower plasma viscosity (4). And, since
this is just testosterone that has been altered to be orally available, some users
actually let the tablet dissolve under their tongue for increased absorbtion. We can
expect many of the same results and side effects that we would with any other
testosterone form such as development of male sexual characteristics in women.
Hence, they should avoid using this compound at any dose, and in men,
aromatization, or conversion to estrogen, is found. This can contribute to hair loss,
87
acne, oily skin, water-retention, gynocomastia, hair growth on the body, and other
side effects. It’s also worth noting that this compound converts to
DiHydroTestosterone, which can cause prostate enlargement and hair loss. Taking
endogenous hormones (AAS) will affect your natural testosterone levels as well as
many interrelated hormones and processes. MethylTestosterone is no exception to
this rule, and taking it will result in significant decreases in plasma levels of
gonadotropins, gonadal steroids, sex hormone binding globulin, free T3 and T4, and
thyroid binding globulin (5). Inclusion of Arimidex at .5mgs/day to help lower
estrogen levels or a similar ancillary, such as Finasteride (1mg/day to help combat
DHT) would be warranted with the use of Methyltest. Also, when considering the
possible side effects and hormonal effects Methyltest can have on a user, proper Post
Cycle Therapy (Nolvadex at 20mgs/day and 500 iu/day of HCG for 3 weeks) is
necessary.
I think that the effect you’ll typically get from Methyltest is most comparable to that
of the short (or no) ester testosterones (i.e. suspension or propionate). Ergo, I
believe you will get a bit stronger but probably will not be impressed with weight
gains unless intolerably high doses are used. A quick survey of the results gained by
members of Steroid.com reveal that none of them were impressed with either weight
or strength gains from Methyl testosterone, but some liked the drug. Hence, I
recommend that you choose a different compound if you are simply trying to get
bigger. Methyltest won’t impress anyone with its ability to add weight to an athlete.
The members of Steroid.com who liked Methyltest generally cited effects such as
increased strength and aggression while using it, especially when it was taken before
workouts. Herein lies the most effective and common use for Methyltest in a cycle.
It is effective for rapid increases in strength and aggression when a dose is taken
prior to a workout or athletic event. Twenty-five mgs taken an hour before working
out or competing should be sufficient for this purpose, while I’d recommend 2-4x
that dose if it’s being used as the primary oral in a cycle. Someone on a cycle may
want to consider the inclusion of this drug into their regimen to make their workouts
more productive, and thus get maximum results from their workouts. This would
allow the other anabolics in their cycle to be more efficient. Powerlifters also love
this drug and it is often used prior to competitions as well as prior ot workouts.
Again, in terms of cost/benefit ratio (side effects vs. results), Methyltest is most
effective for use prior to a weight training workout or athletic competition, (or
possibly to increase aggression in the weight room on a low calorie diet) and not as a
weight gain or strength gain drug. Using Methyltest 3-4x a week before workouts
will help you derive more benefits from those workouts (and this will be especially
important on a cycle) while minimizing possible issues with liver toxicity. Trying to
use this compound multiple times per day and every day of the week (as would be
necessary if this were the primary oral in your cycle) would not produce acceptable
results (in my mind, anyway) when compared with the risks taken.
There are better orals than Methyltest for both size and strength, but perhaps none
are as good at increasing aggression. You can use this drug in conjunction with any
type of cycle as a pre-workout boost. If this drug is used as the main oral in a cycle,
then the use of Methyltest should be limited to 50mgs/day for no more than 6
weeks. After cessation, a long break from all liver-stressing compounds should be
taken (i.e. oral AAS, Alcohol, etc…).
Availability of this drug is reasonably high, as most major pharmaceutical companies
produce it, as do a few UnderGround Labs. It’s reasonably priced since the demand
88
for it isn’t very high. I wouldn’t be able to justify paying more than a quarter
(25cents, American) per tab for this stuff, and it could be found for under that based
on availability, demand, and results.
Here’s how Methyltestosterone is metabolized in your body:
References:
1. Karl Huesler & Jaroslav Calvoda, Pharmaceuticals Division, Ciba-Geigy
2. Westaby, D., Ogle, S.J., Paradinas, F.J., et al Lancet, August 6:261, 1977
3. Lancet, August 6:261, 1977
4. Clin Endocrinol (Oxf). 2002 Aug; 57(2):209-14.
5. Psychoneuroendocrinology. 2003 Apr; 28(3):317-31
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Myagen
(Bolasterone or Dimethyltestosterone)
[7-ALPHA, 17-ALPHA-DIMETHYLTESTOSTERONE]
Molecular Formula: C21H3202
Molecular Weight: 316.4826
Melting Point: 162-167
Manufacturer: N/A
Release Date: N/A
Effective Dose: 50-100mgs
Active Life: 6hours
Detection Time: 4-6 weeks
Androgenic/ Anabolic Ratio: 300:575
Basically, what we have here is DiMethyltestosterone or Methyltestosterone with an
added methyl group (hence “dimethyl”) at the C7 position. I think any further
comparison to Methyltestosterone (except perhaps with regards to hepatoxicity)
wouldn’t really be warranted.
It needs to be noted that a lot of what I’m going to tell you about this drug is
basically speculation for now, although I suspect that since we’ve seen the
reemergence of several drugs which wear gone for decades (Mitolan, OT, etc…), this
one isn’t far behind. Why would this stuff reappear on the market? Well, by taking a
look at its androgenic/anabolic ratio, you should see why. It’s 3x as androgenic as
testosterone and almost 6x as anabolic! This makes it one of the most powerful oral
anabolic steroids ever made.
While writing this book, I contacted several underground Labs to see if they could
produce this drug, for me to test out on myself (as I have done with several
experimental compounds already). Unfortunately, nobody seemed to know where to
get this stuff from, and nobody I’ve spoken to has ever used it.
So, as it stands, we can look at this drug on paper and speculate that it would be a
very useful anabolic compound, it’s going to remain on paper until some resourceful
underground decides to produce it.
This is how Bolasterone is metabolized in your body:
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References:
1. CLINICAL EVALUATION OF A NEW ANABOLIC AGENT 7-ALPHA,17
ALPHA-DIMETHYLTESTOSTERONE (BOLASTERONE). Clin Pharmacol Ther.
1963 Nov-Dec;30:734-9.
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Omnadren
(Testosteone shown, plus testosterone with Propionate, Phenylpropinoate,
Isocaproate, and Caproate esters)
(Testosterone + 4 esters)
[4-androsten-3-one-17beta-ol]
Formula (of Base): C19 H28 O2
Formula (esters)
Propionate:C3 H6 O2
Phenylpropionate:C9 H10 O2
Isocaproate:C6 H12 O2
Caproate:C16 H12 O2
Molecular Weight (of Base): 288.429
Molecular Weight (esters)
Propionate: 362.5082
Phenylpropionate: 438.6058
Isocaproate: 404.5886
Caproate:116.16
Melting Point: 154-155C
Manufacturer: Jelfa
Effective dose: 250-1,000mgs/week
Active Life: 10 days
Detection Time: 3 months
Anabolic/Androgenic Ratio: 100:100
1 milliliter of Omnadren 250 contains:
30mg testosterone propionate
60mg testosterone phenylpropionate
60mg testosterone isocaproate
100mg testosterone caproate
Omnadren 250 is a combination of the 4 separate test esters listed above. Older
versions of the drug, list the final two esters as ‘isohexanoate’ and ‘hexanoate.’
However, it should be noted that hexanoate is simply another word for caproate, so
92
the drug’s esters have not actually been modified. Most commonly, people will
correlate Omnadren 250 with its cousin Sustanon 250, since they are both a blend of
4 test esters. The only difference between the two lies in the last and most
concentrated-ester. Whilst Omnadren contains the caproate ester, Sustanon
contains the decanoate ester in the same concentration. Really, except for price,
there’s no difference between them, and price-wise, you’re going to be paying ½ as
much for Omnadren as you would for Sustanon (or $3-4usd/amp). This is a very
nice price, and for that reason, I typically advise people to purchase Omnadren over
Sustanon if their source carries it.
It is also not uncommon to hear people refer to Omnadren as a superior version
of testosterone since it boasts 4 esters instead of 1 (or none). This should be taken
with a grain of salt. All testosterones produce very similar effects, while the ester
simply delays the release of the compound into the body, which has two immediate
consequences. The first being less important: injection frequency. This has recently
become a hotly debated issue. On one side, there are those who advocate injections
only once or twice a week. Their arguments are supported frequently with cycle
results that have yielded ‘good gains.’ On the other side, perhaps the more scientific
side, are those who advocate injections at least every-other-day (EOD) or everyday
(ED). One only has to glance at the ester constitution in Omnadren to understand
why this is so. Such small concentrations of the shorter esters (propionate and
phenylpropionate) are rendered practically useless when Omnadren is injected once
or twice a week. Furthermore, when injecting only a few times a week the “peaks
and valleys” of concentration in the blood are not desirable. We want our blood
concentration of the drugs to be as high as they can be –relative to dose- as long as
they can be. Obviously, this is not the case when fast acting esters are introduced
and subsequently dissipated before another injection is given.
The longest ester in Omnadren (caproate) is slightly faster acting than the longest
ester in Sustanon (decanoate), and users will notice an increase in their testosterone
levels sooner with Omnadren than with Sustanon. This has a few consequences that
we shall examine now. First of all, since testosterone aromatizes (converts) to
estrogen, a buildup of this female hormone will occur more rapidly. Estrogen
increase follows the inevitability of increased water retention. This is significant for 3
reasons.
First, the user’s strength will increase. Secondly, the user’s size will
increase, and finally, definition in the muscles will begin to dissipate. As a result,
Omnadren is typically used more for bulking than cutting. The extent of these
effects are highly dictated by the user’s diet and training habits; although, it is also
easily controlled with the proper use of anti-estrogen drugs such as Nolvadex,
Armidex, Proviron, and a myriad of others.
As I previously stated, testosterone is a highly anabolic and androgenic hormone,
and it has an anabolic (muscle building) rating of 100, making it a good drug to use
if one is in pursuit of more size and strength. And if you aren’t in pursuit of more
size and strength, then why would you be reading this, right? Well, let’s get on with
it and look at exactly what makes testosterone a good mass builder. First,
testosterone promotes nitrogen retention in the muscle (6). The more nitrogen the
muscle holds the more protein the muscle stores. Testosterone can also increase the
levels of the highly anabolic hormone, IGF-1, in muscle tissue (7)(9). Even the
aromatized part of testosterone that turns into estrogen may increase levels of IGF,
and it may also increase sensitivity to it. Testosterone’s actions come mostly from its
binding to the androgen receptor to promote A.R dependant mechanisms for both
muscle gain and fat loss (5). Thankfully, it also significantly increases the
93
concentrations of the A. R in cells critical for muscle repair and growth and A.R in
muscle (8). Testosterone induces changes in shape; size and also can change the
appearance and the number of muscle fibers (7). Androgens like the testosterone(s)
found in Omnadren can protect your hard earned muscle from the catabolic
hormones (8), whether those hormones occur from exercise or other stress.
There are strong androgenic side effects, which are pronounced with Omnadren (as
with all testosterones). Oily skin, acne, increased body/facial hair, and, depending on
the individual, an increase in aggressiveness can occur. Omnadren can also be hard
on the hairline. This is partly due to the conversion of the testosterone into
dihydrotestosterone (DHT). Test is converted to DHT via the 5-alpha reductase
enzyme. DHT is more potent than test at the androgen receptor (the double bond is
removed from the carbon4-carbon5 bond and replaced with a hydrogen atom on
each) and is responsible for some growth. It can also cause some negative side
effects as well. Because of this bond, Testosterone is actually much more anabolic.
For example: DHT formation in the scalp is suspected of causing/expediting male
pattern baldness. To possibly combat this, one can use finasteride (Proscar®). This
drug will inhibit the conversion of testosterone to DHT, but many users will report
that since DHT is more potent at the androgen receptor than test, gains in muscle
mass, as well as strength, will diminish. On the other hand, a lack of DHT caused by
blocking 5-AR can sometimes cause gynocomastia (4)(5).
Typically, cycles that contain Omnadren 250 will be around 12-16 weeks. The idea is
that it will take at least 2 weeks for the compound to become fully ‘active’ in the
body, and most users will report an additional 1-3 weeks until the effects of
Omnadren are truly felt. As a result, gains from Omnadren are not typically noticed
for about 1 month after the first injection. What most people mean by this is that,
although the actual drug is already active, gains aren’t realized immediately. The
majority of users will supplement a fast acting oral drug such as Dianabol or Anadrol
in the first 4 weeks of a cycle, which is thought of as a ‘kickstart’ until the effects of
the Omnadren are fully felt. As mentioned above, a typical weekly dose of
Omnadren can range from 500mg-1000mg per week. Those who are new to steroids
and cycling should generally start with a minimal dose to better judge how their own
bodies will react to the synthetic testosterone. I suggest that beginners stick with 2
amps per week if they’re inclined to use this preparation.
Omnadren has always been manufactured by Polfa©, who have changed their name
to Jelfa©. The company is based in Poland, and as one might obviously conclude, the
availability and price of Omnadren 250 is different in many places. Often, fake
Sustanon in the 80’s would actually turn out to be Omnadren, which was much less
highly prized (nonsensically).
References:
1. Hypothalamic sites of action for testosterone, dihydrotestosterone, and estrogen in the
regulation of luteinizing hormone secretion in male sheep. Endocrinology. 1997 Sep;
138(9):3686-94.
2. Inhibition of LH Secretion by Localized Administration of Estrogen, but not
Dihydrotestosterone, Is Enhanced in the Ventromedial Hypothalamus during Feed
Restriction in the Young Wether. Biol Reprod. 2005 Jun 22; [Epub ahead of print]
3. Crystalline dihydrotestosterone implants in the lateral septum of male rats. A positive
94
effect on LH and FSH. Endocr Res. 2001 Feb-May; 27(1-2):35-40.
4. Significant role of 5 alpha-reductase on feedback effects of androgen in rat anterior
pituitary cells demonstrated with a nonsteroidal 5 alpha-reductase inhibitor ONO-3805. J
Androl. 1994 Nov-Dec; 15(6):521-7.
5. Case report: finasteride-induced gynecomastia in a 62-year-old man. Am J Med Sci.
1995 Jun; 309(6):322-5.
6. J Clin Endocrinol Metab. 1997 Feb; 82(2):407-13.
7. Am J Physiol Endocrinol Metab. 2002 Mar; 282(3):E601-7.
8. Curr Opin Clin Nutr Metab Care. 2004 May; 7(3):271-7.
9. Comparison of effects of the rise in serum testosterone by raloxifene and oral
testosterone on serum insulin-like growth factor-1 and insulin-like growth factor binding
protein-3. Maturitas. 2005 Jul 16; 51(3):286-93.
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95
Oral-Turinabol
(4-chlorodehydromethyltestosterone)
[4-chloro-17b-hydroxy-17a-methyl-androst-1,4-dien-3-one]
Formula:C20 H27 O2 Cl
Molecular Weight:334.8854
Manufacturer: Underground Labs only
Effective Dose (Men): 10-40mgs/day
Effective Dose (Women): 5-15mgs/day
Active life: 16 hours
Detection Time: 6 weeks
Anabolic/ Androgenic ratio: >100:>0
Oral Turinabol was first developed by scientists in East Germany for their Olympic
and national-level athletes to use. This, plus the eventual removal of it from the
market caused OT to become a very “sexy” drug for athletes to try to obtain. The
East Germans studied this drug pretty extensively for many years and some of the
success of this now defunct country was attributed to this drug. It made its first
appearance to athletes in East Germany as little blue “Vitamins” their coaches gave
to them. This drug has been discontinued by all of the major pharmaceutical houses,
and is only found through certain underground labs. Although some UnderGround
Labs have access to this item and it appears on their price-lists, it’s still rare enough.
I believe it was first produced in the last half decade by a certain cat in Thailand. It’s
my speculation that it’s on the cusp of either becoming very popular, to the point
where every Underground Lab will start carrying their own version of it, or it will
disappear again and only be carried by a select few, if any, suppliers.
The easiest way to explain this drug is that it is a derivative of Dianabol. Though it is
a derivative of our old friend Diana, it’s still quite different. Remember, Equipoise is
estrified Dianabol, and really has nothing in common with it in terms of real-world
effects. Let’s examine OT in relation to D-bol for now. The first similarity between the
two is that they have been 17-alpha-alkylated (a carbon atom was added at the 17th
position) to survive the first pass through the liver. This, of course, increases
hepatoxicity (liver toxicity). OT has a much lower level of androgenic activity
compared to dianabol, but has a better balance/ratio of anabolic and androgenic
effects. It has a rating of a 0 (according to the Vida reference) for androgenic
properties and a 53 for anabolic properties based on a score of 100 each for
testosterone. This promotes more of a "hard" look, or what competition bodybuilders
often call “quality” muscle. You do not get the same "puffy" look as you would on d
96
bol, and many people have thus compared the results they’ve gotten from OT to
Anavar. Actually, though, this stuff is simply dianabol with a 4-chloro alteration, the
same alteration found in Clostebol.
Due to this 4-chloro substitution in the A-Ring of its Steran Nucleus, this drug cannot
be aromatized (3). This is, as you know, quite beneficial and is one of the reasons
Oral Turinabol has been called a "gentle d-bol.” You will probably not get any typical
estrogenic side effects like water retention, acne, gyno, etc. with any dose of this
drug. I read a couple of studies examining male athletes over a period of six weeks
who were given 10 mg OT/day and did not show any indication of health-threatening
effects. It has been recommended that men should take between 20-40mg every-
day and women a 5mg everyday, and I generally think that it is not very strong (as
compared to many other orals) and wouldn't drop below the 40mg mark if I were to
use it personally. It may perhaps be used in low(er) doses if it is simply being used
for its ability to reduce SHBG's binding (1) to other steroids. In this respect, it may
have synergy with other drugs since it has the ability to reduce SHBG and free up
more testosterone for use in the body.
The only negative thing I have heard about this drug is that in high doses (10+mg)
virilization has been seen in women (14) and there has been at least one case of
testicular tumors, and one case of a guy who suffered adverse effects from 5 years
of high-dose use of OT (2)(4). It should be noted that the former East Germans did
many experiments with this drug in high doses though, and found it to be a very
suitable compound for their athletes. Many of the women suffered virilization at
higher dosages, though. During the 68-72 Olympic cycles, the East German Sports
OT program made its biggest impact. It was around this time that the East German
weightlifters were taking over 10g/year of OT, and their leading male sprinter was
taking under 730mgs/year of OT (14). I think this tells me that for real weight gains
and huge gains in the weight room, you’re going to need bank-breaking doses of this
stuff. On the bright side, if you are an athlete looking to get faster, a little bit of OT
will get you there pretty easily and with minimal (if any) side effects. I think that its
inability to cause negative side effects and its ability to produce a favorable increase
in lean body mass, thus, causing a favorable increase in strength/speed makes this
substance popular. An athlete’s strength: bodyweight ratio is what turned the East
German coaches and scientists on. It must be noted that, at the time, this stuff was
mostly undetectable and that was certainly a sought after trait by the East Germans
who were looking to circumvent the drug testing procedures of the IOC. Now, of
course, OT is detectable once it’s administered to man because three major
metabolites are formed: 6 beta-hydroxy-turinabol, 6 betas, 12-dihydroxy-turinabol,
and 6 beta, 16-dihydroxy-turinabol (5)(8)(9). All of those metabolites are now
detectable by drug screeners. In much smaller quantities at least another three
metabolites are excreted, one of which could be identified as 17 epi-turinabol (5),
and is easily detected by modern drug tests. No measurable amounts of OT itself
are detected in any of the urine samples investigated in sport’s doping procedures,
but the presence of the metabolites is enough to warrant a positive result and a
failed test. Keeping all of this in mind, it is still important to note that the rate of
metabolism and urinary excretion or Oral-Turinabol is reasonably fast (5), even
though it is technically eliminated biphastically (in two stages) by the body with a
terminal 16hr ½ life (1). I thank the sports-doping-party-poopers (The NCAA and
IOC). OT is notorious for increasing the time it will take for your blood to clot
because it has spontaneous fibrinolytic properties. “Fibrinolytic effects” means that
the destruction of fibrin (an insoluble fibrous protein produced in the liver from the
soluble protein) is happening in your body. Fibrinogen is important during the blood
97
clotting process. It is a soluble protein in the blood that is converted to insoluble
fibrin by the action of the enzyme thrombin in response to tissue damage. (6)(7)
Thus, you will bleed for longer than usual when on this stuff. Combine that with the
fact that steroids raise your hematocrit and you’ll be spending your entire morning
trying to stop the bleeding if you cut yourself shaving. Well, that’s probably an
exaggeration, but not by much.
I’ve already told you that this stuff is a potent lean tissue builder, and good for
cutting. But that’s mostly of interest for bodybuilders. Now, with regards to athletics,
what kind of results can we expect? Well, I was digging through the old East
German literature, and found that they reported that their world class strength
athletes were making some pretty remarkable improvements on OT over a 4 year
Olympic training period: Male Shot-putters were adding 2.5-4m to their shot throws,
10-12m on their Discus throw, and 6-10m to their Hammer throws. Female athletes
gained even more. Let’s take a look at a chart representing the improvements made
by one particular female strength athlete (she held the World Record for the shot
put, at the time of her beginning OT administration) over the period of July 18 1968
through October 13 1972. During this time, she was taking OT and she improved
her throw from under 18m to over 20m (yes, this is a 2m+ improvement to a world
record holding throw in one Olympic Cycle). She was taking roughly 5-15mgs/day of
OT in the beginning, but worked up to 35mgs/day before she was done with her
Olympic cycle. Her throws even while “off” OT even improved a bit, leading to
speculation that there are a lot of permanent gains to be had with OT. Anyway, here
are the charts representing her intake of OT, as well as her improvements over her 4
year over her 4 year Olympic training regimen:
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Effects of an androgenic-anabolic steroid, Oral-Turinabol, on the shot-put
performance (in meters, y-axis) of a female athlete (code identification 1/68 in a,
1/69 in b, and 1/72 in c) directly photographed from the secret scientific report of
Bauersfeld et al. (13), is one of the numerous examples documented and is chosen
here because of its historic importanc. It is the first documented case of androgenic
doping of a woman (for a detailed account, see ref. (11)). (a) 1968. The rectangle
from July 28 to October 13 shows the period of drug administration, and the
numbers above each date show the number of tablets taken per week (here, 14, or
10 mg per day). The curve presents the results of the specific competitions, showing
the increase of strength and performance in a fully trained woman. At the time of the
first drug application in 1968, the athlete had been well trained for almost 14 years.
Under the influence of the drug, however, she gained unprecedented muscle
strength and improved her records dramatically within a few weeks. (b) 1969. The
steroid was given in three cycles and at various dosages, from 7 to 21 tablets per
week (i.e., 5–15 mg daily). Without the drug, she could not reach 18 m, but when
taking the drug, she improved her world record once more, to 20.10 m. (c) 1972.
She took even more of the androgenic hormone, with daily dosages of up to 7 tablets
per day (35 mg), in four cycles, for a total androgenic load of 1450 mg for the year.
This led to her top performances in the winter indoor season (left curve) as well as in
the summer (right curve) and another personal best (20.22 m). Note the much lower
performance at times off the drug or after only short periods of androgenization.
Also, after 4 years of systematic androgenization, her basic strength level when not
taking the drug had also increased by ~1 m, indicative of a residual effect/
(14).
Did all of this work for anyone else? Well, as I told you, virtually everyone who was
involved with the East German Olympic Training program was on some kind of
steroids, but OT was by far the most popular. They had access to some pretty wierd
stuff, too, like intranasal testosterone, etc…
So, back to OT, it is notable from my readings on this compound that women saw
much more positive effects from OT did than men (this is generally true of all
steroids). Women also showed more side effects and generally found the side effects
to be more severe and unbearable than their male counterparts. Unfortunately, they
sometimes tended to use higher dosages than the men did; often up to 2 xs as high.
Let’s take a look at their typical yearly doses:
Some documented dosages of androgenic-anabolic steroid (Oral-Turinabol)1 taken
by female GDR medal winners (track and field) in Olympic Games, World
Championships, and European Championships (2):
Annual dosage of OT in mgs followed by events
3680 Shot-put
3190 Discus
2900 Shot-put
2615 Shot-put
2590 Shot-put
1670 Sprint
1560 Hurdles
1480 Hurdles
1474 Sprint
1460 Sprint
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1450 Shot-put
1405 Sprint
1380 Heptathlon
1375 Sprint
1340 Heptathlon
1255 Discus
1230 Heptathlon
1230 Hurdles
1185 Javelin
1.Additional injections of testosterone esters have not been considered here.
2. At least 12 of the drug-receiving competitors listed in this table set world records.
In keeping with Journal policy regarding confidentiality of patients and subjects, the
names of subjects have been omitted.
Shocked? Don’t be. This was during the cold war, and victory in the Olympics was
seen as a victory for a certain way of life and a certain ideology; defeat was
unthinkable and unacceptable. Is the recent reappearance of Oral-Turinabol on the
black market going to change athletics or bodybuilding dramatically? No, I doubt it.
A combination of price ($1/10mgs average) and availability may cause this stuff to
remain an understated tool at our disposal. It is, however, a viable tool in a lean
mass cycle, cutting cycle, or any athlete’s drug intake routine.
As a final reference, I'll give you an example (direct from the East German State
Doping Program's reports) on how they used OT throughout the year, and with
various other drugs (like Test Prop, for example):
100
Anabolic and special preparation for the top competition of the year during the
immediate preparation period in the Olympic cycle 1980/84. The example examines
some selected long jumpers (W) and a high jumper (H) in combination with the
results of competitions during this time. Example (from hundreds of evaluations)
showing typical administration patterns of orally taken synthetic anabolic-androgenic
steroids (Oral-Turinabol, periods of application denoted by rectangles) and injections
of testosterone esters [arrows, 10 mg of testosterone propionate (TP); triangles, 25
mg of TP; circles, 100 mg of testosterone enanthate plus 1500 IU of hCG], here
given to high (H) and long (W, Weitsprung) jumpers during the last 10 weeks before
a major international competition in 1981–1984 [immediate preparation period
(UWV), in weeks, is indicated on the x-axis; WS, competition series preceding the
UWV; the competition results (in meters) are shown immediately above the specific
drug application symbols].(14)
Here’s how Oral Turinabol is metabolized in your body:
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References:
1. [The pharmacokinetics of Oral-Turinabol in humans] Pharmazie. 1991 Sep;
46(9):650-4. German.
2. Department of Urology, Universitaetsklinikum "Carl Gustav Carus," Technical
University of Dresden,Dresden, Germany
3. Influence of 1-double bond and 11 beta-hydroxy groups on stereospecific microbial
reductions of 4-en-3-oxo-steroids.
J Steroid Biochem. 1986 Oct; 25(4):561-6.
4. Intratesticular leiomyosarcoma in a young man after high dose doping with Oral
Turinabol: a case report. Cancer. 1999 Oct 15; 86(8):1571-5.
5. GC and capillary column GC/MS determination of synthetic anabolic steroids. II. 4
chloro-methandienone (oral turinabol) and its metabolites. J Chromatogr Sci. 1983 Sep;
21(9):405-10.
6. [Activation of the fibrinolytic system with dehydrochlormethyltestosterone]
Folia Haematol Int Mag Klin Morphol Blutforsch. 1984; 111(4):556-62. German.
7. [Modification of hypofibrinolytic states by dehydrochlormethyltestosterone]
Folia Haematol Int Mag Klin Morphol Blutforsch. 1984; 111(4):563-6. German.
8. [Application of microbial enzymes in studies of steroid metabolism (author's transl)]
Acta Microbiol Acad Sci Hung. 1975;22(4):397-402. Review. German.
9. [Application of microbial enzymes in studies of steroid metabolism (author's transl)]
Acta Microbiol Acad Sci Hung. 1975;22(4):397-402. Review. German.
102
10. [ON THE PHARMACOLOGY OF "ORAL TURINABOL".] Dtsch Gesundheitsw.
1965 Apr 15; 20:690-1. German. No abstract available.
11. Berendonk B. Doping. Von der Forschung zum Betrug. Reinbek bei Hamburg:
Rowohlt Taschenbuchverlag. 1992:448pp
12. [4-CHLORO-DELTA-1-METHYLTESTOSTERONE (ORAL TURINABOL), A
NEW EFFECTIVE ORAL ANABOLIC STEROID.] Dtsch Gesundheitsw. 1965 Apr 15;
20:670-4. German. No abstract available.
13. Bauersfeld K-H. Olek J. Meibner H. Hannemann D. Spenke J. Analyse des Einsatzes
u. M. in den leichtathletischen Wurf/Stob-disziplinen und Versuch trainingsmethodischer
Abteilungen und Verallgemeinerungen. Science Center of the DVfl 1973:41pp.
14. Clinical Chemistry 43:7. 1262-1279 (1997)
Research Anabolic Steroids
and Related Topics at:
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103
Spectriol
(Testosterone and Nandrolone shown, followed by Methandriol)
(Testosterone + Nandrolone + Methandriol)
[17b-hydroxy-4-androsten-3-one + 19-nor-androst-4-en-3-one-17beta-ol + 4 chloro
testosterone]
Testosterone base + cypionate ester. + Propionate ester+ Hexahydrabenzoate ester
Formula: C27 H40 O3.
Molecular Weight: 412.6112
Molecular Weight (base): 288.429
Formula (base): C19 H28 O2
Melting Point (base): 155C
Effective Dose (Men): 200-2000mg+ week.
Effective Dose (Women): Not recommended
Active life: 12 days.
Detection Time: Up to 3 months
Anabolic/Androgenic ratio: 100/100.
Nandrolone base + phenylpropionate ester
Formula (base): C18 H26 O2
Formula (ester): C9 H10 O2
Molecular Weight (base):274.4022
Melting Point (base): 122-124°C
Active life: 15 days
Detection Time: Up to 18 months
Anabolic/Androgenic ratio: 37:125
Methylandrostenediol dipropionate
Formula: C20 H32 O2
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Formula (base): C20 H32 O2
Formula (ester): C3 H6 O2
Molecular Weight: 304.4716
Molecular Weight (base): 304.4716
Molecular Weight (ester): 74.0792
Melting Point (ester):21.5C
Effective Dose (Men):350mg week.
Effective Dose (Women): 25mg per day.
Active life: 3 days
Detection Time: 2 weeks
Anabolic/Androgenic ratio: 30-60/20-60
Spectriol has the dubious distinction of having three totally separate compounds in it,
one having 3 totally different esters, and all three are in an mg/ml concentration that
is too low to do a damn thing! This product is made by RWR in Australia. They have
made a name for themselves by producing interesting and unique blends of different
compounds, esters, and combinations of both.
Let’s see how Spectriol breaks down, per ml:
Methandriol Dipropionate: 20mgs
Nandrolone Phenylpropionate: 15mgs
Testosterone Propionate: 10mgs
Testosterone Cypionate: 10mgs
Testosterone Hexahydrobenzoate: 10mgs
And all of this comes in a 10ml multi use vial. Unfortunately, this equates to 30mgs
of testosterone, 15 mgs of Nandrolone, and 20mgs of Methandriol per ml. You’ll
need a minimum of a bottle (or 2) per week of this stuff. Realistically, that’s 20mls of
oil in your body every week and a lot of sore injection sites that can’t be kept up for
very long. Lets look at it this way: if you shoot this stuff yourself, rotating 4-6
injection sites, you’ll still be shooting it into areas that may not have recovered from
the last shot you put in there. I just don’t think too many people will keep that up for
too long.
This stuff may be useful for women, perhaps shooting one ml per week.
105
Sten
(Testosterone shown, plus testosterone with propionate and Cypionate ester, and
DHEA)
(Testosterone Cypionate &Propionate + DHEA)
[17b-hydroxy-4-androsten-3-one/17-(1-oxopropoxy)-(17beta)-androst-4-en-3-one
+ 3beta-Hydroxy-5-androsten-17-one]
Testosterone base + cypionate ester. + Propionate ester
Molecular Weight: 412.6112
Molecular Weight (base): 288.429
Formula (base): C19 H28 O2
Melting Point (base): 155C
Effective Dose (Men): 200-2000mg+ week.
Effective Dose (Women): Not recommended
Active life: 12 days.
Detection Time: Up to 3 months
Anabolic/Androgenic ratio: 100/100.
Molecular Weight (DHEA): 412.6112
Formula (DHEA): C27 H40 O3,
Melting Point (DHEA) 90, 149 - 151 °C
Manufacturer: Atlantis, MX 120mg/2ml
Effective Dose (Women): Not recommended
Average Active Life: +/- 1-1.5 weeks
(2ml of Sten contains 25 mg testosterone propionate, 75mg testosterone
Cypionate, and 20mg DHEA)
Sten, yet another blended steroid, is similar to Testoviron, but it has different dosing
with the addition of DHEA. Specifically, this blend is made up of testosterone
propionate and testosterone cypionate, as well as a steroid called
dehydroepiandrosterone, or better known as DHEA. DHEA is a hormone produced by
the adrenal cortex as well as the brain. Some of this hormone is actually converted
to testosterone in males and estrodiol in women (1).
The function of DHEA in the body is not clearly understood. For starters, unlike
testosterone, there is no receptor for DHEA or its close relative DHEAS. It is also non
anabolic receptor mediated, meaning its action has nothing to do with the anabolic
receptors in your body. Let’s figure out exactly what it does and how it is beneficial
to us. For starters, Dehydroepiandrosterone is well known to decrease body fat
significantly (3)(4). It has been shown to reduce both abdominal fat as well as
106
visceral fat (5). This makes Sten a very exciting drug, as it contains a steroidal fat
burner as well as a short and long acting testosterone.
Obviously, Sten also contains testosterone, so it would be appropriate to have a brief
review of that compound as well. Testosterone is known to cause strength and
muscle growth. The most obvious mechanism by which testosterone induces muscle
growth is that it promotes nitrogen retention in the muscle (6) and the more
nitrogen the muscle holds, the more protein the muscle stores. Testosterone can also
increase the levels of another anabolic hormone, IGF-1, in muscle tissue (7). This
hormone is the mediator of Growth Hormone and also (as the name implies) causes
muscle growth. Testosterone can help protect your hard earned muscle from the
catabolic (muscle wasting) glucocorticoid hormones (11), thus inhibiting the actions
of them. Testosterone has the ability to increase red-blood cell production (12), and
a higher RBC count may improve endurance by highly oxygenating the blood going
to your muscles. More highly oxygenated blood in your muscles will improve
recovery from strenuous physical activity.
Sten would be used very similar to a Sustanon-type blend. Sten is not nearly as
common as it was 5 years ago, but it can still be found in some parts, especially
Mexico. Male users would want to take a dosage range of 200-400mg/wk for an
effective range. Intermediate users would use a dosage of 400-800mg/wk, while
advanced users could go as high as 1000mg/wk. This compound should not be
recommended to women even in low doses; although the more adventerous women
I know have tried 1/2 an amp/week of it. Remember ladies, testosterone has very
strong virilizing properties in women such as deepened voice, increased body hair,
acne, and clitoral hypertrophy.
The testosterone contained in Sten can be converted to other unwanted by-products
also. The 5-alpha-reductase enzyme can convert the testosterone into
dihydrotestosterone, or as its better known, DHT. DHT is responsible for mens’
hairloss and for prostate hypertrophy. Anti-DHT drugs such as Finasteride can be
taken to block this conversion and offset most of the possible side effects. Some men
will be much more genetically prone for hair loss, which will greatly magnify the
effects of DHT.
A second by-product produced by exogenous testosterone administration is, of
course, estrogen. The aromatase enzyme can convert testosterone into estrogen.
The rate in which it converts will vary depending on the dose and will vary from
person to person. The top symptoms include bloating, gynecomastia, elevated blood
pressure, acne, and increase in cholesterol levels. To combat this, the use of anti
estrogen compounds is highly recommended.
Users of this compound report great gains with testosterone in general. It can be
used in cycles planned to gain mass or lose fat. Gains usually come quickly and are
maintained well with proper post cycle preventions.
Testosterone is usually considered the base compound of any cycle. After all, it is
the primary anabolic hormone in the male body. For this reason, Sten can be stacked
with any other compound desired. The most popular combinations are with Dianabol,
Equipoise, Deca, or Trenbolone.
Sten contains only natural hormones. Partly for this reason, the drugs contained in
107
Sten are only detectable for approximately 3 months. This makes Sten a good choice
for those who are only seasonally tested.
Although a blend of esters, the longest active life is reported to be just around 2-3
weeks. The length of this life is attributed to the testosterone cypionate contained in
Sten. Ideally, Sten should be injected at least every third day in order to properly
utilize the testosterone propionate in it while giving stable levels of testosterone in
the blood.
I have to admit, this is really the only blended testosterone product I will reccomend,
and this is for several reasons, really. For starters, there are absolutely zero known
fakes of this product. The second reason is that it's absurdly cheap When I was last
in Mexico, it was less than $3USD for a box of 2 amps (2mls each), each amp
containing 25mgs of testosterone propionate, 75mgs of Cypionate, and 20mgs of
DHEA. This means you get 200mgs of testosterone, plus 40mgs of the fat-burning
DHEA, for half the price of an amp of Sustanon.
As a final note, I never smuggled a hundred amps of Sten from Mexico back into the
U.S. of A. in an industrial sized suntan lotion bottle.
References:
1. Psychol Neuropsychiatr Vieil. 2003 Jun;1(2):111-9.
2. Endocr Res. 2004 Nov;30(4):667-71
3. Effect of DHEA on endocrine functions of adipose tissue, the involvement of
PPARgamma.Biochem Pharmacol. 2005 May 16; [Epub ahead of print]
4. Effects of dehydroepiandrosterone (DHEA) supplementation on hormonal, metabolic
and behavioral status in patients with hypoadrenalism. J Endocrinol Invest. 2004
Sep;27(8):736-41.
5.Effect of DHEA on abdominal fat and insulin action in elderly women and men: a
randomized controlled trial. JAMA. 2004 Nov 10; 292(18):2243-8.
6. J Clin Endocrinol Metab. 1997 Feb; 82(2):407-13.
7. Am J Physiol Endocrinol Metab. 2002 Mar; 282(3):E601-7.
8. Curr Opin Clin Nutr Metab Care. 2004 May; 7(3):271-7.
9. Curr Pharm Biotechnol. 2004 Oct; 5(5):459-70.
10. J Clin Endocrinol Metab. 2004 Oct; 89(10):5245-55.
11. Anat Histol Embryol. 2003 Apr; 32(2):70-9.
12. J Lab Clin Med. 1995 Mar; 125(3):326-33.
13. Zhonghua Nan Ke Xue. 2003; 9(4):248-51
14. J Clin Endocrinol Metab. 2003 Apr; 88(4):1478-85
108
Sustanon 250
(Testosterone shown, plus Testosterone with Propionate, Phenylpropionate, Isocaproate, and
Decanoate esters)
17b-hydroxy-4-androsten-3-one
Testosterone base + 4 different esters
Propionate, Phenylpropionate, Isocaproate, Decanoate
Formula (base): C19 H28 O2
Molecular Weight (base): 288.429
Molecular Weight, Esters:
Propionate: 362.5082
Phenylpropionate: 438.6058
Isocaproate: 404.5886
Decanoate: 460.6958
Formula (base): C19 H28 O2
Melting Point (base): 155
Manufacturer: Organon
Effective Dose (Men): 500-2000mg/ week
Effective Dose (Women): Not recommended
Active life: Up to 3 weeks
Detection Time: 3+ months
Anabolic/Androgenic ratio:100/100
This product was developed by Organon as an ideal HRT (Hormone Replacement
Therapy) solution, and it was thought at the time that the different esters would be
able to provide a constant release of Testosterone over a months time. Sustanon is a
blend of different estered testosterones (4 of them): testosterone propionate - 30
mg, testosterone phenylpropionate - 60 mg, testosterone isocaproate - 60mg, and
testosterone decanoate -100 mg.
This drug was highly sought after as a “superior” version of testosterone in the late
80’s and through the mid 90’s. No doubt this is partly due to the very nice write-up
Dan Duchaine gave it in his newsletters. However, let’s keep in mind that this drug
was designed for convenience, not athletics or bodybuilding. The advantage to this
drug, according to the manufacturer, is that it can be injected once a month, and the
109
different esters would provide different timed releases over that month, and the
patient would therefore only need to visit the doctor once a month for his shot. For
athletes or bodybuilders (who routinely use between half a gram and a gram of
testosterone per week), this product is really no better than any other form of
injectable testosterone.
Lately, it seems that this product has fallen out of favor with Steroid.com members,
as many feel that the inclusion of the Propionate and phenylpropionate estered forms
of testosterone in this blend would necessitate shooting every other day. This stems
from the fact that testosterone propionate would be shot every other day at least,
and testosterone phenylpropionate would generally be shot every third day.
Sustanon will do exactly what other forms of testosterone will do:
Testosterone will cause both muscle growth as well as fat loss. It sends a message to
muscle cells to store more contractile protein (called actin and myosin), thus making
your muscles grow. It also protects your muscles from catabolic (muscle wasting)
glucocorticoid hormones (1). Thus it is often said that testosterone is not only
anabolic, but it is strongly catabolic. Not only does it cause an increase in size of the
muscle fibres (hyperfascia) but it also can change the appearance and the actual
number of muscle fibres (Hyperplasia) (2). Testosterone has the ability to increase
erythropoiesis (red blood cell production) in your kidneys (4), and a higher Red
Blood Cell (RBC) count may improve endurance by producing more highly
oxygenated blood. More RBCs can also improve recovery from strenuous physical
activity. Agression levels often rise dramatically with the use of any exogenous
testosterone (3). Testosterone improves muscle contraction by increasing the
number of motor neutrons in muscle (5) and improves neuromuscular transmission
(6). It also promotes glycogen synthesis (7)
Since Sustanon is simply a form of (well actually 4 forms of) testosterone, we also
know that administration of this compound will produce a dose respondant curve
(10). A what? Yeah, basically, a "dose respondant curve" is the fancy way of saying
"the more you take, the bigger you get." This is true of Sustanon as well as for
every form of testosterone, up to a point.
Unfortunately, Sustanon will also do all of the bad things that any form of
testosterone is known for: It will convert to the female hormone estrogen (via a
mechanism known as aromatization) by the (you guessed it) aromatize enzyme.
Excessive estrogen can lead to unwanted side effects, such as acne, the growth of
breast tissue (gynecomastia), fat gain and reduced fat breakdown, loss of sex drive,
testicular shrinkage and water retention. Water retention can increase blood
pressure weakening blood vessels over time. Unfortunately, this isn’t all it does: it
can also interact with the 5 alpha-reductase enzyme. This interaction converts the
testosterone to Dihydro-testosterone (DHT), a more androgenic form of the parent
hormone. DHT has a high binding affinity to the tissues of the scalp resulting in hair
loss in loss in users who suffer from male pattern baldness. DHT can affect the
prostate as well, making it larger. This swelling can cause the gland to press against
the bladder causing urinary problems. Drugs called 5alpha-reductase inhibitors can
prevent these symptoms without blocking testosterone’s anabolic effects (8). Higher
dosages of test can also negatively impact cholesterol, lowering HDL (9).
Testosterone is probably the safest steroid around, but it can’t be taken lightly, and
Sustanon is no different.
110
The principal drawback to Sustanon is its cost. It can cost between $5 and $12 an
ampule. Compared with Omnadren, Testoviron, or even Sten (other testosterone
products featuring various blends of Testosterone), the cost makes it prohibitive. An
equal amount of one of the aforementioned products can be had for less than half
the average cost of an amp of Sustanon. Sustanon, therefore, is no better or worse
than any other form of testosterone...if the price is right.
References:
1. J Lab Clin Med. 1995 Mar;125(3):326-33.
2. Anat Histol Embryol. 2003 Apr; 32(2):70-9.
3. Health Psychol. 1990; 9(6):774-91.
4. Zhonghua Nan Ke Xue. 2003; 9(4):248-51
5. Curr Opin Clin Nutr Metab Care. 2004 May; 7(3):271-7.
6. J Appl Physiol. 2001 Mar; 90(3):850-6.
7. Can J Physiol Pharmacol. 1999 Apr; 77(4):300-4.
8. Am J Physiol Endocrinol Metab. 2005 Jan; 288(1):E222-E227. Epub 2004 Sep 14.
9. J Clin Endocrinol Metab. 2004 Dec 21
10.14. Am J Physiol Endocrinol Metab. 2001 Dec; 281(6):E1172-81.
111
Test 400
(Testosterone shown, plus Testosterone with Propionate, Cypionate and Enanthate esters)
(Testosterone + 3 esters)
[17b-hydroxy-4-androsten-3-one]
Testosterone base +enanthate+ cypionate ester. + propionate este
Formula (base): C19 H28 O2
Formula (ester)
Propionate: C3H6O2
Cypionate: C8 H14 O2
Enanthate: C7 H12 O
Molecular Weight: 412.6112
Molecular Weight (base): 288.429
Molecular Weight (ester)
Propionate: 74.0792
Cypionate: 132.1184
Enanthate: 130.1864
Melting Point (base): 155C
Effective Dose (Men): 200-2000mg+ week.
Effective Dose (Women): Not recommended
Active life: 8 day
Detection Time: Up to 3 months
Anabolic/Androgenic ratio: 100/100
Denkall produces this particular testosterone blend, and it has the highest
concentration (and pain) of any of the mass-produced testosterone blends. It comes
in with the following characteristics per ml:
Testosterone Propionate: 25mgs
Testosterone Cypionate: 187mgs
Testosterone Enanthate: 188mgs
This came out a few years ago, and was received very well by the average smuggler.
You see, since it was available in Mexico for a reasonable price, and had 4 grams of
testosterone per bottle, you could actually bring back double the amount (mg-wise)
of testosterone in the same space. Really, this product is a smuggler’s dream, and it
flooded the streets of Venice and other steroid hot-spots soon after it hit the market.
I suppose the good thing about this product is that you can get a whopping dose of
testosterone in a few milliliters of product. Other than that, it’s very painful to inject
and not really anything special over any other form of testosterone.
112
Testolent
(Testosterone shown with phenylpropionate ester)
(Testosterone Phenylpropionate)
[4-androstene-3-one, 17beta-ol]
(Testosterone Base + Phenylpropionate Ester)
Formula (base): C19 H28 O2
Formula (ester): C9 H10 O2
Molecular Weight(base): 288.429
Molecular Weight (ester): 150.174
Melting Point (base): 155
Melting Point (ester): 20°C
Manufacturer: Organon
Effective Dose (Men): 350-1,000mgs/week
Active life: 5 days
Detection Time: Up to 6 weeks
Anabolic: Androgenic ratio: 100:100
This is a pretty rare version of testosterone, as it has the phenylpropionate ester
attached. This ester is much more commonly attached to the nandrolone base
compound, giving us Durabolin (often called NPP, which is short for Nandrolone
Phenylpropionate). Here, the ester is attached to the testosterone base compound,
giving a short/medium estered product, which results in an active life of 4-5 days.
Clearly, you’d get best results shooting this compound every fourth day, or twice a
week. Other than the ester, there’s not much to say about Testosterone
Phenylpropionate (TPP), which hasn’t been said already about testosterone in
general. Here’s a refresher course on it, nevertheless.
You may experience less water retention with TPP when compared with other, longer
acting versions of test, probably somewhere between that experienced with
testosterone propionate and cypionate. Anyway, testosterone promotes nitrogen
retention in the muscle (1), which is highly desirable because the more nitrogen the
muscle holds the more protein the muscle stores, and the bigger the muscle gets.
And that’s why we’re jabbing ourselves with a needle full of TPP, right? Testosterone
also has the ability to increase the levels of the highly anabolic hormone, IGF-1, in
muscle tissue (2). IGF-1 is highly anabolic and can promote muscle growth, and is
thought to mediate the effects of Growth Hormone (GH). IGF-1 is also one of the few
hormones positively correlated with both muscle cell hyperplasia and hyperphasia,
113
and this means it both creates more muscle fibers as well as bigger pure mass, IGF
1, GH, and testosterone would be a very nice combination for muscle growth.
Testosterone also has the ability to increase the activity of satellite cells (3). These
cells play a very active role in repairing damaged muscle, and remember, exercise is
perceived by your muscles as a form of damage. Testosterone also binds to the
androgen receptor (A.R.) to promote all of the A.R dependant mechanisms for
muscle gain and fat loss (4), although it has many important effects independent of
this mechanism. Some of those AR-independent effects are Testosterone’s ability to
protect your hard earned muscle from the catabolic (muscle wasting) glucocorticoid
hormones (6), and increase red blood cell production (7). Glucocorticoid hormones
eat away muscle and a higher RBC count may improve endurance via better
oxygenated blood.
Testosterone, once in the body, can be converted to both estrogen (via a process
known as aromatization) as well as DHT. Estrogen is the main culprit for many side
effects such as gyno, water retention, etc. DHT is often blamed for hair loss and
prostate enlargement. Unfortunately, reducing estrogen will often reduce some of
your gains, and reducing DHT will do the same, but doing so is preferable to going
bald, or having prostate problems and/or unsightly acne.
I suppose you can use this stuff in conjunction with Nandrolone Phenylpropionate
and you’d have a pretty cool cutting cycle with minimal water retention and the
added benefit of having your injection frequency being exact, since both compounds
you would have the same active life. Other than that, TPP has its place in a cycle as
any testosterone would, and is no better or worse than others.
References:
1. J Clin Endocrinol Metab. 1997 Feb; 82(2):407-13.
2. Am J Physiol Endocrinol Metab. 2002 Mar; 282(3):E601-7.
3. Curr Opin Clin Nutr Metab Care. 2004 May; 7(3):271-7.
4. Curr Pharm Biotechnol. 2004 Oct; 5(5):459-70.
5. Metabolism. 1991 Apr; 40(4):368-77.
6. Am J Physiol Endocrinol Metab. 2002 Mar; 282(3):E601-7.
7. Curr Opin Clin Nutr Metab Care. 2004 May; 7(3):271-7.
114
Testosterone Cyclohexylpropionate
(Testosterone shown without ester)
(Testosteronebase + cyclohexylpropionate ester)
[17b-hydroxy-4-androsten-3-one]
Formula (base): C27 H40 O3
Formula (ester): C9 H16 O2
Molecular Weight (base): 288.429
Molecular Weight (ester): 156.222
Melting Point (base): 155
Manufacturer: Theramex
Effective Dose: 400-1000mgs/week
Active life: 13.5days
Detection Time: 3 months
Anabolic/Androgenic ratio: 100:100
Basically, what we have here is a French testosterone preparation. This means it
comes in all sorts of weird dosing schemes, which are actually not too weird once
you understand why they exist. See, this stuff comes in 296mgs, 148mgs, and
37mgs ampules, of one milliliter each. Why the weird dosing? Well, actually, it’s
much less weird than you think. Those amps provide a very sensible 200mgs,
100mgs, and 25mgs respectively with this particular ester, combined with
testosterone, at those available doses. As we all know, esters delay the release of a
hormone, and Test-CHP has 9 carbons, which hints that it is a long acting ester
comparable cypionate (8 carbons) or decanoate (10 carbons) with an active life of
about 13.5 days. Obviously, this is a very long acting version of testosterone, and
anecdotally, the longer esters, tend to produce more water retention. Therefore, this
stuff would be good for bulking, therefore, and not really for cutting.
Testosterone, even with this absurdly long ester, is the hormone responsible for the
different physical and mental (sexual) characteristics males tend to have in
abundance (and females less so). It promotes sex drive, fat loss, helps with gaining
and maintaining lean muscle mass and bone density and may even protect against
heart disease (1). All other anabolic steroids are actually the testosterone molecule
that has been altered in one way or another to change the properties of the
hormone. But lets get back to testosterone. Test-CHP (or any form of testosterone)
will bind to the A.R on fat cells resulting in fat breakdown and also prevents new fat
formation (15). Testosterone CHP will also promote nitrogen retention in the
muscle(2), which is good, as the more nitrogen the muscle holds the more protein
the muscle stores, and the bigger the muscle gets. Testosterone has the ability to
increase red blood cell production (9), and a higher RBC count may improve
115
endurance via providing more highly oxygenated blood to working muscles. More
RBCs can also improve your recovery from strenuous physical activity, and has a
“volumizing” effect on your muscles. Testosterone’s anabolic/androgenic effects are
dose-dependant, the higher the dose the higher the muscle building effect (10),
regardless of ester. Testosterone can also increase the levels of another hormone
(one of the super family of anabolic hormones), IGF-1, in muscle tissue (3).
Testosterone also has the profound ability to increase the activity of satellite cells
(4), which play a very active role in repairing damaged muscle. Testosterone binds
to the androgen receptor tightly to promote A.R dependant mechanisms for muscle
gain and fat loss (5), and it also significantly increases the concentrations of the A. R
in cells critical for muscle repair and growth and A.R in muscle (4)(6). Testosterone
induces changes in both shape and size of muscle cells, and also can change the
appearance and the number of your muscle fibers (7). Testosterone-CHP
administration will also protect your hard earned muscle from the catabolic (muscle
wasting) glucocorticoid hormones (8). Testosterone greatly improves muscle
contraction by increasing the number of motor neutrons in muscle (4) and also
improves neuromuscular transmission (12). This is of special interest to strength
athletes and sprinters.
Test-CHP will also promotes glycogen synthesis (13)
providing more fuel for intense workouts thus having a positive effect on endurance
and strength. Finally, Testosterone-CHP will promote aggressive and dominant
behavior (14), even though it is a still basically a French version of testosterone.
Testosterone-CHP use does have some unwanted side effects. It will convert to the
hormone estrogen (via aromatization) by the now-infamous aromatize enzyme. This
can lead to breast tissue growth in men (gynecomastia), increased fat gain and
reduced fat breakdown, possible loss of sex drive, almost certain testicular shrinkage
and finally water retention. Water retention with this product (because of its ester)
will probably be very pronounced, and can increase blood pressure weakening blood
vessels over a period of time. Testosterone can also interact with the 5 alpha
reductase enzyme, which converts the testosterone to Dihydro-testosterone (DHT), a
more androgenic form of the parent hormone. This new compound has a high
binding affinity to the tissues of the scalp resulting in hair loss in loss in users who
suffer from male pattern baldness. DHT can affect the prostate as well, making it
swell. This swelling can cause the gland to press against the bladder causing urinary
problems, especially urinary difficulty.
Although Steroid.com has nearly 40K members, I haven’t found any who have used
this particular version of test, possibly because it was discontinued in 1991. If it
were still on the market, or a UG began producing it, then it would be a good buy for
those who are squeamish about needles, since once a week injections would be more
than sufficient. Until then, though, it’s of note purely as an academic object.
References:
1. Heart. 2004 Aug; 90(8):871-6.
2. J Clin Endocrinol Metab. 1997 Feb; 82(2):407-13.
3. Am J Physiol Endocrinol Metab. 2002 Mar; 282(3):E601-7.
4. Curr Opin Clin Nutr Metab Care. 2004 May; 7(3):271-7.
5. Curr Pharm Biotechnol. 2004 Oct; 5(5):459-70.
6. J Clin Endocrinol Metab. 2004 Oct; 89(10):5245-55.
116
7. Anat Histol Embryol. 2003 Apr; 32(2):70-9.
8. J Lab Clin Med. 1995 Mar; 125(3):326-33.
9. Zhonghua Nan Ke Xue. 2003; 9(4):248-51
10. J Clin Endocrinol Metab. 2003 Apr; 88(4):1478-85
11. steriod.com/forums
12. J Appl Physiol. 2001 Mar; 90(3):850-6.
13. Can J Physiol Pharmacol. 1999 Apr; 77(4):300-4.
14. Health Psychol. 1990; 9(6):774-91.
15. Biochim Biophys Acta. 1995 May 11; 1244(1):117-20.
16. Am J Physiol Endocrinol Metab. 2005 Jan; 288(1):E222-E227. Epub 2004 Sep 14.
17. J Clin Endocrinol Metab. 2004 Dec 21
18. Sports Med. 2004; 34(12):809-24.
19. Heart. 2004 Aug; 90(8):871-6.
20. Pol J Pharmacol. 2004 Sep-Oct; 56(5):509-18.
21. Proc Natl Acad Sci U S A. 2002 Feb 5; 99(3):1140-5. Epub 2002 Jan 22.
Completely Cleanse Steroids From Your
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http://www.SteroidCleanse.com
117
Testosterone Cypionate
(Testosterone shown with Cypionate ester)
(Testosterone base + cypionate ester)
[17b-hydroxy-4-androsten-3-one]
Formula (base): C19 H28 O2
Formula (ester): C8 H14 O2
Molecular Weight: 412.6112
Molecular Weight (base): 288.429
Molecular Weight (ester): 132.1184
Melting Point (base): 155
Melting Point (ester): 98 - 104 C
Manufacturer: Various
Effective Dose (Men): 300-2000mg+ week
Effective Dose (Women): Not recommended
Active life: 15-16 days
Detection Time: 3 months
Anabolic/Androgenic ratio:100/100
Testosterone is the hormone that makes men, well, men! Since it’s basically the
most commonly used form of testosterone in America at this time, let’s take a look
at testosterone cypionate, and examine the pros and cons of its ability to improve
performance in athletics and bodybuilding,
Testosterone is the hormone responsible for many different physical and mental
characteristics in males. It promotes sex drive, fat loss, helps with gaining and
maintaining lean muscle mass and bone density, and may even protect against heart
disease (1). All other steroids are actually the testosterone molecule altered soas to
change the properties of the hormone. This would make testosterone the "father" of
all other steroids employed by athletes today. In fact, testosterone is the standard
for the anabolic/androgenic ratio we use—it’s a “perfect” 100 score, against which we
measure all other steroids.
As I previously stated, testosterone is a highly anabolic and androgenic hormone, it
has an anabolic (muscle building) rating of 100, making it a good drug to use if one
is in pursuit of more size and strength. And if you aren’t in pursuit of more size and
strength, then why would you be reading this, right? Well, let’s get on with it and
look at exactly what makes testosterone a good mass builder. First, testosterone
118
promotes nitrogen retention in the muscle (2). The more nitrogen the muscle holds
the more protein the muscle stores. Testosterone can also increase the levels of
another anabolic hormone, IGF-1, in muscle tissue (3). Testosterone also has the
amazing ability to increase the activity of satellite cells (4). These cells play a very
active role in repairing damaged muscle. Testosterone also binds to the androgen
receptor to promote A.R dependant mechanisms for muscle gain and fat loss, (5) it
also significantly increases the concentrations of the A. R in cells critical for muscle
repair and growth and A.R in muscle (4)(6). Testosterone induces changes in shape
and size, and also can change the appearance and the number of muscle fibres (7).
Androgens like testosterone can protect your hard earned muscle from the catabolic
(muscle wasting) glucocorticoid hormones (8), thus inhibiting their action. In
addition, Testosterone has the ability to increase red blood cell production (9), and a
higher RBC count may improve endurance via better oxygenated blood. More RBCs
can also improve recovery from strenuous physical activity. As you may have
suspected, testosterone’s anabolic/androgenic effects are dose dependant; the
higher the dose the higher the muscle building effect (10).
Steroid.com members report massive strength gains while using testosterone (11).
Testosterone improves muscle contraction by increasing the number of motor
neutrons in muscle (4) and improves neuromuscular transmission (12). It also
promotes glycogen synthesis (13) providing more fuel for intense workouts thus
increasing endurance and strength. Also note that the water retention from
testosterone use will cause the muscle to spring back when compressed during the
lowering of a weight. Testosterone promotes aggressive and dominant behavior
(14); this explains the boost of confidence that gives athletes the mental edge they
need to move the heavy iron.
Testosterone is also good at promoting fat loss. Having an anti-estrogenic effect, it
creates an ideal fat loss environment. Test binds to the A.R on fat cells resulting in
fat break-down, and also prevents new fat formation (15). Another indirect action of
fat loss that test produces is the nutrient portioning effect it has on muscle and fat.
Since the body is building muscle at an accelerated rate, more of the food you eat is
shuttled to muscle tissue and away from fat.
Is there anything testosterone can't do?
Testosterone use does have some unwanted side effects that Steroid.com members
should be aware of. Testosterone can convert to the female hormone estrogen (via
aromatization) by the aromatize enzyme. Excessive estrogen can lead to some nasty
side effects: breast tissue growth in men (gynecomastia), fat gain and reduced fat
breakdown, loss of sex drive, testicular shrinkage and water retention. Water
retention can increase blood pressure weakening blood vessels over a period of time.
A class of drugs, called aromatize inhibitors, to stop the testosterone from converting
to estrogencan easily stop the estrogenic side effects. The use of HCG during a
testosterone cycle can prevent the testicular shrinkage. Testosterone can also
interact with the 5 alpha-reductase enzyme. This action converts the testosterone to
Dihydro-testosterone (DHT), a more androgenic form of the parent hormone. DHT
has a high binding affinity to the tissues of the scalp resulting in hair loss in loss in
users who suffer from male pattern baldness. DHT can affect the prostate as well,
making it swell. This swelling can cause the gland to press against the bladder
causing urinary problems. Drugs called 5alpha-reductase inhibitors can prevent these
symptoms without blocking testosterone’s anabolic effects (16). Higher dosages of
119
test can also negatively impact cholesterol, lowering HDL (17). Constantly ignoring
this can lead to a series of serious health problems down the road.
Testosterone levels decrease as we age, with levels dramatically falling at 50-60
years of age (18). Low test levels lead to loss of muscle mass and stregth, gains in
fat, and loss of sex drive (18). So, it is a good idea to replace testosterone with an
outside source. Supplementing testosterone in older adults with sub-optimal levels
may prevent or delay Alzheimer's disease and other cognitive diseases, protect
nerves, and regenerate motor units; improve mood, memory, appetite, sex drive,
and bone mass; and may decrease the risk of heart attack and stroke (19)(20)(21)
(22). This shows that test replacement significantly improves the quality of life and
may be a good option for middle-aged men. Caution should be taken when using
higher dosages because of an increased risk of adverse side effects (23).
Testosterone cypionate is an injectable oil, which contains testosterone with the
cypionate ester attached to the testosterone molecule. The ester denotes the release
pattern of the test after it is injected into the body. This particular ester gives the
testosterone an active life of 15-16 days, although blood levels of this drug fall
sharply five days after post-administration, testosterone levels are still above
baseline after a week (24). Stable blood levels can be achieved with injections once
per week. Steriod.com members often administer the drug twice weekly or every
three to five days. On a funny note, many steroid users believe that test cyp is more,
or less powerful, than the other popular injectable testosterone enanthate. The truth
is that they are almost identical in release patterns, so there is virtually no difference
between the two. However, as far back as the printing of the first Underground
Steroid Handbook, there has been speculation that Cyp has more “kick” than Enth.
Testosterone is highly versatile and should be considered the “base” of
anabolic/androgenic steroid cycles because of its muscle building potential as well as
for the fact that it prevents the loss of sex drive that sometime affects those who
neglect to use it with other HPTA suppressive anabolics, (especially the 19-nor
family). Test can be used for any body-building goal whether it’s fat loss or muscle
gain. An excellent drug for beginners, it’s also cheap, making it a top-notch choice
for anyone interested in utilizing anabolics to reach their bodybuilding or athletic
goals. With regards to this particular version of testosterone, you should be paying
no more than $75 for a 10cc bottle of it, dosed at 200mgs/ml. Of course, as usual,
prices fluctuate, but I’d recommend sticking with a reputable underground Lab,
rather then Organon, UpJohn, or one of the many other expensive (and often
counterfeited) companies.
References:
1. Heart. 2004 Aug; 90(8):871-6.
2. J Clin Endocrinol Metab. 1997 Feb; 82(2):407-13.
3. Am J Physiol Endocrinol Metab. 2002 Mar; 282(3):E601-7.
4. Curr Opin Clin Nutr Metab Care. 2004 May; 7(3):271-7.
5. Curr Pharm Biotechnol. 2004 Oct; 5(5):459-70.
6. J Clin Endocrinol Metab. 2004 Oct; 89(10):5245-55.
7. Anat Histol Embryol. 2003 Apr; 32(2):70-9.
120
8. J Lab Clin Med. 1995 Mar; 125(3):326-33.
9. Zhonghua Nan Ke Xue. 2003; 9(4):248-51
10. J Clin Endocrinol Metab. 2003 Apr; 88(4):1478-85
11. steriod.com/forums
12. J Appl Physiol. 2001 Mar; 90(3):850-6.
13. Can J Physiol Pharmacol. 1999 Apr; 77(4):300-4.
14. Health Psychol. 1990; 9(6):774-91.
15. Biochim Biophys Acta. 1995 May 11; 1244(1):117-20.
16. Am J Physiol Endocrinol Metab. 2005 Jan; 288(1):E222-E227. Epub 2004 Sep 14.
17. J Clin Endocrinol Metab. 2004 Dec 21
18. Sports Med. 2004; 34(12):809-24.
19. Heart. 2004 Aug; 90(8):871-6.
20. Pol J Pharmacol. 2004 Sep-Oct; 56(5):509-18.
21. Proc Natl Acad Sci U S A. 2002 Feb 5; 99(3):1140-5. Epub 2002 Jan 22.
22. J Gerontol A Biol Sci Med Sci. 2001 May; 56(5):M266-72.
23. J Clin Endocrinol Metab. 2005 Feb; 90(2):678-88. Epub 2004 Nov 23.
24. Fertility and Sterility 33. (1980) 201-3
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
121
Testosterone Enanthate
(Testosterone shown with Enanthate ester)
(Testosterone base + Enanthate ester)
[17b-hydroxy-4-androsten-3-one]
Formula (base): C19 H28 O2
Formula (ester):C7 H12 O
Molecular Weight: 412.6112
Molecular Weight (base): 288.429
Molecular Weight (ester): 130.1864
Melting Point (base): 155
Manufacturer: Various
Effective Dose (Men): 300-2000mg+ week
Effective Dose (Women): Not recommended
Active life: 8 days
Detection Time: 3 months
Anabolic/Androgenic ratio:100/100.
Testosterone Enanthate is probably the most commonly used form of testosterone by
both athletes and bodybuilders. Although I don’t have any hard statistics on this, I’d
be willing to bet that this form of testosterone is the most commonly used form of
testosterone on the black market today. It’s very effective for building muscle and
strength, losing fat, and is cheap and readily available.
To understand exactly how Testosterone Enanthate (a.k.a. “test enth” or just “enth”)
builds muscle and burns fat, we’ll take a look at androgens and what they do in the
body. You see, hormones are substances secreted by one cell, which has an effect on
the functions of another cell. Testosterone is manufactured in the Leydig’s cells of
the testes (in men). The adult male produces between 2.5 and 11mgs of Test per
day.
Testosterone induces changes in shape and size, and also can change the
appearance and the number of muscle fibres (7). Androgens like testosterone can
protect your hard earned muscle from the catabolic (muscle wasting) glucocorticoid
hormones (8), thus inhibiting their ability to send a message to muscle cells to
release stored protein. Remember, Testosterone sends a message to muscle cells to
store more contractile protein (called actin and myosin); glucocorticoid hormones
send the opposite message. In addition, Testosterone has the ability to increase
122
erythropoiesis (red blood cell production) in your kidneys (9), and a higher Red
Blood Cell (RBC) count may improve endurance via better oxygenated blood. More
RBCs can also improve recovery from strenuous physical activity. Agression levels
often rise dramatically with the use of exogenous testosterone (15).
All of these great benefits are to be had with the use of test enth alone, but
realistically, it will be part of a cycle containing one or more drugs. People who are
bulking will probably choose Deca or Eq (possibly with Dbol as well) and those who
are cutting will probably steer towards Eq and perhaps Trenbolone. Very often users
will shoot this drug once or twice a week, but blood levels are still above baseline
with this drug at around day eight (16). Common wisdom holds that the
testosterone portion of any such cycle should be equal to or greater than any other
injectable drug(s) portion (on a mg basis). I believe that you can get away with
less, but in general, this is a good guideline.
As you may have suspected, Testosterones' anabolic/androgenic effects are dose
dependant, the higher the dose, the higher the muscle building effect (10). Lets take
a look at exactly what kind of results we can expect from administration of
Testosterone Enanthate:
Effects of 20 wk of GnRH agonist plus TE administration on relative changes (mean ±
SEM) in total LBM (A), appendicular LBM (B), and trunk LBM (C) (percent change
from baseline) measured by DEXA. P values are results for ANOVA: *, P < 0.05 vs.
all other dose groups for the multiple comparison tests using Student-Newman
Keuls; a, P < 0.05 vs. zero change (11).
123
These charts show that the subjects in this test made a roughly 15% gain in Lean
Body Mass from 20 weeks of 600mgs/week of testosterone Enanthate. That’s pretty
impressive, but I feel the following set of charts are more so:
Change in fat-free mass (A), fat mass (B), leg press strength (C), thigh muscle
volume (D), quadriceps muscle volume (E), sexual function (F), insulin-like growth
factor I (G), and prostate-specific antigen (H). Data are means ± SE. *Significant
differences from all other groups (P < 0.05); significant difference from 25-, 50-, and
125-mg doses (P < 0.05); +significant difference from 25- and 50-mg doses (P <
0.05); and significant difference from 25-mg dose (P < 0.05)(14).
Now this is very interesting. You’ll note that the most fat was lost by the group in
this study who used the highest dose (600mgs/week), and the most fat free mass,
strength, and muscle volume was gained when compared to any of the lower doses
studied (14). Basically, the more testosterone you use (and this holds true for almost
all steroids), the more you’ll gain! I know that the last statement will ruffle some
feathers in the “less is more” club, but that’s too bad: more test = more muscle,
more strength, more size, and less fat.
Did the men in this study experience side effects at the 600mg dose? Well, HDL
cholesterol was lowered (but not total cholesterol or triglyceride levels), and two
men got acne. Not exactly cause for a Senate Investigation, huh? (14). Of course,
the usual nasty side effects you can get from any form of injectable testosterone are
possible with testosterone enanthate (acne, hairloss, prostate enlargement, and
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shutting down your body’s own natural hormonal system, etc.), but they are very
overstated or controllable in many instances.
A large percentage of those side effects occur from the body’s ability to turn
testosterone into estrogen via a metabolic pathway mediated by the aromatase
enzyme. This process, known as aromatization causes a portion of testosterone to be
converted to estrogen. Aromatase inhibitors (Arimidex and Letroaole, for example)
can combat this effectively, and are usually necessary with doses over ½ a gram per
week.
Now that I’ve told you all about this drug, let’s talk about cost. You should be paying
no more than $75 for a 10cc bottle of it, dosed at 200-250mgs/ml. This drug is
relatively cheap to produce, the raw materials are very inexpensive, and should be
reasonably cheap, especially since this drug should be a consideration for inclusion in
any cycle. Of course, as usual prices fluctuate, but I’d recommend sticking with a
reputable underground Lab, rather then Organon, UpJohn, or one of the many other
expensive (and often counterfeited) companies.
References:
1. Am J Physiol. 1998 Nov;275(5 Pt 1):E864-712
2. J Clin Endocrinol Metab. 1997 Feb; 82(2):407-13
3. Am J Physiol Endocrinol Metab. 2002 Mar; 282(3):E601-7.
4. Curr Opin Clin Nutr Metab Care. 2004 May; 7(3):271-7.
5. Curr Pharm Biotechnol. 2004 Oct; 5(5):459-70.
6. J Clin Endocrinol Metab. 2004 Oct; 89(10):5245-55.
7. Anat Histol Embryol. 2003 Apr; 32(2):70-9.
8. J Lab Clin Med. 1995 Mar; 125(3):326-33.
9. Zhonghua Nan Ke Xue. 2003; 9(4):248-51
10. J Clin Endocrinol Metab. 2003 Apr; 88(4):1478-85
11. J Clin Endocrinol Metab. 2004 Feb; 89(2):718-26.
12. Am J Physiol. 1998 Jun; 274(6 Pt 1):C1645-52.
13. Biochim Biophys Acta. 1995 May 11; 1244(1):117-20.
14. Am J Physiol Endocrinol Metab. 2001 Dec; 281(6):E1172-81.
15. Health Psychol. 1990; 9(6):774-91.
16. Fertility and Sterility 33.
125
Testosterone Propionate
(Testosterone shown with Propionate ester)
(Testosterone + Propionate ester)
[4-androstene-3-one, 17beta-ol]
Formula (base): C19 H28 O2
Formula (ester): C3 H6 O2
Molecular Weight (base): 288.429
Molecular Weight (ester): 74.0792
Melting Point (base): 155
Melting Point (ester): 21C
Manufacturer: Various
Effective Dose (Men): 350-2000mg+ week.
Effective Dose (Women): 50-100mgs/week
Active life: 2-3 days
Detection Time: 2-3 weeks
Anabolic/Androgenic ratio: 100/100
As we all know, Testosterone was the first steroid to be synthesized. Now, it remains
the gold standard of all steroids. First, we’ll discuss Testosterone in general, then
we’ll examine exactly what the propionate ester is and how it works (together,
testosterone propionate is often referred to as just “prop” or “test prop”).
Testosterone’s anabolic/androgenic ratio is 1:1. It is as much anabolic as it is
androgenic. Actually, testosterone is the steroid on which all anabolic/androgenic
ratios are based. If a steroid is 2:1, then compared with testosterone's ratio, it is
twice anabolic as it is androgenic. Hence, we see from testosterone's ratio, it is both
anabolic as well as androgenic.
So how exactly does testosterone build muscle? Well, Testosterone promotes
nitrogen retention in the muscle (6), the more nitrogen the muscle holds, the more
protein the muscle stores and the bigger the muscle gets. Testosterone can also
increase the levels of another anabolic hormone, IGF-1, in muscle tissue (7). By
itself IGF-1 is highly anabolic and can promote muscle growth. It is responsible for
much of the anabolic activity of Growth Hormone (GH). IGF-1 is also one of the few
hormones positively correlated with both muscle cell hyperplasia and hyperphasia
(this means it both creates more muscle fibers as well as bigger fibers). All of this
leads me to speculate that for pure mass, IGF-1, GH, and Testosterone would be a
very effective combination. Testosterone also has the amazing ability to increase the
126
activity of satellite cells (8). These cells play a very active role in repairing damaged
muscle. Testosterone also binds to the androgen receptor (A.R.) to promote all of the
A.R dependant mechanisms for muscle gain and fat loss (9), but as we’ve seen, this
isn’t the only mechanism that promotes growth.
Testosterone has a profound ability to protect your hard earned muscle from the
catabolic (muscle wasting) glucocorticoid hormones (11), and increases red blood
cell production (12). As you may know, a higher RBC count may also improve
endurance via better oxygenated blood. The former trait increases nitrogen retention
and muscle building while the latter can improve recovery from strenuous physical
activity, as well as increase endurance and tolerance to strenuous exercise.
Testosterone occurs naturally in both the male and female body, and as far as
testing for it, typical tests don't work (i.e. testing for metabolites). Testosterone can
be tested on a testosterone/epitestosterone ratio, a failing result usually being
anything over 6 to 1, but there are other more effective tests currently in use and
being developed by the usual party-poopers in the IOC and FDA. If you are using
low doses of this drug and stop taking it 36-48 hours before a Test/EpiTest analysis,
you can still pass!
Testosterone, once in the body, can be converted to both estrogen (via a process
known as aromatization) as well as DHT. Estrogen is the main culprit for many side
effects such as gyno, water retention, etc., while DHT is often blamed for hair loss
and prostate enlargement. Naturally there are ways to combat this, such as using an
anti-estrogenic compound along with testosterone, or even an estrogen blocker. DHT
can be combated (on the scalp, to prevent hair loss) with compounds such as
Ketoconazole shampoo (sold under the trade name Nizoral) as well as Finasteride
(sold as Proscar in the 5mg version and as Propecia as 1mg tablets). Interestingly,
this shampoo can also be used topically to combat acne on the face (or even the
back if you’re really flexible). Both of these methods for preventing hair loss and
acne are reasonably effective. However, if you are not prone to hair loss, they may
be wholly unnecessary. Male Pattern Baldness (MPB) is carried by the X
chromosome, so if your mother’s family boasts men with full heads of hair, then you
are probably safe (unless those full heads of hair are all mullets). Naturally, as with
most other steroids, your lipid profile and blood pressure are going to suffer a bit
while on testosterone. This, of course is nothing that can’t be controlled by watching
your diet and doing your cardio, at least for the duration of the typical cycle (which
for arguments sake, I’ll assume is +/- 12 weeks). Let’s be totally honest here, even
a modest amount of exercise will improve your blood pressure and lipid profile (10),
and if you aren’t exercising, then why are you taking steroids?
To combat the aromatization of testosterone, you can simply take an aromatase
inhibitor such as Arimidex. This and other Anti-estrogenic compounds are generally
considered a must with testosterone doses over ½ a gram per week (500mgs).
Amother side effect (as if acne and going bald aren’t enough) is increased
aggression. This is a hotly debated issue in steroid-culture. Generally the consensus
is that if you are prone to being a jerk, you'll be a bigger jerk, if you aren't, then
your temper will not get much worse (this is supported by research as well). Also,
high levels of testing are generally associated with aggression and anti-social
behavior in males with lower intelligence (1)(2). Guess what? Dumb people
shouldn't use steroids at all, especially testosterone!
127
For many, the increased aggression found from increased testosterone levels is often
a bonus, in the weight room as well as on the playing field. Let’s not get started on
its benefits in the bedroom!
Testosterone is also a relatively safe steroid to use, with some studies showing no
adverse effects from 20weeks at 600mgs/week (3)! Personally, I have used up to 2
grams per week of various testosterones but now I prefer to keep my dose of it
around ½ a gram.
Testosterone is usually attached to an ester (i.e. when you buy testosterone propionate, the
subject of this profile, you are buying testosterone with a propionate ester attached). The ester
determines how long it takes your body to dispose of the steroid in question, and propionate is
the shortest ester available with a testosterone base (of course, testosterone suspension has no
ester). There are enzymes, called esterases, in your body that have the function of removing the
ester from steroids and leaving you with just the steroid molecule with the ester cleaved off. The
heaviness of the ester chain, determines how long it takes the esterase to remove it. And that
amount of time determines how long the drug stays active in your body. Great, right? Not really;
the ester takes up "room" in the injection. Check out this chart:
Chemical = Formula = Molecular Weight = Mg of Testosterone
Testosterone (no ester) = C19 H28 O2 = 288.4mg = 100mg
Propionate = C3 H4 O = 56.1mg = 83.72mg
Cypionate = C8 H4 O = 124.2mg = 69.90mg
Here, we’re comparing testosterone with no ester (suspension) to Test Propionate
and Cypionate (basically the longest vs. shortest esters available with testosterone).
So you see, the longer the ester on the testosterone, the longer the steroid is active
in your body, and the less actual test you get. This is because for every 100mgs of
testosterone cypionate you inject, only 69.90mgs of it is actually testosterone—the
rest is the cypionate ester, which must be removed. On the other hand, with the
propionate ester, you’ll get 83.72mgs of testosterone! The advantage to longer
esters is that they need to be injected less frequently (test prop needs to be injected
every other day while you can shoot test cyp once a week). The disadvantage to long
estered steroids is that they contain less actual steroid. Anecdotally, most people
from Steroid.com and other discussion boards who have tried differing esters on
their various cycles agree: Testosterone Propionate causes the least side effects and
the least bloating. For this reason, it’s often the testosterone of choice in cutting
cycles. On a personal note, it’s the only form of testosterone I ever use, and it’s the
only one most women will use, due to the previously mentioned factors (as well as
it’s ability to clear your body quickly upon cessation in the case of side effects).
Testosterone levels when you’re using injectable testosterone propionate begin to
decline sharply after the second day of use (5). Obviously this is not the drug of
choice for those who are squeamish about injections; you’ll be shooting this stuff
every other day at least.
Also, as with most steroids, injected testosterone will inhibit your natural test levels
and HPTA (Hypothalamic Pituitary Testicular Axis). A mere Hundred mgs of
test/week takes about 5-6 weeks to shut the HPTA, and 250-500mgs shuts you
down by week 2 (4).
Realistically, every cycle should contain testosterone. Go back and read that
sentence again. A beginner’s dose of testosterone (i.e. someone on their first or
second cycle of AAS) would be in the 250-500mgs range. I wouldn't recommend
128
much less than 400mgs of test per cycle for anybody, beginner or not. And guess
what? The more you use the more results you get.
Frequently, the more side
effects, too (3).
What stacks well with testosterone propionate? Everything! Many people’s favorites
are Eq (boldenone undeclyenate) or Deca (nandrolone decanoate), but anything will
stack well with test prop. Tren (Trenbolone Acetate), Masteron, and/or Winstrol are
also favorites for many on a cutting cycle, myself included. It’s important to
remember that since test prop has such a short ester, most people stack it with
other short estered drugs. They need to endure frequent injections for the test prop
to be effective, so they may as well be using other drugs requiring the same dosing
protocol.
Finally, it’s worth noting that sometimes a phenomenon strategy known as
"frontloading" is employed with testosterone propionate. This is where double or
triple the intended dose for the cycle is injected for the first two weeks; the user
then switches to a longer ester. The reasoning behind this is presumably to get the
blood levels of the drug up quickly in the hopes of seeing rapid results.
Of all testosterones available on the market today, Testosterone Propionate is the
most expensive. This is both because it is in high demand (due to it’s ability to avoid
bloating the user as other testosterone’s tend to do) and because the actual chemical
is expensive compared to other tests. Expect to pay roughly $40-60 for a 10-20ml
bottle dosed at 100mgs/ml, when buying from a reputable underground lab, expect
to pay at least double that amount if you are buying human grade ampules or bottles
from a major pharmaceutical company.
References:
1. Pope, H.G, Kouri, E.M., & Hudson, J.I. (2000). Effects of supraphysiologic doses of
testosterone on mood and aggression in normal men: A randomized controlled trial. Archives of
General Psychiatry, 57, 133-140
2. Chance, S.E., Brown, R.T., Dabbs, J.M., & Casey, R. (2000). Testosterone, intelligence and
behavior disorders among young boys. Personality and Individual Differences, 28, 437-445
3. Am J Physiol Endocrinol Metab 2003 Jan 7; [epub ahead of print] Related Articles, Links
"Development of Models to Predict Anabolic Response to Testosterone Administration in
Healthy Young Men."
4. J Investig Med. 1997 Oct; 45(8):441-7
5. J Clin Endocrinol Metab. 1986 Dec; 63(6):1361-4.
6 .J Clin Endocrinol Metab. 1997 Feb; 82(2):407-13.
7. Am J Physiol Endocrinol Metab. 2002 Mar; 282(3):E601-7.
8. Curr Opin Clin Nutr Metab Care. 2004 May; 7(3):271-7.
9. Curr Pharm Biotechnol. 2004 Oct; 5(5):459-70.
10. Metabolism. 1991 Apr; 40(4):368-77.
11. J Lab Clin Med. 1995 Mar; 125(3):326-33.
12. Zhonghua Nan Ke Xue. 2003; 9(4):248-51. Effect of androgen on erythropoientin in patients
with hypogonadism] [Article in Chinese]
129
Testosterone Suspension
(Testosterone)
[17b-hydroxy-4-androsten-3-one]
Formula: C27 H40 O3
Molecular Weight: 288.429
Melting Point: 155
Manufacturer: Various
Effective Dose (Men): 350-1000mg/week
Effective Dose (Women): Not recommended
Active life:+/-1 day
Detection Time: +/-1day
Anabolic/Androgenic ratio:100/100
Testosterone Suspension is an injectable hormone in a water base that was
developed and used for decades and is actually the first anabolic, androgenic steroid
used. For the purpose of building mass, Testosterone Suspension has never been
surpassed since it was first developed in the 1930's. Many underground Labs also
suspend this product in propylene glycol or oil as well (which makes for a very
painful injection). It has no ester attached; therefore no ester is calculated into the
weight. This is extremely beneficial to the user since 100mg of testosterone
suspension will yield 100mg of testosterone. This is unlike the other esterfied
testosterones such as testosterone enanthate, which only yields 72mg of actual
testosterone per 100mg of total weight. Testosterone suspension rises the storing of
glycogen in the muscle cells and because it is dissolved in water it becomes effective
immediately. Making it different from other esterfied hormones, it only keeps
sustained and elevated testosterone levels for 2-3 days due to its micro-crystal
design. This forces the user to inject on a daily basis, with better results coming from
twice-three times a day use due to its short active-life with the effective dose
ranging from 350-1000mg per week (50-140mg/day). One should practice site
rotation and should practice injecting in the same spot only once per week at most.
It should be noted that test suspension is usually a very painful shot, so it is often
cut with something else, such as B-12, or other steroids. And yes, you can mix a
water-based steroid with an oil based steroid in the same syringe. It looks like a lava
lamp. There's no problem with injecting a mixture like this.
Note that due to the water base (not an issue if using a product suspending in
propylene glycol or oil) the testosterone will most likely settle to the bottom of the
vial and shaking the vial is needed in order to insure even dosing. This is true for all
water based steroid suspensions.
130
As was noted before, testosterone can be considered one of the most powerful mass
builders and testosterone suspension can be considered one of the most powerful of
the testosterones simply due to the fact that it has no attached ester. This means
that you are getting 100mgs of Test per 100mgs you inject. Suspension is the only
version of Testosterone that can boast that claim. A growing reason why many
athletes are choosing to use testosterone suspension instead of enanthate or other
forms (besides the fact that it has a higher amount of pure testosterone resulting in
greater results) is that it may be responsible for localized growth at the injection site,
like winstrol. Most athletes will only use this form of testosterone in a bulking cycle
because it usually is accompanied by high water retention, severe bloat, adipose
storage, and gynomastia. This product also has a high level of aromitization into
estrogen and coverts to DHT (dihydrotestosterone) as well. Of course, adding
endogenous testosterone to your body will result in the shutting down of your own
exogenous testosterone levels, as well as the hormones secreted which cause
testosterone to be secreted by your testes.
Many times testosterone is not used by women because male secondary sex
characteristics may start to appear in female users. However, testosterone
suspension will allow women to site-inject and help problem areas common in
women such as calves and inner thighs, and can be used in small enough doses,
clearing the system quickly if sides develop. This advantage also means that one can
pass a drug test a couple of days after the last injection. This is a great advantage to
athletes who will be tested and still want the benefits of a mass drug which can not
be tested for easily, many other forms of testosterone (such as Cyp or Enanth) can
take 3 months to become undetectable.
One should be very happy with the results of the cycle, as long as the diet and
training regimen are good. As I previously stated, testosterone is a highly anabolic
and androgenic hormone, it has an anabolic (muscle building) rating of 100. This
makes it a good drug to use if one is in pursuit of more size and strength. And if you
aren’t in pursuit of more size and strength, why would you be reading this, right?
Well, let’s get on with it and look at exactly what makes testosterone a good mass
builder. First, testosterone promotes nitrogen retention in the muscle (2), the more
nitrogen the muscle holds the more protein the muscle stores. Testosterone can also
increase the levels of another anabolic hormone, IGF-1, in muscle tissue (3).
Testosterone also has the amazing ability to increase the activity of satellite cells (4).
These cells play a very active role in repairing damaged muscle. Testosterone also
binds to the androgen receptor to promote A.R dependant mechanisms for both
muscle gain as well as fat loss (5). Testosterone significantly increases the
concentrations of the A. R in cells which are critical for muscle repair and growth.(4,
6). Testosterone induces changes in shape and size of your muscle fibres, and can
change the actual appearance and the number of muscle fibres (7). Also, a note to
both bodybuilders and athletes, many anabolic/androgenic steroids (like testosterone
susprnsion, in this case) can also protect your hard earned muscle from the catabolic
(muscle wasting) glucocorticoid hormones (8) that your body employs to maintain
homeostasis. In addition, Testosterone has the added ability to increase red blood
cell production (9), and a higher RBC count may improve endurance via better
oxygenated blood. More RBCs can also improve recovery from strenuous physical
activity, and this has obvious benefits for the hard training bodybuilder or athlete. As
with 99% of other steroids, Testosterones' anabolic/androgenic effects are dose
dependant, the higher the dose the higher the muscle building effect (10).
Testosterone suspension is best run for at least 8 weeks and depending on the
131
experience of the user one may choose to run much longer. Since this hormone is
primarily used by more advanced users, other drugs are usually incorporated into
the cycle. One should opt. for other mass drugs such as dianabol and deca
durabolin, since the goal of this cycle will most likely and should be for mass. The
user should expect to see rapid muscle growth, water retention, and possibly extra
fat deposits. Some athletes will also choose to inject Suspension before a workout or
competition (this would increase aggression, and would be especially important for
MMA competitors or those in a sport where aggression is a benefit). I’ve used it for
this purpose and found it to be very useful. Many other athletes will also use it solely
for this purpose; every day (painful) shots are not much fun for a typical 12 week
cycle. It is for this reason that most people who use this drug employ it pre-workout
and/or competition, and not much more often. A mere 100mgs pre-workout or
competition is sufficient and would benefit competitive athletes enough to justify its
inclusion in an in-season-cycle.
Lastly, you should be paying roughly $50 for a 10cc bottle of 100mgs/ml from any
reputable underground lab.
References:
1. Heart. 2004 Aug; 90(8):871-6.
2. J Clin Endocrinol Metab. 1997 Feb; 82(2):407-13.
3. Am J Physiol Endocrinol Metab. 2002 Mar; 282(3):E601-7.
4. Curr Opin Clin Nutr Metab Care. 2004 May; 7(3):271-7.
5. Curr Pharm Biotechnol. 2004 Oct; 5(5):459-70.
6. J Clin Endocrinol Metab. 2004 Oct; 89(10):5245-55.
7. Anat Histol Embryol. 2003 Apr; 32(2):70-9.
8. J Lab Clin Med. 1995 Mar; 125(3):326-33.
9. Zhonghua Nan Ke Xue. 2003; 9(4):248-51
10. J Clin Endocrinol Metab. 2003 Apr; 88(4):1478-85
132
Testoviron
(Testosterone shown + Teststerone with Propionate and Enanthate ester)
(Testosterone Propionate + Testosterone Enanthate)
[17b-hydroxy-4-androsten-3-one]
Formula (base): C19 H28 O2
Formula(Enanthate ester):C7 H12 O
Molecular Weight: 412.6112
Molecular Weight (base): 288.429
Molecular Weight (Enanthate ester): 130.1864
Molecular Weight (Propionate ester): 74.0792
Formula (Propionate Ester): C3H6O2
Melting Point (base): 155
Manufacturer: Schering
Effective Dose (Men): 300-2000mg+ week
Effective Dose (Women): Not recommended
Active life: 8 days
Detection Time: 3 months
Anabolic/Androgenic ratio:100/100.
Testoviron is a blend of two different products, namely testosterone with the
propionate (short) ester attached, and testosterone with the Enanthate (long) ester
attached. Confusingly, Schering, who produces this product, also has a pure
testosterone Enanthate product of the same name. Testosterone is usually attached
to an ester (i.e. when you buy testosterone propionate, or Enanthate the
components of this particular drug, you are buying testosterone with a propionate
ester attached and testosterone with an Enanthate ester attached, both in the same
milliliter of drug). These esters determines how long it takes your body to dispose of
the testosterone, and propionate is the shortest ester commonly available with a
testosterone base (of course, testosterone suspension has no ester), whereas
Enanthate is the longest, generally available with a testosterone base. Within your
body, there are enzymes called esterases, which have the function of removing the
ester from steroids. This leaves you with just the steroid molecule with the ester
cleaved off. The heaviness of the ester chain, determines how long it takes the
esterase to remove it. With this product, you have testosterone with a heavy chain
(which will take your esterases awhile to remove) as well as with a short chain
(which your esterases will quickly remove).
What happens when those esters are removed?
133
Well, then the Testosterone you injected induces changes in shape as well as in the
size of your muscle fibers. It can also change the appearance and the number of
those (7). Testosterone is also noted for its ability to protect your hard earned
muscle from catabolic (muscle wasting) glucocorticoid hormones (8), inhibiting their
ability to send a message to muscle cells to release their stored protein.
Concomittantly, Testosterone sends a message to muscle cells to store more
contractile protein (called actin and myosin); glucocorticoid hormones send the
opposite message. In addition, Testosterone has the ability to increase erythropoiesis
(red blood cell production) in your kidneys (9), and as we all know, a higher Red
Blood Cell (RBC) count would most likely improve endurance via bringing more
highly oxygenated blood to your muscles. Having more RBCs can also improve
recovery from strenuous physical activity. It should be noted that agression levels
often rise dramatically with the use of exogenous testosterone (15).
All of these great benefits are to be had with the use of either testosterone
Enanthate or propionate alone. Realistically, Testoviron will be part of a cycle
containing one or more other drugs. People who are bulking will probably choose to
use another drug like Deca or Eq (possibly with Dbol as well) and those who are
cutting will probably steer towards Eq and perhaps Trenbolone. Very often users will
shoot this drug three or four times a week, but blood levels of testosterone from the
testosterone Enanthate component would still above baseline with this drug at
around day eight (16), even though we know the other component would peak and
fall much more rapidly.
The advantage to longer esters is they need to be injected less frequently (test prop
needs to be injected every other day while you can shoot test cyp once a week). The
disadvantage to long estered steroids is they contain less actual steroid. However,
most people from Steroid.com and other discussion boards who have tried differing
esters on their various cycles agree: Testosterone Propionate causes the least side
effects and bloating, while Enanthate causes the most. Also, any injected
testosterone will inhibit your natural test levels and HPTA (Hypothalamic Pituitary
Testicular Axis). A hundred mgs of test/week takes about 5-6 weeks to shut the
HPTA, and 250-500mgs shuts you down by week 2 (4).
What stacks well with Testoviron? Well, since it’s a testosterone with both a short
and long acting component, I suppose the answer is everything and nothing. Since it
has a short ester in it, you would have to inject it every other day, so you may as
well run another short acting drug with it (Trenbolone Acetate, or whatever).
However, since its got a long acting component to it, you may consider using a
longer acting drug with it (Deca or Eq, perhaps); the downfall here is that you don’t
get the full benefit of shooting test prop alone (less water retention, etc…). You still
have to shoot as frequently as if you were only using prop. The testosterone
Enanthate is long acting, but you’re still going to be shooting this compound every
other day to make use of the propionate component. The advantage of testosterone
Enanthate (reduced shooting frequency) is negated. Many people’s favorite’s are Eq
(boldenone undeclyenate) or Deca (nandrolone decanoate), but anything will stack
well with testoviron. Tren (Trenbolone Acetate), Masteron, and/or Winstrol are also
favorites for many on a cutting cycle. It’s important to note that a product to fight
water-retention and other estrogenic sides would be warranted if Testoviron were
used for a cutting cycle.
Finally, it’s worth noting that sometimes a strategy known as "frontloading" is
employed with products like this one, since it contains both testosterone propionate,
134
and Enanthate. This is where double or triple the intended dose for the cycle is
injected for the first two weeks, and the propionate ester gives a very quick rise in
blood plasma levels of testosterone, and then the Enanthate ester is relied on for a
more even blood level in the ensuing weeks. The reasoning behind this is
presumably to get the blood levels of the drug up quickly in the hopes of seeing
results more quickly, and then have the blood levels even out and stay constant.
Of all testosterones available on the market today, blended ester products like this
one are the most unjustifiably expensive. This is both because they are in high
demand, as well as more rare than single estered products. You can only find
Testoviron in the Dominican Republic and Italy (135mg versions available in both
countries). Expect to pay up to $5-7 for an amp of this stuff and if your source is
asking for more, expect to walk away. When the price of testosterone is so low, I
can’t justify purchasing a blended product for any more than you would purchase a
single estered test.
References:
1. Pope, H.G, Kouri, E.M., & Hudson, J.I. (2000). Effects of supraphysiologic doses of
testosterone on mood and aggression in normal men: A randomized controlled trial.
Archives of General Psychiatry, 57, 133-140.
2. Chance, S.E., Brown, R.T., Dabbs, J.M., & Casey, R. (2000). Testosterone,
intelligence and behavior disorders among young boys. Personality and Individual
Differences, 28, 437-445
3. Am J Physiol Endocrinol Metab 2003 Jan 7; [epub ahead of print] Related Articles,
Links "Development of Models to Predict Anabolic Response to Testosterone
Administration in Healthy Young Men."
4. J Investig Med. 1997 Oct; 45(8):441-7
5. J Clin Endocrinol Metab. 1986 Dec; 63(6):1361-4.
6. J Clin Endocrinol Metab. 1997 Feb; 82(2):407-13.
7. Am J Physiol Endocrinol Metab. 2002 Mar; 282(3):E601-7.
8. Curr Opin Clin Nutr Metab Care. 2004 May; 7(3):271-7.
9. Curr Pharm Biotechnol. 2004 Oct; 5(5):459-70.
10. Metabolism. 1991 Apr; 40(4):368-77.
11. J Lab Clin Med. 1995 Mar; 125(3):326-33.
12. Zhonghua Nan Ke Xue. 2003; 9(4):248-51. Effect of androgen on erythropoientin in
patients with hypogonadism] [Article in Chinese] 1.Am J Physiol. 1998 Nov; 275(5 Pt
1):E864-712
13. Biochim Biophys Acta. 1995 May 11; 1244(1):117-20.
14. Am J Physiol Endocrinol Metab. 2001 Dec; 281(6):E1172-81.
15. Health Psychol. 1990; 9(6):774-91.
16. Fertility and Sterility 33.
135
19-nortestosterone
Derived Steroids
136
19-nortestosterone Derived Steroids
As you know, some steroids are derived directly from 19-nortestoserone this includes
Nandrolone, Trenbolone,Nilevar, and many more. related compounds. Below is a
partial list of some traits and effects that most, if not all, 19-nor-testosterone
Derived Steroids have attributed to them
• Very favorable anabolic:androgenic ratio
• Minimal water retention
• High quality gains have been reported
• High strength gains reported
• Generally regarded as very safe
• Low side effects
• Excellent ability to retain gains post-cycle
• Low/No reduction to DHT
• (Nandrolones) Cause favorable actions to blood lipids
• (Nandrolones) Improve immune function
• (Nandrolones) Only convert to estrogen at 1/5th the rate of testosterone
• Increased Creatine Phosphate metabolism
• Increased insulin sensitivity
• Positive effects on joints and favorable on collagen/bone-mineral content
• Known to have progestenic activity
• Inhibition of HPTA at very low doses
• Difficult recovery of HPTA post-cycle
137
Anabolic DN
(Nandrolone shown without Cypionate ester)
(Nandrolone Base + Cypionate Ester)
[19-nor-androst-4-en-3-one-17beta-ol]
Formula (base): C18 H26 O2
Formula (ester): C8 H14 O2
Molecular Weight(base): 274.4022
Molecular Weight (ester): 132.1184
Melting Point (base): 122-124°C
Melting Point (ester): 98 - 104 C
Manufacturer: SYD Group
Effective Dose (Men): 200-600mgs/week (2mg/lb of Bodyweight)
Effective Dose (Women): 50-100mgs/week
Active life: 8 days
Detection Time: Up to 18 months
Anabolic/Androgenic ratio: 125:37
This is an underused product, for one reason or another. It’s currently produced by
SYD Group who had some very inconsistent lab reports posted on the ‘net, with
regards to their product line. It was also produced previously by Jurox, under the
name Dynabol. It’s also under used, I think, because it’s an obscure buy for most
people outside of Australia, where those aforementioned companies reside. Let’s
have a look at Nandrolone, then we’ll discuss the addition of the Cypionate ester in
opposition to the much more commonly used Decanoate ester (the ester used with
Deca-Durabolin). First of all, Nandrolone doesn’t produce many estrogenic or
androgenic side effects. This is because it has a very low rate of aromitization
(conversion to estrogen via the aromatase enzyme); roughly equal to 20% the rate
of Testosterone. Nandrolone is a very nice anabolic, in my estimation (even though I
don’t use it anymore), and a 100mg/E2W (every 2 weeks) injection of it has been
shown to provide a “significant increase in weight” (3). I’d never recommend that
low a dose for an athlete, but it’s evidence of Deca’s strong anabolic properties. All of
the Nandrolones are very nice anabolics, causing high-quality (albeit slow) gains in
muscle. This could be due to its moderately strong binding to the Androgen Receptor
(stronger than testosterone, actually), or possibly its many positive non-Androgen
Receptor mediated effects. One such non-receptor mediated effect is nitrogen
retention, which is a major factor in muscle growth. Even with low-doses of
Nandrolone (65 mg/week), Nandrolone produces significant nitrogen retention (5).
Nandrolone is also well known to impove collagen synthesis (1), and increases bone
mineral content (2). For these purposes, studies on Nandrolone use very low doses
and were generally far too low to promote muscle growth.
138
In another study of HIV+ men (4) we can see that Nandrolone (200mgs on week 1,
400 on week 2 and 600mgs for weeks 3-12) actually caused NO negative side effects
in total or LDL cholesterol, triglycerides, or insulin sensitivity. In addition, there was
a reduction of HDL cholesterol (8-10 points) in both groups. Also, in these studies
with HIV+ subjects, Nandrolone improved immune function (5).
Judging from Steroid.com members’ feedback, as well as my own personal
experience, long-estered Nandrolones are known for producing quality weight gains,
but have to be used for 12 weeks at a minimum. This shouldn’t cause any problems,
since they are very mild drugs in terms of side-effects, and I don’t think they would
cause many adverse effects over this period of time. Nandrolone Cypionate has a
very long active life, of roughly 8 days or so, slightly less than the far more common
Nandrolone Decanoate (Deca). This would mean we want to shoot it 1-2xs a week,
along with our other compounds because we’d probably be running Testosterone
Cypionate with it.
Many members of Steroid.com also complain of water-retention with this the use of
longer-estered Nandrolones, and again, I’m inclined to agree. Letrozole seems to be
a preferred choice to combat this and it’s been my favorite for this use, on cycles of
12-16 weeks. This water retention would seem to make something like Anabolic DN
more suitable for bulking rather than cutting, although it can be succesfully used for
either with a proper diet and use of ancillary compounds.
So where are we? How would I use this stuff personally? Well, I'd be comfortable
recommending this compound for either a bulking or cutting cycle, and I think its
real utility would be that you can use it along with Testosterone Cypionate and inject
them on the same day because they’d have the same active life.
References:
1. Metabolism. 1990 Nov;39(11):1167-9.
2. Effects of nandrolone decanoate on bone mineral content. R, Righi GA, Turchetti V,
Vattimo A
3. AIDS. 1996 Jun;10(7):745-52.
4. Sattler et al J Physiol Endocrinol Metab 283: e1214-22
5. J Acquir Immune Defic Syndr Hum Retrovirol. 1999 Feb 1;20(2):137-46.).
139
Anadur
(Nandrolone shown with Hexyloxyphenylpropionate ester)
Nandrolone base + Hexyloxyphenylpropionate ester
Formula (base): C18 H26 O2
Molecular Weight(base):274.4022
Melting Point (base): 122-124°C
Manufacturer: Various
Effective Dose (Men): 200-600mgs/week (2mg/lb of Bodyweight)
Effective Dose (Women): 50-100mgs/week
Active life: 15 days
Detection Time: Up to 18 months
Anabolic/Androgenic ratio: 125:37
Anadur is steroid that is very closely related to Deca Durabolin. The base compound
in both drugs is 19-nor-testosterone, which is more commonly known as nandrolone.
The base compound is similar to testosterone except the absence of a carbon-atom
in the 19th position. The significance of a 19-nor-testosterone compound is that the
conversion to estrogen is very low, and while the bond strength with the anabolic
receptor (AR) is higher. The difference between this drug and that of Deca Durabolin
is that Anadur contains the Hexyloxyphenylpropionate ester. This particular ester is
very large, making this steroid very slow acting, and may be the slowest acting of all
the nandrolone compounds. The downside to this large ester is that on a mass to
mass basis, there is less nandrolone hormone than compared to Deca Durabolin.
Anadur is used in a very similar fashion to Deca Durabolin and is mostly for those
looking for gradual gains with lower side effects. Anadur is not a commonly found
steroid but still exists in some parts of the world, as listed later on. Nandrolone in
general is more anabolic than testosterone and has a very low androgenic
expression. It is reported to have an anabolic to androgenic ratio of 37:125.
Typically, males would take a dosage range of 200-600mg/wk, with higher doses
sometimes found in more advanced users. This compound normally would not be
recommended for women due to the virilization effects this compound may cause
such as increased body hair, deepened voice, acne, and clitoral hypertrophy.
However, some female members at Anabolic Review have used it at ultra low doses
of 25-50mg/wk with success.
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This steroid can be affected by Anadur’s chemical structure, the 5-alpha-reductace
enzyme producing dihydronandrolone (DHN). DHN is a compound similar to that of
DHT, however, unlike DHT, DHN is a much weaker drug and has a much lower
affinity for binding to the AR. Furthermore, the rate at which nandrolone is
converted to DHN will be much lower than testosterone. Because DHN is a weaker
compound, those with concerns for the prostate and hair loss can still take Anadur
with little side effects. Most members report no hair loss while using nandrolone
products.
Also, again, based on structure, Anadur can be converted to estrogenic compounds
via the aromatase enzyme. Although some estrogen is produced, both the amount
and the rate of Anadur are much lower than testosterone, approximately less than
20% than that of testosterone. Although estrogen is low, the use of anti-estrogen
compounds is highly recommended.
While the levels of estrogen and DHN production are low, there is a third mechanism
that Anadur can convert. Nandrolone has been shown to have agonistic effects and
a high affinity when binding with the progesterone receptor and acts as a progestin
throughout the body. Ideally, one would want an anti-progesterone compound;
however, there are no widely available products at this time.
Since Anadur has a high affinity toward the androgen receptorand has a lower
androgenic expression, it is usually not recommended that it be taken without
testosterone. Without a high androgenic expression and having a strong bond to the
AR, side effects of low testosterone are possible such as the infamous “Deca-Dick”
(impotence), lethargy, and low sex drive. Furthermore, because of the three
conversion products listed above, this compound is generally very suppressive to the
body and can make it difficult to restart natural testosterone production during post
cycle therapy. Most Anabolic Review members report loss of libido and retention of
gains after a nandrolone only cycle, and the addition of testosterone combats these
problems. By adding testosterone, the balance of androgenic expression is raised in
the body due to more competition and more binding with the AR. Remember,
nandrolone binds very heavily to the AR and shows little androgenic expression.
Hence, an androgenic compound is needed to counteract this.
Users of nandrolone report a soothing sensation in their joints. This is most likely
attributed to the mild water retention caused by nandrolone. For this reason, Anadur
would most likely not be found in high concentrations of a cycle for those looking to
lose fat, and is more suitable for those looking to gain mass. Also, because of the
different aromatizing products (estrogen, progesterone, and DHN), some Anabolic
Review members report gains of fat when strict diets are not followed. Gains usually
come steadily and are quality gains that are easy to hold with proper post cycle
therapy.
Anadur is a good steroid to be stacked with a few other steroids, and as mentioned
above, testosterone is highly recommended. Other compounds commonly stacked
with Anadur or other nandrolone compounds are Equipoise, Dianabol, Winstrol, and
Anavar.
When ending a cycle containing Anadur, most of the Anabolic Review members run
testosterone for a couple weeks longer than the nandrolone. Since nandrolone is so
suppressive, this gives the body time to clear the AR; binding with nandrolone so
that it can prepare for testosterone. The Anabolic Review members report that this
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helps recovery very much by doing so. For post cycle therapy, most follow the typical
regimen of Clomid and/or Nolvadex. Others like to add HCG prior to ending the cycle.
Since Anadur is a nandrolone, it is to be expected that some of the metabolites
produced will stay in the body for up to 18 months, making Anadur and all
nandrolone compounds a very poor choice for athletes who are drug tested.
Given the large fatty ester on Anadur, the active life is reported to be around four
weeks long. This also allows for very few injections as low as one injection per week
for Anadur, although due to the relatively low concentrations either high volumes or
more frequent injections are required. It is possible to only inject weekly, but the
volume required would be 6-8ml which would not be advised with one injection.
References:
1. Comparison of the receptor binding properties of nandrolone and testosterone under in
vitro and in vivo conditions.Bergink EW, Janssen PS, Turpijn EW, van der Vies J.
2. Metabolism and receptor binding of nandrolone and testosterone under in vitro and in
vivo conditions.
Bergink EW, Geelen JA, Turpijn EW.
3. New iodinated progestins as potential ligands for progesterone receptor imaging in
breast cancer. Part 2: In vivo pharmacological characterization.
4. Rijks LJ, van den Bos JC, van Doremalen PA, Boer GJ, de Bruin K, Janssen AG, van
Royen EA. E-17 alpha-(2-[125I]iodovinyl)-19-nortestosterone: the synthesis of a
gamma-emitting ligand for the progesterone receptor.
5. Hochberg RB, Hoyte RM, Rosner W
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Cheque Drops
(Mibolerone)
[7-alpha, 17-alpha-dimethyl-19Nor-androst-4-en-3-one,17b-ol
17-hydroxy-7,17-dimethyl-estr-4-en-3-one
17beta-Hydroxy-7alpha,17-dimethylestr-4-en-3-one]
Molecular Formula: C20 H30 O2
Molecular Weight: 302.455
Melting Point: N/A
Manufacturer: Upjohn
Release Date: (Has been released and re-released numerous times)
Effective Dose: 200-400mcg
Active Life: 2-4hours
Detection Time: Immediate (only)
Anabolic/Androgenic Ratio:: 590:250
Mibolerone was initially used as a veterinary product used to keep female dogs under
control while they were in heat. It did so by shutting down the cycling of their
ovaries. With proper timing, breeders are able to regulate the heat cycles of their
bitches. Eventually, athletes began to utilize the product in order to boost aggression
before events. It was even rumored that Mike Tyson was on Cheque Drops during
the infamous ear biting incident during his bout with Holyfield. However, the late
great guru Dan Duchaine discovered the application of Cheque Drops in modern
bodybuilding far before that. The drops went in and out of production several times,
before making a recent insurgence due to the piqued interest in the product thanks
to the growing popularity of ultimate fighting circles.
Cheque Drops are extremely potent, certainly one of the most potent androgens
known to man. According to the manufacturer, “When compared to testosterone, it is
5.9 times more potent as an anabolic agent and 2.5 times more potent as an
androgen.” The most probable usage of Cheque Drops is for administration to
athletes 30 to 40 minutes prior to an event that requires extreme aggression and
adrenaline. To adapt the drug to bodybuilding purposes requires a much more
complicated dosing regimen. Due to its toxicity, Cheque Drops should not be used
longer than two weeks at a time, and at low dosages. However, for an anabolic
effect, Cheque Drops should be used at 5mg (5,000mcg) a day or more. However,
that would possibly lead to prompt physical illness. In order to find a medium that is
possible for the modern bodybuilder, it is important to remember a few key aspects
of the compound. Keep in mind that the dosages appropriate are only used to
increase aggression, which can subsequently increase strength. The actual anabolic
effect at these low doses is limited. Furthermore, long term use (beyond two weeks)
143
will lead to testosterone suppression and liver damage. Using the drops sparingly
(1-2 drops at a concentration of 200-250mcg 30 minutes prior to a workout for no
more than 2 weeks at a time) will provide a boost in training and aggression. Many
users report breaking personal lift records when utilizing the compound. If the drops
are used short term, testosterone levels should bounce back rather quickly.
However, due to the risk of suppression, it is best to use the drops while on an
anabolic stack in order to ensure elevated test levels. The drops are only used as a
supplement to lifting, and they can be used when bulking or cutting. I would never
recommend using this stuff without other compounds; however…the increased
aggression without the increased performance provided by other compounds may be
dangerous. They do not aromatize (convert to estrogen), so if used in the context
above, Nolvadex, Armidex, or other such agents are not necessary, nor is the use of
Clomid. It is highly progestenic, but in the doses we’re talking about, that won’t be a
concern either. Unfortunately, this stuff blocks LH secretion, which will wreak havoc
with your natural hormone production with prolonged use.
The half-life of the compound is very short (about 4 hours), so along with its
immediate impact on the body, it leaves quickly as well. The drug has had enough of
an impact, however, to be included in most all banned substance lists in most
athletic organizations, so precaution should still be utilized. Several metabolites of
this compound may still be detectable however (1), if you are tested immediately.
While it is sometimes touted as the most androgenic compound on the planet, it
might subsequently be the most toxic as well. A 19 nor-androgen it can possibly
cause progesterone related gynocomastia (you don’t want that) if used out of the
recommended dosage and time frame. A 17AA compound, it can also severely affect
liver function. Precaution MUST be used when dealing with Mibolerone. Side effects
include but are not limited to, increased aggression, hypertension, insomnia, and
severe liver damage.
Female athletes should avoid this compound at all costs. Remember, it’s used to
regulate ovulation in bitches (ok, that was a gratuitous use of that word again).
Side effects include, but are not limited to: severe acne, deepened voice, depression
of menstruation and clitoral enlargement,and…err…vaginal secretion (if that’s an
issue). If taken by a pregnant female athlete, it would have possible effects on the
fetus, as well as alter serum lipids. Remember, this stuff is used to control bitches in
heat (and no, that wasn’t slang; it’s really used to control female dogs that are
ovulating).
For those that are naturally aggressive, this compound will elevate aggression to
dangerous levels. It may affect some users more severely than others, and should
the athlete still be experiencing elevated aggression levels after the estimated time
of physical exertion, they may displace aggression on others. Cheque Drops should
not be stacked heavily with other 17AA compounds. Let’s be honest, though, this
stuff is powerful, but not deadly. The LD50 (the dose at which 50% of the Lab rats
died) is 1,600,000mcg/kg! You’d need to take bottles and bottles of this stuff per
day to replicate anything nearing that dose.
Cheque Drops are manufactured by Upjohn, and are available in a 100 mcg per cc,
55-cc bottles. There are 3 Chinese manufacturers of Mibolerone powder, which offer
the crystalline form for anywhere between 200-350 dollars/gram. Several
underground Labs have also began to produce Cheque Drops, such as Supra, with a
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concentration of 200mcg/ml, but the prices remain high, and the availability low.
Currently, Supra is the leader in Cheque drop production for athletes today.
Reference:
1. J Vet Pharmacol Ther. 2000 Apr;23(2):57-66
Completely Cleanse Steroids From Your
Body in Just 5 Days!
http://www.SteroidCleanse.com
145
Deca-Durabolin
(Nandrolone shown with Decanoate ester)
(Nandrolone Base + Decanoate Ester)
[19-nor-androst-4-en-3-one-17beta-ol]
Formula (base): C18 H26 O2
Formula (ester):C10 H20 O2
Molecular Weight(base):274.4022
Molecular Weight (ester):172.2668
Melting Point (base): 122-124°C
Melting Point (ester):31 - 32 C
Manufacturer: Organon
Release Date (in USA): 1962
Effective Dose (Men): 200-600mgs/week (2mg/lb of Bodyweight)
Effective Dose (Women): 50-100mgs/week
Active life: 15 days
Detection Time: Up to 18 months
Anabolic/Androgenic ratio: 125:37
Deca-Durabolin (“Deca”) is actually the brand name for Organon’s version of the
compound Nandrolone Decanoate. This is a 19-Nor compound (some would say that
it is the 19-nor compound), and as such, it shares basically the same characteristics
with all of them. One thing that is unique about Deca above nearly all steroids is the
mystique it has had for the last quarter of a century. On a personal level, I've
included Deca in cycles at doses ranging from 100mgs/week to 2,000mgs per week.
Suffice to say, I have my fair share of experience with this compound. This drug was
regarded very highly by Dan Duchaine in his Underground Steroid Handbooks, as
well as many of his later writings. For many, this was, and is, the final word on Deca.
Let’s dive into some of the reasons that Deca’s mystique may be well deserved.
First of all, Deca (and Nandrolone in general) doesn’t produce many estrogenic or
androgenic side effects. This is because Deca has a very low rate of aromitization
(conversion to estrogen via the aromatase enzyme). Its rate is roughly equal to
20% the rate of Testosterone.
Also, I’ve read in many places that Deca stores water in connective tissue, thus
alleviating joint pain. I have no idea what “storing water in the joints” means. I have
no idea how to really quantify that statement, or where it started. However, in one
146
study of postmenapusal women, Deca impoved collagen synthesis (1), and in
another study, it increased bone mineral content (2). Both of these studies used
VERY low doses, which were far too low to promote muscle growth. In my
estimation, based on these 2 studies, an athlete attempting to use Deca only for
these two effects (increasing bone mineral content and collagen synthesis) should be
using 100mgs every week. That’s actually a higher dose than those two studies used
successfully. Even at ½ of this dose, in HIV+ patients who have experienced
significant wasting, a 100mg/E2W (every 2 weeks) injection of Deca resulted in a
“significant increase in weight” (5). I’d never recommend that low of a dose for an
athlete, but it’s evidence of Deca’s strong anabolic properties. Deca is a very nice
anabolic, causing nice (albeit slow) gain in quality muscle. This could be due to its
moderately strong binding to the Androgen Receptor, or its many positive non
Androgen-Receptor mediated effects. One such effect is nitrogen retention, which is
a major factor in muscle growth and lean mass gains. In one study, with low-doses
(65 mg/week) and high-doses of Deca (200 mg/week), both low-doses and high
doses resulted in significant nitrogen retention (33-52 g nitrogen/14 days,
representing gains of 0.5 to 0.9 kg lean tissue/week), and body weight increased by
4.9 +/- 1.2 kg, including 3.1 +/- 0.5 kg lean body mass, and treadmill exercise
performance (cardiovascular fitness) also improved (7). The higher doses in this
study produced more gains. Steroid.com members who have posted their results
with Deca confirm this in many posts and threads, with their average
reccomendation being to take 400-600mgs/week for muscle gain.
Deca also has a very long active life. We can see from the chart below that a 100mg
shot (represented by the circles) produced relatively active and stable plasma
nandrolone levels almost until day 10, hence, once a week shots are all that’s
necessary for stable levels of nandrolond decanoate (as a side note, the nandrolone
phenylpropionate used in this study was active, and only experienced a severe drop
off around day 5—shooting NPP every 4th day is the way to go). You’ll also note that
higher blood plasma levels of Nandrolone are found with Gluteal injections as
opposed to Deltoid injections (this is true for all oil-based steroids, I suspect).
In another study of HIV+ men (6) we can see that Ddeca (200mgs on week 1, 400
on week 2 and 600mgs for weeks 3-12) caused no negative side effects in total or
LDL cholesterol, triglycerides, or insulin sensitivity and there was a reduction of HDL
147
cholesterol(8-10 points) in both groups. Also, in most studies with HIV+ subjects,
Deca also improved immune function.
So what do we know so far about this compound? So far, we know that Deca is a
very safe drug for long term use, will help with joint problems, could improve
immune function, and is highly (!) anabolic and not very androgenic. That’s the
good news (and there’s a lot of it)…now for the bad news. Judging from Steroid.com
members’ feedback, as well as my own personal experience, Deca is known for
producing quality weight gains, but it has to be used for 12 weeks at a minimum.
This shouldn’t cause any problems, since it is a very mild drug in terms of side
effects. Many members of Steroid.com also complain of water-retention with this
drug, and I’m inclined to agree. Letrozole seems to be a preferred choice to combat
this, and it’s my favorite for this use. This water retention would seem to make Deca
more suitable for bulking rather than cutting; although, it can be succesfully used for
either.
Now for the worst news: unfortunately, Deca is a progestin (as are all nandrolones),
and it happens to stimulate the progesterone receptor 20% as well as progesterone
itself (3). This opens the door for many possible unwanted side effects (water
retention, acne, etc…). It must be noted that most of those are rare, though. This
also may be the major reason why Deca is such a suppressive drug when it comes to
your natural testosterone levels. We can see from the chart below that a single
measly 100mg injection of Deca caused a total (100%) reduction of natural
testosterone levels, and it took roughly a month to return those testosterone levels
to baseline! All from 100mgs of Deca!
The moral of this story? Always use testosterone with your Deca! I suggest 200mgs
minimum to avoid impotence and sexual dysfunction. For an anabolic effect from
that of Testosterone, I recommend at least double that, with an equal amount of
Deca (minimum). I’d also recommend taking an anti-progesteronic drug with deca
148
(or at least having it on hand): Cabergoline and Bromocriptine are both good
choices.
So where are we? Well, I'd be comfortable recomending Deca for a bulking cycle with
a dosage of up to 600mgs/week for an extended duration (12-16 weeks), or up to
400mgs/week in a cutting cycle (again, for 12-16 weeks), as long as something to
combat water retention was present. Whatever purpose you decide to use Deca for,
you still need to include Testosterone in your cycle and have some anti-progesteronic
drugs on hand (see paragraph above), just in case.
Post Cycle Therapy (PCT), though beyond the scope of this profile, needs to be
discussed. Due to the highly suppressive nature of Deca, I will speculate that
testosterone in a deca-inclusive cycle must run for at least 2 additional weeks upon
cessation of Deca. We remember from the chart above that baseline testosterone
levels took roughly a month to return. Hence, a nice long estered testosterone
should run for an additional 2 weeks. This is to prevent having a lag in time when
the Deca is not producing an anabolic effect, yet is still suppressing your natural
testosterone levels. I'd also suggest that a particularly agressive PCT be run after
your cycle; nolvadex, HCG, and perhaps clomid should all be utilized in an effort to
restore your natural hormone levels as quickly and efficiently as possible.
Buying this product as a human-grade pharmaceutical from a dealer who stocks the
Organon brand will be an expensive proposition. You could end up paying well over
$10usd per amp or 2ml vial, not to mention that this product is (in my estimation)
probably the most faked steroid in the world. Buying veterinary grade will lower the
cost, with an average price of $75 for a ten milliliter bottle. There are also many
underground labs who produce this drug and usually 10-20mls of a 200mg/ml
concentration will never run over $100.
Here’s how Nandrolone is metabolized in your body:
References:
1. Metabolism. 1990 Nov; 39(11):1167-9
2. Effects of nandrolone decanoate on bone mineral content R, Righi GA, Turchetti V,
Vattimo A.).
149
3. Cancer Res 1978 Nov; 38(11 Pt 2):4186-98
4 (Charts) from Minto et al
5. AIDS. 1996 Jun; 10(7):745-52
6. Sattler et al. Am J Physiol Endocrinol Metab 283: e1214-22
7. J Acquir Immune Defic Syndr Hum Retrovirol. 1999 Feb 1; 20(2):137-46.
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
150
Diandrol
(Nandrolone shown + w/ Phenylpropionate ester and Decanoate ester)
(Nandrolone Base + 2 esters)
[19-nor-androst-4-en-3-one-17beta-ol]
Formula (base): C18 H26 O2
Formula (esters)
Phenylpropionate: C9 H10 O2
Decanoate:C10 H20 O2
Molecular Weight(base):274.4022
Molecular Weight (esters)
Phenylpropionate: 150.174
Decanoate:172.2668
Phenylpropionate: C9 H10 O2
Melting Point (base): 122-124°C
Manufacturer: Xelox
Effective Dose (Men): 200-600mgs/week (2mg/lb of Bodyweight)
Effective Dose (Women): 50-100mgs/week
Active life: 15 days
Detection Time: Up to 18 months
Anabolic/Androgenic ratio: 37:125
This is an interesting product, simply because it combines the two most popular
Nandrolone preparations, namely, Nandrolone Decanoate (Deca) and Nandrolone
Phenypropionate (Durabolin). I guess from a marketing point of view, it’s a good
idea, because a lot of people like both of those versions of Nandrolone. Let’s take a
look at what we’re dealing with here, in terms of concentration:
Nandrolone Phenylpropionate: 40mgs
Nandrolone Decanoate: 60mgs
(100mgs/ml, presented in a 2ml vial)
So basically, we have a nice little combination of slow and fast acting Nandrolone in
a reasonable concentration. If you are inclined to use blends, and you can find this
one cheaply; I’d say it’s a decent buy. It’s produced in the Phillippines and Labeled
for export only, so the various economic factors involved tend to make this a cheap
product, price-wise. If I were to speculate, I’d say that labeling it for “export only”
was a way to export a loophole and get this stuff from the manufacturer onto the
black market and into athlete’s bodies with minimum interference from the local and
federal authorities of that country.
151
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152
Durabolin
(Nandrolone shown with Phenylpropionate ester)
(Nandrolone Base + Phenylpropionate Ester)
Formula (base): C18 H26 O2
Formula (ester): C9 H10 O2
Molecular Weight(base):274.4022
Molecular Weight (ester): 150.174
Melting Point (base): 122-124°C
Melting Point (ester): 20°C
Manufacturer: Organon
Effective Dose (Men): 200-600mgs/week (2mg/lb of Bodyweight)
Effective Dose (Women): 50-100mgs/week
Active life: 5 days
Detection Time: Up to 12 months
Anabolic: Androgenic ratio: 37:125
Effective Dose (Men): 300-600mgs/week
Effective Dose (Women): 50-100mgs/week
Nandrolone is a modification of testosterone (carbon atom removed from the 19th
position). With an Anabolic/Androgenic ratio: 37:125 it is highly anabolic (muscle
building) and moderately androgenic (male characteristics). Due to nandrolone’s
chemical structure, it only aromatizes (converts to estrogen) slightly, at about 20%
the rate of testosterone when it interacts with the aromatase enzyme. Ergo,
estrogenic effects are not a major concern with its use. Of note, however, is that
nandrolone is a progestin with a binding affinity of 20% to the progesterone receptor
(15) (PgR), so side effects are still possible, though rare. The development of breast
tissue in males (gynecomastia) has been reported by some Steroid.com users.
Besides being one of the most popular anabolic steroid used in bodybuilding cycles,
nandrolone is also (medically) used to treat severe debility or disease states, and
refractory anemias (1). It promotes tissue building processes, reverses catabolism
(muscle destruction) and stimulates erythropoiesis (red blood cell production). This
makes it a very useful drug to treat wasting disorders such as advanced H.I.V. (2)
(16), and also, makes it highly sought after by bodybuilders and athletes.
Nandrolone is most commonly found with a cypionate, laurate, decanoate or
plenylpropionate ester. Briefly explained, the ester determines how much of the
given hormone is released over a period of time. Longer esters such as decanoate
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peak slowly and can keep stable blood plasma levels up to ten days. Shorter esters,
such as the phenylpropionate, peak more rapidly but the half-live is shorter. Shorter
esters usually release much more active hormones per mg than longer esters, and of
course, allow the drug’s effects to leave your system more quickly. Surprisingly, NPP
(Durabolin) and ND (Deca) release almost the same amount of active nandrolone per
100mgs: 69% and 65% respectively; this does not correlate exactly though because
blood levels of nandrolone are much higher (about doubled) post NPP usage
compared to the same 100mg dose of ND (see chart). NPP also has more distinct
advantages over ND. One of the most common complaints about adding ND (Deca)
to a cycle is the water retention that accompanies its use (3). Gains from NPP are
reported to be “clean” with minimal water retention and fat gain. While ND is usually
used in “bulking” cycles, NPP is used in “cutting” cycles, although either drug can be
used in either regard. Being an oil based anabolic it is injected intramuscularly (into
the muscle); many users inject it ED or EOD, however, NPP can be administered E4D
without problems.
NPP and nandrolone in general have a number of benefits for athletes; they increase
levels of serotonergic amines in the brain. These chemicals contribute to aggressive
behavior. This could help athletes train harder and improve speed and power (4).
Nandrolone also increases levels of IGF-1 in muscle tissues (5). This may be another
reason why nandrolone is highly anabolic. NPP also benefits the athlete by increasing
the number of androgen receptors (AR). One study showed that when nandrolone
was given to rats at a dosage of 6mg/kg of bodyweight and was combined with
muscle functional overload (muscle functional overload gives a similar effect to
resistance training) it had a 1,300% (!) increase in AR protein concentrations (6).
There is a direct link to muscle growth and AR levels. NPP also seems to be a
promising fat loss agent. Men who were given the drug had reduced levels of
subcutaneous (under skin), adipose (fat) tissue, and visceral (gut) however, fat loss
was not as good (7). The fat loss effect seems though to be dose dependant. In one
study, NPP at a daily dose of 1, 4, or 10mg per kg of bodyweight, the 10mg dose
had the greatest effect on fatloss (8). NPP is used to treat anemia by stimulating red
blood cell production (1). An increase in RBC count can improve endurance during
exercise via better lactic acid clearing and oxygen delivery. The blood is also better
enabled to carry nutrients to muscle tissue to aid in repair. Administration also
increases the rate of muscle glycogen repletion after exercise, helping the athlete to
dramatically recover after strenuous physical exercise (9). Athletes who require a
high level of endurance in their chosen sport can benefit from the use of NPP (15). A
favorite with bodybuilders who suffer with sore joints, NPP can also improve collagen
synthesis (10), which may improve joint function and alleviate joint pains. Many
members of Steroid.com swear by nandrolone’s ability to allow them to train in
comfort.
Many nandrolone lovers claim that it is one of the safest anabolic steroids, if not the
safest. It does have side effects that can be bothersome to hypersensitive individuals
such as acne, excitation, insomnia, nausea, diarrhea and bladder irritability (1). More
serious (and common) side effects include testicular atrophy (shrunken balls),
impotence (Deca dick) and gynecomastia (bitch tits) (1). Nandrolone use has been
shown to be safe and easy on the lipid profile, often improving HDL Cholesterol (16)
Impotence can be offset by stacking the nandrolone with a higher testosterone.
Nandrolone also causes the “shut down” (total stoppage) of endogenous (natural)
testosterone production. Thus an exogenous (outside) source must be provided. The
increased prolactin levels from the use of a progestinic steroid contribute to HPTA
shut down and testicular atrophy, which can be treated with a combination HCG (a
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female hormone that acts like LH when introduced into the male body) and
bromocriptine (a dopamine receptor agonist that, among other things, can lower
prolactin levels) (1)(11).
NPP can be highly useful in either “bulking” or “cutting” cycles, and it would seem
that diet and dosages are the determining factors of whether a cycle with this drug
will be one or the other. Due to its highly anabolic nature, coupled with low
androgenic properties, it can be incorporated into a mass cycle that is usually
stacked with testosterone and a powerful oral like, possibly, oxymetholone (Anadrol)
or methandrostenolone (Dianabol). NPP can thus be part of a classic bulking cycle.
For a cutting cycle NPP is usually be combined with other short-estered injectable
anabolic steroids (testosterone propionate and boldenone acetate come to mind as
likely choices) and one of the DHT derived orals such as stanozolol (winstrol) or
oxandrolone (Anavar). NPP is said to produce good mass and strength gains in both
cutting and bulking cycle phases (3). When one is planning a cutting cycle one must
take caution if combining the 19-nor-testosterone derivative trenbolone with
nandrolone. Trenbolone Acetate, although a powerful drug for lean muscle gains,
strength, and fat loss, is also a strong progestin with a binding affinity to the PgR of
60% (3x that of nandrolone). The elevated prolactin can worsen HPTA insult, often
causing the user to spend more money on preventative measures. The combo may
also result in a difficult PCT protocol to regain natural testosterone production. So
far, few Steroid.com members have had any first- hand experience with NPP because
it is limited to the few who know which UGLabs sells this particular form of
nandrolone. This increases the popularity of “home brewing” since the powder
comes out of China at very affordable prices. It is only a matter of time before NPP
(or Durabolin) takes a special place in the arsenal of Steroid.com members in their
quest for more muscle.
References:
1. Nursing2003 drug handbook.
2. Am J Physiol Endocrinol Metab. 2002 Dec; 283(6): E1214-22.
3. Steriod.com/steroid forums.
4. Med Sci Sports Exerc. 2003 Jan; 35(1): 32-8.
5. Am J Physiol Endocrinol Metab. 2002 Feb; 282(2): E483-90
6. J Appl. Physiol.94 1153-61 2003
7. Int J Obes Relat Metab Disord. 1995 Sep; 19(9): 614-24.
8. Ann Nutr Metab. 1991; 35(3): 141-7.
9. J Vet Med A Physiol Pathol Clin Med. 2001 Aug; 48(6): 343-52
10. Metabolism. 1990 Nov; 39(11): 1167-9.)
11. Pharmacol Biochem Behav. 1988 Mar; 29(3): 489-93.
12. Cancer Res. 2003 Oct 1; 63(19): 6523-31.)
13. Expert Opin Pharmacother. 2004 Dec; 5(12): 2549-58.
14. Cancer Res 1978 Nov; 38(11 Pt 2): 4186-98
15. Med Sci Sports Exerc. 1995 Oct;27(10):1385-9.
16. Am J Physiol Endocrinol Metab. 2002 Dec; 283(6):E1214-22. Epub 2002 Aug 27.
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Dynabolan
(Nandrolone shown with Undecanoate ester)
(Nandrolone + Undecanoate ester)
[Nandrolone: 19-Nor-4-androstene-3-one, 17b-ol]
Formula (of base): C18H26O2
Formula (of ester): C11 H22 O2
Molecular Weight (Nandrolone w/o ester): 274.4022
Melting Point (of base): 122-124°C
Manufacturer: Farmasister (Italy), Theramex (France-Discontinued)
Release Date: 1992
Effective Dose: 200-600mgs/wk (men); 40-80mgs/wk (women)
Active life: 8-10 days
Detection Time: Up to 18 months
Anabolic/Androgenic Ratio: 125:37
For readers who are getting used to my (lack of?) style with regards to writing
anabolic profiles, it will come as no surprise that the first thing we’ll need to do in
examining Dynabolan (Nandrolone Undecanoate) is have a quick look at its
structure. First, we can see that this is a 19-nor steroid. In fact, this is just another
type of Nandrolone, which means that it will share many, if not all, of its traits with
“Deca” (Nandrolone Decanoate, trade name: Deca-Durabolin). As we know,
Nandrolone is similar to testosterone, with the exception of the alteration of the 19th
carbon atom. And the “Undecanoate” part of this drug’s name (that’s the ester, or
the thing that slows its release into your bloodstream) provides a slightly longer
release time than Deca has. If I were to suggest that everyone take one thing away
from this profile, it’s that this drug is more or less a slightly longer acting version of
Deca, which means you need to employ it for a extended length of time to see
results (12 week cycles are recommended when using this compound). Also, this
long release time and the ubiquitous nature of Nandrolone’s metabolites make it
unsuitable for drug-tested athletes.
Before we go into all of the wonderful characteristics of this drug, let’s discuss some
of its less-than-wonderful aspects. Most side effects common with most AASs are
also common with this drug: possible virilization (development of male sexual
characteristics in women), gynocomastia, water retention, acne, hairloss, and
possibly even sexual dysfunction. Being a nandrolone, Dynabolan is also going to
have the ability to stimulate the progesterone receptor 20%, as well as progesterone
156
does (1)(2). This stimulation of the progesterone receptor is primarily responsible for
the suppressive effects that this drug will have on the body’s natural endocrine
system. Progesterone (and synthetic progestins, like nandrolone) can reduce
luteinizing hormone production. This hormone is secreted from the pituitary and
stimulates testicular testosterone production. Anabolic/androgenic steroids (AAS)
can also suppress this hormone’s pituitary borne production by interfering with the
Gonadatropin Releasing Hormone signal sent from the hypothalamus to the pituitary;
this, in turn, also stimulates lutenizing hormone secretion. So, it should be clear that
this compound, through various mechanisms, will act to halt the production of
testosterone, as well as other important hormones, in your body. The now infamous
“Minto” studies on nandrolone have shown us that even a single 100mg injection of
Nandrolone (although Undecanoate was not used, both a short as well as long ester
Nandrolone product were used) will shut down endogenous (natural) testosterone
production for a week and will not return to baseline values until roughly 3 weeks
later (3). Dynabolan will also aromatize (convert to estrogen) at a reasonably low
rate, much lower than that of testosterone. Given the estrogenic/progesteronic side
effects that this drug will cause, use of an anti-progesteronic drug (such as
Bromocriptine at 2.5mgs/day) as well as perhaps some Letrozole (1mg/day) should
be warranted. Regarding Nandrolone, most veterans of Steroid.com recommended
the concurrent use of exogenous (injectable) testosterone to avoid the possible
sexual dysfunction associated with Nandrolone. In general though, it’s difficult to
imagine someone getting any side effects if dosages are kept at 400mgs/week or
less (women would do well to keep dosages at or under 1/4 of that).
Now, if all of that didn’t scare you off or put you to sleep, we can get into the good
parts of this drug. It binds well to the Androgen Receptor (AR), which has been
positively correlated with enhanced fat-burning (4). This property makes it a great
addition to a cutting cycle; although, it can also be used with great success in a
bulking cycle as well. And, since this is a Nandrolone (albeit not with the ester we
are used to seeing it with), we can probably expect to reap all of the benefits that
nandrolones have been shown to have on bone mineral content and collagen (5).
When using nandrolone, little nagging injuries seem to go away for many athletes,
and Steroid.com members consistently report that their joints feel better when using
it.
Dynabolan is also, being a nandrolone, very easy on the liver, although if
someone has a pre-existing liver condition, it should be avoided. Also, lipid profiles
(your HDL/LDL cholesterol) won’t suffer, and could possibly improve a bit with use of
this drug.
Weight and strength gain with this drug is moderate and users report more of a
“kick” than they usually get with regular Deca. Besides, binding well to the AR, this
drug also operates via several non-androgens receptor mediated mechanisms, such
as increasing protein synthesis and increasing creatine phosphate synthesis. This is
also one of the few drugs that won’t negatively impact your lipid profile (cholesterol).
Most users report that weight gains are of a high quality with this drug and represent
a favorable change in body composition. This would be especially true if it were
stacked with testosterone and proper ancillaries.
Hypothetically, if I were to use this compound to bulk up, I’d use 400mgs/week with
500mgs of a long-estered testosterone (Cypionate or Enanthenate), and the
ancillaries I’ve previously mentioned. If I were to use it in a cutting cycle, I’d use a
short estered testosterone (most likely Propionate) at that same dose
(500mgs/week), as well as Oxandrolone at 50mgs/day, and I wouldn’t forget the
ancillaries. I’d also consider this drug to be appropriate for use in a 12-16 weeklong
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cycle. Due to the highly suppressive nature of this drug, a very aggressive post
cycle therapy would be necessary, and I’d recommend taking Clomid at 100mgs/day
as well as Nolvadex at 30mgs/day for a month and HCG at 500iu/day for 3 weeks.
I’d also caution anyone who is going to use this drug to avoid stacking it with a
trenbolone product. Combining 2 steroids, which stimulate the progesterone
receptor, isn’t a great idea.
And that leaves us with the final question: Is this stuff actually available? The
answer is yes and no. Actual Dynabolan is very hard to obtain although it is still in
production, and fakes would be an issue, as would cost. On the other hand,
nandrolone undecanoate (not the brand-name product “Dynabolan”) is made by
several underground labs (Dpharm, for example, produces it), and is relatively
cheap. Expect to pay slightly more than you would for nandrolone with the
decanoate ester; anything under $50 for a 10ml bottle of 100mg/ml strength is a fair
black market price.
References:
1. Methods Find Exp Clin Pharmacol 1997 May; 19(4): 215-22
2. Cancer Res 1978 Nov; 38(11 Pt 2): 4186-98
3. The Journal of Pharmacology And Experimental Therapeutics, Vol 281, No. 1; 93-102,
1997
4. Xu X, et al. "The effects of androgens on the regulation of lipolysis in adipose
precursor cells." Endocrinology 1990 Feb; 126(2): 1229
5. Effects of nandrolone decanoate on bone mineral content R, Righi GA, Turchetti V,
Vattimo A. and Metabolism. 1990 Nov; 39(11): 1167-9
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Laurabolin
(Nandrolone shown with Laurate ester)
(Nandrolone + Laurate ester)
[ 17beta-Hydroxyestra-4-en-3-one]
Formula (base): C18 H26 O2
Formula (ester): C12 H24 O2
Molecular Weight (base): 274.4022
Melting Point: 44-46C
Manufacturer: Various
Effective Dose: (men) 200-400mg/week (women) 50-100mgs/week
Active life: 10 days
Anabolic/Androgenic Ratio: 125:37
Laurabolin is an oil based injectable steroid, which was allegedly intended for
veterinary use in animals such as cats, dogs, pigs, lambs and horses. I found very
little information while searching in various medical journals for the use of Laurabolin
in any of those animals. This, plus the fact that this steroid is primarily available in
Mexico, leads me to believe that it is basically made for humans making the trip into
Mexico from the US. I mean, I can't imagine a doctor prescribing steroids for
someone's cat. Unfortunately, as with many useful steroids, Laurabolin was never
approved or even marketed toward humans in the USA.
Let’s take a look at Laurabolin and see what we’re dealing with: this compound is a
19-nor-testosterone based steroid, specifically a nandrolone, which means that
nearly anything that is true of Deca-Durabolin (or any other nandrolone) will be true
of Laurabolin. Of course, here we're talking about all of the things you’re probably
familiar with regarding Deca: the positive effects on joints, collagen, and bone
mineral content (1)(2), and the unfortunate progestinic effects that nandrolones
have (remember, nandrolone is a progestin). Progestins have the ability to wreak
havoc with your natural hormone levels, as well as amplifying many of estrogen’s
effects (5). Fortunately, nandrolone is not subject to much aromatization so it will
be amplifying the estrogen (most likely) engendered by other steroids in your
system. Don't forget to have on hand an anti-progestenic ancillary drug. Personally,
if I were going to run any form of nandrolone, I’d be using Letrozole at .25mg/day.
While it’s true that Letrozole can cause some problems with blood lipids, I think that
when you consider the positive effects that nandrolone has on them (6), you’ll find
159
that they can both run together safely and actually provide many complimentary
actions. Letrozole will also help you with any possible estrogenic and progesteronic
effects from Laurabolin (more on this later). Also, in a cycle containing Laurabolin,
adding in some form of injectable testosterone is going to probably be necessary for
most people. This is to replace the endogenous testosterone levels that Laurabolin’s
progestenic properties will have depleted. A good rule is to use roughly equal
amounts of both compounds.
Laurabolin will help you recover more quickly from exercise (3) via replenishing
muscle glycogen, increasing protein synthesis, etc. The only true difference is the
duration of its effectiveness. Laurabolin can remain effective many days after the
injection, but realistically, only slightly more than Deca. Nandrolone’s structure is
very similar to that of testosterone. The only difference is it lacks a carbon atom at
the 19th position. This causes it to have much lower androgenic properties than
testosterone. The primary reason for low androgenic side effects associated with
nandrolone is that although it is altered by 5a-reductase enzyme just like
testosterone, the altered product is dihydronandrolone, which is much weaker in
action then dihydrotestosterone. What do all of these big words mean to you? Well,
none of them are particularly important. They’re just geek-speak for stating that
nandrolone generally produces less side effects than testosterone. Unfortunately,
the main place where nandrolone causes more side effects than testosterone is in its
ability to shut down and inhibit your HPTA. This is despite much lower tendency for
estrogen conversion, since the rate at which the nandrolone converts to estrogen is
estimated at a mere 20% of testosterone’s conversion. The primary disadvantage of
Laurabolin over Deca-Durabolin is it’s generally found in a very low concentration
level of 25-50mg per cc/ml. This in turn forces the athlete to take multiple and
voluminous injections, making it quite a bit less desirable than Deca. However the
price of Laurabolin is generally much lower than that of Deca-Durabolin, somewhat
making up for the voluminous and frequent injections. Unfortunately, while the price
of is lower than that of Deca, the water retention experienced is the same, if not
more. This is possibly due to the longer ester. Using Letrozole (which I
recommended previously to help with progestenic/estrogenic side effects) will
combat this, but I still think that Laurabolin must be relegated to use in bulking
cycles.
Laurabolin has a strong anabolic action (rated more highly than testosterone, for
anabolic properties) and this is coupled with minimal androgenic properties.
Remember, nandrolone was synthesized to provide fewer side effects than
testosterone and more anabolic effects by allowing enhanced cellular protein
synthesis, thus allowing the prevention of protein loss through the urea and
promoting lean tissue build up. In animals, this compound has also been used to
correct metabolic deficiencies, malnutrition, anemia, and slow maturation (8). It
will, again, like all nandrolones, increase your bodymass, FFM, and strength (7). A
few other important characteristics of Laurabolin include maintenance of proper
levels of calcium & phosphorous and the production of red blood cells (8). This
compound is unlikely to be counterfeited, due to its low demand in the nandrolone
market place, where Deca and NPP are the reigning champs. Also, Laurabolin is
mostly available in Mexico where it is sold in very low concentrations, whereas Deca
and NPP are available from several uderground labs, as well as major pharmaceutical
houses.
The gains with this compound are much slower than with testosterone; however,
they are of higher quality and are easier to maintain once the use of Laurabolin has
160
been discontinued. And of course, as with any nandrolone, proper post cycle therapy
regimen should be incorporated at the end of cycles consisting of Laurabolin.
The average doses for male athletes are in the range of 200-400mg per week (which
would entail putting more oil in your body than there is in your average Indy 500
car). Female athletes can also find this item useful as it has low androgenic
properties and high anabolic properties, that will limit virilizing effects (effects which
make a woman take on male characteristics). The average dose for a female athlete
would be in the range of 50-100mg per week. Laurabolin is a good choice for female
athletes, as it is usually sold in a very low concentration (Mg/Ml), is rarely
counterfeited, and is not in high demand, thus, making it cheap (you should never
pay more than $2-4 per ml). Sadly, this drug will never really be very useful for
men, except perhaps for its effects on bone mineral content and collagen, which can
be taken at 50mgs/week. This is because it is only available in low dosed
concentrations.
References:
1. Metabolism. 1990 Nov; 39(11): 1167-9.
2. Effects of nandrolone decanoate on bone mineral content (R, Righi GA, Turchetti V,
Vattimo A.)
3. J Vet Med A Physiol Pathol Clin Med. 2001 Aug; 48(6): 343-52.
4. Eur J Endocrinol. 2004 Apr; 150(4): 511-5
5. Cancer Res 1978 Nov; 38(11 Pt 2): 4186-98
6. Sattler et al. Am J Physiol Endocrinol Metab 283: e1214
7. J Acquir Immune Defic Syndr Hum Retrovirol. 1999 Feb 1; 20(2): 137-46
8. Package insert from Laurabolin
161
Nandrolone + Methandriol Blends
(Nandrolone Phenylpropionate)
(Methandriol Dipropionate)
Nandrolone phenylpropionate + Methylandrostenediol Dipropionate (methandriol)
blend
(Trade name: Libriol, Tribolin, and Anabolic NA)
Nandrolone base + phenylpropionate ester (or Decanoate or Cypionate ester,
respectively)
Formula (base): C18 H26 O2
Formula (ester): C9 H10 O2
Molecular Weight(base):274.4022
Melting Point (base): 122-124°C
Manufacturer: RWR
Effective Dose (Men): 200-600mgs/week (2mg/lb of Bodyweight)
Effective Dose (Women): 50-100mgs/week
Active life: 15 days
Detection Time: Up to 18 months
Anabolic/Androgenic ratio: 125:37
Methylandrostenediol dipropionate
Formula: C20 H32 O2
Molecular Weight: 304.4716
Molecular Weight (base): 304.4716
Molecular Weight (ester): 74.0792
Formula (base): C20 H32 O2
Formula (ester): C3 H6 O2
Melting Point (ester):21.5C
Manufacturer: RWR
Effective Dose (Men):350mg week.
Effective Dose (Women): 25mg per day.
Active life: 3 days
Detection Time: 2 weeks
Anabolic/Androgenic ratio: 30-60/20-60
162
Libriol and Tribolan are trade names for another exotic anabolic preparation coming
out of an Australian company, RWR, which is shrouded in mystery. Anabolic NA is
Syd Group’s entry into this bizarre combination of steroids. They all seem to be of
popular demand in bodybuilding circles primarily because of this mystique. I will
look at the pros and cons of this obscure drug and if it qualifies to be in the muscle
building, fat-melting cycles of our future.
Libriol is an injectable veterinary product containing short esters of the drugs
nandrolone and methandriol. Anabolic NA has the rare Nandrolone Cypionate, and
Tribolan contains the very long estered Nandrolone Decanoate. Steroid.com
members should immediately recognize the first drug, nandrolone. A steroid derived
from modifying the testosterone molecule, Nandrolone is one of the most popular
drugs in the world and with good reason; it is a versatile steroid that can be used in
“bulking” or “cutting” cycles. Nandrolone has many benefits for athletes coupled
with an unbeaten safety record. It has an anabolic (muscle building) rating of 125,
making it an excellent drug for adding lean muscle. Neither is it very androgenic
(leading to the development of male characteristics), with an androgenic ratio of only
37. Nandrolone aids the hardcore athlete in various ways: it promotes nitrogen
retention in the muscle cell (1), which in turn promotes the muscle cell to synthesize
and store more protein; it increases levels of the highly anabolic hormone IGF-1 in
muscle tissue (2); and it leads to a significant increase in the amount of androgen
receptors in muscle (3). Nandrolone has been proven to improve endurance (4),
increase the number of red blood cells (5) and speed the rate of glycogen
replenishment after strenuous physical activity (6). One trait Steriod.com members
love about nandrolone is its ability to reduce joint pain and soreness (7)—this is
because the drug increases the rate of collagen synthesis and increase bone mineral
content (8)(9). Shown to be a good drug for fat loss (10), nandrolone can reduce
the amount of fat under the skin and around the abdominal area (10). The amount
lost, however, is dependant on dose, with higher dosages having the greatest overall
effect (11). Nandrolone also has positive effects on the brain. It increases chemicals
in the brain that promote aggressive behavior, which can improve both speed and
power (12). Nandrolone aromatizes (convents to estrogen) slightly, but only at
about 20% the rate of testosterone, so estrogenic side effects such as breast tissue
growth in men (gynecomastia), fat gain and water retention are not major issues.
Steriod.com members who use nandrolone seldom complain of androgenic side
effects such as prostate enlargement, loss of hair and acne. Those who are worried
about their cardio vascular health can use nandrolone without fear; studies have
shown that it does not negatively affect cholesterol (13). The ester of nandrolone
contained in Libriol is the phenylpropionate ester, which provides a rapid, high
concentration of hormone in the blood steadily for up to four days.
Nandrolone is a good drug, but it is not perfect. With its chemical structure it acts
directly on the receptor of the female sex hormone—progesterone—with a binding
rate of 20% of the actual hormone (14). Despite its low aromatizing rate, this can
lead to breast growth in gyno-prone individuals. There is no need for panic though,
because the drugs letrozole (femera) or fulvestrant can easily combat this (15)
reaction. Elevated prolactin levels are also a side effect of nandrolone usage, but
there are readily available drugs like bromocriptine and cabergoline that activate the
dopamine receptor to lower prolactin levels (5). Shrunken balls (testicular atrophy)
may be a problem from elevated prolactin as well; HCG (female hormone that acts
like LH when introduced into the male body) used during the cycle can possibly
remedy or prevent the condition (16). Probably the worst effect nandrolone has is
on natural testosterone production: a single 100mg dose of nandrolone causes
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complete nullificaton of testosterone levels, which remained suppressed for a month
before returning to normal (see chart). This can cause impotence and loss of sex
drive, better known as the dreaded “Deca dick.” The best solution to this problem is
to always use testosterone with nandrolone.
The second drug in these combination steroids is methylandrostenediol dipropionate.
It is a very weak steroid with an anabolic/androgenic ratio of 30-60/20-60. No large
amount of strength or muscle gain should be credited to methandriol, but it does
have a few benefits that are worth mentioning. Studies show the parent hormone
5AD to promote a favorable immune system (17). This would probably prevent
those who are over-trained from getting sick. Methandriol also has a binding affinity
to the sites of the muscle destroying (catabolic) glucocorticoid hormones (18)—
blocking them from doing harm, which makes methandriol anti-catabolic. Most other
profiles would tell you that methandriol somehow amplifies the muscle building
potential of other steroids by “unblocking” the androgen receptor and for this reason
it should be stacked with other anabolics. This statement is total garbage and should
be disregarded by all Steroid.com members. Androgen receptors do not become
“blocked” or “clogged up”; secondly, androgens themselves increase the numbers of
androgen receptors (3), so methandriol would not be needed to do this.
So far the news on methandriol does not look good but wait, it gets worse.
Methandriol’s parent hormone 5AD has been shown to be a steroid with “potent
estrogenic properties” (19). Since methandriol is more potent than 5AD, its
estrogenic effects should cause any Steroid.com member using it grave concern.
Excessive estrogenic activity can lead to gynecomastia, fat gain, water retention,
loss of sex drive, and sluggish natural testosterone production. The bad news does
not end there; methandriol itself binds to the estrogen receptor, needing no chemical
change to exert its nasty side effects. Estrogen combined with an androgen promotes
weight gain in animals better than either alone (20) however, and this is the real
reason the highly estrogenic methandriol is added to other steroids, not because it
“unblocks” the A.R. The “massive strength gains” allegedly from methandriol use
would most likely result from the great deal of water retention inside the muscles,
which would rebound when compressed during the lowering of a weight, similar to
the action of a benching shirt. In addition, methandriol has also been shown to
increase blood pressure (21). In fact, the only good thing about methandriol would
be that it has not been shown to affect lipids, so clogged up blood vessels would be
one of many sides you would not have to worry about on it. Methandriol carries di
propionate esters which are actually two propionate esters attached to the hormone.
So how could you use them in a cycle? Let’s take Libriol as an example; your first
problem would be the weak concentrations of hormone per ml, with 30 mg of
nandrolone phenylpropionate and 40 mg of methandriol dipropionate per ml to get
the recommended 400-600mg of nandrolone per week. This would mean injecting
14-20 cc per week. Adding the other injectables recommended will amount in a
good deal of injection volume. This would also give you a whopping 560-800mg of
the highly estrogenic methandriol. You face the same problem with Tribolan, since it
contains 40mgs of MAD and 35 of nandrolone decanoate. Anabolic NA is not much
better, having only 45mgs of MAD and 30mgs of Nandrolone Cypionate Per ml. If
you are determined (or stupid) enough to use Libriol (or any of these combination
compounds), stacking it with testosterone propionate and the anti-estrogen letrozole
would be the best course of action to control the massive amount of bloat to follow. I
think you’ll be using about a bottle (10mls) every week if you want a real anabolic
effect from Nandrolone/Methandriol. I strongly advise against using them with
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highly aromatizing drugs like dianabol and anadrol, and with longer acting
testosterone like enanthate or cypionate. I fear the sides would be too much for the
average athlete. To be honest, I would not touch Libriol with a ten-foot pole.
References:
1. J Acquir Immune Defic Syndr Hum Retrovirol. 1999 Feb 1;20(2):137-46.
2. Am J Physiol Endocrinol Metab. 2002 Feb; 282(2):E483-90
3. J Appl. Physiol.94 1153-61 2003
4. Med Sci Sports Exerc. 1995 Oct;27(10):1385-9.
5. Drug hand book. 2003
6. J Vet Med A Physiol Pathol Clin Med. 2001 Aug; 48(6):343-52
7. Steriod.com forums.
8. Metabolism. 1990 Nov;39(11):1167-9
9. Am J Ther. 1998 Mar;5(2):89-95.
10. Int J Obes Relat Metab Disord. 1995 Sep; 19(9):614-24.
11. Ann Nutr Metab. 1991; 35(3):141-7.
12. Med Sci Sports Exerc. 2003 Jan; 35(1):32-8.
13. Am J Physiol Endocrinol Metab. 2002 Dec; 283(6):E1214-2.
14. Cancer Res 1978 Nov; 38(11 Pt 2):4186-98
15. Curr Med Res Opin. 2001;16(4):276-84
16. Pharmacol Biochem Behav. 1988 Mar; 29(3):489-93.
17. Int J Immunopharmacol. 2000 Jan;22(1):1-14.
18. Endocrinology. 1994 Mar;134(3):1401-8.
19. J Steroid Biochem Mol Biol. 2003 Sep;86(3-5):423-32.
20. J Anim Sci. 1999 Dec;77(12):3133-9
21. Endocrinology. 1978 Jul;103(1):1-5.
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Nilevar
(Norethandrolone)
[17-alpha-ethyl-19-nor-4-androstene-3-one, 17b-ol]
Formula: C20 H30 O2
Molecular Weight: 302.4558
Melting Point: 130-136
Manufacturer: Searle
Release Date (in USA): 1956
Effective Dose: 20-40mgs/day
Active life: 12-16 hours
Detection Time: 5 weeks
Anabolic/Androgenic ratio (range): 100-200/22-55
Nilevar was one of the first oral steroids available in the United States. It was
essentially Searle’s answer to Ciba’s Dianabol (methandrostenolone), which was
released that same year. In fact, with respect to Nilevar’s effects on weight gain,
anabolism, and water-retention, it is frequently compared to Dianabol. Seven years
prior to the release of Nilevar, the Mayo Clinic heralded the dramatic effectiveness of
cortisone in the treatment of rheumatoid arthritis. This in turn stimulated
tremendous interest in all facets of steroid chemistry, endocrinology, and related
fields. G.D. Searle & Co. promptly initiated a major effort in steroid research, with
the objective of discovering better steroidal compounds than were previously
available, and new steroids that could be used for conditions for which no other
compounds were available. This effort resulted in the introduction of
norethandrolone, marketed in 1956 as Nilevar, the first anabolic agent with a
favorable separation between protein building and virilization (which is the
development of androgynous characteristics) (1). Paradoxically, in men, only weak
androgenic effects are found (possibly because it is deactivated by 5-alpha
reductase, which we don’t need to delve into—just remember that in men, only mild
androgenic effects are generally seen), though in women virilization is very common
(for women this would mean developing male physiological characteristics: a
deepening of the voice, the growth of extra body hair, and a tendency to leave the
toilet seat up). I wouldn’t recommend this drug for use by female athletes, not only
due to these side-effects but also due to some issues with infertility, which are also
possible in females, though probably not with males (5)(6). The anabolic effect of
this drug is moderate, and this is probably due to its moderately strong binding to
the androgen receptor (this makes it quite different from Dianabol, which has a poor
binding to the androgen receptor) as well as it’s ability to stimulate protein synthesis
(which it has in common with Dianabol) and stop protein catabolism (7). Nilevar was
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Searle's first unique entry into the world of AAS, and it was this drug that eventually
led to the research and develpoment of the much less androgenic and estrogenic/
progesteronic oxandrolone (Anavar) a decade later, and the resulting decline in
popularity and use of Nilevar.
As you will see, though, Nilevar still has it's own niche and purpose in athletics and
bodybuilding, and can be an important part of either a cutting or bulking stack, but
I'm getting ahead of myself, and we need to understand a few basics about Nilevar
first.
A quick look at the molecular structure of this drug tells us that it is a 19-nor steroid,
which means that it could/should possess some of the same characteristics as
nandrolone, which is why it is often referred to as “Oral Deca”. Although this is a
gross oversimplification of this drug, it’s the easiest place to start when describing
this compound. Norethandrolone, shares many characteristics with the injectable
nandrolones; it aromatizes and it is also a progestin. This means that it can convert
to estrogen (since it aromatizes) and also fits into and stimulates the progesterone
receptor (being a progestin). Unfortunately, progestins fall into the category of being
severely gonadotrophin suppressive compounds (3), and it also means that most
ancillaries aren't going to have 100% of their desired effect. Nolvadex, especially,
won't help and could actually hurt you by increasing progesterone receptors (4). The
19-nor structure of this compound, very much like injectable nandrolone, indicates
that this drug can shut down your natural testosterone production and HPTA (which
is the term used to describe a whole host of interdependent hormones and processes
within your endocrine system). It does all of this while also causing side effects such
as gyno, acne, and water retention (the dreaded "smooth look"). If I were going to
use Nilevar, I’d strongly consider having anti-progesteronic compounds on hand
(preferably Bromocriptine which I’d take at a dose of 2.5mgs/day, and perhaps some
Letrozole, which I'd use at .5mg/day to fight water retention and estrogen) as well
as the typical ancillaries used with other AAS, as those generally only fight/eliminate
the process that causes AAS to convert to estrogen or fight/eliminate the estrogen
itself.
Sadly, we're fighting side effects from both estrogen and progesterone when we use
Nilevar. On the positive side of being a 19-nor compound, it must be noted that you
also can reap many of the positive effects of other such compounds including a
relatively strong bind to the androgen receptor, which is positively correlated with
lypolysis (fat-burning). (2). Although at first glance, I’d say that you should consider
Nilevar as a “bulking” type of drug, I’m speculating that if you use something to keep
the water-retention to a minimum while using this compound (for this purpose, I've
already reccomended Femera), it can successfully be used in a cutting cycle. Users
who experience joint pains may find similar relief with Nilevar as they would with
Deca. Sadly, though, as Nilevar is an oral steroid, it can’t be used for the same
length of time as Deca, so it’s use for joint relief is probably contraindicated by
possible issues with hepatoxicity (Liver Toxicity) stemming from its being 17 alpha
alkylated. On the bright side, since it is orally active and not estrified like the
injectable 19-nor drugs (like Deca), its metabolites will most likely clear your body in
much less time than with the injectables, the most common estimate being roughly 5
weeks. I’ll also speculate that a novel use for this drug may be in the middle/end
portion of a heavy bulking or powerlifting cycle (which doesn’t include another 19
nor compound), when Nilevar can be used for a month or so when the heaviest
lifting is involved, and the joint relief (and obviously the anabolic effect) it provides
could allow the athlete to lift heavier than would normally be possible. There are
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many other orals on the market which can be used for anabolism, cutting, bulking,
and all related effects, but none that will provide the joint relief that it should/can.
For that reason, Nilevar will always have a purpose in heavy cycles, if it can be
obtained.
Before we consider putting it in our next stack, it should be noted that this
compound is rarely (if ever, anymore) counterfeited, and even more rarely seen on
the black market. It’s not in high demand, and in fact has been taken off the shelves
in the USA (and is primarily marketed in France, but also in Australia and
Switzerland). Taking it off the American shelves certainly doesn’t mean it’s not
useful. Allegedly, Arthur Jones was very fond of putting his athletes on it (instead of
the more popular Dianabol), and Bill Pearl almost certainly used it as his main
bulking agent for an entire cycle (10mgs/day) before a Mr. Universe win, and I
wouldn’t be surprised if Casey Viator and the Mentzer brothers dabbled in Nilevar.
Based on what these guys looked like, I’d venture a guess that this drug was (and
possibly still is) most commonly used for bulking, and by the larger powerlifters and
other athletes not worried about staying in a particular weight class. Your best bet
for finding this stuff is through a source who has a “connection” at a local pharmacy,
and you’ll probably be looking at a price of .20-.40 cents per 10mg tablet (it only
comes in 10mg tablets). As I said, it’s not exactly readily available, so that could
create a bit of a seller’s market. On the other hand, since it’s not in high demand it
could be a buyer’s market. In either case, I wouldn’t be thrilled with paying more
than .25 cents per tab.
So let’s see where that leaves us in terms of designing a cycle using Nilevar?
We’d want to have a form of testosterone in our cycle, regardless of whether we’re
going to use Nilevar to bulk up or to get cut. Remember, Nilevar will probably reduce
your natural testosterone levels to nothing. So let’s say, to start off, we’re looking at
using injectable testosterone at roughly 400-500mgs/week, to make sure that we
replace the testosterone that we’re not going to produce naturally. In a bulking cycle
we’d use a long ester testosterone (testosterone cypionate or testosterone
enanthenate), while in a cutting cycle we’d probably want to consider the use of a
shorter ester (testosterone propionate is the most popular for cutting cycles, as
anecdotally, it seems to produce less water retention). We’re going to avoid any form
of injectable nandrolone (nandrolone decanoate, nandrolone phenyl-propionate,
etc…) as well as any form of trenbolone, in this cycle, as we don’t want to stack 2
progestins together (and nandrolone and trenbolone, are both progestins). So that
leaves us with a host of other drugs we can stack with our Nilevar and testosterone.
I’d suggest using Equipoise (boldenone undeclyenate) on a bulking cycle, at 400
600mgs. This will serve the dual purpose of keeping your red blood count high
(which is important for anabolism) as well as keeping your appetite high. In a cutting
cycle, I’d suggest the use of Masteron (drostanolone), at 400-500mgs/week,
probably injected with the same frequency as your testosterone propionate. Now, I’d
probably suggest keeping Bromocriptine on hand, and using it if you start to hold too
much water or develop gynocomastia. I’d say that 1.25mgs-2.5mgs/day is enough
and will prevent progesteronic side effects (as well as stimulate fat burning), and this
recommendation is regardless of whether you choose to use Nilevar in a bulking or
cutting cycle. We’re not going to use any other orals in this cycle, either, as we’ve
already discussed Nilevar’s hepatoxic properties, and we don’t want to stress our
livers unnecessarily. Unlike most orals, I’d suggest using Nilevar at 20-40mgs/day in
the middle of either cycle, as opposed to the beginning, so that the bulk of your
heavy lifting is done while you reap the benefits of the joint protection Nilevar
provides.
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Proper post cycle therapy needs to be followed after any cyclecontaining Nilevar, and
personally I would use: 500IU/day of HCG for 3 weeks and 20mgs of Nolvadex for 4
6 weeks starting one week after cessation of the cycle. Remember that both of
these cycles should include Bromocriptine’s use at 1.25-2.5mgs/day to combat
progesteronic side effects, and .5-1mg/day of Femera to combat water retention and
estrogenic side effects.
Here’s how Norethandrolone is metabolized in your body:
References:
1. Steroids. 1992 Dec; 57(12):624-30
2. Xu X, et al. "The effects of androgens on the regulation of lipolysis in adipose
precursor cells." Endocrinology 1990 Feb;126(2):1229
3. Clin Endocrinol (Oxf) 2003 Apr;58(4):506-12
4. Gynecol Oncol. 1999 Mar;72(3):331-6.
5. J Reprod Fertil. 1966 Dec;12(3):489-99
6. Contraception. 1975 Feb;11(2):193-207
7. Lancet. 1958 Oct 25;2(7052):885-6
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Methyltrienolone
(Methyltrienolone)
[17beta-Hydroxy-17-methylestra-4,9,11-trien-3-one]
Formula: C19H2402
Molecular Weight: 284.38
Melting Point: 170C
Manufacturer: Negma (never released), Underground Labs
Effective dose: 500-750mcgs/day
Active Life: 4-6hours
Detection Time: Unknown (Probably up to 6 weeks)
Anabolic/Androgenic Ratio (Range, estimated):12,000-30,000/6,000-7,000
Methyltrienolone (MT) is a very potent, reasonably toxic, non-aromatizing steroid.
Ok. Let’s go over those three points again.
First of all, MT is potent. It binds so strongly to the AR (androgen receptor) that it is
often used in studies on other androgens to measure how strongly they bind. In
other words, this stuff binds onto the AR receptor so strongly that it is pretty much
the benchmark for that quality. If you’ve read my profile on trenbolone acetate (TA),
you’ll note that I said TA is the most potent injectable weapon in our arsenal with
regards to ability to bind to the androgen receptor. That’s still true, because this
particular compound is not in our arsenal, and it’s simply the oral version of TA (i.e.
it is trenbolone which has undergone modification to become orally active, via the
addition of a 17-alph-methyl group).
So why is it important that this stuff binds so tightly to the AR? Well, androgen
receptors are found in both fat cells and muscle cells (8); they act on the AR in
muscle cells to promote growth, and in the fat cells to affect fat burning (9)(6). The
stronger the androgen binds to the AR, the higher the lipolytic (fat burning) effect on
adipose (fat) tissue (9)(5). Unfortunately, that strong binding doesn’t also
automatically mean that it will elicit the strongest possible anabolic response, nor
that the weakest bind will elicit a weak anabolic response. Anadrol has the weakest
bind to the AR possible (too low to be measured), and it produces a profound
anabolic response, for example. Don’t be fooled by the anabolic/androgenic ratio of
this (or any steroid) either. The anabolic/androgenic ratio of MT would suggest that it
produces 5x the anabolic and androgenic effect of testosterone (which has a score of
100 and 100 respectively). If one were able to get a bottle of this stuff, I believe it
would be best used as part of a cutting cycle, stacked with some injectables
(testosterone, etc…), but certainly no other orals. It’s just too toxic. Negma (the
French company who brought Parabolan to the market, and then discontinued it)
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never pushed MT to gain approval as a commercially released item, since their
original studies showed it to be highly toxic.
But, remember, AR’s are found in muscle tissue as well. When a muscle’s AR is
stimulated, it can induce hypertrophy. When an adipose tissue’s AR is stimulated,
through various related mechanisms, fat is lost. This is a gross oversimplification.
Whatever. All we need to know is that when you have a steroid that binds to the AR,
it builds muscle and burns fat, and a steroid that binds very tightly to the AR will
stimulate a lot of muscle synthesis and burn a lot of fat. A good example of this is
Trenbolone. And since I mentioned Trenbolone, it’s worth further mentioning that
MT is basically a 17aa (oral) version of (injectable) Trenbolone. AR binding and AR
stimulation is not the only mechanism which stimulates anabolism, however. It’s
important to note that dbol has a very low AR binding ability and A50 has an AR
binding ability that is too low to even measure! Both are very potent oral steroids,
though. So while it’s important, AR binding/stimulation is not the end all and be all of
anabolism.
Methyltrienolone is, of course, a 19Nor compound (as is Trenbolone). It will effect
your sexual drive and performance in a similar way to both Tren and nandrolone,
meaning that temporary impotence and/or a lack of libido is highly possible (aka
Tren-Dick or Deca Dick) (10). Also, it is a progestin, and still binds almost as well to
the progesterone receptor (PgR) (3). As we know, progestins amplify estrogenic
effects of aromatizing drugs. Although MT doesn’t aromatize, you will still need to
worry about its ability to cause side-effects by amplifying the estrogenic issues
caused by the other compounds you may be taking.
How toxic is this stuff? Well, it was never commercially marketed for use in humans,
and has been relegated to Steroid-Purgatory, to be used only in studies. I’d probably
rate it on around the same level as taking high(ish) doses of halotestin or
methyltestosterone. I’d also probably recommend that people keep doses of this
product very low, much lower than reccomended doses typical of the other 2
compounds I just mentioned (i.e. 500-750mcgs/day…for not much longer than 3-4
weeks). I have had the fortune to discuss this product with the owner of an
underground lab. He had given out several samples of this stuff to athletes he knew,
and they all kept records and got regular bloodwork done. People who were in the
2mg/day range developed highly elevated liver enzymes and jaundice (yellowing of
the eyes and skin). They all recovered, and through trial and error, a 500-750mcg
dose was found to be (relatively) safe, and (roughly) as effective as 150-225mgs of
Trenbolone Acetate. For women, a possible side effect of MT is virilization
(development of male sexual characteristics), which is profound with this stuff (11),
so it is entirely off limits for women to use.
With this stuff, you may want to take milk thistle (320mgs/day), ALA (500mgs per
meal) and try some Pygeum Africanum (Permixon, the liposterolic extract of
Serenoa). This stuff will protect your prostate: in one study, it inhibited competitively
the binding of methyltrienolone to the cytosolic receptor of the rat prostate. You’ll
still need to get blood work done, avoid other orals (this includes drinking, or
anything else which could tax your liver), and monitor your health closely. This isn’t
a drug for novices, clearly, and is probably only useful for pre-contest bodybuilders.
I’ve only seen MT available from one underground lab, and it came in a 50ml bottle,
which was 1mg/ml, and was priced at $100. This translates to roughly 100 doses, at
a reasonable cost of fifty-cents per dose. And since you would never want to run
171
this particular drug for longer than 3-4 weeks at a time (maybe it would have use in
the last few weeks before a bodybuilding competition, but not much else), you’ll get
to use one bottle in 4 different cycles. That makes it no less dangerous, just
reasonably cheap.
References:
1. Endocrinology. 1984 Jun;114(6):2100-6.Relative binding affinity of anabolic
androgenic steroids: comparison of the binding to the androgen receptors in skeletal
muscle and in prostate, as well as to sex hormone-binding globulin.
2. Bonne C, Raynaud JP. Methyltrienolone, a specific ligand for cellular androgen
receptors. Steroids 1975 Aug;26(2):227-32
3. Dube JY, Tremblay RR, Chapdelaine P. Binding of methyltrienolone to various
androgen-dependent and androgen-responsive tissues in four animal species. Horm Res
1976;7(6):333-40
4. Tremblay RR, Dube JY, Ho-Kim MA, Lesage R. Determination of rat muscles
androgen-receptor complexes with methyltrienolone. Steroids 1977 Feb;29(2):185-95
5. APMIS. 2000 Dec;108(12):838-46.5. APMIS. 2000 Dec;108(12):838-46.
6. (Xu X, et al. "The effects of androgens on the regulation of lipolysis in adipose
precursor cells." Endocrinology 1990 Feb;126(2):1229 ).
7. J Anim Sci. 1992 Nov;70(11):3381-90.
8. Am J Physiol. 1998 Jun;274(6 Pt 1):C1645-52.
9. Biochim Biophys Acta. 1995 May 11;1244(1):117-20.
10. Baum MJ, Kingsbury PA, Erskine MS. Failure of the synthetic androgen 17 beta
hydroxy-17 alpha-methyl-estra-4,9,11-triene-3-one (methyltrienolone, R1881) to
duplicate the activational effect of testosterone on mating in castrated male rats. J
Endocrinol 1987 Apr;113(1):15-20
11. Biochem Pharmacol. 1984 Apr 15;33(8):1235-41.Changes in the activities of
microsomal enzymes involved in hepatic steroid metabolism in the rat after
administration of androgenic, estrogenic, progestational, anabolic and catatoxic steroids.
172
Orabolin
(Ethylestranol)
[19-Nor-17alpha-pregn-4-en-17-ol]
Formula:C20H22O
Molecular Weight:288.46
Melting Point: 76-78C
Manufacturer: Various, discontinued
Effective Dose (Men): 40mgs(?)
Effective Dose (Women): 10mgs(?)
Active life: 8-12 hours
Detection Time: 6 weeks
Anabolic/Androgenic ratio (range):20-400:200-400
What we’re looking at here is yet another steroid that has been off the market for so
long that I haven’t been able to actually find someone who’s used it. It’s a 19Nor
steroid, meaning it’s been derived from nandrolone. We know that 19nor compounds
all bind well to the androgen receptor, and that this is part of the reason that it
imparts such a strong anabolic effect. It has very good androgen binding properties,
giving it good enough anabolic effect, but is actually androgenically reduced in
androgen responsive tissues like prostate and skin. There are few actual studies that
really examine this compound in any depth, and basically the ones I’ve read actually
seem to suggest that ethylestronol simply exerts it’s anabolic effect by making a 3
keto group and essentially converting to norethandrolone (1). I think this is why it
has such a distressingly broad anabolic/androgenic range. There is also a 17-alpha
ethyl group to contend with, and that gives this compound a degree of hepatoxicity
that makes the cost/benefit ratio very poor for athletes, and thus it’s rarely found on
the black market. The weirdest thing about Orabolin is that it comes as some kind of
bizarre paste for oral administration—I really don’t know why this stuff was ever
brought to the market, but the fact that it comes as an oral paste is just very
bizarre.
Here’s how ethylestranol is metabolized in your body:
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Reference:
1. Metabolism of anabolic steroid drugs in man and the marmoset monkey (Callithrix
jacchus)--I. Nilevar and Orabolin. J Steroid Biochem. 1977 Oct;8(10):1057-63.
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
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Parabolan
(Trenbolone shown without HexaHydroBencylCarbonate ester)
(Trenbolone Base + HexaHydroBencylCarbonate Ester)
[17beta-Hydroxyestra-4,9,11-trien-3-one]
Formula (base): C18 H22 O2
Formula (ester): C2 H4 O2
Molecular Weight: 312.4078
Molecular Weight (base): 270.3706
Molecular Weight (ester): 130.1864
Melting Point (base): 183-186C
Manufacturer: (originally) Negma, Various Underground Labs
Effective Dose (Men): 300-500mgs/week
Effective Dose (Women): Not recommended
Active life: 5-7 days
Detection Time: 4-5 weeks
Anabolic/Androgenic ratio: 500:500
Parabolan is one of those drugs which appeared briefly (Negma eventually pulled it
off the market) and made a huge impact very quickly. Dan Duchaine was the first
person to write about this compound in his Underground Steroid Handbook Update
Newsletter. In his write up, he speculated that you wouldn’t want to go over 2 amps
per week of the original Negma product (each amp was 76mgs, and if you are
wondering why that’s so, it’s because each amp gave the user precisely 50mgs of
trenbolone, once your body’s esterases cleave off the HexaHydroBencyl Carbonate
ester ). Unfortunately, not many people really got a chance to experiment with the
original Parabolan, as it was pulled off the market very quickly by Negma
(discontinued in 1997). That created a very odd situation where the product was
used very successfully by a few people for a very short time, then was basically
unavailable after that. This basically created a bit of a cult following for the drug.
Decades passed, and counterfeits stormed the market until Duchaine (again) wrote
an article on extracting the trenbolone from Finaplex pellets, and then sterilizing
them, in order to create your own trenbolone acetate. Although this wasn’t
Parabolan, it soon curtailed the counterfeit craze for Parabolan. Tren was Tren, in
most people’s eyes, regardless of the ester. “Fina kits” (a kit which enabled the user
to make his own Tren) then flooded the market, utilizing a loophole whereby the
pellets and kit were both legal to buy, although clearly making and using an
injectable steroid in your kitchen is illegal. Flashing forward a few years, trenbolone
acetate became available by many underground labs, then trenbolone enanthate
became available, and now, even Parabolan (which is trenbolone base + a
HexaHydroBencyl Carbonate ester) is easily obtained from most major underground
175
labs. A visit to Steroid.com or any of the major discussion boards will testify that
Parabolan’s cult following still hasn’t diminished. Let’s see why…
Parabolan is neither affected by aromatase or 5alpha-reductase. This means it
becomes neither weaker nor stronger in androgen responsive target tissues, a trait
usually shared by DHT (DyhydroTestosterone) derived steroids; since Parabolan is of
course a trenbolone, it is not actually DHT derived but rather is derived from 19-Nor
testosterone. Parabolan has no estrogenic activity (it may actually reduce serum
estradiol levels in the body), is a very strong anabolic and androgenic compound (5x
stronger than testosterone in both categories!) and binds well to the androgen
receptor. Actually, binding "well" to the androgen receptor is quite an
understatement. There's no injectable AAS in our arsenal that binds to the androgen
receptor (AR) as well as trenbolone does. This is probably a major reason that
Parabolan was so sought after for use as a precontest agent. Androgen receptors
are found in fat cells as well as muscle cells (8), and we all know that they act on the
AR in muscle cells to promote growth, but the androgens act directly on the AR in fat
cells to affect fat burning (9)(6). The stronger the androgen binds to the AR, the
higher the lipolytic (fat burning) effect on adipose (fat) tissue (9)(5). As if that’s not
enough good news, some steroids even increase the numbers of AR in muscle and
fat (9)(10), leading me to speculate that this fat losing effect would be amplified with
the concurrent use of other compounds, such as injectable testosterone.
Another mechanism whereby Parabolan causes muscle accumulation and fat loss is
it’s ability as a nutrient partitioning agent (7). Basically, what this means is that
while using Tren, more of the food you eat will become muscle and less (if any) will
become fat. Really, as you can see, most of Parabolan’s cult reputation is well
deserved, and—as if that’s not enough—Parabolan noticeably increases the level of
the IGF-1 within muscle tissue (2), which in itself is an extremely anabolic hormone.
It’s worth noting that not only does it increase the levels of IGF-1 in muscle over two
fold (2), it also causes muscle satellite cells (cells that repair damaged muscle) to be
more sensitive to IGF-1 and other growth factors (3). This leads me to speculate
that Parabolan (or any version of Tren) would be synergistic within a cycle containing
any form of injectable IGF-1.
Parabolan also happens to bind quite strongly to the glucocorticoid receptor as well,
and this in turn imparts a nice anti-catabolic effect. This, in part, may help to explain
why low(ish) doses of it seem to work nicely, as well as why it aids fat loss. You see,
glucocorticoid hormones send a message to muscle cells to release stored protein
(this is called catabolism), which is exactly the opposite of what we want.
This drug stacks well with mostly everything, especially testosterone (actually, if you
want to avoid sexual dysfunction, stacking it with test is necessary). I have also
found it to be a great addition to a stack containing Eq as well, unfortunately the
insomnia the Parabolan gives me added to the appetite the Eq gives me makes
midnight snacking almost inevitable. Parabolan is most often used in cutting stacks
when "quality muscle" gain is favored over bloat and water retention. Really, I think
Parabolan (or any Tren) is a great "cutting " anabolic, although it has been used
successfully by many in both Cutting and Bulking cycles.
It’’s not all good news, though…
Some users of Para report sexual dysfunction (Tren-Dick) and symptoms of gyno
(probably progesterone related, as Trenbolone acts on progesterone receptor but not
176
the estrogen receptor). As you know, Trenbolone is unfortunately, a progestin: it
binds to the receptor of the female sex hormone progesterone (with about 60% of
the actual strength progesterone) (4). In hyper-sensitive Steroid.com members this
lead to bloat and breast growth when combined with an estrogenic or aromatizable
product, but probably not without one (14); worse still, trenbolone’s active
metabolite (17beta-trenbolone) has a binding affinity to the progesterone receptor
(PgR) that is actually greater than progesterone itself (5). No need to panic though:
the aromatase inhibitor Lertrozole can also lower progesterone levels and combat
any progestenic sides. I would strongly consider its inclusion at .25-.5mgs/day in a
cycle containing Parabolan.
Ironically, even though Para is an excellent cutting drug, it will lower your thyroid
level (11). Doing this, by means of the body’s negative-feedback-loop, also raises
prolactin. Ergo, I recommend taking T3 (25mcgs/day) along with your Tren to avoid
suffering from increased levels of prolactin and the host of unwanted side effects this
could cause. For these reasons, many people avoid stacking Tren with Deca
(nandrolone decanoate), which is also a progestin (4).
Mental changes are a notorious side effect of any type of trenbolone use (12), and
Para is no exception to this rule. Androgens increase chemicals in the brain that
promote aggressive behavior (13), which can be beneficial for some athletes wanting
to improve speed and power, but perhaps detrimental to those trying to hold a job
as a social worker. Luckily, I am not generally known for being an ambassador of
goodwill, so this side effect goes largely unnoticed in me.
For me, the worst effect of any sort of Tren is "Tren cough" which I get for the first 2
weeks of a cycle including this compound. Tren Enanthate does not have this effect
on me, but Parabolan sometimes does; Tren Acetate gives me a crippling Tren-cough
for the first week or so that I’m on it. Also, any kind of Tren gives me a bit of
insomnia, which is common for many users. The most noticeable side effect of
Parabolan for me is that it increases my sweating dramatically, even giving me
vicious "night sweats" that go nicely with my insomnia. Walking up a flight of stairs
can also cause me to break out in beads of sweat when I’m on this product. Also, it
needs to be noted that many people experience a reduced cardiovascular capacity
when using Para (12), and I fall into this category as well. Still, its incredible effects
on my strength and appearance mean that it'll fall into my cycles for off seasons and
in the winter (when sweating won't be as much of a problem).
References:
1. Br J Nutr. 1978 Nov;40(3):563-72.
2. J Cell Physiol. 2004 Nov;201(2):181-9.
3. Endocrinology. 1989 May;124(5):2110-7.
4. Cancer Res 1978 Nov; 38(11 Pt 2):4186-98
5. APMIS. 2000 Dec;108(12):838-46.
6. (Xu X, et al. "The effects of androgens on the regulation of lipolysis in adipose
precursor cells." Endocrinology 1990 Feb;126(2):1229 ).
7. J Anim Sci. 1992 Nov;70(11):3381-90.
8. Am J Physiol. 1998 Jun;274(6 Pt 1):C1645-52.
177
9. Biochim Biophys Acta. 1995 May 11;1244(1):117-20.
10. J Appl. Physiol.94 1153-61 2003
11. Res Vet Sci 1981 Jan;30(1):7-13
12. Steroid.com forums.
13. Med Sci Sports Exerc. 2003 Jan; 35(1):32-8
14. Progesterone is not essential to the differentiative potential of mammary epithelium in
the male mouse. Freeman, Topper. Endocrinology. 1978 Jul;103(1):186-92
15. Eur J Obstet Gynecol Reprod Biol. 2002 Nov 15;105(2):161-5.
16. J Clin Endocrinol Metab. 1995 Sep;80(9):2658-60.
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178
Sanabolicum
(Nandrolone shown with CycloHexylPropionate ester)
(Nandrolone + CycloHexylPropionate Ester)
(17b-Hydroxy-19 -nor -4 -androsten-3-one-17–phenylpropionate)
Formula (base): C18 H26 O2
Formula (ester): C9 H16 O2
Molecular Weight: 412.6112
Molecular Weight (base): 274.4022
Molecular Weight (ester): 156.222
Melting Point (base): 122-124°C
Manufacturer: Nile (Egypt), and others
Effective Dose (Men): 200-600mgs/week (2mg/lb of Bodyweight)
Effective Dose (Women): 50-100mgs/week
Active life: 13.5
Detection Time: Up to 18 months
Anabolic/Androgenic ratio: 125:37
Sanabolicum, or nandrolone CycloHexylPropionate is a rarely found version of the
anabolic androgenic steroid nandrolone, with a CycloHexylPropionate ester.
Nandrolone probably the most talked about anabolic steroid on the planet. It is a
drug derived from the hormone testosterone, with a slight modification taking the
form of a carbon atom removed from the 19th position of the molecule. For this
reason, it is also called a 19-nor testosterone compound. The modification makes
nandrolone more anabolic (muscle building) and less androgenic (producing of male
characteristics) than its parent hormone. Testosterone, the standard for that ratio,
has an anabolic/androgenic ratio of 100:100 (arbitrarily determined as a
benchmark). Nandrolone’s anabolic/androgenic ratio is 37:125.
Nandrolone’s popularity partly stems from its versatility; it can be used to reach
virtually any bodybuilding or athletic goal, and has an outstanding safety record
among its users. The medical industry uses nandrolone to treat anemia, debility,
disease and severe wasting disorders. It is commonly administered to H.I.V positive
patents to reverse muscle break down (catabolism) and improve immune function
(1)(2). It has numerous benefits for the hard training athlete and very few side
effects. First off, nandrolone is an excellent drug for building muscle via different
179
mechanisms of action, some less understood that others. Nandrolone promotes
nitrogen retention in the muscle cell (3), which in turn promotes the muscle cell to
synthesize and store more protein. The drug also increases the levels of the highly
anabolic hormone IGF-1 inside muscle tissue (4). Nandrolone also significantly
increase the levels of androgen receptors in muscle (5). Athletes who participate in
regular strenuous physical activity will appreciate the effects of nandrolone, proven
to significantly improve endurance (6). It can also dramatically improve recovery by
increasing the number of red blood cells (1), which in turn will help in the removal of
lactic acid and improve oxygen delivery to working muscles; it will also speed the
rate of glycogen replenishment after exercise (7). One thing that puts nandrolone
above all other steroids taken by athletes is its ability to improve joint function and
reduce joint pain by improving collagen synthesis and bone mineral content (8)(9).
In fact, a common saying by Steroid.com’s nandrolone fans is “I feel like I’m 20
again!” when on cycle. Muscle building and “lubed” joints are not the only positives
of nandrolone use; it seems to be a good fat loss agent (10), and the amount of fat
loss and from where, is dose dependant, with higher dosages producing overall
better results (11). The good stuff does not end there, as nandrolone does not only
affect your body but your mind as well by increasing chemicals in the brain such as
seratonin and norepinephedrine; this will help an athlete train harder and improve
speed and power, while at the same time is probably responsible for the enhanced
feeling of “well being” many Deca users report (12).
Nandrolone has a safety record that cannot be beat, although it still has some
drawbacks, since its chemical structure aromatizes (converts to the female hormone
estrogen via the aromatize enzyme) slightly, at about 20% the rate of testosterone.
Thus, adverse estrogenic side effects such as breast tissue growth (gynecomastia or
bitch tits) and fat gain are not a major concern. With its low androgenic properties,
prostate and hair loss problems are not commonly reported by Steroid.com
members. One thing that must be mentioned is the notion that nandrolone
aromatizes into the female hormone progesterone. This is not entirely true.
Nandrolone, being a progestin, directly acts on the progesterone receptor (PgR)
without needing to change chemically. Fortunately, the binding rate to the receptor is
fairly low (about 20% of the actual progesterone hormone itself) (13). If you are
prone to progestinic sides there are various drugs to available to combat them.
Fulvestrant or Letrozole can be taken to reduce the number of progesterone and
estrogen receptors (14), and with less receptors to attach to, these hormones will
not be able to exert their actions on the body. Letrozole also has the added benefit of
reducing estrogen levels to nothing—which would certainly cut down on sides—as
without estrogen present, most of the ill-effects of any aromatizing (or even
progestenic) steroids aren’t really possible. The use of a progestin also raises the
level of another female sex hormone, prolactin. Bromocriptine and cabergoline are
drugs that activate the dopamine receptor to lower prolactin levels. Shrunken balls
(testicular atrophy) may be a problem from elevated prolactin as well; HCG (a
female hormone that acts like LH when introduced into the male body) used during
the cycle can best remedy the condition (15). The heart conscious bodybuilder need
not worry about cholesterol if choosing to use nandrolone—in a study, H.I.V+ men
given nandrolone had no negative affects on lipid profile (16).
Sanabolicum, nandrolone CycloHexylPropionate (mouthful huh? We’ll use N-CHP
from now on) is indeed a rare and unusual find anywhere in the athletic world. To
figure out how to use it in a cycle, now the ester itself must be analyzed. As we all
know, esters delay the release of a hormone, and N-CHP has 9 carbons. This hints
that it is a long acting ester comparable to cypionate, (8 carbons) or decanoate, (10
180
carbons) with an active life of about 13.5 days. I would compare its effects to
nandrolone decanoate, aka, Deca-Durabolin thus dosage amount and frequency
should be near the same. Thus, once per week injections can keep blood levels
stable. Most Steroid.com members however inject 2 times per week, or every 3rd
day.
Now that we know the potential usage for anabolism, let us look at how it can be
incorporated into a cycle of a Steroid.com member. Since it is similar to Deca, slow,
high quality muscle gains can be expected along with significant water retention. So,
our first choice would be to use Sanabolicum in a “bulking” cycle, stacked with a
testosterone, of course, and another “bulk” promoting drug like Dianabol or Anadrol.
That’s a formidable stack, and great gains in size and strength can be realized.
Nandrolone, being a compound that promotes fat loss, can also be used in a
“cutting” cycle without problems stacked with testosterone and a low or non
aromatizing oral like stanozolol, (Winstrol, Winny) oxandrolone, (Anavar, Var) or
oral-turinabol (OT). Lean muscle gains with reduced body fat can be attained. It
must be noted that you should avoid combining anabolic steroids with progestin
attributes, e.g. Fina (aka Tren)+Deca, as this will only prove bothersome when you
are shelling out cash on drugs to fight the sides. It's common practice to run
testosterone one week longer than nandrolone to "line up" timing for post cycle
therapy. This is to be recommended with Sanabolicum, as it is going to have a
residual effect when it’s not producing an anabolic effect yet it will still suppressing
your natural testosterone levels. It’s recommended that testosterone be run about 2
weeks longer than the Sanabolicum to combat this. Due to extremely low availability
and a similar drug easily available, sanabolicum may never catch on as the anabolic
of choice for nandrolone lovers.
References:
1. Drug hand book. 2003
2. Int J Cardiol. 2002 Sep;85(1):151-9.
3. J Acquir Immune Defic Syndr Hum Retrovirol. 1999 Feb 1;20(2):137-46.
4. Am J Physiol Endocrinol Metab. 2002 Feb; 282(2):E483-90
5. J Appl. Physiol.94 1153-61 2003
6. Med Sci Sports Exerc. 1995 Oct;27(10):1385-9.
7. J Vet Med A Physiol Pathol Clin Med. 2001 Aug; 48(6):343-52
8. Metabolism. 1990 Nov;39(11):1167-9
9. Am J Ther. 1998 Mar;5(2):89-95.
10. Int J Obes Relat Metab Disord. 1995 Sep; 19(9):614-24.
11. Ann Nutr Metab. 1991; 35(3):141-7.
12. Med Sci Sports Exerc. 2003 Jan; 35(1):32-8.
13. Cancer Res 1978 Nov; 38(11 Pt 2):4186-98
14. Curr Med Res Opin. 2001;16(4):276-84
15. Pharmacol Biochem Behav. 1988 Mar; 29(3):489-93.
16. Am J Physiol Endocrinol Metab. 2002 Dec; 283(6):E1214-20
181
Trenbolone Acetate
(Trenbolone shown with Acetate Ester)
(Trenbolone Base + Acetate Ester)
[17beta-Hydroxyestra-4,9,11-trien-3-one]
Formula (base): C18 H22 O2
Formula (ester): C2 H4 O2
Molecular Weight: 312.4078
Molecular Weight (base): 270.3706
Molecular Weight (ester):60.0524
Melting Point (base): 183-186C
Melting Point (ester):16.6C
Manufacturer: Cattle implants, British Dragon, Various
Release Date (United States): 1987
Effective Dose (Men):50-150mg ED
Effective Dose (Women): Not recommended
Active life: 2-3 days
Detection Time: 5 months
Anabolic/Androgenic ratio: 500/500
The drug trenbolone is, without a doubt, the most powerful injectable anabolic
steroid used by Steriod.com members to gain muscle. However the full properties of
the drug are not always fully understood. This profile will separate fact from fiction
and help Steroid.com members decide if trenbolone is right for them.
Trenbolone is similar to the highly popular steroid nandrolone, in that they are both
19-nor steroids, meaning that a testosterone molecule has been altered at the 19th
position to give us a new compound. Unlike nandrolone however, trenbolone is an
excellent mass and hardening drug with the majority of gains being muscle fiber,
with minimal water retention (1). It has an unbelievable anabolic (muscle building)
score of 500. When you compare that to testosterone, which itself is a powerful
mass builder but has an anabolic score of 100, you can begin to fathom the muscle
building potential of trenbolone. What makes trenbolone so anabolic? Numerous
factors come into play. Trenbolone greatly increases the level of the extremely
anabolic hormone IGF-1 within muscle tissue (2). And, it’s worth noting that not only
does it increase the levels of IGF-1 in muscle over two fold, it also causes muscle
satellite cells (cells that repair damaged muscle) to be more sensitive to IGF-1 and
other growth factors (3). The amount of DNA per muscle cell may also be
significantly increased (3).
182
Trenbolone also has a very strong binding affinity to the androgen receptor (AR),
binding much more strongly than testosterone (4). This is important because the
stronger a steroid binds to the androgen receptor, the better that steroid works at
activating AR dependant mechanisms of muscle growth. There is also strong
supporting evidence that compounds binding very tightly to the androgen receptor
also aid in fat loss. Think of the receptors as locks and androgens as different keys,
with some keys (androgens) opening (binding) the locks (receptors) much better
than others. This is not to say that AR-binding is the final word on a steroid’s
effectiveness. Anadrol doesn’t have any measurable binding to the AR, and we all
know how potent Anadrol is for mass-building.
Trenbolone increases nitrogen retention in muscle tissue (5). This is of note because
nitrogen retention is a strong indicator of how anabolic a substance is. However,
trenbolone’s incredible mass building effects do not end there. Trenbolone has the
ability to bind with the receptors of the catabolic (muscle destroying) glucocorticoid
hormones (6) giving it anti-catabolic properties as well. This has the effect of
inhibiting the catabolic (muscle destroying) hormone cortisol (7).
Yet another amazing trait of trenbolone that must be noted is its ability to improve
feed efficiency and mineral absorption in animals given the drug (8). To help you
understand what this means for you, feed efficiency is a measurement of how much
of an animal’s diet is converted into meat, and the more food it takes to produce this
meat, the lower the efficiency. Conversely, the less food it takes to produce meat,
the higher the efficiency—well you get the idea. Animals given trenbolone gained
high quality weight without having their diets adjusted, thus improving feed
efficiency. Finding new compounds that can improve feed efficiency is a billion dollar
industry, and has spawned many nutritional advances in the bodybuilding world over
the last few decades (CLA, Whey Protein, and HMB are compounds which spring to
mind as having first been introduced by the livestock industry). What does this
translate to for the hard training athlete? The food you eat will be better utilized for
building lean muscle, and vitamins and minerals are also better absorbed, which may
keep you healthier during cycle.
Trenbolone is also a highly androgenic hormone, when compared with testosterone,
which has an androgenic ratio of 100; trenbolone’s androgenic ratio is an astonishing
500. Highly androgenic steroids are appreciated for the effects they have on strength
as well as changing the estrogen/androgen ratio, thus reducing water under the skin.
As if the report on trenbolone were not good enough, it gets better; trenbolone is
extraordinarily good as a fat loss agent. One reason for this is its powerful effect on
nutrient partitioning (9). It is a little known fact that androgen receptors are found in
fat cells as well as muscle cells (10). Androgens act directly on the AR in fat cells to
affect fat burning (11). The stronger the androgen binds to the AR, the higher the
lipolytic (fat burning) effect on adipose tissue (fat) (11). Since some steroids even
increase the numbers of AR in muscle and fat (11)(12), this lypotropic (fat losing)
effect would be amplified with the concurrent use of other compounds, such as
testosterone.
Trenbolone promotes red blood cell production and increases the rate of glycogen
replenishment, significantly improving recovery (13). Like almost all steroids,
trenbolone’s effects are dose dependant with higher dosages having the greatest
effects on body composition and strength. Mental changes are a notorious side effect
of trenbolone use (15); androgens increase chemicals in the brain that promote
183
aggressive behavior (16), which can be beneficial for some athletes wanting to
improve speed and power.
Trenbolone’s chemical structure makes it resistant enzymes that aromatize
(conversion to estrogen), thus absolutely no percentage of trenbolone will convert to
estrogen. Trenbolone administration would not promote estrogenic side effects such
as breast tissue growth in men (gynecomastia, bitch tits) accelerated fat gain,
decline in fat break down and water retention. Trenbolone is also resistant to the 5-
alpha-reductase enzyme; this enzyme reduces some steroid hormones into a more
androgenic form. In trenbolone’s case however this does not matter, trenbolone
boasts an androgenic ratio of 500, it can easily cause adverse androgenic side
effects. In any Steroid.com members who are prone to cases of hair loss, prostate
enlargement, oily skin and acne have been reported. Unfortunately trenbolone’s
potential negative side effects do not end there. Trenbolone is also a noted
progestin: it binds to the receptor of the female sex hormone progesterone (with
about 60% of the actual strength progesterone) (17). In sentitive Steroid.com
members, this can lead to bloat and breast growth or worse still, trenbolones active
metabolite17beta. Trenbolone has a binding affinity to the progesterone receptor
(PgR) that is actually greater than progesterone itself (18). No need to panic
though, the anti-estrogens Letrzole or Fulvestrant can lower progesterone levels, and
combat any progestenic sides. The use of a 19-nor compound like trenbolone also
increases prolactin. Bromocriptine or cabergoline are often recommended to lower
prolatin levels (20). Testicular atrophy (shrunken balls) may also occur; HCG used
intermittently throughout a cycle can prevent this (21). It is also wise for Tren users
to closely monitor their cholesterol levels, kidney function, and liver enzymes as Tren
has the potential to negatively affect all of those functions. Trenbolone, being a
powerful progestin, will also shut down natural testosterone production—even a
relatively small dose will keep the testosterone level suppressed for an extended
period of time. This can lower libido and cause erectile dysfunction (fina dick). It is
essential that you always stack trenbolone with testosterone.
The acetate ester is a very short-chain ester attached to the trenbolone molecule. It
has an active life of 2-3 days but to keep blood levels of trenbolone elevated and
steady, daily injections are often recommended. The acetate ester provides a rapid
and high concentration of the hormone, which is beneficial to those seeking quick
gains. When coupled with a rapid clearing time, the acetate ester can be
discontinued on the onset of adverse side effects.
Now that the properties of trenbolone acetate have been explained, we can better
understand how to use it in order to maximize its advantages. Evidence suggests
that trenbolone stacked with estrogen promotes more weight gain that trenbolone
alone (22). Now I’m not telling you to go pop some birth control with your
trenbolone, but the addition of aromatizing orals such as Dianabol and a long estered
testosterone such as cypionate or enanthate would produce great gains in a bulking
cycle. For a cutting cycle, trenbolone is the best choice you have; trenbolone’s
powerful effect on nutrient shuttling allows a user to restrict calories and remain in a
state of positive nitrogen balance (remember what that means?). The cortisol
reducing effect, and its binding to the glucocorticoid receptor will greatly reduce the
catabolic effects of harsh dieting and excessive amounts of cardio, not to mention
that trenbolone itself may burn fat (due to its strong AR-binding). A good choice to
stack with Tren in a cutting cycle is Winstrol. Winstrol has a low binding affinity to
the AR and thus will act in your body in vastly different ways than the Tren (i.e. in
non-receptor mediated action). In addition, Winstrol is a DHT-based drug and Tren is
184
a 19-nor. Throw in some Testosterone (prop), and you’ll have a cutting cycle which
takes advantage of all 3 major families of Anabolic Steroids (Testosterone, 19-nor,
and DHT), as well as vastly different AR-binding affinities and mechanisms of action.
Ironically, even though Tren is an excellent contest prep drug, it lowers your thyroid
level (this, by means of the body’s negative-feedback-loop, also raises prolactin). I
recommend taking T3 (25mcgs/day) along with your Tren.
Also, this drug is a poor choice for athletes who rely on cardiovascular fitness to play
a sport. Tren, anecdotally at least, reduces many athletes’ ability to sustain high
levels of endurance. Unfortunately, this makes Tren a poor choice for many.
As of now the main source of trenbolone is from implants for cattle being converted
into an injectable or transdermal compound, from powder, and of course
underground labs. “Home brewing” powder or cattle implants seems to be the
preferred method of obtaining injectable trenbolone acetate, because the user would
have much more control over the potency and sterility of the drug. Trenbolone is
much more expensive than other anabolic steroids ranging from 15 U.S dollars per
gram of powder or 150 U.S for a single 10 ml bottle. The cost of trenbolone should
not matter—it is worth every penny.
Here’s how Trenbolone is Metabolized in your body:
References:
1. Br J Nutr. 1978 Nov;40(3):563-72.
2. J Cell Physiol. 2004 Nov;201(2):181-9.
3. Endocrinology. 1989 May;124(5):2110-7.
4. Toxicol Sci. 2002 Dec;70(2):202-11.15
5. J Anim Sci. 1994 Feb;72(2):515-22.
6. APMIS. 2001 Jan;109(1):1-8.
7. J Anim Sci. 1990 Sep;68(9):2682-9.
8. APMIS. 2001 Jan;109(1):1-8.
9. J Anim Sci. 1992 Nov;70(11):3381-90.
10. Am J Physiol. 1998 Jun;274(6 Pt 1):C1645-52.
11. Biochim Biophys Acta. 1995 May 11;1244(1):117-20.
12. J Appl. Physiol.94 1153-61 2003
13. J Vet Med A Physiol Pathol Clin Med. 2001 Aug; 48(6):343-52
185
14. Toxicol Sci. 2002 Dec;70(2):202-11.15
15. Steroid.com forums.
16. Med Sci Sports Exerc. 2003 Jan; 35(1):32-8
17. Cancer Res 1978 Nov; 38(11 Pt 2):4186-98
18. APMIS. 2000 Dec;108(12):838-46.
19. Curr Med Res Opin. 2001;16(4):276-84
20. 2003 drug handbook.
21. Pharmacol Biochem Behav. 1988 Mar; 29(3):489-93.
22. J Anim Sci. 1997 May;75(5):1256-65.
Research Anabolic Steroids
and Related Topics at:
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186
Trenbolone Enanthate
(Trenbolone without Ester shown)
(Trenbolone Base + Enanthate Ester)
[17beta-Hydroxyestra-4,9,11-trien-3-one]
Formula (base): C18 H22 O2
Formula (ester): C7 H12 O
Molecular Weight (base): 270.3706
Molecular Weight (ester): 130.1864
Melting Point (base): 183-186C
Manufacturer: Stark, Dpharm, Various
Effective Dose (Men): 300-600mgs/wk
Effective Dose (Women): Not recommended
Active life: 8 days
Detection Time: 5 months
Anabolic/Androgenic ratio: 500/500
Trenbolone enanthate was the steroid produced by underground labs to take the
place of Parabolan, and its obscure ester. Tren enanthate basically is the longest
acting version of tren we have available on the market right now, and it actually
offers a couple of advantages over the traditional Tren A that’s been available for the
last couple of years as either an UG Product, or from converting Finaplex Pellets into
an injectable.
I had the opportunity to be one of the first athletes in the world to try this product,
from the UG “Stark Labs.” It was so new, in fact, that when I sent it away for
testing, the lab told me that they had nothing to really compare it to, and that they
were simply estimating potency and legitimacy based on the respective values for
the Trenbolone molecule and the Enanthate ester.
I’m not going to go into the various merits of trenbolone, but I would like to discuss
some unique properties the Enanthate version has. For one reason or another, this
stuff doesn’t give me tren cough, and I am particularly susceptible to this side-effect
of Tren, which basically cripples me for the first week I use it. Regardless of whether
I use home-brewed Tren, UG lab Tren, or Vet-Grade, I was basically crippled for the
first week of use. I can’t tell you why, exactly, this was, and can only speculate that
it was due to a rise in prostaglandins. Tren enanthate didn’t have this effect on me,
however. Yeah, that’s right. I know that the ester attached to a steroid doesn’t
dictate any of its properties, but in this particular case, I believe that the enanthate
ester provided less of a sharp rise in prostaglandin levels and allowed my body to not
187
develop the dreaded “tren-cough” that usually side-lines me when I start a cycle
including Tren.
There is a method of prostaglandin production whereby prostaglandins made from
one pathway in particular happen to dictate some muscle constriction as well as
platlet aggregation, while the other method of production dictates bronchial
constriction, and this could possibly be the means by which Tren Acetate causes that
vicious cough. The reason why—though this is speculation—the enanthate version
doesn’t cause this rapid rise in prostaglandins is because of its more steady release,
and my body’s ability to gradually acclimatize itself to this. If you look at the graphs
in the Minto studies (in the Deca profile), you’ll see that the rise and rapid peak in
blood plasma levels afforded by short esters are profoundly higher than those
provided with longer esters, and it’s my belief that the enanthate ester provides a
lower peak level and less rapid rise in prostaglandin levels, especially the ones which
dictate that second form of prostaglandin release which causes bronchial
constriction. I feel that this bronchial constriction never really leaves you while you
use any form of Tren, and this is what causes the shortness of breath experienced by
many athletes on Tren.
Anyway, clearly the long estered Tren is a viable compound for those who wish to
make minimal injections, and still use a nice lean-mass providing, non-aromatizing
anabolic.
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188
Tri-Trenabol
(Trenbolone without Esters Shown)
(Trenbolone Base + Acetate, Hexahydrobenzylcarbonate, & Enanthate esters)
[17beta-Hydroxyestra-4,9,11-trien-3-one]
Formula (base): C18 H22 O2
Formula, esters
Acetate: C2 H4 O2
Hexahydrobenzylcarbonate: C2H4O2
Enanthate: C7 H12 O
Molecular Weight (base): 270.3706
Molecular Weight, esters
Acetate: 60.0524
Hexahydrobenzylcarbonate: 130.1864
Enanthate: 130.1864
Melting Point (base): 183-186C
Manufacturer: British Dragon
Effective Dose (Men):50-150mg ED
Effective Dose (Women): Not recommended
Active life: 8 days
Detection Time: up to 5 months
Anabolic/Androgenic ratio: 500/500
Tri-Trenabol is British Dragon's trenbolone blend. It's been formulated with three
different esters: trenabolone accetate, trenbolone hexahydrobenzylcarbonate, and
trenbolone enanthate (for details on each specific trenbolone ester, see: Trenbolone
Acetate, Parabolan, and Trenabol 200). The acetate ester allows Tri-Trenabol to
display a rapid elevation of blood plasma levels of trenbolone. The other two esters
(hexahydryobenzyclcarbonate and enanthate), which release at differing but slower
rates, prolong the blood plasma levels of trenbolone.
Here’s how it breaks down:
Trenbolone Acetate: 50mgs
Trenbolone Hexahydrobenzylcarbonate: 50mgs
Trenbolone Enanthate: 50mgs
189
Regardless of the ester, trenbolone is a very potent androgen with strong anabolic
activity. It can be used for mass development or it can be used for cutting (which is
more common) and is well suited for either. Due to its progestenal nature,
testosterone must always be stacked with it, altough trenbolone does not convert to
estrogen.
Tri-Trenabol would probably be used for cutting, and one would probably stack it
with an anabolic such as Winstrol or Primobolan (and testosterone, as previously
discussed). Bulking with this product is also highly possible, and with the addition of
compounds like Dianabol and Testosterone, quality muscle mass would be quickly
accrued.
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and Related Topics at:
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190
Dihydrotestosterone
Derived Steroids
191
Dihydrotestosterone Derived Steroids
As you know, some steroids are derived directly from Dihydrotestosterone; these
incluse Oxandrolone, Methenolone, Drostanolone, Stanozolol, Oxymetholone, and
Mesterolone. Below is a partial list of some traits and effects that most, if not all,
dihydrotestosterone derived steroids have attributed to them:
• Does not convert to estrogen (structurally incapable)
• Is not able to be 5-Alpha-Reduced
• Has a nice balance of androgenic and anabolic properties
• Generally considered very safe in terms of side effects
• Possibly the less suppressive than other derivations (either test or 19-nor)
• Possible anti-estrogenic effects
• Possible anti-progestenic effects
• Can cause hairloss
• Can cause acne
• Possibly able to cause joint problems
192
Anadrol 50
(Oxymetholone)
[17 beta-hydroxy-2-hydroxymethylene-17 alpha-methyl-5 alpha-androstan-3-one]
Molecular Formula: C21 H32 O3
Molecular Weight: 332.482
Melting Point: 178-180C
Manufacturer: Syntex (Originally)
Release Date: 1960
Effective Dose: 100mgs (optimal)
Active Life: <16hours
Detection Time: up to 8 weeks
Anabolic/Androgenic Ratio: 320:45
Anadrol (commonly called by athletes “A50” or “A-bombs”) was initially developed as
a compound to help people with anemia, and has since been used very successfully
to aid people who are suffering from many other diseases where weight loss is a
concern. Thus, it is clearly an effective agent for promoting weight gain, increasing
appetite, gaining strength, and increasing red Blood cell count. And, as with most
Anabolic/Androgenic Steroids (AAS), it has its downsides as well. Anadrol will inhibit
your body’s natural production of hormones (testosterone, etc), will negatively affect
your blood lipid profile, can cause water retention, is notorious for causing headaches
and is also highly liver toxic (in fact, it has the worst reputation for hepatoxicity out
of all steroids). Paradoxically, although one of the benefits touted by its original
manufacturer (Syntex) is that it can be used to stimulate weight gain through
increasing appetite, taking too much may actually inhibit your appetite!
I think, in order to gain a complete understanding of this compound, we need to take
a look at its advantages contrasted with its disadvantages. Anadrol is a DHT-derived
compound, and is a 17-Alpha-Alkylated steroid, meaning that it has been altered at
the 17th carbon position to survive oral ingestion. Most oral steroids are 17aa, and
this helps them make it through your liver in a useful form. Sounds great, right?
Let’s 17alpha-alkylate everything! Well…as you can imagine, there’s a down side.
This 17aa alteration, which makes it possible for Anadrol to survive its first pass
through your liver, also makes it very taxing on your liver. How taxing is A50 and
how much weight can you gain from its use? Well, there was a 30 week study done
on A50 and, as you can expect, a reasonable amount of side effects were noted. The
fact that A50 causes some side effects has really never been in debate. But how
effective was the drug? Well, first it should be mentioned that this study was done on
people with AIDS related wasting, and they actually gained weight (8+kg) while the
control group lost weight and had increased mortality rates (1). I suppose, if you’re
in a study because you have a wasting disease which is also a terminal illness, you
193
don’t want to end up in the control group. Anyway, weight gain in this study peaked
at 19-20 weeks, though, so the last 10 weeks weren’t very productive in this
respect. Clearly, you wouldn’t want to run Anadrol for 20 weeks, given its toxicity,
but after that, any effect in terms of weight and strength gains would be negligible
anyway. The sheer fact that this study lasted so long (30 weeks) should make it
apparent that sides can be kept under control and the drug can be used safely.
People are commonly told to limit their intake of A50 to 4 weeks or less. I’m a bit
less conservative and think you can easily run A50 for 6 weeks or more. From
personal experience, however, I can tell you that gains from Anadrol are quite
dramatic for the first 3 weeks, and then quickly level off. Unfortunately, I find that
the side effects experienced from Anadrol (which include, for me, a headache,
bloating, elevated blood pressure, and a general “unwell” feeling) remain for the
entire duration of use, but I find, as usual, side effects for this drug are pretty much
half legend and half truth.
Since Anadrol is derived from DHT, it can’t actually convert to estrogen (via the
aromatase enzyme), and it’s not a progestin or a compound with progestenic
activity, so the estrogenic side effects it produces are of a very mysterious nature. It
has been speculated that perhaps it can stimulate the estrogen receptor without
actually being converted to estrogen, that’s about as plausible an explanation as I’ve
heard. However, things really get strange when Oxymetholone is used in studies to
alter the female reproductive/menstrual cycle; in those cases, it has lowered plasma
progesterone levels (7)! One would expect that an AI (aromatase inhibitor) wouldn’t
be of much use with this drug, but many have found that Letrozole (which has, in
some cases, been shown to reduce estrogen in the body to an undetectable amount)
(6) can greatly reduce or even eliminate many of the more noticeable side effects of
Anadrol, such as the bloating.
As I’ve stated, however, the sides from this drug are certainly no joke, but are easily
preventable and controlLable. One study even showed very few sides for subjects
using up to 100mgs of Oxymetholone (2). In the original UnderGround Steroid
HandBook, Dan Duchaine states that he used it at doses up to 150mgs/day. Clearly,
Anadrol’s hepatoxicity has been a bit exaggerated, in some circles. Be that as it may,
my suggestion is still to limit Anadrol’s use to 6 weeks, at a maximum even if just to
err on the side of caution. Of course, I have personally run this drug for much
longer.
How should we use Anadrol? I’d probably be willing to include Anadrol in a cycle
including injectable steroids, but not other 17aa compounds. I’d make any 6-week
run of this compound begin at the start of a cycle, as a form of “jumpstart” towards
seeing gains quickly. The quick gains you will get from Anadrol (up to a pound per
day for the first 2 weeks are not uncommon in Steroid.com members) are also just
as quick to disappear upon cessation of use, unless you are simply using it as a
kickstarter, while waiting for your other compounds to kick-in. I’ll go out on a limb
here and say that utilizing Anadrol as a “Jumpstart” is the most popular use of this
drug for athletes and bodybuilders today. I’ll also say that this drug is immensely
popular with strength athletes who don’t have to worry about weight classes (field
athletes and strongmen), and with powerlifters in the heavier weight brackets. It’s
also important to note that in one study by Schroder et. al (2), Anadrol showed that
it has the ability to lower serum SHBG (Sex Hormone Binding Globulin, which binds
to your free test and makes it no longer useful for anabolism, among other things)
concentrations by 54.9 ± 25.8 and 45 ± 16.2 nmol/l in the 50- and 100-mg
treatment groups. This means there will be more free test circulating around your
194
body when you take this drug. Clearly, this would produce some synergy when
stacked with other steroids. Given the large amounts of weight and strength which
can be gained in a relatively short time span on this drug, I’m sure this comes as no
surprise to many.
Another important and often understated characteristic of this compound is that
Oxymetholone doesn’t bind well to the androgen receptor (Relative Binding Affinity =
too low to be determined) (3); its rate is the lowest I’ve ever read about. Basically,
what this tells me is that there are a lot of non-receptor mediated effects from this
steroid, making it a very potent addition to ANY BULKING stack, because it won’t be
competing for the receptor sites with the other steroids you’re using. It’s also, as
you may have guessed, a very poor choice for a cutting stack.
How much should you use? Well, this is actually one of the most interesting facts
about Anadrol. You see, most steroids produce what we call a “dose respondent
curve” which is a fancy way of saying, “the more you use, the more you gain.”
Anadrol is one of the few steroids where the dose respondent curve flattens out very
quickly. When you take 50mgs of Anadrol, you’ll make some very good gains. When
you take 100mgs of Anadrol, you’ll make even more gains. However, it has been
found that 100mgs/day is as effective for weight gain as 150mgs/day but produces
fewer side effects and is less toxic (4). The jump from 50mgs to 100mgs constitutes
an acceptable rise in benefit vs. cost, but this is not the case as dosages get over
100mgs. Now, let’s see how 50mgs and 100mgs of Oxymetholone actually effect
strength, when compared with each other:
Relative (%) changes in strength are shown for the groups receiving placebo (filled
bars), 50 mg/day oxymetholone (open bars), and 100 mg/day oxymetholone (gray
bars). Nos. above bars represent relative change (%) from baseline to week 12 for
the 1-repetition maximum tests of strength. Error bars represent ± 1 SE from the
mean. * Significant difference from placebo, P < 0.05; significant difference from
placebo by Wilcoxon test, P < 0.02. See text for additional statistical analyses.
As you can see, in this study, doubling the dose of Anadrol nearly doubled the
strength gains of the test subjects. Now, when we look at changes in body
composition from Oxymetholone (chart below) we can see that although the guys
taking the 100mgs (vs. the 50mgs group) had more fat lost and more lean body
195
mass gained, it wasn’t as dramatic as the differences in strength gains between the
two groups:
Changes in body composition are shown for the groups receiving placebo (filled
bars), 50 mg of oxymetholone per day (open bars), and 100 mg per day (gray bars).
Numbers above the bars represent the mean absolute changes and the error bars
are ± 1 SE. For total lean body mass (LBM) and total fat, differences among the 3
groups were significantly (P < 0.0001, one-way ANOVA) different from placebo, P
0.001.
Although I am usually not inclined to posit speculations on why a particular drug
does or doesn’t do something, in this case I will. I’m guessing that the higher doses
of Anadrol cause enough appetite suppression (at least anecdotally) to make eating
rather difficult. It can also increase insulin resistance and glucose intolerance (5).
This has the effect of making macronutrient absorption more inefficient, and could
also be a factor in reducing gains when the dosage goes over 100mgs/day.
Unfortunately, Anadrol also has a reasonably profound effect on your body’s natural
hormonal system, on par with most other oral steroids, but not as bad as most
injectables, and it’s certainly not as harsh on your lipid profile as many anabolics are
(2). As an interesting side note, some of the medical literature on this compound
suggests a dose of 1-5mgs per kg of bodyweight. I’ll pause a second here for you to
figure out how absurdly high of a dose that would translate to for the average
bodybuilder!
This steroid is very available on the black market in the form of capsules, tablets
(some are even 75mgs!), liquid, and even paper. Prices will vary, and be indicative
of many different factors including the form in which you buy the compound (paper
will usually be the most expensive, and liquid the least), and where you live. In any
case, you shouldn’t be paying more than $2.50-3.00 per 50mgs.
Here’s how Oxymetholone is metabolized in your body:
196
References:
1. Br J Nutr. 1996 Jan;75(1):129-38.
2. Schroeder et al. Am J Physiol Endocrinol Metab 284:E 120-28
3. Endocrinology. 1984 Jun;114(6):2100-6.
4. HIV Clin Trials. 2003 May-Jun;4(3):150-63.
5. J Clin Endocrinol Metab. 1981 Nov;53(5):905-8
6. Epilepsy Behav. 2004 Apr;5(2):260-3
7. Am J Obstet Gynecol. 1973 Sep 1;117(1):121-5.
Charts from reference 2:
Am J Physiol Endocrinol Metab 284: E120-E128, 2003. First published September 24,
2002; doi:10.1152/ajpendo.00363.2002
0193-1849/03
197
Anavar
(Oxandrolone)
[17b-hydroxy-17a-methyl-2-oxa-5a-androstane-3-one]
Formula: C19 H30 O3
Molecular Weight: 306.4442
Melting Point: 235 – 238 Celcius
Manufacturer: BTG, SPA, Originally Searle (1964)
Effective dose: (Men)20-100mgs/day (or .125mg/kg~bdywt); (Women) 2.5
20mgs.day
Active Life: 8-12 hours
Detection Time: 3 weeks
Anabolic/Androgenic Ratio (Range): 322-630:24
Anavar (oxandrolone) is not very toxic, not very androgenic, mildly anabolic, and
pretty mild on the body’s HPTA (Hypothalamic-Testicular-Pituitary-Axis). Those are
its 4 major points, and I’d like to examine each one a bit further; as usual, gym
rumors and Internet conjecture have made this steroid the subject of many
misconceptions.
First of all, and this will come as no surprise to many people, Anavar is quite mild on
your liver. It’s probably the mildest oral steroid available today. Dosages of up to
80mgs/day are easily tolerated by most men, and most side effects often found with
other steroids are not common with ‘var (1). For this reason, Anavar is frequently
the steroid of choice for many top-level female bodybuilders and other athletes.
It’s a very mild steroid in every sense of the word. It binds reasonably well to the
AR, but pretty high doses are still needed and I would never suggest doing less than
20mgs/day. In fact, 20-80mgs are needed to start halting AIDS related wasting (1)
and recovering weight for burn victims (2), so that’s the range I’d recommend for
dasging this compound. Personally, I’d use 100mgs/day if I were ever going to try
this stuff. Any less than this amount (20-100mgs) would be a waste. For women,
however, I think 2.5-10mgs/day would suffice. Virilation is not a concern with this
compound, as it is only very mildly androgenic (3). Water retention is also virtually
nil with it.
Although Anavar is an oral steroid, and has been alpha-alkylated to survive oral
ingestion and the first pass through the liver; it’s still relatively mild in that respect
too. The unique chemical configuration of oxandrolone both confers a resistance to
liver metabolism as well as noticable anabolic activity. It would also appear that
Anavar appears not to exhibit the serious hepatotoxic effects (jaundice, cholestatic
198
hepatitis, peliosis hepatis, hyperplasias and neoplasms) typically attributed to the
C17alpha-alkylated AASs (17). Anavar has even been used successfully in some
studies to heal cutaneous wounds (7), or to improve respiratory function (18). Both
of these novel properties could make it a good choice for in-season use for boxers,
mixed Martial Arts competitors, and other such athletes.
Now here’s some interesting stuff for anyone interested primarily in the fat burning
properties of this stuff: Anavar may be what we’d call a “fat-burning steroid.”
Abdominal and visceral fat were both reduced in one study when subjects in the
low/normal natural testosterone range used it (4). In another study, appendicular,
total, and trunk fat were all reduced with a relatively small dose of 20mgs/day (8)
and no excercise. In addition, weight gained with ‘var may be nearly permanent too.
It might not be much, but you’ll stand a good chance of keeping most of it. In one
study, subjects maintained their weight (re)gains from Anavar for at least 6 months
after cessation (2)! Concomitantly, in another study, twelve weeks after
discontinuing oxandrolone, 83% of the reductions in total, trunk, and extremity fat
were also sustained (8)! If you’re regaining weight, Anavar will give you nearly
permanent gains, and if you are trying to lose fat (and you keep your diet in check),
the fat lost with Anavar basically looks to be nearly permanent. Check this chart
out:
Absolute change in total fat mass (A) and trunk fat (B) by dual-energy X-ray
absorptiometry from baseline to study week 12 (solid bars) and from baseline to
study week 24 (open bars) in the placebo (n = 12) and the oxandrolone (n = 20)
study groups. Values are means ± SE. *Significant decrease from baseline, P <
199
0.001. Significant difference between study groups for change in fat mass from 0 to
12 wk, P < 0.001. (15)(8)
Keep in mind this is all without any post cycle therapy, and without any change in
diet or training! And although many of the studies done on oxandrolone use elderly
men or young boys as the test subjects, some evidence suggests that many of the
effects of oxandrolone are not age dependant (11). If you are following the typical
“time on = time off” protocol, this means you can lose a bunch of fat during your
time on, then keep most (if not all) of it off until your next cycle. That makes it a
great drug for athletes who are drug tested and need to be clean for their season,
yet need to keep off the fat/weight they lost on their cycle off; I’m thinking about
wrestlers and other weight-class athletes. Anavar is also the clear choice for a
“spring-cutting” cycle, to look great at the beach—you can use it up until the
summer starts, and then keep the fat off during the entire beach season!
Anavar is great for strength and cutting purposes, but not for bulking or a lot of
weight gain. In other words, what I'm saying is that everything you gain will be solid.
Personally I am leaning towards a theory that purports that the more solid your
gains are, the more you’ll keep (percentage-wise). It makes sense, when you think
about it; people make a lot of weight gains on the highly water-retentive steroids
(Dbol, A50, long estered testosteones, etc…), but lose the greatest percentage of
their gains afterwards. The same seems to be opposite for the steroids which cause
less (or no) water retention (Anavar, Primo, Winstrol, etc).
So why else may you keep such a high proportion of what you gained on ‘var? Well,
I think it may be due to it’s relatively light impact on the HPTA, which brings me to
my final point: Anavar will not totally shut down your HPTA, especially at lower doses
(unlike testosterone, which will eventually do this even at a 100mg dose, or Deca
which will do it with a single 100mg dose). This could be due, at least partly, to the
fact that Anavar doesn’t aromatize (convert to estrogen). Serum testosterone, SHBG
(Sex Hormone Binding Globulin), and LH (Leutinizing Hormone) will be slightly
suppressed with low doses of Anavar, but less than with other compounds. FSH
(Follicle Stimulating Hormone), IGF1 (Insulin Like Growth Factor 1) and GH (Growth
Hormone) will not be suppressed with a low dose of Anavar and LH will even
experience a “rebound” effect when you stop using it (3). If your endocrine system
and HPTA are funtioning normally, you should be able to use Anavar with minimal
insult to it, and can even keep most of your values within the normal range (5).
Thus, Anavar may even be ideal for use in bridges between cycles, (at very low
doses under 10mgs perhaps), or as previously mentioned, for cutting/strength cycles
at 50-100mgs.
Its relatively high cost is its only major drawback, and tablets can typically sell in
Mexico or on the black market for up to a dollar (US) per 10mgs. Many black market
dealers or underground labs, however, offer capsules, liquid form or, in some cases,
even their own brand of tabs for substantially less money than the legit
pharmaceutical versions, or even veterinary versions found overseas.
200
Here’s how Oxandrolone is Metabolized in your body:
References:
1. Proj Inf Perspect. 1997 Nov;(23):19.
2. Burns. 2003 Dec;29(8):793-7
3. Clin Endocrinol (Oxf). 1993 Apr;38(4):393-8.
4. Int J Obes Relat Metab Disord 1995 Sep;19(9):614-24
5. jcem.endojournals.org/cgi/content/full/84/8/2705
6. Segal S, Cooper J, Bolognia J., Treatment of lipodermatosclerosis with oxandrolone in
a patient with stanozolol-induced hepatotoxicity., J Am Acad Dermatol 2000
Sep;43(3):558-9
7. Demling RH., Oxandrolone, an anabolic steroid, enhances the healing of a cutaneous
wound in the rat., Wound Repair Regen 2000 Mar-Apr;8(2):97-102
8. J Clin Endocrinol Metab. 2004 Oct;89(10):4863-72.
9. Demling RH, Orgill DP., The anticatabolic and wound healing effects of the
testosterone analog oxandrolone after severe burn injury., J Crit Care 2000 Mar;15(1):12
7
10. Hart DW, Wolf SE, Ramzy PI, Chinkes DL, Beauford RB, Ferrando AA, Wolfe RR,
Herndon DN., Anabolic effects of oxandrolone after severe burn., Ann Surg 2001
Apr;233(4):556-64
11. Demling RH, DeSanti L., The rate of restoration of body weight after burn injury,
using the anabolic agent oxandrolone, is not age dependent., Burns 2001 Feb;27(1):46-51
12. Demling RH, DeSanti L., Oxandrolone, an anabolic steroid, significantly increases
the rate of weight gain in the recovery phase after major burns., J Trauma 1997
Jul;43(1):47-51
13. Papadimitriou A, Preece MA, Rolland-Cachera MF, Stanhope R., The anabolic
steroid oxandrolone increases muscle mass in prepubertal boys with constitutional delay
of growth., J
201
14. Doeker B, Muller-Michaels J, Andler W, Induction of early puberty in a boy after
treatment with oxandrolone? Horm Res 1998;50(1):46-8
15. J Appl Physiol 96: 1055-1062, 2004. First published October 24, 2003;
doi:10.1152/japplphysiol.00808.20038750-7587/04
16. James JS., Wasting syndrome: oral oxandrolone re-released in U.S., AIDS Treat
News 1995 Dec 22;(no 237):3-4
17. Drugs. 2004;64(7):725-50.
18. Mt Sinai J Med. 1999 May;66(3):201-5.
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202
Andractim
(Topical Dihydrotestosterone)
Although DHT is much more potent than testosterone in terms of both anabolic and
androgenic effects, it has several possibly nasty side effects, as well as several
problems and a couple of possible advantages inherent with its form of
administration (topical). First, though, a brief discussion of DHT is probably in order,
so bear with me.
For starters, pure DHT is a very poor choice for anabolism of any sort. I know we
can all look at its anabolic/androgenic rating and say that it’s a very good anabolic
steroid, but in actuality, what happens to DHT in the body is far different than what
we’d want, but first I’ll give you the good news about. DHT is a non-aromatizing
androgen, which as you know means it doesn’t convert to estrogen at all. This is
important because estrogen is suppressive of LH production (1), which is of course
going to be an aggravating factor in lowering your endogenous testosterone
production. In addition to not converting to that nasty test-suppressive-estrogen,
DHT will not inhibit LH production or testosterone production (1)(2)(3). DHT may
even have a suppressive effect on estrogen, in some cases. This would certainly
account for its ability to actually have a positive effect (again, in some cases) on LH
and testosterone.
This is all very good news, but unfortunately, there’s a catch. Your body reduces
DHT to inactive metabolites by way of the 3-alpha-hydroxysteroid dehydrogenase
enzyme before a lot of it can reach the androgen receptors in skeletal tissue. This
means that while it reaches your scalp and prostate relatively intact, it doesn’t make
it to your muscles that way. This is why we see so many different alterations of DHT
available on the market, from Anadrol 50 to Anavar, with so many different uses.
Andractim has the most unique use, though, I think.
Andractim has been used with some success to reduce gyno in males. It’s possible
that a lowering of circulating DHT-levels can cause Gyno (5)(6), and certainly
androgen therapy with DHT derivatives has been found useful for treatment of gyno,
so it’s very logical that a topical DHT would be a good bet to address anabolic/
androgenic steroid induced gyno. Here’s the creepy part: You’ll need to rub it on
your nipples several times per day.
Obviously this is problematic for someone with a job, who can’t be going to the
restroom and rubbing his nipples a couple of times every day. Unless rubbing his
nipples is part of his job; anyway….
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Andractim is a topical gel, which comes in a tube, containing 80x 25mg doses of
DHT. The absorbtion rate is going to be similar to testosterone gel, or roughly 10%,
so you’re applying 2.5mgs of pure DHT to your nips every time you use this stuff.
I’d say you want to be doing this 2x per day with an equal amount per nipple, using
25-5mgs of gel each time.
References:
1. Hypothalamic sites of action for testosterone, dihydrotestosterone, and estrogen in the
regulation of luteinizing hormone secretion in male sheep. Endocrinology. 1997
Sep;138(9):3686-94.
2. Inhibition of LH Secretion by Localized Administration of Estrogen, but not
Dihydrotestosterone, Is Enhanced in the Ventromedial Hypothalamus During Feed
Restriction in the Young Wether. Biol Reprod. 2005 Jun 22; [Epub ahead of print]
3. Crystalline dihydrotestosterone implants in the lateral septum of male rats. A positive
effect on LH and FSH. Endocr Res. 2001 Feb-May;27(1-2):35-40.
4. Significant role of 5 alpha-reductase on feedback effects of androgen in rat anterior
pituitary cells demonstrated with a nonsteroidal 5 alpha-reductase inhibitor ONO-3805. J
Androl. 1994 Nov-Dec;15(6):521-7.
5. Case report: finasteride-induced gynecomastia in a 62-year-old man. Am J Med Sci.
1995 Jun;309(6):322-5.
6. Male pseudohermaphroditism due to 5 alpha reductase deficiency associated with
gynecomastia. Rev Hosp Clin Fac Med Sao Paulo. 1987 Mar-Apr;42(2):66-8.
204
Masteron
(Drostanolone shown with Propionate ester)
(Drostanolone Propionate)
[17beta-Hydroxy-2alpha-methyl-5alpha-androstan-3-one propionate]
Formula: C23 H36 O3
Molecular Weight: 360.5356
Melting Point:N/A
Manufacturer:Syntex, Various Underground Labs
Effective Dose (men):350mgs/week (*100mgs Every other day) to 500mgs/week
Effective Dose (women): 25-50mgs Every other Day to Every Third Day
Active Life:2-3 days
Detection time: 3 weeks
Anabolic/Androgenic Ratio:62:25
Masteron is, to be honest, my favorite Anabolic/Androgenic Steroid (AAS). For many
years, this compound was unavailable to the average athlete; it was frequently
counterfeited, often very expensive, and almost never available on the black market.
The most common form of this product, as manufactured by major pharmaceutical
houses, is 50mg/ml ampules with either 1-2mls per amp (or vial). Needless to say,
these products used to be the only game in town, and since this drug was a
particularly sought-after compound for bodybuilding contest preparation, its price
made it prohibitive for all but the highest-level bodybuilders.
Masteron is a derivative of DHT (as you can tell from it's chemical name: 2a-methyl
dihydro-testosterone propionate), but what they fail to tell you is less obvioius is that
DHT and its derivatives are commonly used in treatment of certain forms of breast
cancer (see the etymology here: MASTectomy, gynocoMASTia, MASTeron…get it?).
Masteron is not clinically used for weight gain (as is common with most steroids), so
this makes it a very unique steroid from that perspective. Unfortunately, for that
reason much of the information on Masteron available in medical journals doesn’t
focus on weight or strength gain or even fat loss. Most information on Masteron
focuses on it’s use in treating certain forms of breast cancer, and it does this
reasonably well (4)(5). To give you an idea, Masteron + Tamoxifen actually fared
better than chemotherapy for immediate objective responses from patients (8). So?
What does this tell us? Well, this makes it a very exciting drug for a lot of reasons.
Clearly it won’t aromatize at all, nor will it have progesteronic sides—remember,
Nolvadex (and most ancillaries) are used to reduce estrogen for breast cancer
patients, so a drug used to treat breast cancer obviously wouldn’t convert to
estrogen. In addition, Masteron may in fact interact with the aromatase enzymes to
inhibit aromatization of other steroids into estrogen, and may additionally interact
205
with estrogen (as a “blocker” of sorts) at the receptor site (4)(5). This is how it helps
to combat breast cancer, obviously, but this could also be part of the reason that
Masteron is considered a “cutting” or “Pre-contest” drug. Masteron may actually be
very useful for combating estrogenic/progesteronic side effects. Yes, you read that
right: if you include Masteron in your cycle, you may not need other “ancillary” drugs
like Arimidex or Letrozole. Therefore, much like Proviron, Masteron could be used as
an anti-side-effect-drug (remember, most ancillary drugs we use to combat
estrogenic sides, like Nolvadex, Letroxole, and Arimidex were originally developed to
combat breast cancer). Along a similar line, being a DHT (DiHydroTestosterone)
derivative, it’s got a very nice ability to add muscle hardness to an already lean
physique. Masteron has a deceivingly low anabolic/androgenic ratio, but since DHT
is 5x as androgenic as testosterone and has a 3-4x higher affinity to receptor sites,
Masteron provides a lot of “bang for the Buck” when examined on a Mg for Mg basis.
In my experience, as well as that of many others, Masteron is a stronger androgen
than it appears on paper, and this could cause increased aggression. As we know,
higher androgens also produce that “hard” look prized by competitive BB’ers, and as
we all know, androgens also promote lypolysis (fat loss). The effects of Masteron, in
that regard are consistent with the documented effects of (somewhat heavier)
androgens to decrease lipoprotein lipase and upregulate-adrenergic receptors on
adipocytes, which would inhibit the accumulation of lipid (fat) and enhance the efflux
of lipid from these cells in response to catecholamines (1)(2)(3). So, like I said
previously, don’t let Masteron’s deceptively low anabolic:androgenic ratio fool you.
It helps eliminate fat as well (if not better) than much more highly scored androgens,
in part due to its being a derivative of DHT. This reduction in fat and rise in
aggression (making workouts more effective) could be beneficial for people
competing in a sport or who are on a reduced calorie diet. Sounds pretty good,
right?
Unfortunately, being a DHT derivative means that it can have certain undesirable
sides as well (acne, hairloss, prostate enlargement, etc.; you may want to consider
using Finasteride with this drug). Water retention (and increased danger of high
blood pressure) with this compound is virtually nil, and liver toxicity is not much of
an issue either. Really, you can take heaps of this stuff; the maximum theraputic
dose is pretty high: 167mgs/kg-bdywt/day. So that's 167mgs per day, every day of
the week for a 220lb person—and that's not considered excessive by the FDA, which
hasn't been very traditionally liberal on dosing protocols. So clearly, up to that dose
is very safe for almost anyone. DHT has a bad reputation for causing prostate
hypertrophy, acne, and hairloss, but most people I’ve talked to find that reputation
to be mostly undeserved at least in the case of Masteron.
Remember that year that the Chinese National Swimming Team (women’s) kicked
everyone’s ass? Or the year that the German National Swimming Team (again, I’m
talking about women) took all those Gold medals? They were all using a form of
DHT or a derivative, possibly Masteron. The German Women had very deep voices,
which leads me to believe that Masteron’s virilizing effects on women could be very
bad (there was a famous/funny interview during which the interviewer implied that
they all had deep voices, and one of them replied “Ve came here to svim… not to
sing.”). Anyway, Masteron is a great drug for any type of athlete, but possibly not
for women (at least not at high doses, perhaps 50mgs/E3D is appropriate). Sorry
girls: you can have a go with this drug, but keep the doses low.
Stacking Masteron? Well, I’d say that your best bet is with test, of course, but
206
really, due to Masteron’s reasonable binding to the androgen receptors and its high
androgenic properties, almost any cutting drug (Tren, Anavar, etc.) could be
efficientlty included with it in a cycle. I have a feeling that due to stanozolol’s
(Winstrol) non-AR mediated effects, and it’s ability to reduce SHBG, a stack including
both of these drugs would be very synergistic.
However, don’t forget the
testosterone, as Masteron will reduce your own natural testosterone levels (9), and
since you are going to have to inject Masteron every other day at least (100mgs EOD
is the lowest dose of this stuff I’d consider using), you might as well stack it with
testosterone propionate, and possibly injectable Winstrol (and/or maybe Tren
Acetate if you’re inclined to use a lot of compounds in the same cycle, and I know I
am). Eq is another popular choice to stack with Masteron.
I’d say that optimum effects of this stuff are found with 4-500mgs/week (based on
conversations I've had with people who have used Masteron, as well as my own
results). I happen to have a friend who has gone up to 600mgs/week with Masteron
and didn’t feel that it provided significantly better results than 400-500mgs per
week. I think, for maximum cost effectiveness, 400mgs per week is ideal. It’s also
important to remember to spread those shots out on an every other day basis, as
the Masteron I’m talking about here is the propionate version, and as such, requires
more frequent dosing. Of course I know there is a version of Masteron with an
enanthenate ester dosed at 200mg/ml being produced by a very good underground
lab (I personally used the “alpha” version, as a sort of human guinea pig almost a
year ago), but that’s not the version of Masteron I’m talking about in this profile. In
addition, there is another form of Masteron out there: drostanolone (base)—yeah,
that’s right, Masteron without an ester. It’s called Dromostan and it’s made by the
Xelox company. I’ve never tried this version, and don’t know anyone who has, but
it’s my suspicion that it would be a very potent product, but would need to be
injected every day.
If you are looking for this drug from a major pharmaceutical company, I’d caution
you to reconsider that route, and go with an underground lab instead. There are
many very reputable underground labs operating out there, with no known
counterfits. On the other hand, genuine Masteron is one of the most difficult drugs to
find on the black market if you’re looking for a “Human-grade” product made by a
major pharmaceutical house. In addition, UGLabs commonly offer this product for a
very reasonable $50-75 for a 10ml bottle dosed at 100mg/ml. Trying to find the
Syntex (or comparable Human-Grade) version of this product will bring a mg for mg
cost of 2-5x that amount.
To recap: Masteron is derived from DHT; could be used as an anti-estrogenic drug;
doesn’t convert to estrogen and actually works to reduce it in your body; can
possibly cause hairloss and other DHT-related sides; is great for all types of athletes
and BB’ers, but not women in high doses; stacks well with almost anything; is very
androgenic; is awesome for losing fat and getting “hard”; and should be used at
around 400-500mgs/week. It’s no surprise that it’s the favorite steroid of many
people, myself included.
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Here’s how drostanolone is metabolized by your body:
References:
1. Marin P, Oden B, and Bjorntorp P. Assimilation and mobilization of triglycerides in
subcutaneous abdominal and femoral adipose tissue in vivo in men: effects of androgens.
J Clin Endocrinol Metab 80: 239-243, 1995
2. Rebuffe-Scrive M, Marin P, and Bjorntpor P. Effect of testosterone on abdominal
adipose tissue in men. Int J Obes 15: 791-795, 1991.
3. Xu XF, De Pergola G, and Bjorntorp P.Testosterone increases lipolysis and the number
of beta-adrenoceptors in male rat adipocytes. Endocrinology 128: 379-382, 1991.
4. Eur J Cancer Clin Oncol. 1983 Sep;19(9):1231-7.
5. Cancer Res. 1982 Nov;42(11):4408-12.
6. Gan No Rinsho. 1986 Apr;32(4):345-8. Japanese.
7. Khirurgiia (Sofiia). 1987;40(6):80-6. Bulgarian.
8. Sem Hop. 1982 Sep 23;58(34):1919-23.
9. J Clin Endocrinol Metab. 1965 Apr;25:476-9.
208
Masteron Enanthate
(*Shown Without Enanthate Ester)
(Drostanolone Enanthate)
[17beta-Hydroxy-2alpha-methyl-5alpha-androstan-3-one Enanthate]
Molecular Weight: 360.5356
Formula: C23H36O2
Melting Point:N/A
Manufacturer: Dpharm, others
Effective Dose (men):400-600mgs/week
Effective Dose (women): 100mgs/week
Active Life: 8 days
Detection time: up to 3 months
Anabolic/Androgenic Ratio: 62:25
This is a compound very near and dear to my heart, as I was actually one of the first
people in the world to ever use it! I was contacted by the owner of Dpharm after
writing my original article on Masteron, and asked a bunch of questions concerning
making this drug with the enanthate ester. It seems that another lab had tried to
produce this drug and people were getting sick from it. The attempt to get it right is
really a very cool example of an underground lab pushing the frontier of developing
anabolic steroids beyond those of the major pharmaceutical houses.
So of course, I told him to send me a bunch of the prototype and I’d shoot it, and
we’d see if I got ill. It wasn’t much of a plan, in retrospect, but it’s what we did.
Anyway, I get this stuff in my mailbox a few days later—it’s virtually clear, and in an
unLabeled vial. Well, I shot ½ a cc into each biceps, to see if it made me sore, then
I tried a cc in each delt. Everything seemed ok. It was supposed to be 220mgs/ml,
but the Lab reports said it was only around 90% pure.
So as you may have guessed, I’m still alive. It didn’t get me sick or anything, leading
me and the owner of the Lab to speculate that the other Lab had some unrelated
purity issues, and the Dpharm version didn’t share them.
Anyway, I gave him my feedback on the product, and another fine anabolic steroid
entered the black market!
209
It’s dosed at 200mgs/ml, and comes in a 10ml multi use vial, with (of course) the
enanthate ester instead of Masteron’s traditional propionate ester. Though this
particular compound acts just like the one with the propionate ester, in almost all
respects. Let’s see how it differs.
Now,we know a couple of things from the Minto et. al studies (see the profile for
Deca-Durabolin); the first is that higher mg/ml steroids give higher blood plasma
levels of a given steroid, and we also know that shorter esters do this as well. So
why would anyone make a nice cutting steroid like Masteron (drostanolone
propionate) into a longer estered version? In this case, the higher concentration
(200mgs/ml) and longer ester (enanthate) allow us to do several interesting things
with this compound. One I’ve heard of is people running a gram per week of it, and
that would only require two 2.5ml shots! Another thing I’ve seen is people using this
with a long estered Tren and Test (along with an ancillary compound like Letro) and
having a great cutting cycle that only requires a 1-2 day a week injection schedule.
210
Miotolan
(Furazabol)
[17-alpha-methyl-5-alpha-androsta-2,3-furazan,17b-ol]
Molecular Weight: 330.4692
Molecular Formula: C20H30N2O2
Melting Point: N/A
Manufacturer:Various Underground Labs
Release Date: 1989
Effective Dose: 1-2mg/kg of Bodyweight
Active Life:+/- 4 hours
Detection Time: 3 weeks
Anabolic/Androgenic Ratio: 270-330:73-94
Furazabol was originally manufactured in Japan in tabs of 1 mg strength. Dan
Duchaine was very unimpressed with this drug, noting that he rarely saw any very
large Japanese bodybuilders. I’m inclined to agree, but let’s take a look at it, since it
has become quite popular ever since its reappearance on many underground labs’
price lists.
Finding out information on this stuff was agonizing, since most of it is in Japanese,
and no athletes really use it. Anyway, with respect to its half-life and active life (and
detection time), I’m pretty much estimating from what I’ve seen in studies. One
study said that the half-lives of unchanged Furazabol in two human subjects were
1.87 and 1.29 h respectively, and the recovered amount in 48 h was averaged to
24% (33% for one, 15% for the other, respectively) (4). Unfortunately for tested
athletes, Furazabol is metabolized in the body into 16-hydroxyfurazabol and then
excreted in urine. The presence of this compound in urine can be monitored with a
very simple, standard procedure (4) for urine screening, and this is incorporated into
the general dope testing protocol for anabolic steroids employed by the IOC and
other such no-fun-agencies.
The really interesting thing about this stuff (to me, anyway) is that it’s a DHT
derived steroid, with a decent anabolic rating that lowers cholesterol! It is often
compared with Winstrol, for many good reasons: strucrurally, it is a DHT molecule
with a 17-alpha-methyl group (making it both liver-toxic and orally available, as you
know). Additionally, it has no 3-keto group, which is needed for a strong androgenic
binding ability, so this lack probably impairs its overall androgenic rating. As with
Winstrol, it’s not estrogenic in any way, doesn’t aromatize, and you’ll only have to
worry about DHT-sides from it (acne, hairloss, etc.), and possible liver problems.
However, while Winny really KILLS your cholesterol values, furazabol actually
improves them! In one study, the administration of furazabol at the daily dose of
211
0.04, 0.2 or 1 mg/subject (in this case, rats) for 3 months, there were substantial
increases noted in the plasminogen (a substance found in body fluids and blood
plasma that, when activated, becomes plasmin—an enzyme found in plasma that
catalyzes the breakdown of blood-clotting agents) activator activity in blood.
Furthermore, in the rats’ lung tissue there was an expected decrease in plasma
fibrinogen level. This will, of course, serve to increase your blood-clotting time
considerably. There was also a decrease in plasma cholesterol levels with
administration of Furazabol (8), which certainly means it’s a reasonably safe oral.
One month after cessation of the furazabol treatment, these altered parameters
tended to return to normal (8), as is very common with similar side effects from
most anabolic steroids (notably, this is very similar to Winny, once again).
This steroid is quite confusing to me, as it was found to be a good treatment for
hyperlipemia (it lowers cholesterol), and this was without affecting proteinuria (the
prevention of excretion of amino acids) (12). Generally, steroids affect proteinuria
positively, as you’d expect (and want) them to. This stuff is DHT-derived, and it also
appears to have a relatively low androgen binding ability, which makes the lack of
effect it had on proteinuria when compared with it’s anabolic rating even more
confusing. It should be noted that doses used in this study were oddly high for a
product which comes in 1mg presentation: 1.1 mg/kg/day. That means a 200 lb
bodybuilder would be using about 100 mg/day. I think a reasonable anabolic effect
would be had with furazabol roughly 50-100mgs/day. This may also be a decent
steroid for use in a cycle if one were worried about cholesterol. You’d get an
anabolic effect (remember, its anabolic rating is roughly the same as Winstrol’s);
thus you could build muscle and lower cholesterol with just one pill. Well, actually
about a hundred pills, since it comes in 1mg form. Why make a pill in 1mg form if
you need to take 100/day? I just don’t understand.
Furazabol is not estrogenic in any way. It’s structure and its lack of estrogenic action
make it an appropriate precontest drug, as I can’t imagine anything gained with it
being less than high-quality muscle. There is only a slim chance of androgenic risk,
so this may be a nice drug for women as well as men, although certainly not worth
consideration for the latter as a stand-alone anabolic. The most unfortunate part
about this drug is it’s current availability (low) and cost (high).
As a quick recap, let’s just keep in mind that this stuff is essentially Winstrol that
helps your cholesterol instead of harming it. I looked at the steran nucleus of both
Winstrol and Miotolan (a likely candidate because, as I said, it also lowers
cholesterol). They are both DHT-derived, which I knew off-hand, and this made me
more curious about subbing Miotolan for the Winny. Anyway, they are DHT-Derived
with a 17-alpha-methyl group (making them methylated, or 17aa, for oral
availability). Neither have a 3-keto group; both having instead 2 nitrogen atoms and
2 double bonds—a very weird looking structure—which also makes them both very
weak binders to the AR, perfect for stacking with the strong-binding-Tren. The
difference (that I could see) between the two is that in lieu of the 2,3-pyrazol group
found in the stanozolol structure, furazabol has a 2,3-furazan group (hence the
name). Think of it as Winny, when you can’t use Winny.
212
References:
1. Improvement in steroid screening for doping control with special emphasis on
stanozolol. J Chromatogr A. 2003 Jan 24;985(1-2):375-86. provement in steroid
screening for doping control with special emphasis on
2. Excretion study of furazabol, an anabolic steroid, in human urine. J Chromatogr B
Biomed Appl. 1996 Dec 6;687(1):79-83.
3. 17-Epimerization of 17 alpha-methyl anabolic steroids in humans: metabolism and
synthesis of 17 alpha-hydroxy-17 beta-methyl steroids. Steroids. 1992 Nov;57(11):537
50.
4. Urinary excretion of furazabol metabolite. J Anal Toxicol. 1990 Mar-Apr;14(2):120-2.
5. Inhibitory effect and interaction of stanozolol with pig testicular cytochrome P-450 (17
alpha-hydroxylase/C17,20-lyase). Chem Pharm Bull (Tokyo). 1989 Jul;37(7):1855-8.
6. Changes in the cytoplasmic androgen receptor of rat ventral prostate after
administration of androgens, antiandrogens and anabolic steroids. Endocrinol Jpn. 1980
Aug;27(4):483-93.
7. Pharmacological studies on experimental nephritic rats. (4) Improvement of
hyperlipemic models in rats utilizing anti-rat kidney rabbit serum and effects of anti
hyperlipemic agents on serum lipid levels. Jpn J Pharmacol. 1978 Oct;28(5):729-38.
8. Enhancement of fibrinolytic and thrombolytic potential in the rat by treatment with an
anabolic steroid, furazabol. Thromb Haemost. 1976 Nov 30;36(2):451-64
9. Enhancement of fibrinolytic and thrombolytic potential in the rat by an anabolic
steroid, furazabol.Thromb Res. 1976 May;8(2 suppl):107-14.
10. Some non-hormonal properties of 17 -hydroxy-17 -methyl-5 -androstano(2,3
c)furazan (furazabol). Chem Pharm Bull (Tokyo). 1973 Jan;21(1):21-4.
11. [Influences of testosterone, progesterone and furazabol, an anabolic steroid, on the
cholesterol-shifting response to estrone] Yakugaku Zasshi. 1972 Mar;92(3):316-21.
Japanese
12. Suzuki Y, Honda Y, Ito M. Pharmacological studies on experimental nephritic rats.
(4) Improvement of hyperlipemic models in rats utilizing anti-rat kidney rabbit serum and
effects of anti-hyperlipemic agents on serum lipid levels. Jpn J Pharmacol 1978
Oct;28(5):729-38
13. Kim T, Suh JW, Ryu JC, Chung BC, Park J. Excretion study of furazabol, an anabolic
steroid, in human urine. J Chromatogr B Biomed Appl 1996 Dec 6;687(1):79-83
213
Primobolan
(Methenolone)
(+ acetate)
(Injectable version is Methenolone + Enanthate Ester)
(Oral Version is + Acetate Ester)
(Injectable Version is + Enanthate Ester)
[17beta-Hydroxy-1-methyl-5alpha-androst-1-en-3-one]
Formula: C20H30O2
Molecular weight of base: 302.4558
Molecular weight of Acetate ester: 60.0524
Molecular weight of Enanthate ester: 130.1864
Melting Point: N/A
Manufacturer: Schering
(+Enanthate)
Effective dose(oral): (Men)50-100mgs/day; (Women) 10-25mgs/day
Effective dose (injectable): (Men) 350-600mgs/week; (Women) 100mgs/week
Active Life: 10-14 days (injectable); 4-6hrs (oral)
Detection Time: 4-5 weeks
Anabolic/Androgenic Ratio (Range): 88:44-57
Primobolan is one of those anabolic steroids with a cult following not unlike the old
original version of Masteron. Actually, as you can easily see from it’s anabolic/
androgenic ratio, it’s a pretty weak steroid—but actually stronger(!) than Masteron in
both regards. I don’t know anyone who has run both compounds at the same dose.
We are probably justified in speculating that you’d probably get similar results from
either of them, when you consider the fact that you are getting quite a bit less actual
drug and more ester when you choose injectable Primobolan (which has the very
long enanthate ester attached to it) over Masteron (which has the very short
propionate ester attached to it).
I happen to be one of the few people who have used drostanolone enanthate
(Masteron with the enanthate ester attached) as well as methenolone enanthate
(injectable Primobolan). I can tell you that the results from these two compounds,
when ester and mg potency are the same, are in fact very similar.
Let’s flesh out some of the various general effects of Primobolan, before we get into
the differences between the oral and injectable versions. One study performed on
sheep involved administering 100mgs of Methenolone, and electronically stimulating
their lats (electronic stimulation was used because they kept falling off the chin-up
bars). Anyway, when compared with the control group, the group receiving the drug
gained significantly more muscle mass as well as strength (1)(2). It also has a
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relatively high affinity for binding to the AR, actually binding better than testosterone
(3). This ability to strongly bind to the AR may be why Primobolan is such a good
“fat burner.” Strong AR binding has been positively correlated with lypolysis (fat
burning) (8).
In addition, as this steroid can actually aid in reducing breast tumors, no ancillary
products need be considered for use with Primobolan, and like Masteron, it may
actually be a useful ancillary agent in it’s own right. Also, just like Masteron,
Primobolan has no propensity to aromatize (convert to estrogen).
Although nobody would ever suggest to use Primobolan as a bulking agent, it’s been
studied as an agent to halt wasting and possibly reverse many of the adverse effects
of anemia. It is a shocking failure in both areas, according to some of the case
studies I’ve read (5)(6), and this should come to no surprise to anyone. Anadrol
reigns supreme in this area, and nobody in the athletic community would ever
compare those two drugs. However, Michael Mooney and many other respected
doctors who work with AIDS patients have found sufficient evidence to claim that
Primobolan is an immune enhancer and as such is very useful for AIDS patients.
AIDS patients aren’t really in need of bulking drugs, so an immune enhancer like
Primo which will add small, quality gains in muscle is perfect for them. And since we
aren’t even going to vaguely consider the use of Primobolan as a bulking agent,
clearly this leaves us with considering it primarily for use in gaining and maintaining
lean tissue. It’s a great choice for this purpose, and many competitors have used it
very successfully to retain muscle while on a reduced-calorie diet. The reason Primo
is so useful for this purpose is that one of it’s primary functions is to help your body
retain nitrogen (7) at a greatly enhanced rate. The greater your nitrogen retention,
the more muscle you will build. In the case of using primo as a pre-contest drug,
this nitrogen retention will help you retain muscle and ensure that your dieting
preferentially favors fat loss over muscle loss.
Primobolan is a very unique steroid, as it is one of the few that comes in both an oral
as well as an injectable version. I suppose Winstrol does also, but Primobolan
actually has a different ester on the oral (acetate) and injectable (enanthate)
versions. The oral version is one of the more interesting oral compounds I’ve looked
into. For starters, it’s one of the few compounds available to athletes and
bodybuilders taht is both oral as well as non-17-alpha-alkylation. This alteration is
(as I’m sure you remember from other stuff I’ve written) what generally makes oral
steroids survive their first pass through your liver, but also makes them hepatoxic
(liver–toxic). Well, oral Primo doesn’t have this feature, so it is very mild on your
liver (actually it basically isn’t liver toxic at all), but also is largely destroyed by it,
since 17 beta estrification and 1 alkylation is the method used to make this stuff
orally available. You’ll need to take a lot of this stuff for it to be effective:
100mgs/day of the oral version is a safe estimate for reasonable gains. Women can
get away with less, perhaps 25mgs/day. Even though the acetate ester has a 2-3
day active life, your liver will do some damage to oral primo, so every day dosing will
still be necessary.
When men were given a 30-45mg dose of the oral version of Primo, they
experienced a 15-65% decrease in gonadotropin levels (9). Remember, I said
100mgs is a good dose for gains—well, you’ll also reduce your gonadotropin levels
considerably. I have personally never understood why people recommend either oral
or injectable Primobolan as a possible bridging compound for this reason. Maybe at
215
a too-low-to-do-anything dose of 10mgs it could be used as a bridge. And forget
about using injectable Primo to bridge.
Hey, speaking about injectable Primo…
I’ve used this stuff at 200mgs/week and wasn’t very impressed with it. Generally, I
think injectable primo needs to be used at a dose of at least 350mgs/week (100mgs/
every other day), and preferably at a dose of 400-600mgs/week. I happen to like
running it with testosterone propionate, but for convenience I would imagine most
people would run it with testosterone enanthate, to keep dosing times the same
(shooting it twice per week, in most cases).
The unfortunate truth about injectable Primo is that it’s a very expensive chemical to
obtain, and that price is reflected in the cost to the average consumer. Ten dollars
per 1ml/100mg ampule is not unheard of, and I’ve seen it go for more. This is, of
course, absurd. As if that’s not enough, this is also one of the most commonly
counterfitted steroids on the black market. I recommend buying Primobolan (either
the oral or injectable) from a respected underground lab instead of trying to play a
game of “spot the fake steroid” in Mexico or Europe. The underground versions
should cost between $5-7 for 100mgs of methenolone and I wouldn’t really consider
paying more for it.
Here’s how your body metabolizes methenolone:
References:
1. Anabolic steroids (metenolone) improve muscle performance and hemodynamic
characteristics in cardiomyoplasty. Ann Thorac Surg. 1995 Apr;59(4):961-9; discussion
969-70.
2. Effect of an anabolic steroid (Metenolon) on contractile performance of the chronically
stimulated latissimus dorsi in sheep. Eur J Cardiothorac Surg. 1994;8(4):214-9.
3. Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to
the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone
binding globulin. Endocrinology. 1984 Jun;114(6):2100-6.
216
4. [Anabolic therapy in metastatic breast cancer] Med Klin. 1981 Nov 20;76(24):689-91.
German.
5. Partial remission and severe adverse effect caused by metenolone acetate in a male
patient with aplastic anem Eur J Haematol. 1995 Jul;55(1):57-8.
6. Fatal outcome of a patient with severe aplastic anemia after treatment with metenolone
acetate. Ann Hematol. 1993 Jul;67(1):41-3.
7. Metabolic effects of anabolic steroids. Wien Med Wochenschr. 1993;143(14-15):368
75.
8. Biochim Biophys Acta. 1995 May 11;1244(1):117-20.
9. Comparative Studies about the influence of MetenoloneAcetate and Mesterolone on
hypophysis and male gonads. Arzneimittelforshung. 1970 20(4) 545-7
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
217
Proviron
(Mesterolone)
[1 alpha-methyl-17 beta-hydroxy-5 alpha-androstan-3-one]
Molecular Formula: C20H32O2
Molecular Weight: 304.4716
Melting Point: N/A
Manufacturer: Schering
Release Date: 1960
Effective Dose: 25-200mgs/day
Active Life: up to 12 hours
Detection Time: 5-6weeks
Androgenic: Anabolic Ratio:30-40/100-150
Proviron (mesterolone) is basically an orally active DHT (dihydrotestosterone)
preparation. For comparision, we can think of some other orally prepared DHT
compounds like Winstrol, Anavar, etc. Those both act very similarly in mechanism to
Proviron, but a more accurate way to think of this compound is as something like
“Oral Masteron.” As I’m sure you noticed, their anabolic/androgenic ratio is very
similar. Remember, DHT is 3 to 4 times as androgenic as testosterone and is, of
course, incapable of forming estrogen. Also, Proviron is quite unique in that a simple
look at its 4-ring structure will show us that it is not going to be too liver toxic, since
it is not c17-Alpha-Alkylated, as many orals are. This modification (lacking in
Proviron) makes drugs more liver toxic. Proviron has a 1-metyhl group added,
instead--looks pretty great on paper, right? Well, as usual, things tend to look better
on paper than they do in the body. Your body has a negative feedback loop which
prevents it from having too much DHT floating around (if you’ve been paying
attention up to now, you already know this). An excess of DHT will eventually be
changed into another (largely not anabolic) compound.
So let’s go back to the comparison with being some sort of “Oral Masteron.”
Basically Proviron is 5-alpha reduced and not capable of forming estrogen. More
importantly, however, it has a very high affinity for binding to the aromatase enzyme
(the enzyme responsible for converting all that good testosterone in your body into
all that nasty estrogen). That means if you choose to take Proviron with testosterone
(and I know you wouldn’t even be doing a cycle without including some form of
testosterone) and/or any aromatizable steroid, it should actually serve to prevent
estrogen build up by the aforementioned binding to the aromatase enzyme, which
prevents aromatase from doing its dirty work and making a bunch of estrogen out of
the other steroids you are taking. It should also be noted that Proviron also binds
very well to SHBG (sex hormone binding globulin, a hormone responsible for
218
reducing the amount of circulating free testosterone in your body) (1). As a matter
of fact, in the last study I read, it bound to SHBG better than any other drug studied.
Also, I’d like to note that Proviron bound to the anabolic receptor better than any
oral anabolic (except for the insanely toxic methyltrienolone), better than
testosterone, but not as well as Nandrolone (1). Unfortunately, as we know, DHT
also has a high affinity for binding to receptors in the scalp and prostate, causing
some possible nasty side effects, like male pattern baldness and prostate
enlargement. It’s important to remember that DHT and DHT derived compounds are
used quite successfully to treat gynocomastia, and in this area, Proviron is no
different.
Let’s delve into some of the positive points of this drug before we go any farther.
androgen receptors are found in fat cells as well as muscle cells (5), and while they
act on the AR in muscle cells to promote growth, they also act directly on the AR in
fat cells to affect fat burning (9)(3). The stronger the androgen binds to the AR, the
higher the lipolytic (fat burning) effect on adipose (fat) tissue (6)(2). As if that’s not
enough good news, some steroids (notably, testosterone) even increase the numbers
of ARs in muscle and fat (9)(7). Thus, if you are taking a simple stack of proviron
and testosterone, you’ll have more of the Test you shoot as free testosterone floating
around building muscle (compliments of the Proviron) and more androgen receptors
to be bound to (compliments of your testosterone) by your Proviron, thus causing
more fat loss. Testosterone and Proviron is a very nice synergistic stack, pretty
nearly an “ideal” stack of an oral and injectable, because both drugs will actually act
to enhance each other.
So what we have here is a steroid that can basically make other steroids more
effective by preventing their conversion into estrogen, as well as increasing the
amount of circulating free testosterone in your body. This of course all provides a
more hardened and quality look to muscles. Proviron is very much a “synergistic”
drug in this respect, and its inclusion in any cycle would definitely make all of the
other steroids perform better, and provide better gains. This is all compounded by
the fact that Proviron is a very lipolytic (fat-burning) drug.
Now, as if all of this weren’t enough, let’s talk about how Proviron affects your HPTA
(hypothalamic-pituitary-testicular-axis), the thing that regulates the male hormonal
system. When a reasonable dose of this stuff is given (100-150mgs/day), it had no
depressing effect on low or normal serum FSH and LH levels (6). Follicle Stimulating
Hormone (FSH) and Leutenizing Hormone (LH) are two hormones that send a signal
to your testes to produce testosterone. Thus, by not suppressing those hormones,
your normal testosterone levels will remain intact. This points to a novel use for this
compound during post-cycyle-therapy: a non-suppressive “bridge” between cycles.
In fact, in yet another study, administration of Proviron (basically the same dose as
in the last study) produced no changes in steroids, thyroid hormones, gonadotropins
or PRL (prolactin levels—you want those to remain low) (8).
Unfortunately, this stuff is not too hot on it’s own. It’s a good drug for inclusion in a
cycle containing testosterone and other armoatizable steroids, and it’s a good drug
for a possible “bridge” between cycles. Alone, however, as an androgenic or anabolic
agent its effects have been very weak in both studies (9), as well as in the
experience of everyone I spoke to about it. This may be due to the addition of the 1
methyl-group to DHT, which makes this stuff orally active. Whatever the case, as a
stand-alone anabolic or androgenic compound, it’s not too impressive.
219
This drug is a rare find on the black market, and many underground labs do not
produce it, but if you can find it, I’d say that you shouldn’t be paying more than .50
cents for each 50mg tab.
Here’s how your body metabolizes Mesterolone:
References:
1. Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to
the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone
binding globulin.Endocrinology. 1984 Jun;114(6):2100-6.
2. APMIS. 2000 Dec;108(12):838-46.
3. (Xu X, et al. "The effects of androgens on the regulation of lipolysis in adipose
precursor cells." Endocrinology 1990 Feb;126(2):1229 ).
4. J Anim Sci. 1992 Nov;70(11):3381-90.
5. Am J Physiol. 1998 Jun;274(6 Pt 1):C1645-52.
6. The effect of mesterolone on sperm count, on serum follicle stimulating hormone,
luteinizing hormone, plasma testosterone and outcome in idiopathic oligospermic men.Int
J Gynaecol Obstet. 1988 Feb;26(1):121-8.
7. J Appl. Physiol.94 1153-61 2003
8. Effect of non aromatizable androgens on LHRH and TRH responses in primary
testicular failure.Horm Metab Res. 1984 Sep;16(9):492-7.
9. [Androgen substitution in the andrological disease picture] Andrologia. 1983 May
Jun;15(3):283-6. German.
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Winstrol
Stanozolol
[17beta-Hydroxy-17-methyl-5alpha-androstano[3,2-c]pyrazole]
Molecular Formula: C22H36N2O
Molecular Weight: 344.5392
Melting Point:N/A
Manufacturer: (Originally) Sterling
Release Date:1962
Effective Dose(men): 50-100mgs/day
Effective Dose (women): 2.5-10mgs/day
Active Life:8hours
Detection Time:3 weeks (oral) to 9 weeks (injectable)
Anabolic/Androgenic Ratio:320:30
Stanozolol is a very commonly used anabolic steroid for cutting cycles. While many
people will attempt to use Dianabol or even Anadrol for cutting cycles, I’ve really
never heard of anyone using stanozolol for anything except a cutting cycle. It’s a bit
of a one-trick-pony in this respect. Let me repeat that: stanozolol is a cutting drug.
Not many people will argue for its use in a bulking cycle. It’s certainly not a very
effective compound for treating anemia (1) and thus, one could rightly assume that
it’s role in bulking cycles is very limited.
One novel use for Winstrol in any cycle (perhaps even bulking) would be to use it at
a very limited dose, in order to lower SHBG (2). One of the properties of Winstrol is
it’s profound ability to lower SHBG much more than other steroids. A dose of
.2mg/kg lowered SHBG significantly, which would, in turn, raise the amount of free
testosterone circulating in the body. As with 99% of steroids, however, it’s important
to note that suppression of your natural hormonal levels will occur (though perhaps
not to the extent that it will with many other steroids) (10). As with running virtually
any compound, testosterone supplementation (i.e. running Test in a cycle containing
Winstrol) is warranted to avoid possible sexual dysfunction.
Adding it to a heavy bulking cycle could be problematic, as stanozolol is a 17aa
compound, meaning that it’s been altered to endure the first pass through your liver
without being destroyed. This makes it an orally active compound, so many people
choose to take the pills which are available from both legitimate pharmaceutical
companies as well as underground labs. Unfortunately, since it’s 17aa, it is also liver
toxic; in fact, stanozolol has one of the worst hepatoxicity (mg for mg) of any
steroid. This is the reason adding it to a bulking cycle could be problematic;
generally a bulking cycle will be very heavy, dosage wise as well as toxicity-wise. It
also has undesirable results on Cholesterol, and a mere 6mgs/day of stanozolol can
221
lower HDL by 33% and raise LDL by 29% (3). Cardiac Hypertrophy, even at lower
doses could be a concern with Winstrol as well (4), thus many people limit their
intake of stanozolol to precontest or summer-cutting types of cycles. It’s generally
accepted that due to the toxicity issues of stanozolol, its use should be limited to 6
weeks. As with anything though, many people have run it for up to 12 weeks with no
problems. I ran Winstrol for about 3 months (12 weeks) at a dose of 100mgs every
other day (along with Test Prop at 125mgs, every other day) and I suffered no ill
effects. My joints felt fine, and I can say that the only thing that was undesirable
about that cycle was the injection pain. Generally, people report a "dry" and less
lubricated feeling in their joints when on this drug (fluid retention is nil with
stanozolol), and also a "dry" overall look as regards contest prep. This could be due
to a sort of "reverse-osmotic" effect; of course this is speculation, but people do look
"dryer" on Winnie, and some even look dryer in the site they inject (more on this
later). There are many conflicting reports on tendon strength and stanozolol, even in
medical journals. Some reports state that it weakens tendons, others that it
strengthens them (and some speculation on the Internet among many “guru’s” is
that it strengthens them unevenly, leading to possible injury). For this reason, it
may be best for athletes in explosive or high-impact sports to stay away from this
drug. It has certainly been shown to be beneficial in some bone ailments induced by
glucocorticoid induced stress (5). It also has collagen producing properties (11), but
with all of the anecdotal problems athletes repoert suffered with their joints while on
stanozolol, I simply can not recommend it with confidence to strength/speed
athletes. I can say that personally, it was an effective compound for me and did not
cause joint duress, but I can do without the discomfort of the shots, and have found
other DHT based compounds to be far more effective (Masteron springs to mind).
As previously stated, this compound is unique, as it is available in both an oral form
as well as an injectable form. Both forms contain the exact same compound, but
injecting this compound (and yes, you can drink the injectable version, and no you
shouldn’t) is superior to ingesting it orally in terms of nitrogen retention (6), and
thus one would also imagine, for overall anabolism. Injecting it also has the
advantage of avoiding the “first pass” through your liver, and thus places your liver
under less stress.
Stanozolol is also one of the few compounds that women can take safely, as it’s
anabolic: androgenic ratio is quite skewed towards anabolism. It’s generally accepted
that women can tolerate around 5-10mgs a day of this compound. Men, on the other
hand can dose themselves in the .5-1.5mg/kg range. I find 100mgs injected every
other day to be sufficient, but of course, even with the injectable form, every day
dosing is optimal. I tend to favor DHT based compounds, and have enjoyed great
success with a Winstrol/Masteron/testosterone cycle, but I suspect that replacing the
Masteron in that cycle with trenbolone would prove more beneficial for most
bodybuilders seeking to get ripped.
Although the anabolic ratio of this product is very high as compared to its androgenic
actions, not many people report huge weight gains off of stanozolol. Also,
interestingly, it has a relatively weak AR binding ability (7), which is quite unusual
for a “cutting” steroid. Many of the effects of this drug, as relates to building muscle,
are probably from its very high protein synthesizing ability (6)(8). In addition, since
this compound is derived from DHT, it tends to promote a very nice, “quality” look to
the user’s muscles, with little or no water retention. Winstrol does not aromatize at
any rate and has even been speculated to have anti-progestenic properties (in at
least some cases, where it may “block” that receptor) (9). If one were to run
222
ancillary compounds with stanozolol, perhaps tamoxifen would be appropriate for it’s
beneficial effects on blood lipids, but an anti-estrogen (in it’s classic sense) would be
unwarranted; proper post cycle therapy is still needed, though.
Most underground labs produce Winstrol at very reasonable prices, in both an oral as
well as injectable form. Unfortunately, production value differs vastly due to the
varying size of the stanozolol powder used to make the injectable version; the finer
the powder, the smaller gauge needle it will fit through, and the easier the injection
will be. Of course the opposite is also true. In any case, you should be paying under
$100 for a 10ml bottle of 100mg/ml concentration, and roughly the same for 100 or
so 10mg tablets.
Here’s how Stanozolol is metabolized by your body:
References:
1.Trop Doct. 2004 Jul;34(3):149-52.
2. J Clin Endocrinol Metab. 1989 Jun;68(6):1195-200
3. JAMA. 1989 Feb 24;261(8):1165-8.
4. J Steroid Biochem Mol Biol. 2005 Jan;93(1):43-8. Epub 2005 Jan 25.
5. Di Yi Jun Yi Da Xue Xue Bao. 2003 Nov;23(11):1117-20.
6. Can J Vet Res. 2000 Oct;64(4):246-8.
7. Endocrinology. 1984 Jun;114(6):2100-6.
8. J Am Vet Med Assoc. 1997 Sep 15;211(6):719-22
9. Agents Actions. 1994 Mar;41(1-2):37-43.
10. Chemical Muscle Enhancement
11. J Invest Dermatol. 1998 Dec;111(6):1193-7.
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Chapter 10
Ancillary Compounds
This is a category of products pioneered by Dan Duchaine. He first thought of using
Tamoxifen (Nolvadex) to help prevent gyno, and later, the use of Clomid to restore
endogenous testosterone production after a cycle. The story behind the tamoxifen
discovery, in typical Duchaine fashion is that he found a lonely (gay) doctor and a
male bodybuilder who was willing to be examined for prostate and testicular cancer
in return for a ‘script for some Nolvadex. No, I’m not kidding. Anyway, I didn't know
much about anti-estrogens and their ilk before I started researching them a couple
of years ago, and I'll admit another thing: I didn't care. I knew that 10mgs of
Nolvadex per day was all I ever needed to not get gyno, though 150 mgs/day of
Clomid seemed to work the same for me. Cytadren (remember that stuff?) worked
for me also, at 250mgs/day, but it seemed to make me more prone to joint pain and
problems. HCG worked best for me when I shot 500i.u. every other day post cycle
for about 3 weeks. Arimidex was too expensive. AND THAT'S ALL I NEEDED TO
KNOW!
Now nobody uses Cytadren anymore. We have affordable Arimidex (anastrozole) in
liquid form. We have Letrozole. People were using Cialis to maintain sexual ability
after cycles, and there was this stuff called “Kynoselen” that became very popular for
athletes looking to maintain a little extra edge during their off-time. Finally, some
people were even injecting something called “Adequan” to help their joints out on a
cycle. The whole category of ancillary compounds has been expanded to include not
only anti-estrogens but other similarly useful compounds, like EPO and others, all of
which provide us with more options to achieve our goals, without necessarily taking
more steroids.
But I had a lot of work to do to catch up….
In the long run, I wasn't that interested in what all this other stuff did because I
already knew what worked for me. Well, keep reading and you'll find out why I was
wrong, what my new plan is for during a cycle and post-cycle recovery and some
other interesting stuff about not getting any side effects from ‘roids. I was, of
course, wrong in my initial estimation of this class of drugs.
So, first things first. Some steroids convert to estrogen. As you know, this is through
the aromatase enzyme, and the process is called (duh) aromatization. When this
happens you can get side effects associated with having too much estrogen,
including bloating, gynocomastia, acne, and so on. Some steroids on the other hand,
have progesteronic activity (Deca, for example actually fits into the progesterone
receptor with 20% the efficiency of actual progesterone!) (1). The symptoms (acne,
etc...) are the more or less the same for progesteronic and estrogenic effects. Note
that I didn't say that these other steroids convert to progesterone, but rather that
they have progesteronic effects. That's because the steroid is able to act on the
progesterone receptor without conversion to another substance. Hence, on my old
bulking cycle of 600mgs per week of Deca and 750mgs per week of Test, anti
estrogens would only help with the aromatization of the test and not the
224
progesteronic activity of the Deca, which would amplify the estrogen’s effects!.
Know what else? Here are a bunch of other compounds that don't aromatize
significantly (that’s good news), and hence don't need any amount of anti-estrogens:
methenolone, stanozolol, dromostanolone, oxandrolone, mesterolone, stenbolone,
and trenbolone (though it acts on the progesterone receptor with 60% the efficiency
of progesterone itself, according to the last study I cited). Taking a big dose of any
of these? Anti -estrogens might not help much if at all, per se, but keeping estrogen
levels low is still a good idea. Remember, estrogen still has a role to play, in ways we
don't fully understand yet, and progesterone will only amplify those effects. Not only
that, if you take progesteronic gear and use Nolvadex, you may be at an increased
risk for progesteronic sides, as Nolvadex may increase progesterone receptors (2).
What can you do?
Well, the easy answer is to take bromocriptine (Parlodel) at 2.5 to 5mg every day.
Bromocriptine is one of those drugs that the life-extension crowd was very big on a
few years ago. It is an anti-parkinsons medication that causes higher levels of the
neurotransmitter dopamine, with side effects being an increased sex drive, possible
curbing of appetite, possible stimulation of CNS, and fat loss. It's also indicated for
some forms of male hypogonadism (yeah, so it may increase Test levels on its
own!). However, what we're interested in here is that it can be used to lower
prolactin and progesterone, as can Cabergoline (if you can find it). Anyway, back to
Bromo...it sounds almost perfect, right? Well, unfortunately, bromocriptine is also
used to treat acromegaly (too much GH produced by the pituitary), and ergo may
lower GH levels in your body if they are too high! Fortunately, the dosage needed to
halt overproduction of GH in your body is 10-20mgs/day, so we're safe with our
amount necessary to stop from growing breasts from too much Deca, and yes, all
the cool fat burning, sex drive, and nootropic "side effects" happen at 2.5-5mgs/ day
doses. Another effective method for avoid certain sides from progesteronic drugs
(like Tren, for example) is taking 25mcg of T3 or maybe 50-100mcgs of T4. And
yeah, I have the research to back that statement up, but it involves another page of
reading about TRH, TSH, the negative feedback loop involved with low levels of T4
stimulating TRH, blah blah blah. Trust me, you don't care about the reasons why this
works, just that it does. If you're doing Tren, take some T3 and you'll get increased
fat-burning, no gyno, and more maybe even anabolism. So if I were cutting up,
Tren, T3 (25mcgs), and Bromo would all be part of my stack, and I'd expect to get
really cut really fast (of course, there's other cool drugs I'd add into that mix: Clen,
Test, etc, but this is about ancillaries, not a cutting cycle).
Another idea to reduce progesterone is to take RU486 (yeah, the pregnancy drug).
This drug has anti-progesteronic effects, and in women 600mgs totally blocks
progesterone. Don't even think about taking this dose, however. I'd recommend
taking around 50 mgs a day and working your way up. Remember, cortisol is also
decreased with RU486, so sore joints may be a problem. Considering this, Bromo's
cool secondary effects, and price, I'd consider bromocriptine a better choice.
So what ster
oids do aro
matiz
e? Here some off
ender
s: test
oste
rone,
methandrostenolone, fluoxymesterone, (only in high enough doses). I'm sure you
see a pattern and you get the idea. And Deca, even it aromatizes, besides its being a
progestin, though not much.
You still with me?
225
Okay, so what are some drugs that inhibit aromatization? Cytadren
(aminoglutethimide), at 250-500mgs per day will do the trick, as will Arimidex at .5
1mg per day (more about Arimidex later, and remember, this is all dependant on
what doses of aromatizing drugs you're taking). Cytadren also limits the conversion
of Test to DHT, which may help eliminate any hair loss during a cycle, but may
reduce its effectiveness also. Finasteride (Propecia = 1mg tabs, Proscar = 5mg tabs)
has similar effects with regards to halting some of DHT's negative effects. Cytadren
may also (very) slightly inhibit Test production, so that kinda turns me off to it
especially when other drugs actually increase Test production and will prevent side
effects more effectively. Unfortunately, Cytadren has a really short ½ life, and it
ideally should be taken 2-3x a day. That plus its cortisol inhibiting effects (and the
sore joints you get from that) don't make it really ideal for me. On the bright side,
Cytadren may (theoretically) improve blood lipid profiles. Finasteride, can be
compared with Cytadren, as it also has the added benefit of eliminating some 5-AR
(5-Alpha Reductase), which can cause both male pattern baldness as well as acne.
Reducing 5-AR will reverse 5-AR inspired hypertrophy of the sebaceous glands and
cause a reduction in acne (3), as well as help with hair loss caused by the conversion
(via 5-AR) of testosterone to DHT (4). I would never take this stuff without another
ancillary, as it can also (rarely) cause gyno.
What else can we do to avoid side effects? Well, we can block the receptors that the
estrogen attaches itself to, thus causing the side effects. Clomid (clomiphene citrate)
and Nolvadex (tamoxifen) will do this. As these drugs are selective in their activity,
they are estrogenic to certain receptors (blood lipid profiles are favorably enhanced
by the estrogenic action of these drugs), and antiestrogenic to others (they are anti
estrogenic in terms of their action on breast tissue, for example; yes I know that
Nolvadex is actually a weak estrogen that blocks out the competing stronger
estrogens with regards to attaching to the receptors in breast tissue—I’m trying to
keep things relatively simple, though). Generally Nolvadex is cheaper than Clomid,
and thus more often used. Personally, I've found Clomid attenuates testicular
atrophy during a cycle to a greater degree. So besides competing with estrogen at
the receptor, these drugs both increase serum test levels, and both drugs may also
alter blood lipid profiles. With regards to Clomid and Nolvadex, I’ve found that
20mgs of tamoxifen is equal to 150mgs of Clomid for purposes of testosterone
elevation, FSH and LH, but tamoxifen did not decrease the LH response to LHRH (5).
Thus, I'd recommend Nolvadex over Clomid for most purposes.
As Nolvadex isn't actually an anti-aromatase, but rather a competitor for the
receptor site, and seeing as it increases test levels so much, I'd say that it's actually
a better post-cycle drug than Clomid (which wreaks havoc on my eyesight, due to its
occular toxicity; Nolvadex has some of that property, but in my experience doesn't
mess with my eyesight as much). At least I know that it's what I'll be using post
cycle, even despite its effects on IGF-1. It's important to remember that IGF levels
play an important role in breast cancer (which is what many of our ancillary drugs
were developed for), so many of them will decrease IGF levels, as that could be
desirable for breast cancer survival.
Cyclofenil (remember that drug?) will do just about everything with regards to
halting estrogen's binding to receptors that the other two drugs I just discussed will
do, but helps LH production to a greater degree. Lowering your LH (in addition to
having an adverse effect on the general recovery of your entire hormonal system)
will also contribute to estrogenic-type effects. Raising LH = Good. Lowering LH =
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Bad. Most people take a tab or 2 per day of this stuff, in any case. There's better
stuff on the market, though.
How about Aromasin? Well, it’s totally different than everything else we've looked at
so far. Aromasin (exemestane) it is an aromatase inactivator; it actually makes
estrogen receptors useless. Instead of just inhibiting production (as an anti
aromatase would do) it cuts off production totally. Aromasin can also cause
androgenic sides (8)(9)(10). Aromasin can effectively prevent about 90-95% of
estrogen conversion. Oddly, this compound can actually increase IGF levels (14).
Worth noting is that Aromasin may possibly be less harsh on blood lipids, having no
effect in one study (11) that I looked at. No effect is still not as good as Nolvadex, on
the other hand, which may actually improve HDL & LDL in some cases (12), and
which I’ve also found to help my immune system. Aromasin has also been shown to
have an undesirable effect on blood lipids in some cases…many of these compounds
are simply inconsistent on blood lipid profiles, when comparing different studies.
We’ll discuss the implications of all of these ancillary compounds in just a bit, and
figure out where these pieces fit into our puzzle of creating a perfect cycle and post
cycle regimen. Just bear with me.
I think, at this point I’ll differentiate between the two types of aromatase inhibitors:
or AIs are classified into two types—type I, suicidal or noncompetitive inhibitors, and
and type II—known as competitive inhibitors (16)(17). We just looked at one of the
Type I’s (exemestane). Basically, to further explain, Type I inhibitors are steroidal
compounds, and type II inhibitors totally nonsteroidal drugs. This explains the
possible androgenic side effects found with exemestane and (as you’ll see) the lack
of them with Letrozole and Arimidex. Both type I & II mimic normal substrates
(essentially androgens), competing with the particular substrate for access to the
binding site on the actual enzyme. After this initial binding, the next step is where
things differ for the two types of AI’s. Once a noncompetitive inhibitor has bound, the
enzyme initiates a sequence of hydroxylation, but in this case, hydroxylation
produces an unbreakable covalent bond between the inhibitor and the enzyme
protein. This is important because now, enzyme activity is permanently blocked;
even if all unattached inhibitor is removed. Enzyme activity can now only be restored
by new enzyme synthesis. Nice, huh? Now, on the other hand, competitive inhibitors,
called type II AI’s, reversibly bind to the active enzyme site, and either no enzyme
activity is triggered, or the enzyme is somehow triggered without effect. The type II
inhibitor can actually disassociate from the binding site, eventually allowing renewed
competition between the inhibitor and the substrate for binding to the site. Clearly,
this indicates that the effectiveness of competitive aromatase inhibitors depends on
the relative concentrations and affinities of both the inhibitor and the substrate. We
can safely, therefore, conclude that continued aromatase inhibitory activity requires
constant presence of the type II inhibitor.
Let’s talk about Arimidex (anastrozole), now, which is a type-II AI. From the
research I've done, this seems to be one of the best ancillaries around and I'll tell
you why. First off, 'dex is an aromatase inhibitor (an AI—remember what that is?).
1mg per day of this stuff (9) was shown to decrease estrogen by 50% and increase
testosterone levels by 58%. LH and FSH also went up slightly. Anastrozole also
raises IGF1 and shows a trend towards increasing IGF2 (13). By the way, literature
provided by the original maker of Arimidex states that stable blood plasma
concentrations of the compound are achieved after 7 consecutive 1mg daily doses.
All of that plus the usual blood lipid changes we've seen with most of the ancillaries
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we've looked at! Anyway, that's a pretty hefty decrease in estrogen, even at
.5mg/day.
Now onto Femara (AKA Letrozole, another type II AI), which is more effective than
Arimidex in its ability to pass thru the cell membrane of lipid (fat) cells and inhibit
the activity of aromatase—Arimidex is over 80% effective at inhibiting estrogen (18);
Femara is much closer to 95-97% (19). Levels of estrogen are totally undetectable in
most patients taking Letrozole, and it has even been used to increase testosterone to
normal levels (from sub-normal ones) and increase LH, FSH and SHBG (6). Other
than that, both of these drugs stop the process of aromatization, rather than just
blocking (competing for, if you prefer) the receptors as Clomid and Nolvadex do. An
effective dose of Letrozole is .25-2.5 mg/day (I use .25mgs/day), but be forewarned,
it can kill your sex drive, and could decrease IGF levels. On the other hand, I've seen
studies where it increases IGF levels. Also worth noting is that there's a rebound
effect when you come off Letrozole. Its effects on serum lipids (cholesterol, both HDL
and LDL) are, in the words of one study I read: "inconsistent.” Compared with
Aromasin and Arimidex, in non-cellular systems, Letrozole is 2-5 times more potent
than anastrozole and exemestane in its inhibition of the aromatase enzyme and its
activity, and in cellular systems it is 10-20x more potent! Letrozole (2.5mg daily)
also achieved a much greater suppression of the plasma concentrations of both
estrone and estrone sulphate (estrogens) than anastrozole (1mg daily), and a
greater inhibition of in vivo aromatization (sorry for the geek-speak—it’s over for
now.) (7). I've used Letrozole, and it cleared up my minor gyno lumps to the point
that they are totally gone now, but prolonged use lowered my immune system too
much (due to a lack of estrogen).
Interestingly, it would seem that .5mgs-10mgs of Arimidex is nearly the same thing
(effects-wise), as is .5mgs-2.5mgs of Letrozole (15). This tells me that we can save
some money on them and just take minimal doses, around .5mgs of either.
For my money, if I wanna stop aromatization during a cycle, I’ll typically use
Arimidex or Letrozole at 5mg/day. Arimidex is a nicer choice for long cycles, since it
seems to not cause problems with cholesterol like Letrozole can. They are perfect
during-cycle ancillaries. Incidentally, you need to take anastrozole for a week to get
a steady level of it in your blood (same thing goes for exemestane), whereas you
need to take Letrozole for 60 days to get a steady blood plasma level. Though
anastrozole has a ½ life of 41-48 hours, and exemestane has a ½ life of 27 hours,
Letrozole has a whopping 2-4 day (!) ½ life (8). Thankfully you can take Arimidex or
Letrozole and they’ll reach maximum inhibitory effects on estrogen within 2-4 days
after taking the first dose (15).
Finally, what about using HCG (human chorionic gonadotropin)? For starters, it
increases (stimulates) endogenous (natural) testosterone production by mimicking
LH, which stimulates the Leydigs cells to produce testosterone. It's ideal for post
cycle, when you want to raise testosterone levels by as many mechanisms as
possible, and while you are also taking other drugs to fight estrogen. I've found
personally that 500i.u. every other day or even every day, post-cycle works best for
me. Incidentally, this is the PDR (and Dan Duchaine's) recommendation. In one
study I looked at, 6000IU of HCG elevated Test levels for 6 days. That's why a lot of
people recommend taking it every 3-5 days. We’d have more stable blood levels,
though, if we shot it more frequently. Remember, its non-estrified and a water-based
injectable, after all. In that same study I read, 1500iu of HCG shot test levels up
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between 250 and 300%. Again, though, I'd be more comfortable with the more
stable and slow increase. Also, keep in mind that HCG can suppress FSH and LH
production and has been anecdotally linked to gyno. Thus, it (in combination with
Nolvadex) is ideal for post cycle recovery when gyno is not as much of an issue (due
to the Nolvadex and the cessation of other compounds), but restoring natural Test
levels is. Also, if you are interested in getting a greater testosterone response out of
the HCG you use, I’d recommend taking it vitamin E (no, I’m not joking). Current
research indicates that responsiveness of plasma testosterone levels to HCG is
significantly higher during vitamin E administration than without supplemental
vitamin E (24). My advice? You should be taking at least 400iu of vitamin E year
round, but on the weeks you take HCG (and during PCT) you should bump that dose
to 1000iu. Your testosterone levels will thank you.
So let's review:
During a cycle (because I ALWAYS use Test in my cycles), I think it's a good idea to
use Arimidex at .5mgs per day, or Letrozole at .25-.5mgs/day to take care of
aromatization, thus preventing side effects related to estrogen. If I'm using gear that
has progesteronic side effects, I'm gonna avoid Nolvadex, and I'm gonna have to
throw in some bromocriptine at 2.5-5mgs every day, especially when I'm using lots
of Tren (and perhaps trying to get cut), because I'd want those added "side effects"
we already discussed from the Bromo. I'd thrown in that T3 as well. I may (possibly)
use a small dose of HCG during a cycle too, perhaps at 500iu every other week, just
to try to avoid a little of the inhibition, and maybe make recovery easier.
Now, it becomes really interesting when we try to connect the dots and figure out
how to actually combine these compounds for PCT.
When I'm all done with the cycle, can’t I just use Arimidex at .5-1mg/day (or Letro),
and Nolvadex (at 10-20mgs/day for a month)? Maybe I can just throw in some HCG?
Well, actually, if I use HCG for post cycle, it may slightly inhibit recovery by
desensitizing your HPTA response to certain hormones. In addition, if I use Nolvadex
with Arimidex or Letrozole, the Nolvadex will actually greatly decrease their blood
plasma levels (20)!
Ok, so once I started trying to connect these dots, I had a major problem to solve.
Most of the PCT drugs available to us have interactions with others, which could
render them less useful. This was odd, because my old HCG/Nolvadex protocol
seemed to work for me. What I found when I researched this combination is that It
can be argued that HCG's suppressive effect on endogenous testosterone is (mostly?
totally?) due to to HCG actually blocking the conversion of 17 alpha
hydroxyprogesterone (17 OHP) into testosterone. Nolvadex stops this blocking-action
of HCG from taking place (22). In fact, any suppression of gonadotropins via HCG is
almost totally stopped with concurrent administration of Nolvadex (23)! Ok, so we
can take my old standard (circa 2000-01) PCT, but can we add to it? We know that
the Nolvadex doesn’t work well with Arimidex and Letrozole, as it lowers their blood
plasma levels, and type I aromatase inhibitors are reversible and require constant
blood plasma levels to maintain their effect. I think you know where I’m going with
this: I asked myself, is it possible that we could use a type II AI (exemestane)?
Well, as you already know, although type II AI’s like Letro and Arimidex need to be
present in the blood to maintain their inhibitory effects on the aromatase enzyme,
with a type I AI (like exemestane) enzyme activity is permanently blocked, meaning
229
even if all unattached inhibitor is removed, enzyme activity can only be restored by
new enzyme synthesis. Hence, even if Nolvadex lowered the blood plasma levels of
exemestane, it’ll have done its job on the aromatase enzyme, and lowered estrogen
levels already. Remember, estrogen has an inhibitory effect on your natural
testosterone levels, and it’s thought that aromatization is a large part of HPTA
inhibition and its negative feedback loop. Does the research support Nolvadex and
exemestane combination? Yes! Using those two together doesn’t reduce
exemestane’s effectiveness (21)! And, the androgenic effects of this particular AI will
be appreciated after a cycle to increase aggression when exogenous hormone levels
are suddenly removed. Also, it won’t have any deleterious effects on your joints or
bones, which Letrozole and Arimidex have the potential to engender (25).
So that’s it—we use Exemestane/HCG/Nolvadex for PCT, and .5mgs of Arimidex or
Letrozole during a cycle! It was quick, it was a little dirty, and it was straight to the
point. I’m hoping you continue on to read the profiles on the following pages, but if
you don’t at least you have a cursory knowledge of most of them after reading this.
Before I leave you, I’ll give you a chart of how I run my own Post-Cycle-Therapy,
and how I feel it should be run, according to my research:
Week Nolvadex Exemestane HCG
1 20mgs/day 20mgs/day 500iu/day
2 20mgs/day 20mgs/day 500iu/day
3 20mgs/day 20mgs/day 500iu/day
4 20mgs/day 20mgs/day
References:
1. Cancer Res 1978 Nov;38(11 Pt 2):4186-98
2. Gynecol Oncol. 1999 Mar;72(3):331-6
3. Skin Pharmacol. 1997;10(5-6):288-97
4. Expert Opin Pharmacother. 2004 Apr;5(4):933-40
5. Fertil Steril. 1978 Mar;29(3):320-7
6. Epilepsy Behav. 2004 Apr;5(2):260-3
7. J Steroid Biochem Mol Biol. 2003 Oct;87(1):35-45
8. Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.
9. J Clin Endocrinol Metab 2000 Jul;85(7):2370-7
10. J Steroid Biochem Mol Biol 1997 Nov-Dec;63(4-6):261-7
11. J Clin Endocrinol Metab. 2003 Dec;88(12):5951-6.
12. Br J Cancer. 2004 Aug 2;91(3):476-81.
13. J Steroid Biochem Mol Biol. 2002 Apr;80(4-5):411-8
14. Anticancer Res. 2003 Jul-Aug;23(4):3485-91
15. Pharmacology and Pharmacokinetics of the Newer Generation Aromatase Inhibitors.
Buzdar.
16. Buzdar A., Howell A. Advances in aromatase inhibition: clinical efficacy and
tolerability in the treatment of breast cancer. Clin. Cancer Res., 7: 2620-2635, 2001.
17. Goss P. E., Strasser K. Aromatase inhibitors in the treatment and prevention of breast
cancer. J. Clin. Oncol., 19: 881-894, 2001.
230
18. Geisler J., King N., Dowsett M., Ottestad L., Lundgren S., Walton P., Kormeset P.
O., Lonning P. E. Influence of anastrozole (Arimidex), a selective, non-steroidal
aromatase inhibitor, on in vivo aromatisation and plasma oestrogen levels in
postmenopausal women with breast cancer. Br. J. Cancer, 74: 1286-1291, 1996.
19. Geisler J., Anker G., Dowsett M., Lonning P. E. Letrozole suppresses plasma
estrogen levels in postmenopausal breast cancer patients more completely than
anastrozole. Proc. Am. Soc. Clin. Oncol., 19: 102a 2000.
20. J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):85-91.
21. Inhibitory effect of combined treatment with the aromatase inhibitor exemestane and
tamoxifen on DMBA-induced mammary tumors in rats.
J Steroid Biochem Mol Biol. 1993 Mar;44(4-6):677-80.
22. Andrologia 1991 Mar-Apr;23(2):109-14
23. J Clin Endocrinol Metab 1980 Nov;51(5):1026-9
24. Effect of vitamin E on function of pituitary-gonadal axis in male rats and human
subjects. Umeda F, Kato K, Muta K, Ibayashi H.
25. Clinical Cancer Research Vol. 10, 372S-379S, January 2004
231
Arimidex
(Anastrozole)
Arimidex is what we call an aromatase inhibitor (AI). In medicine it’s used to halt
the progression of breast cancer in women. It works by blocking the aromatase
enzyme, which is responsible for the production of estrogen. In athletics and
bodybuilding, it is used as an ancillary compound to be added to a cycle of anabolic
steroids. In this respect it is also used for its estrogen reducing properties, but it has
the additional benefit of increasing teststerone levels, as we'll see.
Many anabolic steroids aromatize (convert to estrogen via the aromatase enzyme),
and this is responsible for many of the unwanted side effects found with anabolic
steroid use (acne, gynocomastia, water-retention, etc.). In one study, both .5mg and
1mg doses of Arimidex were shown to decrease estrogen by roughly 50%. The
1mg/day dose also increased testosterone levels by 58% (1). In that same study, in
both groups, LH and FSH also went up slightly. Take a look:
Changes in testosterone and E2 concentrations in normal young men (15–22 yr old)
before (filled bars) and after 10 days of oral anastrozole at 0.5 and 1 mg (1).
This would seem to suggest that for use during a cycle, a dose of .5mgs/day would
be sufficient to combat estrogen-related side effects. It is, however, important to
remember that some estrogen is necessary to obtain optimal muscle growth. The
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lower estrogen levels provided by 'dex seems, anecdotally at least, to produce a
more "hard" and "quality" look for bodybuilders who have experimented with it's use
in either a cutting or bulking cycle.
I’d like to point out that the elevation in testosterone provided by Arimidex is so
large that it can be used as a “form” of testosterone replacement therapy for
hypogonadal men (2). Clearly, this suggests its use in a post-cycle-therapy (as well
as its previously discussed use within a cycle) to regain natural testosterone levels
and full HPTA (Hypothalamic-Testicular-Pituitary-Axis) function.
Literature provided by the original maker of anastrozole (Arimidex, produced by
Zeneca Pharmaceuticals) states that stable blood plasma concentrations of the
compound are achieved after a mere 7 consecutive 1mg daily doses. Also, Arimidex
is just over 80% effective at inhibiting aromatase (3). Thus, if you want to take it for
the entire duration of a cycle of anabolic steroids, you can simply start taking it on
the same day you begin your cycle. Those are some pretty good numbers, huh?
But can you use it for the entire duration of a cycle? Is it dangerous? Well, certainly
reducing estrogen levels in your body is good from a body building point of view as it
reduces water-retention and the potential for gynocomastia (if there’s no estrogen in
your body, you can’t get gyno, regardless of how much progesterone is floating
around) (5). Luckily this stuff is very mild on blood lipids (cholesterol) and doesn’t
affect them adversely (2), at least in the studies I’ve seen. As previously mentioned,
those lowered estrogen levels could possibly (eventually) adversely affect your
cholesterol and possibly even your immune function. I am, however, very
comfortable recommending Arimidex for relatively long-term use. This should be the
ancillary compound of choice for those on long and heavy cycles, especially since it
also doesn’t inhibit IGF (insulin-like-growth-factor, an important component of
anabolism) like some other ancillary compounds (4).
Although prices will vary, this is one of the compounds I will caution the reader from
buying in its legitimate pharmaceutical form. The price (up to $5/tab) is absurd when
considering its availability from underground labs, as well as in the form used for
medical research, at less than 1/3rd of that. I’ve used both the tabs from an
underground lab, as well as the liquid version from research-sites, and found the
results from both to be exactly the same.
References:
1. J Clin Endocrinol Metab 2000 Jul;85(7):2370-7, "Estrogen Suppression in Males"
2. Clin Endocrinol (Oxf). 2005 Feb;62(2):228-35.
3. Arimidex package insert
4. J Steroid Biochem Mol Biol. 2002 Apr;80(4-5):411-8.
5. Progesterone is not essential to the differentiative potential of mammary epithelium in
the male mouse. Freeman, Topper. Endocrinology. 1978 Jul;103(1):186-92
233
Aromasin
(Exemestane)
Aromasin (Exemestane)is a steroidal suicide aromatase inhibitor, which means that it
lowers estrogen production in the body by blocking the aromatase enzyme, the
enzyme responsible for estrogen synthesization (1)(2)(3).
This stuff was developed to fight breast cancer in post-menopausal women, who
need a particularly aggressive therapy, and for whom first line defenses such as
SERMS (Selective Estrogen Receptor Modulators, like tamoxifan) have not worked.
This should be our first clue in inferring that this stuff is pretty strong, or at least
stronger than some of the other compounds which are used to fight breast cancer.
Aromasin averages an 85% rate of estrogen suppression (4), so it’s clearly a very
effective agent for bodybuilders and other athletes wanting to avoid estrogen related
side effects such as gyno, acne, or water-retention brought on by aromatizing
steroids. Specifically, exemestane dose this by selectively inhibiting aromatase
activity in a time-dependent and irreversible manner (hence the “suicidal” portion of
its name, I guess) (7).
As with most of the compounds in this class, it also causes a reasonable rise in
testosterone levels (6), and as you may have guessed, this rise in testosterone
means that exemestane can also cause androgenic sides (8)(9)(10). As you can see
from the chart below, exemestane is very effective at both lowering estrogen
(estradiol) and raising testosterone:
234
Estrogen and androgen plasma levels after 10 d of daily exemestane (25 or 50 mg)
in healthy young males (mean ± SD; n = 9–11). To convert to Systeme
International units: estradiol, picomoles per liter (x3.671); estrone, picomoles per
liter (x3.699); androstenedione, nanomoles per liter (*0.003492); and testosterone,
nanomoles per liter (x0.03467) (13).
So we can see from that chart that 25mgs is a very effective dose, right? As an
added benefit, exemestane not only increases testosterone and lowers estrogen but
it also increases IGF levels (11). Additionally worthy note is that Aromasin may
possibly be less harsh on blood lipids (14) than some of the other (similar)
compounds we use (other AIs) in the world of bodybuilding or athletics. It also has,
at best, no effect on IGF, and, at worst, lowers (13) it. AIs are very tricky with
regards to inconsistencies in IGF levels. Unfortunately, you need to take exemestane
for a week to reach steady blood plasma levels, and exemestane has a ½ life of 27
hours (12.).
The ability of exemestane to lower estrogen levels by the aforementioned 85%
makes it a very nice choice for use in any cycle where aromatizing steroids are used.
In addition, since it’s not too harsh at all on blood lipid profiles, it’s a very good
choice for longer cycles. Its ability to raise both testosterone levels also seem to
suggest that it would be a very nice addition to a post cycle therapy (PCT).
Also, as previously mentioned, exemestane is the only currently available aromatase
inhibitor that can be run concurrently (and effectively) with Nolvadex (which usually
lowers blood plasma levels of AIs), making it perfect for PCT:
235
References:
1. A predictive model for exemestane pharmacokinetics/pharmacodynamics
incorporating the effect of food and formulation.Br J Clin Pharmacol. 2005
Mar;59(3):355-64.
2. Exemestane for breast cancer prevention: a feasible strategy?Clin Cancer Res. 2005
Jan 15;11(2 Pt 2):918s-24s.
3. Endocrinology and hormone therapy in breast cancer: Aromatase inhibitors versus
antioestrogens, Anthony Howell1 and Mitch Dowsett2 1CRUK Department of Medical
Oncology, University of Manchester, Christie Hospital, Manchester, UK 2Academic
Department of Biochemistry, Royal Marsden Hospital, London, UK Breast Cancer Res
2004, 6:269-274 doi:10.1186/bcr945 Published 6 October 2004
4. Eur. J. Cancer. 2000, May;36(8):976-82
5. Breast Cancer Res Treat. 1995;36(3):287-97.
6. J Clin Endocrinol Metab. 2003 Dec;88(12):5951-6.
7. Nippon Yakurigaku Zasshi. 2003 Oct;122(4):345-54.
8. Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.
9. J Clin Endocrinol Metab 2000 Jul;85(7):2370-7
10. J Steroid Biochem Mol Biol 1997 Nov-Dec;63(4-6):261-7
236
Clomid
(Clomiphine
Citrate)
Clomid is a drug given to women for use as a fertility aid. It is a SERM (Selective
Estrogen Receptor Modulator) which acts by actually binding to the estrogen receptor
and thereby blocking estrogen from doing the same. Clearly, this is advantageous
when it binds to breast tissue, and prevents estrogen from binding there to cause
gynocomastia (although it is not nearly as effective as Nolvadex for this purpose). It
also opposes the negative feedback loop that the body has with regards to estrogen
and the HPTA (hypothalamic-pituitary-testicular-axis), and this in turn stimulates LH
(leutenizing hormone) and FSH (follicle stimulating hormone). LH and FSH, in turn
stimulate the release of testosterone. Clearly this is advantageous to bodybuilders
and athletes coming off of a cycle, and beginning their post cycle therapy. What we
have in Clomid is essentially a drug that acts as a preventative measure against
gynocomastia, as well as a drug that acts to raise endogenous (natural) testosterone
levels. Usually, it is compared with another SERM, Nolvadex, for those reasons.
Clomid, however, is much weaker than Nolvadex in a mg for mg comparison, with
roughly 150mgs of Clomid being equal to 20mgs of Nolvadex (1). It should be
noted, however, that 150mgs of clomid will still raise testosterone levels to
approximately 150% of baseline value (1). You don’t have to use 150mgs, however;
my research shows that doses as low as 50mgs will show improvements and
elevations in testosterone levels (4). In fact, my original post cycle therapy regime
(as suggested by Dan Duchaine in the original Underground Steroid Handbook) was
100mgs per day for a week and 50mgs/day for a week. Don’t laugh…for the late
90’s, when most anabolic steroid users didn’t even know how to use Clomid, it was
considered a “state of the art” PCT. I suspect that Duchaine originally introduced
this compound to the steroid using community.
Clomid, just like Nolvadex, is very safe for long term treatment of lowered
testosterone levels (2), with some studies showing its safety and efficacy for up to
four months. And post cycle, when steroid users are suffering form lowered
testosterone levels, Clomid is most effective.
I used to run Clomid for about 3 weeks post cycle, at 100-150mgs. Any more than
that, and I experience emotional side effects (no, really) due to the excess amount
of circulating estrogen I have in my body. All of that extra estrogen tends to make
me moody, and it gets hard to squeeze workouts and cardio in-between reruns of
Sex and the City (ok, I’m exaggerating).
A problem arose during a very aggressive Clomid PCT routine once. I was taking
pretty high doses (150mgs/day) of clomid for an extended time (over a month) and
was having vision issues. When I looked into the subject more closely, this was a
common occurrence with Steroid.com members. Upon further investigation, I found
out the optic neuropathy (a fancy way of saying “vision problems”) was actually very
common with Clomid use (5)(6). Since I already wear contact lenses, I’ve had to
remove Clomid from my PCT routine.
Clomid has fallen out of favor as late for post cycle routines, but if you aren’t prone
to vision problems or emotional issues, then it is just as good as Nolvadex for raising
testosterone when appropriate doses are used. I recommend 150mgs/day for ten
237
days, and decreasing the dose by 50mgs every ten days until you’re finished at day
30. Many of the bodybuilders and athletes I've spoken to have used it in a similar
fashion and found that it restores their testosterone levels to normal.
This drug is widely available from many research supply companies, generally in
liquid form, as well as from most underground labs who produce their own version in
capsules. In either case, you shouldn't be paying more than $1 per 50-100mgs
(generally this is 2 caps or 1-2mls of the liquid stuff).
References:
1. Fertil Steril. 1978 Mar;29(3):320-7.
2. Int J Impot Res. 2003 Jun;15(3):156-65.
3. Understanding sex biases in immunity: effects of estrogen on the differentiation and
function of antigen-presenting cells. Immunol Res. 2005;31(2):91-106.
4. The effects of normal aging on the response of the pituitary-gonadal axis to chronic
clomiphene administration in men. J Androl 1991 Jul-Aug;12(4):258-63
5. Optic neuropathy associated with clomiphene citrate therapy. Fertil Steril. 1994
Feb;61(2):390-1
6. Visual disturbance secondary to clomiphene citrate. Arch Ophthalmol. 1995
Apr;113(4):482-4
238
Cialis
(Tadalafil Citrate)
Cialis (tadalifil) is the second-generation Viagra, more or less. While the little blue
pill may work to give you an erection for 6-8 hours, Cialis is good for 36-48 hours.
This obviously makes it much more practical. Why are we talking about this? I
doubt anyone using endogenous testosterone would need to consider the use of such
a compound, but this drug can still have some uses during post cycle therapy. A lot
of men find that once they go off steroids and begin post cycle therapy (PCT), they
suffer reduced libido as well as erectile dysfunction. Cialis may be useful for helping
this, at least during PCT.
The efficacy and safety of tadalafil for the treatment of erectile dysfunction was
assessed in a 6-month study. Men with mild, moderate or severe ED were given
tadalafil (20 mg) as needed or placebo (“any minute now, baby, no, really”).
Tadalafil significantly improved erectile function compared with placebo (which only
succeeded in embarrassing the men who took it and tried to get laid). At the end of
the study, sexual intercourse attempts success rate for those using Cialis was 73.5%
(this only refers to the ability to achieve erection and have intercourse, not the
actual success rate of those attempting to get laid on a given night) (1).
Of particular interest to those considering the use of Cialis is that lack of sexual
activity due to erectile dysfunction actually decreases testosterone levels through a
central effect on the hypothalamic-pituitary axis (2). Cialis was given to men for a
month, and at the end, they had considerably higher testosterone levels, because
they got laid more (2). It is unlikely that the drug has a different direct effect on the
pituitary-testis axis.
This stuff is actually very safe, and was even given 3x a week to men (1) for an
extended length of time, was well tolerated, had very few sides, and was very
effective (1). Thus, it could be another potential compound for inclusion in PCT.
Tadalafil (20 mg) significantly improves erectile function, could increase
testosterone, and is well tolerated (3)—certainly something to think about after your
next cycle.
References:
1. A 6-month study of the efficacy and safety of tadalafil in the treatment of erectile
dysfunction: a randomised, double-blind, parallel-group, placebo-controlled study
in Australian men. Int J Clin Pract. 2005 Feb;59(2):143-9.
2. Type V phosphodiesterase inhibitor treatments for erectile dysfunction increase
testosterone levels. Clin Endocrinol (Oxf). 2004 Sep;61(3):382-6.
3. Efficacy and treatment satisfaction with on-demand tadalafil (Cialis) in men
with erectile dysfunction. Eur Urol. 2004 Sep;46(3):362-9; discussion 369.
239
Cyclofenil
(Cyclofenil)
This is the least popular of the three Selective Estrogen Receptor Modulators (SERM)
being used in athletics today. I actually used this stuff about half a decade ago, when
it was just as easy to get as Clomid, and was a bit cheaper. As we already know,
SERMs cause ovulation in women and (more importantly to us) increase testosterone
and other beneficial hormones. This drug actually works by simulating the effects of
testosterone via inhibiting the negative feedback loop caused by estrogen, with
regards to testosterone production. This in turn causes the increased secretion of
gonadotropin releasing hormone, which increases output of luteinizing hormone
which (finally!) increases secretion of testosterone from your testes.
So what we have here is a compound which, being a SERM, will prevent gyno by
binding to the estrogen receptor in breast tissue and thus preventing stronger
estrogens from binding to those tissues. This should be familiar territory if you
remember your facts on Clomid and Nolvadex.
The results indicate that cyclofenil, paradoxically, has two opposing actions on the
hypothalamic-hypophyseal axis; one of them is estrogen-like, in that it depresses
serum FSH levels and competitively binds to breast tissue (this is good, remember),
and the other action is antiestrogen-like, in that it depresses serum PRL levels and
raises LH levels (4). Overproduction of prolactin, as you recall, will suppress
testosterone, and could induce lactation (gross!) in male breast tissue.
From the reading I’ve done on this compound, I think 400-600mgs/day would be an
appropriate dose for use in post cycle therapy, or during a cycle (4). Dan Duchaine
estimated roughly the same, saying that twice as much is necessary when compared
to Clomid, twice as often. Due to its relative expense and unavailability when
compared to other SERMs, such as Nolvadex and Clomid, I can’t see this stuff
making its way into many people’s ancillary regimen.
References:
1. Effect of cyclofenil on hormonal dynamics, follicular development and cervical mucus
in normal and oligomenorrhoeic women. Hum Reprod. 1992 Jan;7(1):39-43.
2. [Cyclofenil-induced acute hepatitis. A retrospective diagnosis of a case during acute
hepatitis B] Recenti Prog Med. 1991 Apr;82(4):236-9. Italian.
3. [Induction of ovulation in 1985] J Gynecol Obstet Biol Reprod (Paris).
1985;14(7):899-913. Review
4. Plasma FSH, LH and prolactin levels in postmenopausal women undergoing cyclofenil
treatment. Acta Obstet Gynecol Scand. 1982;61(6):487-90.
240
EPO
(Erythropoietin)
EPO is a glycoprotein that regulates red cell (RBC) production. In the human, EPO is
produced by the kidneys of the adult and by hepatocytes in the fetus. Roughly a
century ago, two researchers, Carnot and Deflandre, figured out that a humoral
factor, which they called "hemopoietine," regulates red blood cell production. This
eventually made it possible to synthesize and eventually clone the gene for EPO and
to develop recombinant EPO for use in clinical anemias. EPO binds to an erythroid
progenitor cell surface receptor to regulate several functions in your body, such as
bone marrow erythroid cell proliferation, differentiation, and survival.
EPO, as a performance enhancing drug, gained notoriety in 1998 when a bunch of
cyclists in the Tour de France got caught posessing it.
EPO, when taken exogenously, increases RBC in the blood. This will basically raise
your energy levels (1), and thus will improve recovery, etc. Anadrol was developed
for a very similar purpose as EPO, and I suspect that a lot of the muscle enhancing
effects/potency of A50 (increased muscle fullness, etc.) can be attributed to many of
the same mechanisms which are at work in it. It’s worth noting that EPO also
increases protein synthesis, just like A50. Primarily, though, its effect is to increase
RBCs.
Having more RBCs, and thus having more oxygen delivered to muscle tissues, is
directly associated with a substantial improvement in athletic performance, i.e
speed, endurance, strength, etc.(2). EPO is associated with improved bodyweight,
excercise capacity, oxygen uptake, respiration, whole body metabolism and energy
efficiency (3). In addition, cognitive function (learning, etc.) is also improved with
EPO (4).
Ok, so how much do you take? I'd say you'll need to get about 8,000-10,000IU/wk
for 2 weeks. Thats it. You take it all at once over 2 weeks (maybe a little over
1,000IU or so per day for 14 days) and you’re done. Then, sometime in week 3,
you'll start feeling the results, which will last for 3-6 months! Yeah, you read that
right.
Watch your BP, and don't let it get out of hand, because that could mean your
hematocrit is getting too high—from interaction with various athletes, I think that we
generally want hematocrit around 50 just over. Also remember to keep well hydrated
to avoid any possible issues with clotting, and keep some aspirin on hand just in case
you find that you need to thin your blood out a bit.
Currently, there is no 100% reliable test for EPO doping, although Lance Armstrong
will be accused of using it nonetheless, for the rest of his life, foundlessly.
Sorry…that was a little aside…
Recently, a new EPO-related molecule has been synthesized called "novel
erythropoiesis stimulating protein” (NESP), which contains a higher content of
carbohydrate and provides a new antianemia agent with a longer circulating plasma
half-life in vivo than native EPO. I suspect that it would be even more potent, and
this may become the doping drug of the future for endurance athletes.
241
References:
1. Cancer. 2003 Sep 1;98(5):1072-9
2. Sports Med. 2003;33(3):187-212
3. Semin Oncol. 2002 Jun;29(3 Suppl 8):69-74
4. Clin Breast Cancer. 2002 Dec;3 Suppl 3:S116-20
5. Exp Biol Med (Maywood). 2003 Jan;228(1):1-14
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242
Esiclene
(Formebolone)
Although technically Esiclene (formebolone) is a steroid, not many bodybuilders use
it for any sort of muscle building property. Formebolone is yet another form of
methandrostenolone (Dianabol). It’s basically the same structure, with an
attachment of a 2-carboxaldehyde group and an 11-hydroxyl group. The 11
hydroxyl-group keeps the steroid from aromatizing (converting to estrogen), and
from what I can see, the 2-carboxaldehyde group keeps it from being highly
androgenic or anabolic. Another thing that is actually more important for our
purposes here though, is that the 2-carboxaldehyde group makes formebolone very
irritating to inject. That’s exactly what made the injectable version of this drug very
popular with competitive bodybuilders, especially after Bill Phillips wrote about it.
Basically, it’s a very weak steroid, with no real anabolic/androgenic activity, in a vial
at only 2 mg/ml, and it hurts like hell to inject. There’s also no virilization (3)
possible, and it’s 17-alpha-alkylated and thus toxic to the liver. No anabolic effects, it
hurts to inject, and is liver toxic…sign me up! I have, however, decided to make its
profile quite different from the other anabolic steroid profiles, because its use is not
as an anabolic at all.
It’s no wonder that this drug is only popular with bodybuilders, and not athletes. It’s
purely a cosmetic enhancer for all intents and purposes. Maybe I’m being too hard
on formebolone though. Let’s take a look at it from an anabolic point of view.
Medically, formebolone was mostly used on kids with growth deficiency. It’s basically
a mild and non-aromatizing methandrostenolone, which at first sounds great. There
is an absence of an estrogenic component which could potentially stunt growth, and
it was found that ultimate height was not affected by the increases in bone age
caused by formebolone treatment. A very mild anabolic effect was all that was noted
(1). Unfortunately, another study only indicated that same very mild anabolic activity
(2). Also, unfortunately, formebolone can increase nitrogen retention only slightly
(3).
Anyway, you can clearly see why Formebolone is really a bit of one-trick-pony. It’s
really only injected by precontest bodybuilders into lagging body parts prior to a
competition, to take advantage of the localized swelling it causes. Swelling caused by
formebolone should subside in 3-4 days, roughly the same as with injectable
Winstrol or testosterone suspension, after which the injected muscle will return to its
original size.
This also comes in oral form, but I can only imagine that it won’t really do much, as
injectable versions of given steroids are often much more effective. In this case, the
oral version doesn’t offer us the one thing the injectable version is used for, which is
irritation at the injection site.
References:
243
1. Cuatrecasas Membrado JM, Bosch Banyeres JM. Study of non-hypophysiary growth
retardation treated with formebolone. An Esp Pediatr 1985 Jan;22(1):27-32
2. Esposito R, Pluvio M, Giordano D. Anabolic agents in kidney disease: the effect of
formebolone on protein synthesis in patients with renal insufficiency or nephrosis. Curr
Med Res Opin 1975;3(1):43-5
3. Cerutti S, Forlani A, Galimberti E. Anticatabolic action of formebolone in the castrated
rat treated with dexamethasone. Arzneimittelforschung 1976;26(9):1673-7
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
244
Falsodex
(Fulvestrant)
Falsodex is an estrogen receptor antagonist, which has no agonist effects at all.
What it does is downregulate estrogen receptors (kinda like how Clen downregulates
beta receptors, so you get decreased effects from the stuff). Basically, it binds to the
Estrogen Receptor more strongly than tamoxifen, but still has no estrogen agonist
effects. Here's the interesting part: the resultant downregulation of your estrogen
receptors from the use of Falsodex results in decreased expression of the
progesterone receptor as well! Tamoxifen, as we all know, can increase the sides
from progesteronic drugs because of an increase in progesterone receptor
expression. So you can take this stuff as both an anti-estrogen and an anti
progestin! No more buying Arimidex or whatever, and Bromocriptine! Sweet, huh?
The stuff is administered via an IM injection of 250mgs once per month! And at that
dose, it has most if not all of the same estrogen lowering effects of 1mg/day of Arim
or 2.5mgs per day of Letrozole, but has the added benefits of lowering progesterone
receptor expression.
I haven’t seen this anywhere on the black market, and actually can claim to be the
first person to mention it on the Internet, generating quite a bit of interest but still,
cost remains high, and availability low.
References:
1.Br J Cancer. 2004 Mar;90 Suppl 1:S15-8
2.Drugs. 2004;64(6):633-48
3.J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):209-12
245
Fareston
(Toremifene citrate)
This is yet another SERM, which means it will display both estrogen antagonist/
agonist properties in the body. This puts it in the same category as Nolvadex and
Clomid, the two most popular drugs in this category. This is, however very different,
and you’ll soon see why…
Some scientists at a party were bored one day, so they hooked up some time-lapse
video to breast cancer cell cultures treated with with toremifene (the chemical in
Fareston). Ok, the part about them being bored one day is made up, but they really
did hook up time-lapse photography to breast cancer cell cultures treated with
Fareston. Anyway, they observed this for 3 days, and it caused approximately 60%
of the cells to exhibit morphologic characteristics typical of cells undergoing
apoptosis or programmed death. The significance of this to you and me is that this
is roughly the same thing that would happen to your gyno if you were taking
Fareston. Anyway, the number of mitoses gradually decreased to zero over only a 3-
to 4-day period. So this stuff causes growth inhibition of estrogen-sensitive breast
cancer cells by inducing some cells to die and by inhibiting other cells from entering
mitosis (i.e. from replicating) (1). This stuff will KILL your gyno, from everything
I’ve read (which also means that I’ve had to read into everything I’ve read, if you
kinda follow me). Now where was I? Oh yeah…kill, that’s right. This is certainly
good news for someone who wants to get rid of gyno, but since it also prevents the
cells from replicating, it will stop gyno from progressing as well as kill existing gyno.
Also of note is that it will reduce prolactin (2), and as you probably guessed, this
may raise your Testosterone levels, since prolactin can not only cause lactation, but
it also has an inhibitory effect on your Test levels. The unfortunate part about this
potentially exciting new compound is that it will also raise sex hormone binding
globulin (SHBG), which will in turn lower circulating levels of testosterone in your
body (3).
Perhaps this drug, if it can be found, may be used successfully to treat existing gyno,
or as an adjunct during a cycle, but certainly not for an effective post cycle therapy.
References:
1. Apoptosis in toremifene-induced growth inhibition of human breast cancer cells in
vivo and in vitro.J Natl Cancer Inst. 1993 Sep 1;85(17):1412-8.
2. Hormonal effects of toremifene in breast cancer patients. J Steroid Biochem. 1990 Jun
22;36(3):243-7.
3. Influence of toremifene on the endocrine regulation in breast cancer patients.
Eur J Cancer. 1994;30A(2):154-8.
246
Femara
(Letrozole)
Letrozole is the chemical name of Novartis’ selective third generation aromatase
inhibitor (AI). This drug was developed to fight breast cancer by inhibiting
aromatization. It is usually used as a part of an aggressive treatment in post
menopausal women to fight and reverse the spread of breast cancer after other
treatments (such as tamoxifen therapy) has failed. It’s probably the most efficient
product on the market for this purpose currently (5). It is very similar in structure
and action to it’s predecessor Arimidex.
Letrozole also does quite a few things which would be of interest to both
bodybuilders and athletes. First, it has been shown to reduce estrogen levels by 98%
or greater (1). In at least one documented incidence, Letrozole reduced estrogen in
the test subject to undetectable levels, and increased LH, FSH and SHBG (4).
Clearly this is all of interest to bodybuilders, as less estrogen in the body means less
chance of certain side effects such as water-retention, gynocomastia, and acne. This
makes Letrozole an appropriate choice for even the heaviest bulking or cutting cycles
including harsh androgens. Also, if you are a competitive bodybuilder, letrozole is a
must have product for contest prep; no other Ancillary compound will produce a dry
and tight look like Letro will.
An effective dose of Letrozole is .25-.5mg/day (I use .25mgs/day), but be
forewarned, if you go over that amount, it can kill your sex drive. Also worth noting
is that there's a rebound effect on your estrogen when you come off letrozol.
Maximum inhibition of the aromatase enzyme has been found to happen at doses as
low as 100mcg (2)!
Letrozole's effects on serum lipids (cholesterol, both HDL and LDL) are, in the words
of one researcher: "inconsistent." Clearly, however, you’ll eventually suffer an
impaired lipid profile and immune system if you keep your estrogen levels too low for
too long. Your sex drive will also probably suffer from extraordinarily low levels of
estrogen present.
As previously mentioned, letrozole can be used to raise LH and FSH (which are
hormones that signal your testes to produce more testosterone). It also, of course,
will raise your testosterone levels (6) via this mechanism. Again, this is of interest to
athletes and bodybuilders for obvious reasons. Letrozole can be used for post cycle
therapy (PCT) to raise test levels, but for various reasons, tamoxifen may be a better
choice. Still, I have successfully used letrozole for this purpose.
How good is this compared with Aromasin and Arimidex, its two other main rivals?
Well, in non-cellular systems, letrozole is 2-5 times more potent than anastrozole
and exemestane in its inhibition of the aromatase enzyme and activity, and in
cellular systems it is 10-20x more potent! It also lasts quite a long time in your
body, but takes awhile to get going--letrozole has a whopping 2-4 day (!) ½ life, and
you need to take Letrozole for 60 days to get a steady blood plasma level (8).
247
Those are impressive numbers, but here’s one of the most interesting things about
Letrozole: it may reduce/eliminate/reverse existing gynocomastia!
In a study conducted on mice (no, I know it’s not perfect), gyno-like-changes in the
mammary gland were totally destroyed! Here’s a direct quote from that study:
“Our results also indicate aromatase overexpression-induced changes in mammary
glands can be abrogated [destroyed] with very low concentrations of the aromatase
inhibitor, letrozole.” (7)
In addition, I’ve used Letro to get rid of my own gyno, as has a friend of mine, and
we both used it at a dose of 2.5mgs/day, tapering down to .25mgs/day, and then
finally off—the gyno never returned in both our cases.
I’d say that this stuff is pretty great, considering its availability and cost (when you
consider the fact that .25mgs/day is more than enough protection from estrogen
related sides on most cycles) not to mention it’s overall utility for a variety of
functions (destroying gyno, preventing estrogenic sides, and for PCT).
References:
1. Clin Cancer Res. 2005 Apr 15;11(8):2809-21.
2. J Clin Endocrinol Metab. 1995 Sep;80(9):2658-60.
3. Eur J Obstet Gynecol Reprod Biol. 2002 Nov 15;105(2):161-5
4. Epilepsy Behav. 2004 Apr;5(2):260-3
5. Semin Oncol. 2004 Dec;31(6 Suppl 12):3-8.
6. Diabetes Obes Metab. 2005 May;7(3):211-5.
7. J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):27-34. Aromatase overexpression
transgenic mice model: cell type specific expression and use of letrozole to abrogate
mammary hyperplasia without affecting normal physiology.
8. (Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.)
248
Finasteride
Finasteride was available for years as Proscar (5mg tabs), but only recently became
available as Propecia (1mg tabs). It is in a class of chemicals known as 5alpha
reductase inhibitors. It is based on the progesterone skeleton (4) and has a high
inhibitory activity for the enzyme 5alpha-reductase (5-AR). 5-AR, as you may recall,
is the enzyme responsible for converting certain steroids into 5-Alpha–Reduced
versions of themselves (such as turning testosterone into dihydrotestosterone).
Finasteride and similar compounds are used for the treatment of androgen
dependent diseases such androgenic alopecia (hair loss), benign prostatic
hyperplasia (prostate enlargement) and prostate cancer. Dihydrotestosterone is a
5alpha-reduced metabolite of testosterone and has been implicated as a causative
factor for the onset and progression of these problems. This was discovered when
males who are genetically deficient of the enzyme steroid 5alpha-reductase were
shown to have much lower incidences of these problems (1)(2). Of course, these
problems can be a major annoyance, and nothing to toy around with, but by using
finasteride you risk reducing your gains on a given cycle, and can even suppress
reproductive function (3). I’m not a big fan of this, as you could guess. However, if
you are worried about your hairline, or have incidences of prostate issues in your
family, then 1mg/day of Finasteride may be the answer you’ve been looking for.
It needs to be noted that there are actually 2 different 5-AR enzymes, and
Finasteride specifically blocks the type-II variety. The type-II 5-AR enzyme is the
one responsible primarily for hairloss and prostate enlargement, while type-I is often
the culprit behind acne and hirsutism. In either case, type-II is responsible for
around 2/3rds of the circulating DHT in your body, so it’s no surprise that Finasteride
typically reduces your total DHT levels by around 65%.
There is also some novel information about this compound regarding the conversion
of testosterone into DHT via the 5-Alpha-reducatase enzyme. It’s come to my
attention that the actual conversion process of testosterone into DHT via this enzyme
may act in some way to inhibit luteinizing hormone release (and ergo would inhibit
your HPTA and natural testosterone production). Check this out:
249
Basically, this chart above shows the baseline level of LH in male sheep given a 5
Alpha-Reductase inhibitor (such as Finasteride), then one showing the LH levels in
sheep given testosterone propionate, and finally a chart showing LH levels of sheep
given testosterone propionate + the inhibitor (graph 3).(5) You’ll note that although
using the inhibitor alone produced no discernable effects on LH, when administered
with testosterone, it seems to have allowed LH pulsality to continue nearly
unaffected. This may indicate that you can use Finasteride on a cycle (1mg/day) and
250
possibly keep your LH levels normal (and thus your HPTA), ergo making recovery
much easier. This is, of course only my speculation.
Reference:
1. Steroidal antiandrogens and 5alpha-reductase inhibitors. Curr Med Chem.
2005;12(8):927-43.
2. New 5alpha-reductase inhibitors: in vitro and in vivo effects. Steroids. 2005
Mar;70(3):217-24.
3. [Effect of selective 5alpha-reductase inhibitor or/and testosterone undecanoate on the
reproductive function of male rats]
Zhonghua Nan Ke Xue. 2005 Jan;11(1):38-41. Chinese.
4. New aromatic esters of progesterone as antiandrogens.
J Enzyme Inhib Med Chem. 2004 Apr;19(2):99-105.
5. Biology of Reproduction 50, 1244-50 (1994)
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251
HCG
(Human Chorionic Gonadotropin)
Scientists first recognized a specific hormone now called Human Chorionic
Gonadotropin (HCG) in the 1920’s (1). HCG is no doubt one of the most misused,
misunderstood and underutilized tools in bodybuilding pharmacology we have
available. HCG is not a steroid, but a naturally occurring peptide hormone, produced
by the embryo in the early stages of pregnancy and later by the trophoblast (part of
the placenta) to help control a pregnant woman’s hormones. This makes the uterine
lining ready for implantation of the fertilized egg. HCG is a glycoprotein composed of
237 amino acids and has a mass of 36.7kDa. HCG basically “acts” as leutenizing
hormone (LH) in your body. LH is a Gonadotropin. These were first extracted from
the human, more precisely—the pituitary glands, in 1958. A gonadotropin is any
substance that stimulates the gonads (ovary, testes). It is heterodimeric (initiates
prophase of mitosis) with an alpha subunit identical to LH, FSH (follicle stimulating
hormone) and TSH (thyroid stimulating hormone). LH is produced in the pituitary
cells and is made up of a beta chain of 115 amino acids and an alpha chain of 89
amino acids. In the testes, the LH binds to receptors on the Lydig cells, which, in
turn, stimulate the synthesis and secretion of testosterone. Like LH, FSH is also a
gonadotropin. It consists of a beta chain of 115 amino acids and an alpha chain of 89
amino acids, the same as LH. Production and release of FSH is controlled by GnRH
(gonadotropin releasing hormone). FSH stimulates testicular growth and supports
the function of sertoli cells, which are needed for sustaining maturing sperm cells.
TSH is also known as a thyrotropin and is secreted by cells in the anterior pituitary
glands. TSH is comprised of a beta chain of 112 amino acids and an alpha chain of
89 amino acids. The alpha chain is the same as that found in the two other pituitary
hormones, LH and FSH, and HCG as well. TSH is produced when the hypothalamus
releases TRH (thyrotropin releasing hormone). TRH then causes the pituitary gland
to release TSH. TSH makes the thyroid gland produce triiodothyronin (T3) and
thyroxine (T4), which controls the body’s metabolism.
HCG is clinically used to induce ovulation and treat ovarian disorders in women, as
well stimulate the testes in hypogonadal (underproduction of testosterone) men. It
is also used in the treatment of undescended testicles in young males. HCG offers no
potential performance enhancement in female athletes, but does prove to be very
useful in male athletes especially those that use AAS. As stated above, HCG in males
is similar to LH, because LH binds to receptors on Leydig cells stimulating synthesis
and secretion of testosterone. The use of HCG would be an added bonus to ASS
users even if there is a lack of endogenous LH. Since HCG increases the body’s
natural testosterone levels, its use during long or extremely high dosed cycles can be
most beneficial were the effects on the hypothalamus causes a depressed signal to
the testicles. The result of the depressed signal leads to what is known as testicular
atrophy (shrunken balls). The use of HCG will send an artificial signal to the testes
(again, as if it were actually LH), thus preventing (to some degree) atrophy. It not
only helps to maintain testicular size and condition but it will also help in restoring
testicles back to their original size. At a time when below normal androgen levels
(due to ASS use) could become costly, restarting natural testosterone production as
quickly as possible is of a special concern in males at the end of a cycle. The price
paid by bodybuilders for failing to raise natural Test levels is the loss of most if not
252
all the hard earned muscle gained; the main cause is cortisol. Cortisol sends a
message to the muscles that is opposite to that of testosterone. If cortisol is not
dealt with (because of an extremely low testosterone level), it will quickly strip away
the new and hard earned muscle you have just obtained.
Some users find that they have better gains and quicker recovery while using HCG
during a cycle of AAS. This first claim is more than likely due to the fact that the
body has a high level of natural testosterone as well as that provided by the use of
AAS, and the second may be somewhat justifiable, as stimulating the testes to
secrete testosterone intermittently may aid recovery. Perhaps this is due to the
maintenance of a higher level of Inter-Testicular-Testosterone (ITT) provided by the
intermittent use of HCG, which should greatly aid recovery of the hypothalamic
testicular-pituitary-axis. An average dose of HCG during a cycle is between 500 to
1000iu every week to every other week while on a cycle. In one study I reviewed, a
single injection of 6000IU of HCG elevated Test levels for 6 days. That's why a lot of
people recommend taking it every 3-5 days. We'd have more stable blood levels,
though, if we shot it more frequently. Remember, it's non-estrified and a water
based injectable, after all. In that same study I just spoke of, 1500IU of HCG shot
Test levels up between 250 and 300%. Taking it all at once however will cause an
increase in estrogen levels caused by the aromatization of normal testosterone; the
result may be a case of gynecomastia for the user.
As regards HCG's use of post cycle therapy (PCT), smaller and more frequent doses
after a cycle of AAS would give the best results with the least amount of side effects.
A dose of 250iu to 500iu everyday (ed) for 2 to 3 weeks is plenty and should vary
little from person to person. The Physician’s Desk Reference recommends 500iu/day,
as did the late, great, Dan Duchaine. The smaller doses are sufficient enough to
begin reversal of testicular atrophy, and used in conjunction with nolvade will help
the already present problem of recovery without raising the levels of estrogen too
high and increasing the risk of gynecomastia in the user. Lower doses of 250iu to
500iu also avoid the further risk of downregulating LH receptors in the testes. The
old saying “more is better” definitely does not apply to the use of HCG. You don’t
want to finish PCT after using too much HCG only to find out your back at the
beginning again. Your best bet is to start at 250iu or 500iu ed for 5 or 6 days, and if
you don’t notice anything happening (nuts dropping and getting bigger) up the dose
slightly. Small doses like 500iu two days a week aren’t going to cut it like some
people think. The only thing small doses of HCG may be useful (sublingually) for is
reducing symptoms of benign prostatic hyperplasia (7). Yeah, that’s right, you can
probably reduce some symptoms of an enlarged prostate with the use of small doses
of HCG.
As stated above, the cycles of HCG should be in the 2 to 3 week range with a least
one month off in between, you could stretch your cycle out to four weeks without
any major concern if you are using lower doses. One should, however, take care
when using HCG as prolonged use could repress the body’s natural production of
gonadotropins permanently, but this is mostly just pure speculation as has yet to be
reported—nor has there been a case of an overdose. To be on the safe side, shorter
cycles of HCG seem to be that of the norm. Most users cycle HCG near the end of a
steroid cycle; you should start your HCG therapy on the last week of yours. For best
results, you should also run nolva while you run HCG as taking HCG by itself will do
little to nothing and gyno, even though rare, may also flair up. Once the HCG cycle is
finished you continue with your usual Clomid or Nolvadex (preferably the latter) for
PCT as it is more effective when used in conjunction HCG. With an AAS cycle of 6 to
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10 weeks, HCG may not be necessary unless extreme doses of AAS were used, when
there is an existing problem of testicular atrophy, or when you are running a heavy
oral only cycle. AAS cycles of 12 or more weeks should have HCG as a part of post
cycle plan.
Since HCG is used to stimulate testosterone production, side effects can be the same
as those associated with AAS, although gyno may be more common. Possible side
effects of HCG use are water and sodium retention following higher doses. This is
usually a result of higher androgen production. It may cause gyno (again, if doses
are too high). Any athletes worried about failing urine tests because of low levels of
epitestosterone may find that using a dose of 500iu of HCG will increase
epitestosterone levels. However, the problem with HCG is that it is also banned by
the IOC and can also be detected in a urine test; the half life of HCG is
approximately 4 to 5 days. Another possible downside to HCG is that it to can be
suppressive to natural testosterone because it takes the place of LH. LH is
manufactured in the pituitary because of the response of GnRH (gonadotropin
releasing hormone), which in turn is secreted by the hypothalamus. Because the
HCG mimics LH and is being supplied exogenously, the hypothalamus will be given a
signal to still stop producing GnRH, so no natural LH will be produced. This is why it
should always be used with a compound such as Nolvadex. Let me explain: HCG's
suppressive effect on endogenous testosterone is (mostly? totally?) due to to HCG
actually blocking the conversion of 17 alpha-hydroxyprogesterone (17 OHP) into to
testosterone. Nolvadex stops this blocking-action of HCG from taking place.
So although HCG is essential after long or heavy cycles, it should not be used
without an ancillary such as (specifically) Nolva. Also HCG therapy should be
discontinued at least 2 weeks prior to stopping the use of Nolva, or it may suppress
natural testosterone itself. This should not be a problem if you are running it towards
the end of your cycle of AAS and before PCT.
The average price of HCG is between 10$ to 40$ per 5000iu with solvent; it comes in
doses of 100, 125, 250, 500, 1000, 1500, 2000, 2500, 3000, 5000, 10000, 20000—
all iu (international units).
HCG is readily available and can be found in almost all the places where you may
find AAS. If you have a good source you should have no problems in obtaining this
product. There are currently only a few fakes of HCG around, mostly few and far
between. Since the powder of HCG is similar to the powder of somatropin, often
cheaper HCG is sold and marketed as the more expensive HGH (human growth
hormone) on the black market.
References:
(All references for the claims made about HCG are found in the introduction to this
chapter)
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Ketotifen
(Ketotifen)
Ketotifen was made popular by its ability to inhibit the down regulation of beta
receptors caused by drugs like clenbuterol. Clenbuterol, albuterol, and ephedrine
used to be cycled on and off because they desensitize the various receptors they act
on to produce their lipolytic effect. Ketotifen would therefore allow the use of these
fat burning drugs for much longer periods. If you’ve read my writings on clenbuterol,
you already know that Benadryl (the anti-histimine) can also be used for this same
purpose, and is 10x cheaper and infinitely more available to most people. So why
am I bothering to write about Ketotifen at all?
Ketotifen, in medical circles, is also recognized for its ability to lower levels of the
cytokine tumor necrosis factor-alpha (TNF-alpha), which is a catabolic hormone, and
this is a property that Benadryl does not have, to my knowledge. TNF-alpha lowers
both testosterone and IGF-1 levels (3)(4), and strenuous exercise elevates TNF
alpha levels (5). TNF-alpha has also been shown to increase insulin resistance,,
which we certainly don’t want.
Ketotifen is used by people suffering from wasting diseases partially caused by TNF
alpha. I think, however, its ability to lower TNF-alpha is going to be overshadowed
by anabolic effects produced by anabolic steroids. In one study involving AIDS
patients, combining ketotifen and oxymetholone (Anadrol 50) showed that the
ketotifen didn’t add much to the oxymetholone induced weight gain (1). Hence, you
are reading this profile in the “Ancilliaries” portion of this book, and not the “Fat
Burning” part, even though Kktotifen is typically used as part of a fat burning cycle
including Clen. Benadryl is simply too much cheaper and readily available to use
ketotifen in it’s place with Clen. However, for post cycle therapy, ketotifen and its
ability to lower TNF-alpha, is a very valuable tool. You see, hypogonadism (low
testosterone) often accompanies elevated TNF-alpha levels (6), and after a cycle of
anabolic steroids, you are going to be in a hypogonadal state, with elevated TNF
alpha. Thus, taking ketotifen with your PCT is probably a very good idea. I
recommend 1-3mgs/day before bed because this stuff will make you pretty drowsy.
References:
1. Oxymetholone promotes weight gain in patients with advanced human
immunodeficiency virus (HIV-1) infection.Br J Nutr. 1996 Jan;75(1):129-38.2.
Smart T. GMHC Treat Issues. 1995 May;9(5):7-8, 12.
3. Mauduit C, et.al Endocrinology 1998 Jun;139(6):2863-8
4. Lang CH et.al Growth Horm IGF Res 2001 Aug;11(4):250-60
5. Pedersen BK et. al. Exerc Immunol Rev 2001;7:18-31
6. Malkin CJ et.al. J Clin Endocrinol Metab. 2004 Jul;89(7):3313-8.
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Kynoselen
Kynoselen was one of those weird quasi-legal, grey market drugs that used in horse
racing that its way into the anabolic arsenal of many athletes and bodybuilders. I
will be frank and say that its effects are generally more profound in those who are
already reasonably lean and muscular. I’ve noticed, through my research, that the
biggest mitigating factor in this stuff’s use is that its not doing mych (cosmetically)
for those whose bodyfat is too far over 12%. Over 15% and I’d go so far as to say
kynoselen is a waste. Its fat burning properties are felt proportionately with how lean
you already are. It will help with vascularity if you’re lean also. Women seem to be
much bigger proponents of this stuff than men, generally, but that’s probably
because they tend to aim for comparatively less gains than men, and thus are much
more satisfied with a few lean pounds or a few solid strength increases. Again, on a
lean 125lb female, 5lbs of lean mass is very noticeable—much more so than on a
male twice that size.
Lets unpack a bottle of Kynoselen and see what’s in it:
• AMP (adenosine monophosphate) is what I’d consider to be the primary active
ingredient of Kynoselen. This is a source of phosphorous. It combines with 2
phosphate atoms to become ATP (adenosine triphosphate), which provides an
immediate source of cellular energy. AMP aids lipolysis (1), or fat-burning,
and it’s probably the inclusion of this ingredient that makes Kynoselen’s
effects in this area the most profound. It also has the ability to convert to
ATP, or adenosine tri-phosphate. ATP is the primary carrier of energy within
cells, and most cells die quickly in the absence of it. ATP in turn powers
muscles. This is probably why users of Kynoselen report an increase in
“energy levels.”
• Magnesium aspartate has a major role in muscle contraction (5)(6), and this
is why it’s in high demand with many strength athletes. When Dan Duchaine
made his supplement recommendations nearly a decade ago in Muscle Media,
this was on the list. Magnesium also activates enzymes necessary for the
metabolism of carbohydrates and amino acids, which leads to protein
synthesis.
• Heptaminol is also included in this preparation. It aids in dilation of coronary
blood vessels and could thereby act as a sort of transport aid for oxygenated
blood (4). I’m sure this is partly why it’s given to race horses as a kind of
“wellness tonic.”
• Cyanocobalamin (vitamin b-12) has been included in Kynoselen, and
bodybuilders and other athletes have known about this substance’s role in
increasing energy and appetite stimulation. A deficiency in this vitamin leads
to anemia, so it’s always a good idea to include it in your diet. The injectable
version is also very popular.
• Selenium is an anti-oxidant, and has been used as a protective agent in spinal
cord injuries. I would imagine that keeping racehorses free from injury would
be very important to their owners; hence its inclusion in this preparation.
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• Potassium aspartate: Mainly, we know that potassium keeps you from
cramping, and again, since we are examining a compound given to
racehorses, it’s logical to assume that a smart breeder/owner would like to
prevent his horse from cramping when millions of dollars are on the line in a
race. Potassium also assists in many cardiac functions, and will probably act
synergistically with magnesium to aid in muscle contractions (7).
Looking over the ingredients of Kynoselen, it’s easy to see why it’s used for horse
racing, and I think its similar use in athletics is pretty obvious. Sprinters and
strength athletes would greatly benefit from its various energy producing substrates,
as well as the ingredients added to increase contractile strength in skeletal muscle. I
have heard about some pretty decent increases in strength from the sole use of this
compound, and certainly it has found its way into many powerlifters’ cycles.
For bodybuilders, its benefits are pretty different. It seems to be most widely used
for PCT, when it can be used in conjunction with our SERMs and AI’s to hold onto
gains by increasing our ability to continue using the weights that got us to the size
we were while on anabolics.
Kynoselen comes as a 100ml multi-use vial. Typically, athletes and bodybuilders pay
$50-$75 for it, and inject between 1-3mls per day. The only complaint I’ve heard
about it is that it’s painful to inject it, so I would recommend injecting it with an
equal amount of b-12. If I were to use it personally, I’d use Syntheselen, which is
actually an injectable product containing all of the above ingredients, but
manufactured to human grade standards.
References:
1. Extracellular cyclic AMP-adenosine pathway in isolated adipocytes and adipose tissue.
Obes Res. 2005 Jun;13(6):974-81.
2. Effect of prolonged anaerobiosis on 125I-insulin binding to rat soleus muscle:
permissive effect of ATP. Am J Physiol Gastrointest Liver Physiol, Dec 1978; 235: 606 -
613.
3. Decreased fatty acid synthesis due to mitochondrial uncoupling in adipose tissue.
FASEB J. 2000 Sep;14(12):1793-800.
4. [Heptaminol hydrochloride as an epithelium transporter]
Can J Physiol Pharmacol. 1990 Jul;68(7):791-9. French.
5. CaATP as a substrate to investigate the myosin lever arm hypothesis of force
generation. Biophys J. 2000 Mar;78(3):1474-81.
6. Effects of osmolality and ionic strength on the mechanism of Ca2+ release in skinned
skeletal muscle fibres of the toad.J Physiol. 1993 May;464:629-48.
7. Decreased muscle strength and contents of Mg and Na,K-pumps in chronic alcoholics
occur independently of liver cirrhosis.J Intern Med. 2003 Mar;253(3):359-66.
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Nolvadex
(Tamoxifen Citrate)
This drug is used as a first line defense against breast cancer. In the late 80’s, Dan
Duchaine speculated that it could also be used by bodybuilders to halt the
development of another type of tumor in the mammary gland—gynocomastia. He
introduced this find to the steroid-using-community in his “Contest Prep” issue of the
UnderGround Steroid Handbook Update Newsletter (the contest prep-issue was
actually 3 issues in one, for those who had a subscription to the newsletter).
Nolvadex is commonly referred to in quite a few ways: as a SERM (Selective
Estrogen Receptor Modulator), as an anti-estrogen (that is actually incorrect, as we
will later see), and finally as a triphenylethylene. I happen to stick with calling
Nolvadex a SERM, because out of my three options, it happens to be correct (as we
know that calling it an anti-estrogen is incorrect), and pronouncable (as we know
that I have no idea how to say "triphenylethylene"). Selective estrogen receptor
modulators (SERMs) act as either estrogen receptor agonists or antagonists in a
tissue-selective manner. Let’s see what that means to us.
Nolvadex actually has quite a few applications for the athlete using steroids. First
and foremost, its most common use is for the prevention of gynocomastia. Nolvadex
does this by actually competing for the receptor site in breast tissue, and binding to
it. Thus, we can safely say that the effect of tamoxifen is through estrogen receptor
blockage of breast tissue (1), especially since total body estradiol increases with its
use. Clearly, if you are on a cycle including steroids that convert to estrogen, you
may want to consider Nolvadex as a good choice to run along side them. Nolvadex,
however, is not the most potent ancillary compound we can use on a cycle, but it is
probably the safest considering it doesn’t actually reduce estrogen in your body;
keeping some estrogen floating around can have many benefits on muscle growth,
as well. Estrogen is also important for a properly functioning immune system. Not
only that, but your lipid profile (both HDL and LDL) should also show marked
improvement with administration of tamoxifen (4). Many bodybuilders actually use
this stuff during their cycles for the health benefits it provides. If, however, you are
preparing for a bodybuilding contest, you need to use something that will suck most
(if not all) of the estrogen out of your body. I am speculating that you may be able
to use Nolvadex for the majority of a contest prep cycle, to keep yourself relatively
healthy, and then switch over to letrozol for the last 8 weeks.
Nolvadex also has some other interesting features for steroid users. In hypogonadic
and infertile men given nolvadex, increases in the serum levels of LH, FSH, and—
most importantly—testosterone were all observed (2)(3). The best (rough) estimate
I can give you from my research is that 20mgs of Nolvadex will raise your
testosterone levels about 150% (5), and this would of course greatly aid post cycle
recovery. What this means to us is that if you take nolvadex after a cycle when you
are trying to raise your levels of testosterone, LH, and FSH back to normal, it will
greatly aid recovery. In fact, if I were limited to just one compound to aid me in post
cycle recovery, nolvadex would be my choice. If you want a comparison, it would
require 150mgs of Clomid to accomplish that type of elevation in testosterone, but
nolvadex also significantly increased the LH (Leutenizing Hormone) response to LHRL
(5), after 6 weeks.
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Some of the more harsh ancillary compounds available today will give you a more
“dry” look that nolvadex can’t, but nolvadex is simply safer to use in long (over 16
week) cycles.
Unfortunately, nolvadex isn’t perfect. Anecdotally, it has been linked to reduced
gains in some bodybuilders. This isn’t due, as previously thought, to its reducing
estrogen levels (which it doesn’t), but rather to it’s ability to possibly reduce IGF
(Insulin-like-Growth-Factor) levels, which are important for muscle growth (6)(7).
This lowering of IGF levels is probably due to lowering of GH at the pituitary.
Personally, I’ve had many successful cycles with nolvadex as well as without, but I
can certainly testify to its effectiveness in preventing gynocomastia. Back in the late
90’s I purchased 30 tabs of 10mg Nolvadex for $30, and recently I have found it for
much less on various Internet sites. It’s well worth the money.
References:
1. Klin Padiatr. 1987 Nov-Dec;199(6):389-91.
2. Stimulation of calcitonin secretory capacity by increased serum levels of testosterone
in men treated with tamoxifen. Int J Androl. 1987 Dec;10(6):747-51.
3. Hormonal changes in tamoxifen treated men with idiopathic oligozoospermia Exp Clin
Endocrinol. 1988 Dec;92(2):211-6.
4. 2 Bruning PF, Bronfer JMG, Hart AAM, Jong-Bakker M, tamoxifen, serum
lipoproteins and cardiovascular risk, Br. J. Cancer 1988 Oct, 58 (4) 497-9
5. Fertil Steril. 1978 Mar;29(3):320-7.
6. J Clin Endocrinol Metab. 1993 Jun;76(6):1407-12.
7. Eur J Cancer. 1992;28A(4-5):788-93
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PSGAG
Polysulfated Glycosaminoglycan (Adequan), manufactured by Luitpold
Pharmaceuticals, Inc
Got sore joints? This stuff might be the answer for you. Don’t get me wrong, there’s
tons of stuff out there that’s pretty good (ibuprofen, naproxin, etc.) and could relieve
some pain and inflammation. I’d recommend trying all of the NSAIDS available OTC
before you start shooting up. With that said, here’s the deal on PSGAG:
This is a water-based injectable and is used for treating animals (dogs and horses)
who have degenerative-type or joint problems. From the research I’ve seen, this
drug is much better at treating degenerative type joint problems in animals (hip
dysplasia, tendonitis, arthritis, etc.) than it is at treating traumatic injuries. It does,
however, work for both. Basically, in every measured area that’s relevant to treating
a joint problem (range of motion, flexion, increase in synovial fluid, etc.), this drug
has been shown to display improvements in test subjects. Get it? When this drug
was given to test animals, all of them showed improvement in their joint-related
problems.
Now, check this out: As a side effect IM administration of 500mgs E4D for 12 weeks
of PSGAG, the mean test subject showed roughly a 13.5% increase in bodyweight!
Yeah, you read that correctly. Not only does this stuff help heal joint injuries, it may
be anabolic! This may be due to the fact that it elevates both white blood-cell count
as well as the polymorphonuclear cells. Also of note is that it elevates lymphocytes.
So how much of this stuff should a 200lb bodybuilder take? Well, ideally, I’d say
125mgs, IM, every 4 days. This should be done for at least 28 days, and possibly for
as long as twice that.
How much will it cost? Well, a 5ml, 100mg/ml bottle is going to set you back about
$50. If you’re taking it as I recommend, then each bottle (vial) will last you 16 days,
so you’ll need at least 2-5 bottles. Its also sold similarly priced in the ever
inconvenient 5ml amps.
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Teslac
(Testolactone)
[17 alpha-oxa-D-homo-1,4-androstadiene-3,17-dione ]
Molecular Formula: C19 H24 O3
Molecular Weight: 300.3968
Melting Point: N/A
Manufacturer: Shering
Release Date: 1970
Effective Dose: 250mg/.day
Active Life: up to 24hours
Detection Time: 4-6 weeks
Androgenic: Anabolic Ratio:N/A
Teslac is one of the very first drugs approved by the FDA to fight estrogen
dependant breast cancer, back in 1970. It does this by possibly inhibiting the
aromatase enzyme in what appears to be both a noncompetitive and an irreversible
manner.
I have to admit, when I first went to research this compound, I had thought I was
researching a useless old Anti-Estrogen. Anyway, I took a quick look at its chemical
structure, and realized that it was actually an anabolic steroid, but still decided to put
it in this chapter. Oddly, its D-ring (usually pictured as the upper-right hand ring in
models) is a weird 6 members lactone ring, instead of the usual 5 ring one that
testosterone has. So, now I know it’s an anabolic steroid, but what kind? And what
would it do? Primarily, it’s an Anabolic Steroid whose claim to fame is being used
primarily for it’s antiestrogenic effects (much like Proviron), and I think that it’s been
wrongly assumed to be simply an antiestrogen by many athletes. This is not the
case, and as you’ll soon see, there’s really no reason why this stuff has been pushed
out of use by bodybuilders and athletes for the last decade.
The first study I looked at (1) showed that Teslac increases testosterone (by 47%)
and it’s precursor androstenedione (70%) levels in the body. In the second study I
looked at, it raised testosterone levels in men up to 290ng/dl (almost enough to
bring you from 0 Test to the lowest end of normal/acceptable range), as well as
raising LH (leutenizing hormone) levels, and even FSH (Follicle Stimulating Hormone)
levels slightly (2). So as you can see, not only is this stuff not suppressive of your
natural hormones, it actually stimulates your body to produce more testosterone as
well as the hormones that produce it (2). It has been shown to reduce aromatization
by 90-95%, with regards to decrease in the overall rate, in some instances (7). In
another study, aromatase inhibition by testolactone, at a dose of 500 mg twice daily
(so a total of 1,000mgs/day) for 4 weeks lowered circulating estradiol (E2) levels by
roughly 1/3rd and enhanced the secretion of follicle-stimulating hormone and
testosterone by approximately the same amount (1/3rd each) (6). Basically, we’re
looking at pretty decent reductions in both aromatization, as well as reduction in
total estrogen floating around your body.
So far, we have seen that, in different studies it has been shown to increase LH as
well as FSH, respectively. In addition it raises testosterone levels and lowers
estrogen levels in all of the studies we’ve examined. Raising FSH, LH, and
testosterone while lowering estrogen is a pretty good deal considering most steroids
lower endogenous (natural) production of the first three, and raise estrogen.
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In fact, I’ll go so far as to say that if you don’t want to do any shots (injections)
during your post cycle therapy (PCT), Teslac may be perfect for you, since it will
raise LH as well as HCG in most cases! And it has the added benefit of not
desensitizing your Leydig cells as much as HCG has the potential to do. Another
important benefit of using Teslac over HCG during your PCT is that HCG actually may
raise estrogen levels and/or act as an estrogen in certain tissues (8) (9), while we
know that Teslac lowers estrogen levels and acts as (of course) an androgen.
This means, of course, if you are one of those people who inclined to bridge (use a
low dose of an anabolic compound between higher dose cycles), then this is perfect
for you. In addition, you’ll be able to use Teslac during a cycle as an ancillary
compound that will eliminate aromatasation.
Possibly the most exciting thing I read about Teslac is that it has been PROVEN (!) to
be an effective and safe treatment for gynocomastia (3) (development of breasts in
male mammary glands, often ineloquently referred to as “bitch tits” in gym-speak).
So yeah, if you get a bit of gyno on a cycle, you may want to include Teslac in your
PCT for both the (very good) reasons I revealed above, as well as it’s potential to
treat your gyno.
The only prohibitive thing about Teslac is cost. Currently, I don’t know of any online
pharmacies that carry it, nor UG labs. It generally sells for anywhere between a
dollar and $5 for a 250mg tab. If there’s anything preventing this stuff from
becoming the “must have” drug for PCT overnight, it’s cost.
References:
1. Vigersky RA, Glass AR. Effects of delta 1-testolactone on the pituitary-testicular axis
in oligospermic men. J Clin Endocrinol Metab 1981 May;52(5):897-902
2. Reversal of the hypogonadotropic hypogonadism of obese men by administration of
the aromatase inhibitor testolactone.Metabolism. 2003 Sep;52(9):1126-8.
3. Acta Endocrinol Suppl (Copenh). 1986;279:218-26
4.Vigersky RA, Mozingo D, Eil C, Purohit V, Bruton J. The antiandrogenic effects of
delta 1-testolactone (Teslac) in vivo in rats and in vitro in human cultured fibroblasts, rat
mammary carcinoma cells, and rat prostate cytosol. Endocrinology 1982 Jan;110(1):214
9
5. Martikainen H, Ruokonen A, Ronnberg L, Vihko R. Short-term effects of testolactone
on human testicular steroid production and on the response to human chorionic
gonadotropin. Fertil Steril 1985 May;43(5):793-8
6. Effect of aromatase inhibition by delta 1-testolactone on basal and luteinizing
hormone-releasing hormone-stimulated pituitary and gonadal hormonal function in
oligospermic men.. Fertil Steril. 1985 May;43(5):787-92.
7. The effects of the aromatase inhibitor delta 1-testolactone on gonadotropin release and
steroid metabolism in polycystic ovarian disease.J Clin Endocrinol Metab. 1985
Apr;60(4):773-8
8. Pituitary-testicular responsiveness in male hypogonadotropic hypogonadism.
J Clin Invest. 1974 Feb;53(2):408-15.
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9. Winter JS, Taraska S, Faiman C. The hormonal response to HCG stimulation in male
children and adolescents. J Clin Endocrinol Metab 1972 Feb;34(2):348–353
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
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Chapter 11
Sympathomimetics
(And other Fat-Burners)
Ok—first things first: a sympathomimetic is simply a drug that stimulates the
sympathetic nervous system. Basically, what I’m going to tell you about here are
stimulants and their effects on fat-burning, and their use as pre-workout enhancers.
Lets get to it!
There are two types of adrenergic receptors, alpha and beta, as well as various sub
types of each. The first we’ll talk about is the alpha adrenoreceptors.
The most well known adrenoreceptors are the ever-popular beta receptors. Beta
receptors are embedded in the cell's outer phospholipid membrane. These can be
divided into subtypes 1, 2, & 3, while their less popular cousins, the alpha receptors
are broken into subtypes 1 & 2. Alpha receptors are activated at lower catecholamine
levels than are the beta receptors. A catecholamine is an organic compound (an
amine, obviously) that affects the sympathetic nervous system. Dopamine,
norepinephrine and epinephrine are all catecholamines.
Activation of the alpha2 receptor inhibits the release of norepinepherine. This is of
course a “fight or flight” hormone. Ever get nervous? If you’re like most people, you
got physically agitated, started sweating, and lose your appetite. That’s your “fight
or flight” hormones at work. It is the differences in regional distribution of alpha2
and the beta receptors that is responsible for a large part of the gender differences
in body fat storage.
Males have a noticeably greater alpha2 density in abdominals as compared to
women—which contributes to our increased adipose storage there—but the main
difference is caused by higher lower-body alpha2 activity in women, as well as by
beta receptors, which are more highly expressed in males. Women experience the
lipid storing phenomenon in their butt/hips because women have a 3 quarter higher
alpha2 binding in lower body adipose than men, and have a pronounced decreased
energy expenditure in gluteal obesity versus abdominal adipose. Men have this
phenomenon in their abdominals, as we’ve already covered. Ever wonder why men
and women carry fat differently? This is why.
Adipose (fat) tissue has very poor vascularity (blood flow). Take a look at the fat on
the next steak you have; it’s white—very little other. That means there’s not much
blood in it. When triglycerides are broken down into free fatty acids (and glycerol)
during lipolysis, your body has to then get them out of the area, or they’ll just be
reincorporated into the existing fat that’s still there. Sucks, right? Well, when you
stimulate your beta receptors, it causes vasodilation, thus increasing blood flow. As
264
I’m sure you can guess, that will aid in transport of fatty acids out of the area, as
well as their break down. Alone, beta receptor stimulation will not increase
vasodilation enough to get rid of 100% of the free fatty acids released during
lipolysis.
Enter alpha receptor activation. Alpha receptor deactivation causes a
decrease in blood flow, while antagonism of the alpha receptors increases blood flow,
and thus increases the mobilization and disposal of these fatty acids. Clearly,
combining alpha and beta stimulation would be ideal in a fat burning stack of drugs
or supplements.
Now that we have a decent understanding of alpha receptors and what they’re
about, let’s briefly talk about Beta Receptors. Beta receptor stimulation can increase
your body temperature a bit by increasing heat production in the mitochondria,
increase your basal metabolic rate, and decrease your appetite. This only in part
explains how beta agonists directly stimulate fat cells and increase lypolysis (fat
loss).
Although it’s counterintuitive, let’s first go over the actions of beta-3
adrenoreceptors. These beta receptors are the black sheep of the beta receptor
family, so much so that they were previously called the “atypical” beta-AR. The
mechanism of beta-3 action is still, at this point, poorly understood. From what is
currently understood about them, the beta-3’s stimulate uncoupling protein 1, 2, &
3, which greatly influences mitochondrial uncoupling, leading to increased heat
production and energy expenditure. This mechanism is how DNP works, although to
a much (much!) greater degree than any beta-activator ever studied (including those
which stimulate the beta-3’s). Beta-3 stimulation also increases mobilization of fatty
acids from triglyceride stores. All of this would be great, but currently the only beta
3 action we can see is from carry-over effects gleaned from other traditional beta-1
& 2 agonists like ephedrine and clenbuterol. There are no currently available beta-3
agonists in circulation. In addition the preliminary studies on beta-3 agents in
rodents were very misleading, since beta-3 receptor activation in rats and humans is
very different. For practicality’s sake, I’m going to cut the beta-3 discussion a little
bit short, since we don’t know too much about it, and can’t really get anything to
take advantage of the little knowledge we do have on it.
Both beta 1 & 2 receptors have the ability to increase energy expenditure when they
are stimulated, though the differences (and similarities) between them can be
discerned from the following: In humans, both Beta-1 adrenergic stimulation and
Beta-2 adrenergic stimulation also increase energy expenditure. However, in contrast
to rodents, this type of adrenergic-stimulated thermogenesis in humans is mainly
located in skeletal muscle. For rodents, the major site of thermogenesis is actually
brown adipose tissue, as opposed to skeletal muscle, where it occurs for humans.
Besides increasing energy expenditure, both beta-1 & 2 adrenergic stimulations also
increase adipose tissue lipolysis. It has also been pretty reasonably proven that the
increased lipolysis is responsible for a large percentage part of the increase in energy
expenditure after the beta-1 adrenergic stimulation. In contrast (and this is possibly
their biggest difference), beta-2-adrenergic receptors are mainly localized in skeletal
muscle and not in adipocytes; it can be reasonably concluded that stimulation of
beta-2 receptors may actually exert a more direct effect on energy expenditure than
beta-1’s do. This may even be the primary difference in the “how does this happen?”
difference between the very similar effects of beta-1 & 2 agonists. In fact, in all of
the following charts, you’ll see this effect in the “SAL+ACL” portions of the charts,
which is where a beta-2 agonist (salbutamol noted as “SAL” in all the charts) was
combined with a compound to inhibit fat oxidation (thus showing salbuterol’s true
265
effects on energy expenditure absent of increased lipolysis), compared with energy
expenditure of a beta-1 agonist (dobutamine, noted as “DOB” in all the charts).
In the chart below, beta-1 stimulation (DOB) resulted in a 0.58 ± 0.20 kJ/min (P <
0.05) increase in energy expenditure, whereas the beta-2 stimulation (SAL) showed
a 0.72 ± 0.12 (P < 0.001) and 0.62 ± 0.12 (P < 0.001) kJ/min increase. And, as I
previously stated, the SAL+ACL group’s energy expenditure was similar to the SAL
group, telling us that energy expenditure with beta-2 agonists is not dependant on
fat oxidation. Thus, beta-1 & 2 receptor stimulation produce different energy
expenditure through different means. Here’s that chart (and a few more after it):
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Fig. 1. Energy expenditure during Beta-adrenergic stimulation. Values are means ± S
dobutamine (DOB) (indicated by dark circle), salbutamol (SAL)
(triangle)SAL+acipimox (ACI) (open circle).
(Basically the same chart, but maybe easier to understand…)
267
In addition, Beta-1 stimulants may oxidize more fat than beta-2’s though less
glucose (shown in the next two charts respectively):
Solid bar, DOB (beta-1); gray bar, SAL; hatched bar (beta-2), SAL+ACI. *P < 0.05
vs. baseline; #P < 0.05 vs. SAL and SAL+ACI.
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Now Plasma Free fatty acids, comparing beta-1 & 2 stimulation (it’s very similar, as I
already explained):
Plasma free fatty acids (FFA) during beta 1 or 2 adrenergic stimulation. Values are
means ± SE.
It becomes interesting, because you can combine the information on beta 1, 2, & 3
receptors you’ve just read with the information you have on alpha 1 & 2 receptors
discussed at the start of this chapter, and you’ll have enough information to proceed
into the following profiles on various compounds which stimulate those receptors.
And after you’ve read all of the following profiles, you’ll have the information on what
your adreno-receptors do, and what compounds you can use to stimulate them to
take advantage of that information and affect your physique for the stage or beach,
and/or your performance on the field.
Let’s go over what all of this means, in the simplest terms. Yeah, I know, this is the
part I could have said in the beginning, but I’d rather explain it first, rather than just
issuing semi-profound declarations with no support.
Here’s what we just went over, regarding stimulation of the various adrenoreceptors,
as relates to our goals in particular:
Alpha-2 Receptors: inhibit the release of norepinepherine.
Beta-1 Receptors: increase adipose tissue lipolysis and energy expenditure. It has
also been pretty reasonably proven that the increased lipolysis is responsible for a
large percentage part of the increase in energy expenditure after the beta-1
adrenergic stimulation.
Beta-2 Receptors: Increases adipose tissue lipolysis and energy expenditure. These
receptors are mainly localized in skeletal muscle and not in adipocytes; it can be
269
reasonably concluded that stimulation of beta-2 receptors may actually exert a direct
effect on energy expenditure, which is not dependant on fat oxidation.
Beta-3 Receptors: stimulate uncoupling protein 1, 2, and 3, which greatly influences
mitochondrial uncoupling, leading to increased heat production and energy
expenditure. Beta-3 stimulation also increases mobilization of fatty acids from
triglyceride stores.
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270
Albuterol
(Salbutamol)
This stuff is clenbuterol’s shorter acting brother. Essentially, it has all of the effects
of clenbuterol, but actually may be better for athletes. See, where Clen has a very
long lasting effect in the body, Albuterol actually has a comparatively short active
and half-life. Since we know that we can expect all of the fun fat-burning effects Clen
has, when using Albuterol, let’s take a look at some of the more interesting effects
it’s had on strength.
In one study, subjects performed 9 wk of isokinetic knee extensions twice weekly.
Albuterol was given to one group, and placebo to the other, for 6 wks; groups
received 16 mg.d-1 of either treatment, they were strength trained, and the results
recorded. Anyway, making a long story short, the Albuterol group at both midtesting
and post-testing had higher scores than the non-Albuterol group. These results give
clear indications that even theraptic doses of Albuterol administered with resistance
exercise may augment strength gains above and beyond those experienced without
Albuterol (2).
Anecdotally, clenbuterol and ephedrine have both shown themselves capable of
temporarily increasing strength, and I would bet most beta-agonists have this effect,
but I don’t think has been shown as conclusively as it has been with Albuterol.
There’ve also been more than a few complaints of Clen causing athletes to lose their
wind, especially those whose sports require a higher Vo2 max than most. Albuterol,
perhaps due to its short half-life, may not have this deleterious effect (1) and
therefore may actually be a more effective choice for athletes, though not
bodybuilders, who can benefit from Clen’s long-lasting lipolytic effect.
References:
1. Effect of salbutamol on muscle strength and endurance performance in nonasthmatic
men. Med Sci Sports Exerc. 2000 Jul;32(7):1300-6.
2. The effects of Albuterol and isokinetic exercise on the quadriceps muscle group.Med
Sci Sports Exerc. 1995 Nov;27(11):1471-6
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Caffeine
Yeah, caffeine….the stuff that you get at Starbucks. Caffeine (1,3,7
trimethylxanthine) is yet another sympathomimetic, and a member of the xanthine
family. Luckily for us, most of the United States (and the world) is addicted to the
stuff, so the FDA will probably leave us alone on this issue. Also, it’s over 99% orally
bioavailable, so a cup of black coffee is still socially acceptable, and basically is as
good of a delivery method as a pill is.
Caffeine will raise your body temperature a bit, and also increase your ability to
focus and concentrate on simple tasks. It’s got both (slight) strength
(neuromuscular) enhancing effects as well as endurance enhancing abilities. Those
effects are noticeable enough that caffeine, in large doses, has been banned by both
the IOC and NCAA. Of course, take too much, and you’ll just be jittery and anxious.
Tolerance, therefore, needs to be assessed by the individual (you) ingesting it.
Performance decreases seem to occur past 500mgs in a serving, though they
following a bell curve. Let’s go over that a bit more.
There is an inverted-U shaped curve (like a glass with the open side on the table,
instead of sitting properly). Ergo, more isn’t always better. Anxiety seems to set in
at doses of 1,000mgs/day, and performance can suffer after 500mgs/day. 1
2mgs/kg of bodyweight seems to be optimal for strength, endurance, and cognitive
ability enhancement, not to mention being within the acceptable range for stacking
with ephedrine in a 1:10 (E:C) ratio.
Still, caffeine is a cheap and legal stimulant that will enhance performance…unless,
like me, you ingest it via the Energy-Drink you mix with your Vodka….
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Cimaterol
(Cimaterol)
Cimaterol is a stimulant, a fat burner, and similar to clenbuterol in many ways—and
different in some very important ones. Both Clen and cimaterol are beta-adrenergic
agonists, and thus are both anabolic as well as thermogenic (1)(5). Also, both
stimulate your adrenal glands, increase your body temperature, raise your heart
rate, etc., i.e. they mimic the “Fight or Flight” response quite well. Cimaterol,
however, may stimulate the beta-1, 2, and 3 receptors while Clen only stimulates
the beta 2 and 3 receptors. This may cause increased fat burning by cimaterol when
compared with clenbuterol. Also, a far greater portion of brown adipose tissue is
burned with the use of Cim over Clen, as far as I can tell.
Cimaterol stimulates both lypolisis (burning fat, the release of free fatty acids and
glycerol) as well as inhibit lypogenesis (gaining fat, the incorporation of 14C into
fatty acids from [14C] glucose) and may even do both more effectively than Clen,
possibly making it a more potent fat burner. In addition, it stimulates protein
synthesis and thus could increase fat free mass via this mechanism (1) while at the
same time burning fat. After a couple of weeks, however, the anabolic effects might
lessen, as one study showed that weight gain (with fat loss, ergo a PURE muscle gain
concurrent with fat loss) halted after 14 days (3). Energy metabolism has been
shown to be greatly increased as well (4). Cimaterol also stimulates blood flow and
causes acute mobilization of nitrogen (alanine), significantly increases amino acid
uptake in muscles, and mobilizes lactic acid out of muscles (2). Thus, it may not
have the athletic performance (endurance and possibly speed) decreasing effects of
Clen (which I’ve written about and alluded to previously, so I won’t get into that
here—it’s beyond the scope of this article). This is pure speculation on my part, and
Cim may still have some of the performance decreasing effects of Clen, but as other
beta-andrenergic-agonists like ephedrine don’t, I see no reason to think Cim does
(as I haven’t read any studies which indicate it does). In any case, a lot of the
studies I’ve read and compared with those on clenbuterol seem to indicate that
cimaterol is actually more potent for fat burning than Clen is.
Ok, so now you know what I have to say about cimaterol, let’s see what some other
people have said. Here's what Dan Duchaine had to say about cimaterol:
"Until some new synthetic beta-3 agonist is commercially available, the beta agonist
of choice is still clenbuterol (although the STRONGER cimaterol is available as a
research chemical in the U.S.)."
Doug Kalman, author of Fat Attack, has written about cimaterol and said:
"Though it's yet to be tested in humans, animal studies have determined that
Cimaterol is a more powerful beta-agonist than clenbuterol, promotes protein
retention and accretion, and has shown powerful anti-catabolic properties in cases of
cancer or burns."
So not only is this stuff a great fat-burner, it's anti-catabolic.
Looks promising, huh? Unfortunately, it downregulates the beta receptors just as
Clen does (3), so a 3 week on/1 week off type of schedule may be appropriate, as
273
would the addition of ketotifen after every 3 weeks (and not going off the cimaterol;
so in 4 weeks on cimaterol, every 4th week you’d be adding in 2-3 mgs of ketotifen
every night before you go to bed). You could also use 50mgs of benadryl instead of
the ketotifen, in the same manner.
As with any new drug, caution should be taken with this stuff.
A dose of 0.15 milligram/kilogram administered subcutaneously is the standard dose
in a lot of human studies, so I'd be comfortable trying that dose myself, but I'd
prefer a tablet (which are also available). That’s a fraction of any sort of dangerous
dose, as you can see.
LD50:
1973 mg/kg (male)
and 1745 mg/kg (female)
References:
1. Domest Anim endocrinol. 1990 Oct;7(4): 477-84.
2. J Anim Sci. 1998 Apr; 76(4): 988-98.
3. J Anim Sci. 1992 Jan; 70(1): 115-22.
4. Am J Physiol. 1988 Dec; 255(6 Pt 2): R952-60
5. Reprod Nutr Dev. 1988; 28(1):61-84
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Clenbuterol
Clenbuterol (Clen) is a selective beta-2 agonist/antagonist and a bronchodilator.
What this means, is that it stimulates your beta-2 receptors. Of great importance is
that clenbuterol is a selective beta-2 agonist (because it works selectively on the
beta-2-andrenergic-receptors). The thing is, clenbuterol is selective—like hitting a
tack (the tack being your beta-2 receptors) with a small hammer (the hammer being
the Clen): thus, it hits the beta-2 receptors selectively. Sorry if that seems
repetitious, but it’s very important to understand that fact before we move on. Since
clenbuterol has very little beta-1 stimulating ability, it has the ability to reduce
certain kinds of airway obstruction without much in the way of cardiovascular effect
(more about that later), and this is why it is used as an asthma medication.
So what exactly dose a stimulant like Clen (or Ephedrine) do when it stimulates
those Beta Receptors? Well, it serves to increase your body temperature a bit by
increasing heat production in the mitochondria, increase your basal metabolic rate,
and decrease your appetite (1). This partly explains how Beta-2 agonists directly
stimulate fat cells and increase lypolysis (fat-loss) (1)(13). However, because it is a
beta-2 agent, Clen can decrease insulin sensitivity (2), unfortunately.
Clen is a very effective repartitioning agent, and this is what it’s most often used for
in athletic circles. It will increase your ratio of fat free mass (FFM) to fat mass, by
decreasing your fat and possibly increasing your FFM (3). Let’s quantify that a bit:
In one study, horses given a semi-reasonable dose of Clen (slightly over 1mcg/lb x2
a day) and excercised for 20mins, 3x a week (I suppose they were Mentzer disciples)
had significant decreases in % fat (-17.6%) and fat mass (-19.5%) at week 2, which
was similar to Clen given to horses who didn’t excercise; in contrast, the excercised
group had a different FFM response, which significantly increased (+4.4%) at week 6
(3). Week 6! Here’s a chart illustrating the changes in % of body fat experienced in
the various test groups, followed by a chart showing the increase in Fat Free Mass
experienced by the same groups:
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Changes in percent body fat (%fat) over time in clenbuterol and exercise (ClenEx;
A), clenbuterol only (Clen; B), exercise only (Ex; C), and control (Con; D) groups.
Means with different letters (a and b) are significantly different.
Changes in fat free mass (FFM) over time in ClenEx (A), Clen (B), Ex (C), and Con
(D). Means with different letters (a-c) are significantly different.
I think those charts should clearly illustrate the repartitioning effects of Clen, even
though it is known that it’s effects on animals are typically much more dramatic than
in humans. There’s still no doubt about it, in my mind, Clen will help you lose fat
and gain muscle.
276
So Let’s re-examine that first point I made: Clen vs. Clen+excercise produce roughly
the same results for the first 2 weeks! This tells me that the 2 weeks on and 2
weeks off schedule for Clen dosing is far from optimal, and if you want the quasi
anabolic effect from the Clen, it’ll take more than 2 weeks on (6 weeks apparently).
In addition, since Clen alone is similar to Clen+excercise for those first 2 weeks, why
would anyone ever use a 2 on/2 off protocol? Keep in mind that animal responses to
beta-agonist/antagonists differ a bit from ours, but I’m sure that you get the idea
that 2 on/2 off is not a great dosing protocol. If I were using Clen, I’d be using it for
6-12 weeks at a time if I expected to get maximum results from it, but certainly the
most dramatic effects on fat loss appear to be in weeks 1-2. The reasons for the
further increase in FFM around week 6 despite no changes in % fat or fat mass are
not easily explained. It might be that clenbuterol can increases FFM through another
nonreceptor-mediated pathway, which would be very good for us, since the anabolic
effects would also be applicable in humans, despite the fact that animals often
respond more dramatically to beta-agonist/antagonists, due to receptor properties.
However, clenbuterol is highly lipophylic and can also enter muscle tissue (12), so
that could indicate a possible mechanism of work. Maybe that would explain the
significant increase in FFM of 13 kg in at 8 wks in the study? Certainly, muscle
protein synthesis (MPS) must be a part of it, since Clen will increase MPS in your
body (17), but it has even been speculated that the growth-promoting effect of
clenbuterol may be specific to muscle and that the drug may act in a not-yet
understood manner which circumvents (!) the physiological mechanisms responsible
for the control of muscle growth (13). This may mean that clenbuterol can help blast
you past “sticking points” in your training by circumventing the usual mechanisms by
which anabolism is experienced! Perhaps related to this is that both muscle
composition and fibre size has been shown to increase with administration of Clen
(14).
In any case, Clearly the results you want to reproduce for yourself are those to be
gained by Clen + exercise, for 6 weeks or more. This type of dramatic anabolic effect
hasn’t been confirmed in human studies (8), but the anabolic effects of Clen in
animal (specifically equine and rodent) studies are clearly quite astounding.
Now that I told you how great Clen is, I’ll tell you how to take it. Clen has a biphastic
elimination, which means that it is technically reduced in your body in 2 different
stages. This isn’t particularly important, as a recent study has shown that for most
intents and purposes, Clen concentrations in the body decline with a ½ life
(approximately) equivalent to 7-9.2hours and again up to as much as 35 hours later
(4)(5). If you’re really interested, though, Clen technically declines biphastically at
10 and then 36 hours. But really, in our little world, where we use ½ life to tell us
when to take our next dose, who the hell is going to take Clen, then a dose 10 hours
later, then a dose 36 hours later? We’ll stick with the earlier 7-9 hour ½ life for
dosing purposes, and take our clen every 3.5-4.5 hours that we’re awake, stopping
early enough to still be able to get to bed. Clen can, in some people, cause insomnia
(and as with all stimulants, can cause anxiety). Recently, it’s become popular to take
a whopping dose of Clen in the morning, and that’s it for the day. There’s nothing
wrong with this, I guess, but I’d rather not go through that kind of roller-coaster of
sweating and shaking until it wore off.
Based on it’s rate of elimination from the body, and how much is usually needed to
be effective for athletes, my recommendations are the same for both men and
women. You’ll need to take 20mcgs upon rising, and then repeat that same dose
again later in the day, and then once again in that day (if you find you can tolerate
277
the effects). So you’ll start with 20mcgs, and then repeat that dose 2 more times
that same day if you can tolerate it (classic stimulant side effects will determine this:
hand shaking, sweating, etc.). You can then start increasing the dose gradually.
Personally, I wouldn’t work my way up to more than 200mcg/day. 60-120mcg/day is
an average dose, but keep your blood pressure at (or under) 140/90, while on Clen,
just to be safe. If you go over that, lower the dose. You’ll also want to know your
body temperature, upon rising, for the week before you start taking your Clen, and
then monitor it (again, as soon as you wake up) throughout your regimen. When it
returns to the level it was at before you began taking the drug, you’ll need to start
taking your benadryl or ketotifen, as the decrease in body temperature back to
original levels indicates the thermogenic effect is beginning to decline.
Clenbuterol can also cause a downregulation in testicular androgen receptors and in
pulmonary, cardiac and central nervous system beta-adrenergic receptors (6),
possibly making steroids less effective (if there is androgen receptor downregulation
elsewhere as well, then it's highly probable) while you are on it. It definitely makes
Clen less effective if you keep taking it as time goes on. To counteract this, you can
take some ketotifen every 3rd or 4th week that you remain on Clen. It’s a
prescription anti-histimine, so it’ll make you drowsy (take before bedtime).
Basically, the way this works is to reduce beta-2 receptor activity, and restore
receptor function (15).
Another option, if you are worried about receptor downgrade, is taking benadryl, at
around 50-100mgs/night before bed (every 3rd week or so, for that week).
Benadryl is sold as an anti-histimine in the United States, and/or a sleep aid
elsewhere in the world. However, beta receptors are embedded in the cell's outer
phospholipid membrane. The stability of the membrane has a lot to do with the
proper function of the receptors. Methylation of the phospholipids is stimulated by
the binding of beta agonists to their receptors. Methylated phospholipids are foreign
to the body, and when the body recognizes tham as foreign, it breaks them down
with phospholipase A2. This changes the structure of the outer membrane, which
results in desensitizaton of the beta receptors. On the other hand, agents that inhibit
phospholipase A2 slow desensitization. Cationic ampiphylic drugs are known for
their ability to inhibit phospholipase A2. Benadryl (diphenhydramine) is a cationic
ampiphylic drug, ergo benadryl slows desensitization of beta receptors (i.e. upgrades
them) by inhibiting phospholipase A2, which is the enzyme that breaks down
methylated phospholipids. This action, in turn, keeps the phospholipid membrane
stable, and thus keeps the receptors functioning properly (7). This will allow you to
use Clen for much longer with the same effects. Also, since benadryl is an anti
histamine, and histamines have a direct effect on beta-adrenoreceptors (not just
beta-2’s but all of them), using an anti-histamine will have a direct effect on
reducing beta-receptor stimulation (16), thus upregulating your beta-receptors.
Since we’re speaking about beta-receptors and upregulation here, let me address the
claim that you can use ephedrine (or the ECA stack), alternating with Clen, in order
to avoid receptor downgrade. I’m not sure where this rumor came from, but it is
totally incorrect.
To dispel this myth, let’s examine ephedrine for a second. Remember when I said
that using clenbuterol to stimulate the beta-2 receptors is like hitting a tack with a
hammer? Well, ephedrine is like a sledge-hammer; it hits the beta-2's and
everything around them. Thats because it's not selective, but rather it stimulates
other receptors to a significant degree as well.
278
Anyway, one of those receptors that ephedrine hits is the beta-2 (yeah, the same
one as Clen). As you can see from the graph below (ephedrine is represented by the
the solid circles), it reduced beta-2-AndrenergicReceptor (what we call, in laymen’s
terms, the "beta-2 receptor") levels to 32% of the control level after 24 hours. Read
this again:
Ephedrine, in this study, reduces Beta-2 receptor levels to 32% of control after 24
hours.
(See, the solid circles in this graph represent ephedrine)
Granted, it's not perfect; it's not in vivo, etc., but there's no denying that ephedrine
will downregulate beta-2 receptors. For this reason you will not be able to use it on
the weeks in between your Clen to upgrade your receptors.
Also, bear in mind that Clen isn’t great for your heart, and can cause some issues
there (enlargement of ventricles, etc.). Most studies showing Clen to cause heart
problems are with animals, and even though the dosing is almost similar to what
humans take (in some studies it’s within the range of what would be double of a
large human dose). It’s important to remember that animals have more beta-2
receptors and they cause certain event chains that human beta-2 receptors may not.
Clen causes cardiac hypertrophy and cardiac necrosis (cell death) to some degree, in
some cases. Again though, many studies showing the more significant, possibly
irreversible, heart problems are with mg dosing. We humans take Clen in mcg
279
doses. If we want to duplicate those “theraputic” levels of Clen seen in the more
conservative studies, we’d still be taking just over 1mcg/lb of bodyweight twice a
day. I’d suggest a bit less than half of that dose, however, even if just to avoid
cardiac complications.
Performance issues with Clen also vary. Some studies show reduced exercise
(cardiovascular) performance (9), while some show that Clen can alleviate exercise
induced asthma (10)! Clearly, this compound will have different effects on different
people, and I suspect that a lot of it is sports specific. Many bodybuilders claim that
Clen makes it difficult for them to do cardio, yet I can play a full game of rugby on it.
You need to figure out how it affects you, and tailor your dose personally.
Finally, this brings me to the issue of cramps while on Clen. I don’t get them. My
friends don’t get them. Most of us are athletes who use Clen during the season as
well as the off season, and one of my friends even claims that it gives him more
“wind” (cardiovascular stamina). Take on enough water every day and you should be
fine. If you’re really concerned, you can take some extra minerals and taurine, since
Clen depletes taurine (11) as do most if not all beta-agonists. I don’t take anything
more than my usual vitamins and minerals.
1st Graph Reference:
ASPET Journals, Vol. 58, Issue 2, 421-430, August 2000
Kinetic Analysis of Agonist-Induced Down-Regulation of the 2-Adrenergic Receptor in
BEAS-2B Cells Reveals High- and Low-Affinity Components Bruce R. Williams, Roger
Barber, and Richard B. Clark
2nd set of Graph references:
J Appl Physiol 91: 2064-2070, 2001; 8750-7587/01
Chronic administration of therapeutic levels of clenbuterol acts as a repartitioning
agent Charles F. Kearns1, Kenneth H. McKeever1, Karyn Malinowski1, Maggie B.
Struck1, and Takashi Abe2
Other References:
1. Int J Obes Relat Metab Disord. 1994 Jun;18(6):429-33.
2. Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E146-53
3. J Appl Physiol. 2001 Nov;91(5):2064-70
4. J Anal Toxicol. 2001 May-Jun;25(4):280-7.
5. J Pharmacobiodyn. 1985 May;8(5):385-91.
6. J Anim Physiol Anim Nutr (Berl). 2004 Apr;88(3-4):94-100
7. Prog Clin Biol Res. 1981;63:383-8
8. Ann Pharmacother. 1995 Jan;29(1):75-7
9. Med Sci Sports Exerc. 2002 Dec;34(12):1976-85.
10. Respiration. 1987;51(3):205-13.
280
11. Adv Exp Med Biol. 1996;403:233-45
12. Food Addit Contam 13: 259-274, 1996
13. Biochem J. 1989 Jul 1;261(1):1-10.
14. Biosci Rep. 1987 Feb;7(2):143-9.
15. Z Erkr Atmungsorgane. 1990;175(3):141-6
16. Comp Biochem Physiol C. 1989;92(1):143-8.
17. Biosci Rep. 1984 Jan;4(1):83-91.
Research Anabolic Steroids
and Related Topics at:
http://www.Steroid.com
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DNP
(2,4-dinitrophenol)
DNP was first introduced to the bodybuilding world by Dan Duchaine. In the late 90s,
the body building magazine Muscle Media 2000 was offering this special deal to
anyone who subscribed. If you subscribed, you got a bunch of audio cassettes
containing interviews with 10 bodybuilding experts. Those cassettes included
interviews with noted bodybuilding experts, and I’m sure they were very interesting.
I only listened to two of them, and the other eight collected dust in a drawer
somewhere in my bedroom, I’m sure. But one of the two I listened to had an
interview with Dan Duchaine, which ended with him promising to tell the
bodybuilders about a new substance which would revolutionize the bodybuilding
world. Fast-forward a year, and there was a question in MM2K asking him to let the
cat out of the bag.
What he did was tell us about DNP. Since then, we have a lot more experience with
it, due to feedback from bodybuilders, and figured out the optimal doses and such
from trial and error. The first thing that I will tell you about DNP is the first thing Mr.
Duchaine said about it:
DNP is dangerous.
If you screw up using it, you may go blind, or end up in the hospital on an ice bed
receiving ice-water enemas as the doctors frantically try to make the temperature of
your yellow and sweaty body go back down. I’m not joking. On the positive side,
very few people have died from DNP, although it remains a distinct possibility. Some
DNP related fatalities have been reported (14)(23).
Outside the bodybuilding world, DNP is used to make certain dyes—break open a
capsule and you’ll see that the distinct color you get on your hands is nearly
impossible to wash off. It can also be used as a fungicide, herbicide, and insecticide.
Before that, in the early part of the 1900’s it was used as an explosive.
Clearly, this is stuff you don’t want to take lightly.
DNP works by uncoupling oxidative phosphorylation, which increases the body’s
temperature and metabolic rate (1). Synthesis of fatty acid in adipose tissue requires
cooperation of mitochondrial and cytoplasmic enzymes. Mitochondria release energy
from food molecules and transform energy into useable form via the production of
ATP. ATP is the primary carrier of energy within your cells, and most cells die quickly
in the absence of it. ATP in turn powers your muscles. What does DNP have to do
with all this? DNP depletes your muscle’s ATP (4), thus requiring your mitochondria
to convert more energy from food molecules, and thus create more ATP to replace
what was lost. This makes your body use more energy to do anything, from walking
the dog to benching 315lbs. In addition, since cellular levels of all these metabolites
depend on the efficiency of mitochondrial energy conversion, a mitochondrial proton
leak via uncoupling proteins (UCPs) could modulate Fatty Acid synthesis (8).
Paradoxically, DNP inhibits muscle contraction, even though it accelerates the
ATPase activity activity of isolated myosin (13). ATPase is the enzyme that causes
ATP molecules to release the energy they store, and myosin is a protein that (along
with actin) is responsible for both muscular contraction and relaxation.
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All of this tells me that your body will need to create more energy than usual to keep
up with the demands DNP is placing on it. In addition, it will have to use more of the
food you take in to produce that much-needed energy, and less of that food to
create and store fat. In fact, you’ll start using stored fat as energy to attenuate the
energy deficit DNP creates. I’ve seen studies on animals where a +60% increase in
metabolic rate is achieved with DNP use (9), although I feel that in humans, the rate
may actually be higher. My speculation is that proper DNP use in humans can net a
40-80% rise in BMR (basal metabolic rate). This is all from hypermetabolism, or the
increase in metabolism, or your body’s need to use more energy to perform tasks.
So what happens when your body requires more energy to do today the same things
it did yesterday? You lose more fat today than you did yesterday, in this case a lot
more. What else? You get tired more quickly as your body struggles to convert food
into energy. Your endurance will suffer. Your staying power in the last few reps of a
set will vanish. Your ability to complete the same amount of sets as you did
yesterday, with the same intensity and weights, will suffer. But that won’t seem like
much of a big deal to you at the time, because you probably won’t get much of a
“pump” at all from the workouts you are completing because DNP reduces the
amount of available glycogen in your muscles (4)(5)(6). DNP will also increase your
rate of ventilation, as your lungs try to get oxygen into your muscles (16). Your
blood will be moving a bit slower than usual, as DNP will increase its viscosity
(thickness). Basically, it will increase your body’s need for oxygen as well as your
blood viscosity (3), and it nearly doubles the rate of oxygen consumption in muscles
(11). Thus, your body will have to work much harder to oxygenate your blood, and
then transport it to working muscles. Cardiac output will then increase proportion to
this new rate of oxygen consumption (15).
If you are an athlete, you’ll play like garbage on DNP because of all that stuff I just
mentioned. For these reasons, I see it as very useful for a bodybuilder (who only has
aesthetics to be worried about, not functional ability or performance), but not very
useful for an athlete. If (and this is a big if), you are badly out of shape and fat
before you have training camp for your sport’s preseason, then I suppose you can
try to use this stuff to lose some fast weight. But in all honesty, a 20 day cycle of
DNP no less than a month away from training camp is all I’d risk. You’ll lose some
weight, and only have to keep it off for a month until training camp starts. I really
want to stress, though, that this stuff is an exceptionally poor choice for use by an
athlete. And remember that part I told you about earlier—DNP inhibiting muscle
contraction? Yeah, that’ll make you weaker, also.
Speaking about getting weaker, DNP will lower thyroid (T3) and thyroid stimulating
hormone levels (7). Lower thyroid levels are positively correlated with lethargy
(tiredness) and muscle weakness. So it’s as fair to say that just as DNP makes you
lose fat via several mechanisms, it will make you feel like garbage through several
mechanisms. Don’t get me wrong, not everyone feels like total garbage on DNP, but
it’s by far the most common side effect I’ve heard of. Err…Next to bad breath. No,
really. Oh, and I almost forgot, yellow(ish?) sweat and body odor that’s brutal. Then
there’s this weird taste in your mouth. On the bright side, we’re talking about fat loss
of almost a half a kilogram per day (1lb/day), when DNP is properly used.
One of the most worrying side effects of DNP use is its ability to cause vision
problems (19)(20). Realistically, you should be alright if you keep your doses and
duration of use reasonable.
283
A lot of the side effects (at least the more dangerous ones, including the ones
associated with vision problems) need to be addressed before I tell you how much
DNP you can use, and for how long. First of all, you will want to make sure you are
taking in enough carbs. Yeah, that’s right, a ketogenic diet (that’s a diet with no
carbs, essentially) is too dangerous to consider with DNP use. In fact, I recommend
taking in a good amount of carbs after your workouts, at least 1-2g/kg of
bodyweight. Glucose metabolism is enhanced in less than a week (21), and I’m wary
of depriving your body of carbs while using DNP. All of these extra carbs are going to
make you sweat more, as your body literally burns them up. I’d still say you can
take in as many carbs as you want, and you’ll want a lot (carb-cravings are a side
effect of DNP use).
The other thing you want to use is pyruvate, which at the very least will have
ocularprotective properties (yes, I made that word up, and it means something that
protects your eyes) (22). Pyruvate will also have some other cool effects on your
body’s energy production ability, but here, we’re primarily concerned with not
developing cataracts or floaters in our vision.
Thankfully, DNP is not particularly hard on your heart, blood pressure, or liver. The
only reason you’ll experience increases in cardiac output is as a response to the
increased ventilation DNP will cause while you are exerting any kind of muscular
force, and even then it isn’t particularly dangerous (3)(6)(11)(15). Most DNP users
feel this effect only vaguely, certainly nothing compared to what would be
experienced with use of ephedrine or maybe even caffeine. So we’re really only
dealing with the lowering of thyroid values and the possible eyesight problems. Oh,
and that pesky “death” thing.
So far, we know we need to keep some carbs in our body, and take some pyruvate.
I can only assume you will also be taking a multivitamin/mineral while using DNP,
just to keep all of your bases covered. There’s also some good reasons to take an
energy supplement with DNP, since it will sap energy out of you. I recommend
something in the morning, and pre-workout, as a minimal insurance against feeling
too tired all the time. Also, you want to take some T3 with your DNP, because of
DNP’s aforementioned ability to lower conversion of T4 into T3. 50-100mcgs/day
should suffice. Taurine and potassium are popular additions to a DNP cycle for many
experienced users. They may not help, but if cramping becomes an issue, then they
could. You’d never even consider using DNP and not taking in enough water, right?
I’d suggest water intake be kept obscenely high, and as close to two gallons per day
as you can get.
So now that you know all about DNP, and how to avoid most of the negative side
effects, I’ll tell you how much to take. From my research, I’d say 2mgs/kg-5mgs/kg
is optimal. If I were going to use this stuff personally, I’d stay on the low end of that,
but I am aware that the “Underground Standard” is 600mgs/day. That’s still a
reasonably safe dose, for most. I’ll also say that were I to personally use DNP, I
would limit it’s use to less than 3 weeks….20 days is the longest I’m comfortable
recommending.
Even at a high(ish) dose, this stuff is very cheap. The underground lab most popular
for this stuff sells it for around a dollar per 200mg pill, so you’re looking at $20-60 to
lose 10-20lbs of fat. It’s a bargain, by any standard, if you do it properly and safely.
284
References:
1.Effects of salicylate and 2,4-dinitrophenol on respiration and metabolism
J Appl Physiol, Oct 1982; 53: 925 - 929.
2. Role of peripheral tissue receptors in stimulation of ventilation by 2,4-dinitrophenol.
Journal of Applied Physiology, Vol 47, Issue 5 1066-1073, 1979
3. Regional hemodynamic responses to hypoxia and hypermetabolism in polycythemic
dogs. Journal of Applied Physiology, Vol 67, Issue 1 96-102, 1989
4. Effect of prolonged anaerobiosis on 125I-insulin binding to rat soleus muscle:
permissive effect of ATP. Am J Physiol Gastrointest Liver Physiol, Dec 1978; 235: 606 -
613.
5.Effect of prolonged anaerobiosis on 125I-insulin binding to rat soleus muscle:
permissive effect of ATP Am J Physiol Endocrinol Metab, Dec 1978; 235: 606 - 613.
6. Studies on the Effects of 2:4 Dinitrophenol on Liverless and Diabetic Dogs
Am J Physiol -- Legacy Content, Sep 1951; 167: 224 - 232.
7. Dnitrophenol--a dangerous doping agent. Tidsskr Nor Laegeforen. 2002 May
30;122(14):1363-4. Norwegian.
8. Decreased fatty acid synthesis due to mitochondrial uncoupling in adipose tissue.
FASEB J. 2000 Sep;14(12):1793-800.
9. The effect of 2,4-dinitrophenol on the metabolic rate of bobwhite quail.
Toxicol Appl Pharmacol. 1993 Dec;123(2):226-33.
10. The mitochondrial uncoupling agent 2,4-dinitrophenol improves mitochondrial
function, attenuates oxidative damage, and increases white matter sparing in the contused
spinal cord. J Neurotrauma. 2004 Oct;21(10):1396-404.
11. The mitochondrial uncoupling agent 2,4-dinitrophenol improves mitochondrial
function, attenuates oxidative damage, and increases white matter sparing in the contused
spinal cord.J Neurotrauma. 2004 Oct;21(10):1396-404.
12. Mitochondrial coupling in vivo in mouse skeletal muscle.
Am J Physiol Cell Physiol. 2004 Feb;286(2):C457-63. Epub 2003 Oct 1.
13. Probing actomyosin interactions with 2,4-dinitrophenol.Biochim Biophys Acta. 2005
May 15;1748(2):165-73. Epub 2005 Jan 19.
14. Dying to be thin: a dinitrophenol related fatality.
Vet Hum Toxicol. 2004 Oct;46(5):251-4.
15. Regulation of cardiac output during 2,4-dinitrophenol-induced tissue
hypermetabolism in the dog.Clin Sci Mol Med. 1977 Jul;53(1):17-25.
16. Role of tissue hypermetabolism in stimulation of ventilation by dinitrophenol.
J Appl Physiol. 1977 Jul;43(1):72-4.
17. Comparison of cardiac output responses to 2,4-dinitrophenol-induced
hypermetabolism and muscular work.J Clin Invest. 1973 Sep;52(9):2283-92.
18. Mitochondrial uncoupling as a target for drug development for the treatment of
obesity.Obes Rev. 2001 Nov;2(4):255-65.
19. Energy substrate requirements for survival of rat retinal cells in culture: the
importance of glucose and monocarboxylates.J Neurochem. 2005 May;93(3):686-97.
285
20. 2,4-Dinitrophenol pharmacologically promotes retinal detachment in rabbits.
Retina. 2005 Apr-May;25(3):339-44.
21. Effect of 2,4-dinitrophenol on the energy metabolism of cattle embryos produced by
in vitro fertilization and culture.
Reprod Fertil Dev. 2002;14(5-6):339-43.
22. Energy substrate requirements for survival of rat retinal cells in culture: the
importance of glucose and monocarboxylates.
J Neurochem. 2005 May;93(3):686-97.
23. Tainter, M. L. et al., "A Case of Fatal Dinitrophenol Poisoning," JAMA 102, pp.
1147-1149 (1934).
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286
Ephedrine
(Ephedrine Hydrochloride)
When I started writing this book, ephedrine was one of my favorite legal
stimulants/fatburners. Halfway through finishing, ephedrine (Ephedra, actually)
became one of my favorite outlawed fatburners; now it’s my favorite legal one again.
Who knows what it will be by the time you have this book in your hands? Tiki Barber,
running back for the NY Giants once speculated that while it was legal, 80% of the
players in the NFL used ephedrine. For my part, I’ll speculate that the number using
it will pick right back up now that it’s legal again, and that this time, NFL players will
be stocking up just in case it goes off the market again.
Ephedrine is a stimulant that belongs to the sympathomimetics family. It’s both an
alpha and beta adrenergenic, as opposed to Clen, which only works on your beta
receptors. Ephedrine releases norepinephrine, which is basically very similar to
adrenaline, your fight or flight hormone, which is an endogenous alpha agonist. First,
when you take ephedrine, your body temperature will rise. This is a good thing, as it
indicates more fuel being burned for energy. That’ll help you shed some of your
subcutaneous body fat stores, and this is basically ephedrine’s main use in athletics.
Its other use is for it’s stimulant properties. The stimulant effect of ephedrine will
increase the contractile strength of skeletal muscle; for this reason ephedrine is
commonly used by powerlifters and Olympic lifters. It also helps many people focus,
similar to caffeine, with which many choose to take their ephedrine. The touted stack
of ephedrine (25-50mg), caffeine (200-300mg) and aspirin (100mg) is shown to be
extremely synergistic for fat loss. In this combination, the ephedrine and caffeine
both act as notable thermogenic stimulants, while the added aspirin helps to inhibit
lipogenesis by extending the duration of their effect and blocking the incorporation of
acetate into fatty acids. The best synergy is when the ephedrine/caffeine ratio is
actually 1:10.
Finally, Ephedrine also seems to slow gastric emptying, which is why it is very
popular as an appetite suppressant, and was included in many diet pill preparations
until it was pulled from the market.
References:
1. [Experimental research of Ephedra sinica's influence on lipid metabolism of lipocyte]
Zhongguo Zhong Yao Za Zhi. 1999 May;24(5):302-4, 320. Chinese.
2. Direct effects of ephedrine isomers on human beta-adrenergic receptor subtypes.
Biochem Pharmacol. 1999 Sep 1;58(5):807-10.
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Yohimbine
This a naturally occurring alpha-2 antagonist. Yohimbine promotes sympathetic
activity by central as well as peripheral mechanisms, however, in moderately high
doses does not usually raise heart rate, increase blood pressure, or induce anxiety.
When you take this stuff prior to exercise, it boosts lipolysis for the duration of, and
following, your workout; pre-exercise administration of yohimbine can also lower the
respiratory quotient during and following exercise, thus promoting fat loss. It may
also be synergistic with Caffeine.
Dan Duchaine postulated that you could inject tiny amounts of the prescription
yohimbe into lower body fat stores (where alpha receptors are abundant) to produce
localized fat loss.
Another more secondary mechanism by which yohimbine can induce lipolysis (still
via the adrenergic system) is by increasing peripheral blood flow, which would thus
burn more fat.
Reference:
1.Pre-exercise administration of yohimbine may enhance the efficacy of exercise training
as a fat loss strategy by boosting lipolysis. Med Hypotheses. 2002 Jun;58(6):491-5.
288
Chapter 12
Thyroid Drugs
(And Thyroid Function)
Before we get into the specifics of thyroid medications, I feel that it’s only
responsible to explain what your thyroid is and what it does before we start talking
about manipulating it. After you read this chapter, you will understand all about your
thyroid, and how to manipulate thyroid hormones to optimize your metabolic rate.
The first thing we’re going to have to do is get a digital thermometer so we can
check our basal body temperature when we wake up. A lot of people say they can
use a mercury one, and it’s just as good (or better) than a digital, but I don’t like the
room for human error that they allow (misreading, misjudging where the mercury
level is, etc.). It is of course, up to you, as to whether saving the $5 from buying a
mercury thermometer over a digital is worth it. But since you spent a lot more than
that on this book, I doubt it is. I will leave the choice entirely up to you as to
whether you purchase a thermometer for rectal or oral use. I monitored my morning
body temp (called basal body temperature or BBT, from here on), a few years ago
when I was messing around with thyroid hormones a lot, and found it to be a very
valuable tool to give me some kind of indicator as to how my thyroid was
functioning. I went the oral route, thank you.
Anyway, what you’ll need to do is take your temperature every morning, before you
get up out of bed, for a week without being on any medications (steroids, etc…) or
thermogenics (Clen, ephedra, etc.). This will give you a score to work with to tell
how much work you need to do in order to bring up your “average” score to
“optimal.”
So what score are you striving for? Ideally you’re looking for a score between 97.7F
and 98.3F, with the latter being “on the money” ideal. I’m willing to bet that yours is
slightly or moderately lower than that.
So what do we do? Well, we want to raise it, ideally. This is relatively easy given
the arsenal of compounds we have to work with. You could take supplemental
Synthroid, which is a T4 medication. I don’t like going this route, and I’ll tell you
why. Your body needs to convert T4 into T3. T4 is converted peripherally into T3 via
the deiodinase enzyme. The T3 could then raise your body temperature to the
hypothetical “ideal” of 98.3. And if there is something insufficient or deficient with
your T4-T3 conversion process, then you are taking a bunch of synthroid, which
won’t be turned into T3. It’s simply too haphazard for my liking to take a drug and
hope your body does what you want it to do with it. I don’t like leaving things to
chance.
So what we’re going to have to do is buy a whole bunch of tricana, or a bit of
Cytomel. I’m going to focus on Cytomel, since it’s what I use, and it’s currently very
easy to get via several different Internet pharmacies and research companies.
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Now before you start popping Cytomel like it’s pez until your BBT reaches 98.3, I’m
going to explain a bit about your thyroid.
Your thyroid is a very vascular structure with two lobes connected by a broad
isthmus. It’s located around your larynx, on both sides and in front of your trachea.
It secretes 3 hormones, only 2 of which will be of concern right now. The first is
thyroxine (traiodothyronine) or T4; its molecule contains 4 iodine atoms. The
second is T3 also called triiodothyronine (yes, it’s the same word as for T4 with the
exception of an “i” instead of an “a”, and yes, you guessed it, there are 3 iodine
atoms in T3).
Both of these hormones regulate the metabolism of carbohydrates, fats, and
proteins. They increase the rate at which cells release energy from carbs, enhance
protein synthesis, and mobilize lipids (fats).
T3 is the more physiologically active hormone, and as I already told you, T4 is
converted into T3. Eighty Percent of your body’s T3 comes from this conversion.
Thyroid stimulating hormone (TSH) (produced by the pituitary gland) controls the
secretion of T4 through release of thyrotropin releasing hormone (TRH), which is
produced in the hypothalamus. Another hormone, T2, is then produced from T3.
T2 acts on the mitochondria directly and increases the rate of mitochondrial
respiration, with a consequent increase in ATP production (similar to what DNP
does), and has similar beneficial effects on your cells’ mitochondria (the cells’
powerhouse). If you have a low thyroid level, you will probably be tired and listless.
On the other hand, a high thyroid level can make you energetic. Now hopefully you’ll
start to understand why I recommend optimizing your thyroid level. I mean, it’s
cheap (a couple of months of thyroid meds will run you under $100), and it’s
effective. You get better macronutrient assimilation, a nice fat-burning effect and
higher energy levels. You also get a possible synergy with Clen or ephedrine if you
should choose to run them with your T3. Using T3 will upregulate the beta-2
adrenergic receptor in adipose tissue (fat). Clearly there is a synergy here between
clen, beta-drugs and T3. One research company has even begun selling them pre
mixed!
As you suspected, there’s a catch. Remember the negative feedback loop that your
body has for the HPTA? Well, it has one for thyroid hormones too. When your T3
levels go up, your TSH secretion is suppressed, so there will be a short lag time from
when you stop taking thyroid meds until your body recovers. I wouldn’t be too
concerned with this, as you can schedule it to happen during the winter months
when you’ll be covered up anyway. There have been studies where patients on
thyroid medication for 30+ years have quickly recovered their normal thyroid
function upon cessation of thyroid hormone therapy. And more recently, several
fitness competitors have gone off thyroid meds after several years on them and were
able to recover fairly quickly.
Ok, so now we know where we are (because we’ve checked BBT for the last week)
and where we want to be (98.3F), and now we even know what the thyroid gland is.
So, now can you start popping Cytomel like pez? No, not yet. What you are going
to do is start taking 20mcg of Cytomel per day for a week, and upping the dose by
10mcg/week until your BBT reaches 98.0-98.1. Try not to go over 100mcgs, though.
Then you can start adding in other thermogenics if you are trying to get cut or if you
are in a pre-contest phase, or you can simply continue adding Cytomel until your
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BBT reaches 98.3. Without further ado, here’s the profiles on all currently available
thyroid medications!
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Cytomel
(Liothyrine Sodium )
This drug is a synthetic T3 hormone. As you may already know, most natural T3 is
not produced directly by your thyroid gland, but rather is converted from the T4
thyroid hormone (8).
Natural T3 is a regulator of the oxidative metabolism of energy producing substrates
(food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The
mitochondria, as you will recall from your high school biology class, are usually
referred to as the "cells’ powerhouses" because they produce ATP. Taking Cytomel
(supplemental T3) greatly increases the uptake of nutrients into the mitochondria
and their oxidation rate (i.e. the rate at which they are burned for energy), by
increasing the activities of the enzymes involved in the oxidative metabolic pathway.
Everything is working harder, in other words, and more fuel is needed to supplement
this increased work rate. Therefore, as you can guess, taking supplemental Cytomel
will increase your body’s energy demands. And if you are in a hypocaloric state, you
will begin burning even more fat, primarily due to an increase in ATP. This increased
ATP causes an increase in overall metabolic activity (8)(9). This is exactly what we
want, and is why we would be taking thyroid hormones like Cytomel in the first
place. If you aren’t taking anabolic steroids with your Cytomel, however, your body
may start to eat away muscle to provide energy for you to function. Remember
mitochondria/ATP aren’t very picky, but they are very efficient. What I mean by this
is that they will use whatever is on hand to generate energy for your body to
continue functioning—fat, protein, glucose—it doesn’t matter to ATP, as long as
there’s something to give them energy. Taking this drug will increase their need to
find something to burn to create this energy. Ergo, if we aren’t taking anabolic
steroids while taking our T3, we may lose too much muscle, especially while dieting.
Thus you can see that there are many advantages to using Cytomel to optimize your
metabolic rate. It will also increase your body’s ability to synthesize protein, but
from what I’ve seen personally, it acts as a catabolic when it isn’t administered with
anabolic steroids. It is often the last thing added into a precontest diet, as it has a
reputation for getting rid of the last few percentages of body fat, the “sticky fat” as
it’s called in bodybuilding, the fat that just doesn’t want to leave you in the last few
weeks of dieting. I think this is a poor use for this drug, and that it should be the
first thing added into a diet to lose fat, as it will optimize your metabolic rate, which
should be done at the outset of a diet, not after the calorie restriction has diminished
your thyroid output and you are adding it in simply to replace what was lost.
Unfortunately, in all of the studies I’ve seen, T3 also increased growth hormone
production (5)(6). As we all know, GH is also a strongly lipolytic compound, and this
is another mechanism by which T3 may exert its effects, although I suspect this
would only be a small percentage of it’s overall effects. This being the case, it has
always been somewhat problematic to me to note that when GH and T3 are used
together, the increased nitrogen retention normally found with GH use is negated.
(7). If you were only using T3 and GH this may be a problem, but as I’ve already
stated, you are going to need some anabolic agents if you are using T3. And as you
have read previously, I recommend the veritable anabolic/lipolytic orgy of insulin,
T3, Anabolic Steroids and GH for 100% maximum results in minimal time.
292
On the brighter side, and of special note to dieters, administration of T3 has been
shown to upregulate the beta 2 receptors in fat tissue. As you know clenbuterol and
similar compounds downregulate this receptor, so using T3 with your Clen will help
stave off or reverse this downregulation (1)(2)(3)(4). I would still recommend
taking your benadryl every third week, though.
Finally, I would like to address the issue of recovery of your natural thyroid function
after you stop taking Cytomel. The horror stories of people on permanent thyroid
replacement just aren’t true. I remember a few years ago, the rumor was circulating
that the current Ms.Fitness had permanently shut off her thyroid gland, and was now
fat and on thyroid hormone permanently. This is just another horror story based in
nothing but conjecture and rumor. The studies I’ve looked at have shown people
recovering their thyroid hormone relatively quickly (within months, at most) after
going off of several YEARS (!) of thyroid replacement therapy (10)(11). I speculate
that you can optimize your metabolic rate with Cytomel for 9-10 months a year, and
just normalize yourself for 2-3 months (perhaps the winter, when you are mostly
covered up), and then go right back on. Some people in the studies I read were on
T3 for 30 years and recovered their natural thyroid function in short order. I think
we can safely spend an athletic career using Cytomel 9-10 months out of the year,
and just taking those few months off to normalize ourselves. Is this aggressive? Yes.
Unsafe? No.
References:
1. Catecholamines inhibit Ca(2+)-dependent proteolysis in rat skeletal muscle through
beta(2)-adrenoceptors and cAMP. Navegantes LC, Resano NM, Migliorini RH, Kettelhut
IC Am J Physiol Endocrinol Metab 2001 Sep;281(3):E449-54
2. Regulation of human adipocyte gene expression by thyroid hormone J Clin Endocrinol
Metab 2002 Feb;87(2):630-4 Viguerie N, Millet L, Avizou S, Vidal H, Larrouy D,
Langin D.
3. Alpha 2- and beta-adrenergic receptor binding and action in gluteal adipocytes from
patients with hypothyroidism and hyperthyroidism Metabolism 1987 Nov;36(11):1031-9
Richelsen B, Sorensen NS
4. Regulation of beta 1- and beta 3-adrenergic agonist-stimulated lipolytic response in
hyperthyroid and hypothyroid rat white adipocytes Br J Pharmacol 2000 Feb;129(3):448
56. Germack R, Starzec A, Perret GY
5. Role of thyroid hormone in the control of growth hormone gene expression Braz J Med
Biol Res 1994 May;27(5):1269-72. Volpato CB, Nunes MT.
6. Low-dose T(3) improves the bed rest model of simulated weightlessness in men and
women. Am J Physiol 1999 Aug;277(2 Pt 1):E370-9 Lovejoy JC, Smith SR, Zachwieja
JJ, Bray GA, Windhauser MM, Wickersham PJ, Veldhuis JD, Tulley R, de la Bretonne
JA.
7. Effects of long-term growth hormone (GH) and triiodothyronine (T3) administration
on functional hepatic nitrogen clearance in normal man. Wolthers T, Grofte T, Moller N,
Vilstrup H, Jorgensen JO.
J Hepatol 1996 Mar;24(3):313-9
8. Human Anatomy and Physiology, 6th Edition. John w. Hole jr.
293
9. Physicians Desk Reference
10. Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid
suppression therapy. N Engl J Med 1975 Oct 2;293(14):681-4 Vagenakis AG, Braverman
LE, Azizi F, Portinay GI, Ingbar SH.
11. Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of
chronic thyroid therapy. J Clin Endocrinol Metab 1975 Jul;41(1):70-80 Krugman LG,
Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN
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Synthroid
(Levothyroxine Sodium)
Synthroid is the less powerful of the two most popular thyroid replacement drugs on
the market. It is synthetic T4, and is actually the more prescribed thyroid medication
in America, but the lesser used of the thyroid drugs which are popular with
bodybuilders. If you have naturally low T3 levels, then you may be able to
supplement with T4, and have it convert to T3 via your body’s natural metabolic
pathways, which involves the deiodinase enzyme. However, There have been a
number of studies that have shown that during reduced caloric intake, and/or when
carbohydrate intake is reduced dramatically, levels of deiodinase decline, hindering
the conversion of T4 to the physiologically active T3(1). So, if you are dieting (which
would necessarily mean you have a reduced caloric intake and/or reduced
carbohydrate levels), then you have less deiodinase enzyme (still with me?) and
thus, that T4 you are taking in hopes of getting it to convert to T3, is not getting
converted. This is not what we want, clearly, and is why most pre-contest dieters
include Cytomel in their drug regimen instead of Synthroid. In fact, Synthroid may
be particularly bad for dieters on Cyclic Ketogenic Diets.
When you earn your living off of your body, as many fitness models, models, and
bodybuilders do, it’s just too haphazard to trust Synthroid. This is especially true if
you are not monitoring your Basal Body Temperature or (preferably) shelling out the
money for a thyroid function test every month.
As compared to Cytomel, Synthroid requires significantly higher doses to be
effective. Most bodybuilders don’t exceed 100mcgs of Cytomel during a precontest
phase of dieting, but with Synthroid the doses climb significantly higher to achieve
the same results. From interviews I’ve done with bodybuilders who have used
Synthroid, I’ve heard of it being used at up to 300mcgs/day. When you compare that
to the mere 25-100mcgs/day of Cytomel that bodybuilders are typically using, we
have another strike against Synthroid. It isn’t really economically feasible to do that
much Synthroid and remain cost effective, at least when compared with Cytomel. To
give you a fair estimate, you could run an effective dose of both Cytomel and
Clenbuterol for the same price as an effective dose of Synthroid.
My advice? Use it if you have to, but only if that’s the case, and you can’t get
Cytomel or Tricana. It works, and will eventually get you to the desired body
temperature for optimal fat burning, but it just isn’t as elegant as the less
suppressive Tricana, or the more effective Cytomel.
Reference:
1. The effect of a low-calorie diet alone and in combination with triiodothyronine therapy
on weight loss and hypophyseal thyroid function in obesity. Koppeschaar HP,
Meinders AE, Schwarz F.
Int J Obes 1983;7(2):123-31
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Triacana
(3,5,3'-triiodothyroacetic acid)
Tiratricol
Triacana is a naturally occurring thyroid product containing the substance known as
Tiratricol. Tiratricol is a metabolite of the iodiferous thyroid hormone, L
triiodthyronine (T3) (1), and is available at health-food stores, sold over the
Internet, and is quite popular in Europe. The drug is marketed under the brand
names Triax, Tri-Cuts, and Triacana.
In order to provide you with a sound understanding of Triacana, I’ll first briefly
remind you of the function of the two main hormones produced by the Thyroid gland.
The two main hormones produced by the thyroid are L-triiodthyronine (T3), and L
thyroxine (T4). T4 is the hormone which the thyroid produces the lions share of, and
is converted by a deiodinase enzyme into what is known as T3 (2).
When a person is involved in a calorie-restricted diet, the body produces less
deiodinase enzyme, and hence produces less T3. When our bodies lack the effects of
T3 (the more potent of the two hormones) our BMR decreases. An abundance of T4
is still present, however, T4 simply isn’t potent enough to maintain the high
metabolic rate we seek while trying to burn fat. When our metabolism is slower,
fewer calories are burned, and our dieting struggles to remain productive. This is all
described as the infamous “negative feedback loop.”
Now, with a bit more information, you can begin to draw the connection between fat
loss, and the use of Triacana (tiratricol).
Triacana has held a solid reputation since the 1970’s among athletes and
bodybuilders for being a strong fat-burning drug. While it can aid lipolysis, the
effects are extremely mild when compared to stronger thyroid hormones, namely T4
and T3. One exception would be Triacana’s higher thermogenic potency in brown
adipocytes (3). The misconception that many people possess regarding Tiratricol is
that the effects are harmless. Simply put, this is untrue. Tiratricol can significantly
suppress Thyroid Stimulating Hormone (4). Although the effects are mild when
compared to those caused by T3, they’re still present. Thyroid recovery generally
takes up to 6 weeks; however, extreme cases have shown to take up to 5months to
fully recover from the TSH suppression (4). Thankfully, TSH recovery is very quick
(5), and there has yet to be a documented case of the Thyroid being permanently
shut down from the use of Tiratricol.
Common dosages of this product range from 10-14 tablets per day. Generally, two
0.35 mg tablets are taken on the first day of intake and with two tablets added each
successive day until 10-14 tablets/day are taken. The half-life time of tiratricol is 5-7
hours, so Triacana should be taken 3-4 times daily (7)(8). Doing so will allow a
constant amount of the substance in the blood, so the effects are continual. There
are also many athletes who prefer to combine Triacana with Clenbuterol, or another
type of thermogenic. Popular choices include a stack of Ephedrine, Caffeine, and
Aspirin/Yohimbine. Many feel that the addition of one of these choices substantially
increases the effects of Triacana, and provide better fat loss results when combined.
Additionally, by adding a stimulant, it is easier to sustain hunger pains which can
296
occur with the use of Triacana. Something of additional note, is the common
inclusion of Triacana while exogenous Growth Hormone is being administered. This is
performed in order to meet the body's increased requirement for thyroid hormone.
Additionally, Triacana is superior to T3 the treatment of thyroid hormone resistance
(9), and is often favoured for treating Hyperthyroidism (10).
Regarding duration of application, the range of opinions varies by a large amount.
Athletes have taken Triacana from one week, ranging up to many months. The
reason behind most people straying from long duration use, is the fear of their
thyroid shutting down permanently. As mentioned above, the likelihood of this
happening is slim to none, however, it is still a possibility many consider. In fact,
Triacana is often considered more TSH suppressive than the more potent T4 (11). A
suggested duration for moderate usage would be up to 12 weeks; however, there is
little evidence that running longer cycles have any different effects versus shorter
durations. Something to keep in mind, is that you shouldn’t slowly decrease dosages
in fear of a sudden rebound effect. By doing so, you only prolong the amount of time
until your thyroid can recover. Stopping abruptly allows your thyroid to begin
recovery right away.
If you’re interested in making the commitment that taking thyroid
hormones/derivatives requires, and the risks involved, Triacana isn’t your best
choice. The side effects are very similar to that of T3, yet lacking the potency by a
substantial amount. In fact, it has been observed by some that the effects were non
existent, even at a TSH-suppressive dose of 3mg split throughout the day (12).This
is a substantial reason as to why the drug’s popularity and usage by the bodybuilding
and sport communities has dropped immensely in past years, as it’s quite inferior
when compared to T3.
One hundred tablets are packaged in a box containing four push-through strips of 25
tablets each. The tablets are white and have neither an imprint nor a break
indentation. The price on the black market is usually $60 - 80 per box.
References:
1. Neth J Med. 1991 Jun;38(5-6):193-8.
2. Neuroendocrinology. 1984 Mar;38(3):254-60.
3. Cell Mol Life Sci. 2003 Sep;60(9):1957-67.
4. Int J Sport Nutr Exerc Metab. 2003 Mar;13(1):112-6.
5. J Clin Invest. 1984 Feb;73(2):570-5.
6. Roger PP, Servais P, Dumont JE. Exp Cell Res 1990;172:282–92.
7. Thyroid. 1996 Dec;6(6):563-70.
8. www.Steroid.com/
9. J Clin Endocrinol Metab. 1995 Jul;80(7):2033-40.
10. Monatsschr Kinderheilkd. 1993 Feb;141(2):100-2.
11. J Clin Endocrinol Metab. 1993 Jul;77(1):221-8.
12. Nuklearmedizin. 1989 Dec;28(6):217-20.
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Recovering Thyroid Function
Now that I told you how to get your metabolism to the optimal level, I’ll tell you how
to quickly recover your natural thyroid function in the months following your self
imposed thyroid adjustment. There are many supplements available which will help,
but I am going to concentrate on the three which I feel will help you recover your
thyroid hormones to baseline levels. Coleus forskohlii is the first one I’ll tell you
about. Basically this stuff stimulates your thyroid gland to increase it’s output (1).
Needless to say, this is good. The second supplement of importance here is
Guggulsterones. This is the extract from the tree resin of Commiphora Mukul. In
essence, it stimulates the uptake of iodine and also the output of thyroid hormones
(1)(2)(3). As a nice added benefit, guggul lipids may have some kind of benefits to
your lipid profile.
And the final supplement I’m going to tell you about is Tyrosine (yeah, the amino
acid). Tyrosine is simply a precursor to the thyroid hormone T3 (5)(6). You want to
have this in your body when you are trying to bring your thyroid hormones back to
normal.
References:
1. J Clin Invest. 1984 Feb;73(2):570-5.
2. Thyroid stimulatory action of (Z)-guggulsterone: mechanism of action.
Planta Med. 1988 Aug;54(4):271-7.
3. The hypolipidemic natural product guggulsterone acts as an antagonist of the
bile acid receptor.Mol Endocrinol. 2002 Jul;16(7):1590-7.
4. Thyroid stimulating action of Z-guggulsterone obtained from Commiphora
mukul. Planta Med. 1984 Feb;(1):78-80.
5. [Thyroid hormone production and its regulation]
Rev Prat. 1998 Nov 15;48(18):1987-91. French.
6. Factors regulating triiodothyronine (T3) and thyroxine (T4) in blood.
Mayo Clin Proc. 1972 Dec;47(12):944-52..
7. Iodoamino acid synthesis in thyroid lobes in vitro with excellent yield of
iodothyronines.
Acta Endocrinol (Copenh). 1979 Oct;92(2):286-94.
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GH/IGF/Insulin
299
Chapter 13
GH/IGF/Insulin
As you’ll see from the following profiles, it’s almost counterproductive to talk about
one of these compounds without entering into secondary conversation about the
others.
I’ve also decided to place these profiles directly after the ones concerning Fat
Burning, but more specifically, the ones about thyroid function and thyroid
medications, because it’s my hope that if you’ve read the book in order, you’ll find
that it’s been arranged to build a base of knowledge in a certain order, so the next
chapters are more understandable, and the previous chapters help you to grasp
more fully the ones to come.
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Human Growth Hormone
(Somatotropin)
Human growth hormone is produced in the body by the pituitary gland. Before this
happens, Growth Hormone Releasing Hormone (GHRH) and Somatostatin (SST) are
released by the hypothalamus, and that determines whether more or less GH is
produced by the pituitary.(1) Many factors influence the release of GH, however,
including nutrition and exercise (6)(7).
Once it is released, Growth Hormone (GH), which is also called Somatotropin (STH)
has many functions in the human body. GH is a protein that stimulates the body cells
to both increase in size, as well as undergo more rapid cell division than usual. In
addition, it enhances the movement of amino acids through cell membranes and also
increases the rate at which these cells convert these molecules into proteins. Clearly,
you can see that this would amount to an anabolic (muscle building) effect in the
human body. GH also has the ability to cause cells to decrease the normal rate at
which they utilize carbohydrates, and simultaneously increase the rate at which they
use fats.(1) Fat loss and lean mass increases with GH have been found at a dose as
low as . 0.028 iu/kg/daily for 24 weeks(4)…however, in my estimation, that would be
insufficient for a bodybuilder trying to gain muscle. Lets use .028iu/kg as a working
number; thats 2.8iu for a 100kg (220lbs) bodybuilder. That’s certainly not
unreasonable, and I would say that that dose to 2x that dose is the range most
bodybuilders and athletes are finding their best results with. Also, that length of time
used in the study I just mentioned (24 weeks) is very typical of GH use, and in
conversations with my friends who have used this compound, have told me that they
experience consistent results starting well after the 2-month-mark, and they tend to
either run this stuff for 6 months at a time, or year-round (if they have sufficient
funds). One of my friends is able to consistently retain a shredded 6-7% body fat all
year round with the assistance of GH, whether he is on steroids or off. He also has
noted that his cardio (fast walking, for an hour a day) was much easier while on GH
than when off, and certainly the research I’ve done would support his claim that
submaximal aerobic ability is improved with GH use (5) (15).
How anabolic is this stuff? Well, even endurance athletes at rest (!) were observed in
one study to be in an anabolic state (8). Yeah…so you can basically run marathons
and take this stuff, and still build some muscle. Pretty impressive, right?
Growth Hormone is usually secreted in rhythmic pulses while you are sleeping, as
two peptides, GHRH and Somatostatin (SST) are alternately released. As you can
guess, GHRH (Growth Hormone Releasing Hormone) is the one responsible for the
Release of Growth Hormone (And who said scientists have funny ways for naming
things…?).(1)
Growth hormone also has the ability to stimulate the production (or reproduction, in
the case of an injury) of cartilage. This, however, requires the presence of a
mediator substance, Somatomedin (IGF), which is released from the liver in
response to GH…and the IGF, in turn, actually promotes the growth of cartilage.(1)
Although it requires IGF to actually grow new cartilage, GH is directly able to
stimulate the elongation of bone tissue.(1), and GH has also been shown to elicit a
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positive effects on erythropoeisis (9), which is great for both anabolism as well as
endurance.
Remember the negative feedback loop I always tell you about? Well, of course, your
body has one which can stop the secretion of GH, and it involves IGF. When your
liver receives secretes IGF-1, it sends a message to both your Hypothalamus as well
as your Pituitary to stop producing GH. (1)
As you have probably guessed by now, your body produces the majority of it’s GH
during your early years, when you are experiencing growth spurts. As you get older,
however, you just produce less of this stuff, and it’s effects are much less
pronounced. This was the driving force behind the (always weird) life-extension
crowd embracing GH in the early 90’s. And, as usual,. The driving force behind the
athletic world embracing GH was Dan Duchaine, which I’m sure comes as no surprise
to many. He first wrote a teaser about it in his Underground Steroid Handbook, and
then wrote extensively about it for the next couple of decades. At that time, Grorm,
was being used. This nasty stuff was GH extracted from (are you ready?): the
pituitary of dead bodies. That’s real “Dawn of the Dead” style science, in my opinion.
I guess it’s an advance from a couple of centuries ago, when Descartes (the “I think
therefore I am” guy) declared the pituitary the part of the human body where the
soul resides. Anyway, back to the cadaver-thing…the GH extracted from the
cadavers were found to be able to (in rare cases) carry a rare brain disease. This of
course, infected the kids who received the infected GH. The use of GH from cadavers
was subsequently discontinued. Back then (the 80’s) there was also a fake version of
some purple looking GH going around (it was HCG I believe, mixed with B-12) called
“Rhesus Monkey Growth Hormone”…which is pretty funny, looking back on it. To this
day, however, if you get fake GH, it’s still probably HCG, since both come presented
as a powder and bacterioistatic water you need to use to reconstitute it (and then it
needs to be refrigerated).
Even if you are using the non-cadaver-derived stuff (and at this point, I’m 100%
sure that there’s none of the old Grorm left on shelves anywhere), it’s possible that
you experience some side effects like carpal tunnel syndrome, acromegaly (a
thickening or growth of bones, most noticeable in the feet, hands, and forehead),
and enlarged organs. Gynocomastia is also possible as a side effect of GH use, as
well as Fluid retention(16) (the later being initially pointed out to me by a female
colleague who had a pre-contest bodybuilder using GH as part of his contest prep).
Now for some really interesting stuff:
Although GH can easily produce very nice, high quality weight and muscle gains, it’s
a very poor compound for inducing strength gains(2)(3)(4). That’s very
counterintuitive, and certainly many strength athletes have experienced great results
in both strength as well as muscle size and fatloss from GH. Generally, many studies
have focused on GH vs. GH and exercise, and without the exercise LBM increases but
not usually maximum voluntary strength output. It should also be noted that most
athletes utilizing GH are using it in a “cocktail” with (at least) anabolic steroids, and
usually with IGF, thyroid meds, and other goodies such as an Aromatase Inhibitor.
Lets discuss exactly why this is.
Most people who are taking the plunge into GH use have reached a dead end with
their use of anabolics, and need to push through that wall. I’m sure you’ve heard
302
about the synergistic combination of using GH along with Anabolic Steroids, IGF,
insulin and T3 (* usually synthroid, a thyroid medication). The reason is that when
these hormones are used correctly together, they'll produce a large amount of
synergy…the insulin is able to shuttle nutrients into your muscle, the thyroid
hormone increases your fat-burning capability, the IGF will cause muscle growth as
well as helping to grow new cartilage (thus preventing injury), and the anabolic
steroids like testosterone, specifically (in addition to being anabolic) can increase
IGF-1, in muscle tissue(11), and maybe even increase your body’s ability to use it.
Also, usually, an increased amount of IGF usually tells your body to stop producing
GH…but testosterone actually blunts this part of the Negative FeedBack Loop (12)!
And the addition of an Aromatase Inhibitor will also stop conversion of testosterone
into estrogen; estrogen reduces IGF levels.(13)(14) Finally, the GH does …well
everything I just spent the last few pages telling you about!
Thus, IGF, Testosterone (and of course other steroids), Insulin, thyroid meds, and
GH will all combine to produce a pretty damned effective fat-burning and muscle
building cycle! You know what else? GH is virtually undetectable on any sort of
currently used drug-screening tests. GH, Insulin, Thyroid meds, and IGF may also be
used pretty safely by those who may be subject to drug screening tests, or as a non
HPTA suppressive “bridge” between cycles.
Finally, I’ll tell you how I’d take GH, personally. There was a study done on
continuous GH use vs. every other day injections (ED vs. EOD for the sake of
brevity), with a equal total weekly dose. Although it’s counterintuitive, every other
day injections produced better total growth in the kids in this (2 and 4 year long)
study. Take a look at these graphs:
Growth velocity of children treated with alternate day GH (the darker bars) or with a
daily GH regimen before, during, and 2 yr after stopping therapy. Values are the
mean ± SD. *, P < 0.05; **, P < 0.01.(10)
Here’s another:
Pretreatment and cumulative 4-yr growth velocity of children treated with alternate
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day GH ( the darker bars) or with a daily GH regimen. Values are the mean ± SD. *,
P < 0.00 (10)
Shooting GH every other day more accurately replicates the pulsile frequency of GH,
and thus gave better results for growth (height) deficient children… GH pulsatility is
necessary for proper function of the GH receptor.(10) Dosing in the EOD nature
reduces incidence of any sort of withdrawal problems associated with normal GH use,
including regression or retardation of growth after cessation of therapy.
Therefore, I feel very comfortable speculating that the use of GH in this manner,
which more closely simulates the natural secretion pattern of it, allows the GH
receptors and the rest of the body to to more efficiently recover from it, and this will
result in much more muscle growth over time (although height was examined in the
previous study). My recommendations, therefore are 2 shots per day of .028iu/kg of
bodyweight, taken every other day, for a minimum of 3months, and preferably for 2
3x that long….and preferably with the other synergistic compounds we’ve just taken
a look at.
You should be paying between $1.75-2.75 per IU of GH, and since you are going to
(necessarily) be buying it in bulk, you should be paying closer to the lower end of
that.
References:
1. Human Anatomy and Physiology, 6th Edition, John W. Hole jr.
2. J Appl Physiol 94: 2273-2281, 2003. First published February 14, 2003; doi:10.1152
3. Journal of Applied Physiology, Vol 77, Issue 1 23-29,
4. EFFECTS OF RECOMBINANT GROWTH HORMONE ON VISCERAL FAT
ACCUMULATION: PILOT STUDY IN HIV-INFECTED ADOLESCENTS.
J Clin Endocrinol Metab. 2005 Apr 19; [Epub ahead of print]
5. Measures of submaximal aerobic performance evaluate and predict functional response
to growth hormone (GH) treatment in GH-deficient adults. J Clin Endocrinol Metab.
1999 Dec;84(12):4570-7.
6. Hormonal responses to consecutive days of heavy-resistance exercise with or without
nutritional supplementation. J Appl Physiol, Oct 1998; 85: 1544 - 1555.
7. Hormonal and growth factor responses to heavy resistance exercise protocols
J Appl Physiol, Oct 1990; 69: 1442 – 1450
8. High dose growth hormone exerts an anabolic effect at rest and during exercise in
endurance-trained athletes.J Clin Endocrinol Metab. 2003 Nov;88(11):5221-6.
9. Christ ER, Cummings MH, Westwood NB, Sawyer BM, Pearson TC, Sonksen PH,
Russell-Jones DL. The importance of growth hormone in the regulation of erythropoiesis,
red cell mass, and plasma volume in adults with growth hormone deficiency., J Clin
Endocrinol Metab 1997 Sep;82(9):2985-90
10. The Journal of Clinical Endocrinology & Metabolism Vol. 87, No.8 3573-3577
11. Am J Physiol Endocrinol Metab. 2002 Mar;282(3):E601-7.
12. Testosterone blunts feedback inhibition of growth hormone secretion by
experimentally elevated insulin-like growth factor-I concentrations.J Clin Endocrinol
304
Metab. 2005 Mar;90(3):1613-7. Epub 2004 Dec 7.
13. Comparison of the Metabolic Effects of Raloxifene and Oral Estrogen in
Postmenopausal and Growth Hormone-Deficient Women.J Clin Endocrinol Metab. 2005
Apr 26; [Epub ahead of print]
14. Serum insulin-like growth factor I levels in growth hormone-deficient adults:
influence of sex steroids.Horm Res. 2004;62 Suppl 1:73-6.
15. Growth hormone enhances effects of endurance training on oxidative muscle
metabolism in elderly women. Am J Physiol Endocrinol Metab, Nov 2000; 279: 989 -
996.
16. J Gerontol A Biol Sci Med Sci 1998 May;53(3):M183-7
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305
IGF-1
(Insulin Like Growth Factor 1 a.k.a. somatomedin C)
IGF1 is a polypeptide hormone about the same size as insulin, or 70 amino acids; it’s
a member of the “super family.” No, this is not the same family Clark Kent belongs
to, but rather it’s a family of substances identified as growth factors. It’s a highly
anabolic hormone released primarily in the liver (but also in peripheral tissues) with
the stimulus of Growth Hormone (GH). It is responsible for much of the anabolic
activity of GH, including nitrogen retention and protein synthesis (12) as well as
muscle cell hyperplasia (increase in number of muscle cells), as well as mitogenesis
(the growth of new muscle fibers). It can also induce skeletal muscle hypertrophy by
activating the phosphatidylinositol 3-kinase (PI3K)-Akt pathway(9). In fact, IGF-1
acts on several different tissues to enhance growth via several mechanisms. It’s also
important to note that GH and IGF-1 are interrelated, they produce a host of
divergent effects (5).As you may already know, GH and IGF levels are both elevated
dramatically following exercise, and this may be a primary factor in the anabolic
effects of weight training. In fact, IGF-1 may be possibly used as an anabolic
substitute for GH (2) in many instances. IGF-1 is, therefore, necessary as well as
sufficient in muscle growth (anabolic)(1) and has been shown to also be highly anti
catabolic agent as well (2)(3). As with all anabolic substances, IGF-1's anabolic
effects are still limited only by the protein (amino acid) supply within muscle cells (6)
(7). Thus, as you may expect, IGF works much better when you are eating enough
protein.
IGF1 may be of particular interests to athletes, as it may improve their ability to
learn new skills and techniques relevant to their sport. You see, IGF is a known
neuroprotector and neuropromotor(13)(14)(15), which means new skills could be
learned more quickly with IGF use, and for the elderly, some of the cognitive effects
of aging could be staved off or possibly halted entirely with administration of IGF1.
This also has exciting implications for the medical community studying Alzheimers
and other such diseases. This is because there are IGF receptors within the brain
(16) and in motor neurons (17).
Also of note, and of special interest to both athletes and bodybuilders who are
rehabbing an injury is that IGF is vital to the proper production of connective tissue,
and exogenous IGF administration may improve collagen formation and aid in the
repair of cartilage. (19)(18). IGF is also vital to proper bone density and bone
density regulation (20). IGF administration may be highly useful for rehabilitation of
any kind of joint injury experienced by athletes and bodybuilders, and would greatly
decrease recovery time as well as increase the strength of the recovered area.
So now we have a basic idea of what IGF does and how it works, so I think we can
start looking at how well it works, and what kind of results we can expect from it.
While I was (exhaustively) researching this compound, I found a study which
provided just the type of answers we are looking for…This study examined the
injection of a compound which was responsible for directing overexpression of
insulin-like growth factor I (IGF-I) in differentiated muscle fibers. The researchers
concluded that IGF-I expression promotes an average increase of 15% in muscle
mass and a 14% increase in strength in young adult mice. It’s nice to be able to put
some numbers on this compound, huh? But those effects are not all that the
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researchers have found. IGF also seems to prevent aging-related muscle changes in
old adult mice! These old mice experienced a 27% increase in strength as compared
with uninjected old muscles. Muscle mass and fiber type distributions were
maintained at levels similar to those in young adults. The researchers have
speculated that these effects are primarily due to stimulation of muscle regeneration
via the activation of satellite cells by IGF-I (8). Regardless of the mechanism of
action, the results from this study are pretty exciting. A 15% increase in muscle
mass, and a 14% increase in strength are no small increases. Consider this, if you
are a typical 100kg (220lb) bodybuilder, you would be a 115kg (250lb) bodybuilder
after those kinds of results from IGF-1! If you were a powerlifter who’s best bench
press effort was previously 200kgs (440lbs), then you could expect to be able to
bench press 500lbs after using IGF1! Ok, so you can’t exactly use that study on mice
to justify those numbers, but you get the idea. IGF-1 works and it works very well.
Even if we could realistically expect 7% gains in muscle mass and strength (half of
the gains experienced in the study), then this drug would be able to blast many
bodybuilders and athletes through the plateaus that experienced trainers often
endure.
So how can we use this stuff? Well first let’s talk about creating an ideal environment
for IGF1 to function. See, as you’ve already read, there is a very great
interdependence and synergy between IGF, Insulin, and GH. It has been clearly
observed in studies that when GH and IGF1 are used together, you’ll get greater
results in the accumulation of Lean Body Mass than you would by using either of
them alone (10).In addition, there is a very strong probability that testosterone
would be synergistic to GH (4), and would also increase IGF levels in muscle (11).
Let’s take a look at a chart showing what happens when you use IGF-1, IGF-1+GH,
or GH alone:
Changes in body weight, lean body mass, and fat mass 6 and 12 weeks after
therapy. Values are the mean changes and 95% Cls. * = significant differences
compared with baseline (P < 0.01). The following are the numbers of patients in
each treatment group at weeks 6 and 12: recombinant human growth hormone plus
insulin-like growth factor 1 (rhGH + rhIGF-1), 13 and 9, respectively; rhGH, 12 and
11, respectively; IGF-1, 1D and 4, respectively; placebo, 14 and 11,
respectively(10).
As that chart clearly shows, you will lose more fat and gain more muscle when you
combine GH and IGF-1 than you would using either alone. The subjects in this study,
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over 12 weeks gained around 3kgs of lean mass, and lost around 2kgs of fat.
Clearly, when we use IGF, we are going to want to use it with GH. And we know that
GH functions best when used in conjunction with testosterone. And since we know
that GH increases insulin sensitivity, we can throw in some insulin with that GH….and
if we are using insulin and don’t want to get fat, I’d be most comfortable if I could
add in a fat burner like T3 with it.
So there we have a laundry list of items essential to get the most out of our IGF
use…but lets be honest, if you have the money to use IGF (and IGF is expensive
stuff), then you should really be including these other items to maximize it’s effects.
So how much IGF do we use? What kind do we buy? How much will it cost? Well, the
most popular type available on the Black Market right now is Lr3igf-1 (Long R3
Insulin-like Growth Factor-I or Long R3IGF-I) which is an 83 amino acid analog of
human IGF-I comprising the complete human IGF-I sequence with the substitution of
an Arg for the Glu at position 3 (hence R3…clever name, right?), as well as a 13
amino acid extension peptide at the N-terminus. Huh? Well, that all adds up to make
Long R3IGF-I significantly more potent (2-3x) than IGF-I in studies, because it has a
lower affinity to be rendered inactive by IGF binding proteins (22) (23). Yeah,
everything you’ve read about IGF-1 still holds true for this version, but it’s just a bit
more active in the body, and hence more potent. Also, it’s basically the only type you
can get your hands on at this time…nobody carries the “lesser” versions of it
anymore. SO, you’ll pay around $150.00 for 1mg (1000mcgs/mg). And how much
do you use? From the people I’ve spoken to, I’ve noticed that the magic happens
between 60mcgs and 120mcgs per day, in divided doses. In general, people who
have used less, and even up to 50mcg/day have had mediocre results. People who
have used more have suffered headaches and nausea, and generally not much more
in the way of results.
References:
1. Hormonal Responses and Adaptations to Resistance Exercise and Training.
Sports Med. 2005;35(4):339-361.
2. Clinical uses of insulin like growth factor I (IGF-I).Ann Intern Med. 1994 Apr
1;120(7):593-601.
3. PROTEIN BREAKDOWN IN MUSCLE FROM BURNED RATS IS BLOCKED BY
IGF-I AND GSK-3{beta} INHIBITORS.
Endocrinology. 2005 Mar 31; [Epub ahead of print]
4. Growth Hormone and Testosterone Interact Positively to Enhance Protein and Energy
Metabolism in Hypopituitary Men.
Am J Physiol Endocrinol Metab. 2005 Feb 22; [Epub ahead of print]
5. Are the metabolic effects of GH and IGF-I separable?
Growth Horm IGF Res. 2005 Feb;15(1):19-27.
6. Murphy MG, Plunkett LM, Gertz BJ, He W, Wittreich J, Polvino WM, Clemmons DR.
MK-677, an orally active growth hormone secretagogue, reverses diet-induced
catabolism. J Clin Endocrinol Metab. 83(2):320-5, 1998
7. Fryburg DA, Jahn LA, Hill SA, Oliveras DM, Barrett EJ. Insulin and insulin-like
growth factor-I enhance human skeletal muscle protein anabolism during
308
hyperaminoacidemia by different mechanisms. J Clin Invest. 96(4):1722-9, 1995
8. Viral mediated expression of insulin-like growth factor I blocks the aging-related loss
of skeletal muscle function.Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15603-7.
9. Molecular mechanisms modulating muscle mass.
Trends Mol Med. 2003 Aug;9(8):344-50. Review.
10. Recombinant human growth hormone, insulin-like growth factor 1, and combination
therapy in AIDS-associated wasting. A randomized, double-blind, placebo-controlled
trial.
Ann Intern Med. 1996 Dec 1;125(11):865-72.
11. 3 Am J Physiol Endocrinol Metab. 2002 Mar;282(3):E601-
12. Growth hormone and IGF-I therapy in the hypercatabolic patient.
Baillieres Clin Endocrinol Metab. 1996 Jul;10(3):447-63. Review.
13. IGF-I neuroprotection in the immature brain after hypoxia-ischemia, involvement of
Akt and GSK3beta?Eur J Neurosci. 2005 Mar;21(6):1489-502.
14. Interdependence of oestrogen and insulin-like growth factor-I in the brain: potential
for analysing neuroprotective mechanisms.
J Endocrinol. 2005 Apr;185(1):11-7.
15. Neuroprotective gene expression profiles in ischemic cortical cultures preconditioned
with IGF-1 or bFGF.
Brain Res Mol Brain Res. 2004 Nov 24;131(1-2):33-50.
16. The role of the somatotropic system in cognition and other cerebral functions.
Semin Vasc Med. 2004 May;4(2):167-72. Review.
17. Insulin-like growth factor type 1 prevents hyperglycemia-induced uncoupling protein
3 down-regulation and oxidative stress.
J Neurosci Res. 2004 Jul 15;77(2):285-91.
18. Role of insulin like growth factor-I in repair response in immature cartilage.
Knee. 2005 Apr;12(2):113-9
19. Oxidative stress induces IGF-I receptor signaling disturbances in cultured human
dermal fibroblasts. A possible mechanism for collagen biosynthesis inhibition.
20. Age-related femoral bone loss in men: evidence for hyperparathyroidism and insulin
like growth factor-1 deficiency.J Gerontol A Biol Sci Med Sci. 2004 Dec;59(12):1285-9.
21. Metabolic effects of growth hormone in humans. Metabolism. 1995 Oct;44(10 Suppl
4):33-6.
22. IGF-I variants which bind poorly to IGF-binding proteins show more potent and
prolonged hypoglycaemic action than native IGF-I in pigs and marmoset monkeys.J
Endocrinol. 1997 Nov;155(2):377-86.
23. In vivo actions of IGF analogues with poor affinities for IGFBPs: metabolic and
growth effects in pigs of different ages and GH responsiveness.
Prog Growth Factor Res. 1995;6(2-4):385-95. Review
309
Insulin
Insulin is one of the most powerful anabolic agents in the world. Used properly, it
can help you add weight more quickly than any other compound at your disposal.
Used improperly, insulin will kill you.
Before I delve too deeply into explaining this compound, I feel that it’s important to
stress that last part: Screw up with this stuff, and you die. You will go into a coma
and die. And I'm talking about simply taking too much of this stuff once.
Ok?
This drug needs to be treated with caution. If you aren't willing to read as much as
possible on insulin before using it, then you aren't ready to use it at all.
So first, lets talk about the insulin that’s floating around in your body right now, and
what it does, then we’ll talk about how adding exogenous insulin (insulin from
outside your body) could possibly help you.
Insulin is a protein secreted by the pancreas that acts on the liver to stimulate the
formation of glycogen from glucose and to inhibit the conversion of non
carbohydrates into glucose. Insulin also promotes facilitated diffusion of glucose
through cells with insulin receptors, and, of course, this means muscle tissue (1). As
you may expect, very high concentrations of insulin have resulted in markedly
stimulated muscle protein synthesis (2)(3)(4)(9). It does this mainly at the
translational level by enhancing peptide chain initiation (11). This property and its
consequent results are probably the things which makes it most interesting to
bodybuilders and athletes. This is because those factors combine to make ingested
protein more efficient by promoting the transport of amino acids into muscle cells.
Ergo, we can clearly say that insulin is undoubtedly anabolic in muscle tissue. It also
has an anabolic effect in bone, and thereby increases bone density as well (8).
Another mechanism by which insulin is anabolic is via increasing your body’s IGF
(Insulin-like Growth Factor) levels (6). IGF is an extremely anabolic hormone.
Another unexpected aspect of insulin use is its ability to increase both LH
(Leutenizing Hormone) and FSH (Follicle Stimulating Hormone), both of which—in
turn—stimulate testosterone production. What I’m getting at here is that insulin
stimulates gonadotropin secretion, meaning that its use may actually provide an
anabolic effect through increasing your HPTA’s ability to stimulate the production of
testosterone (Hypothalamic-Pituitary-Testicular-Axis) (11). This effect is often
manifested as virilization (development of male sexual characteristics) in women.
Insulin also increases the binding ability of anabolic steroids to the androgen
receptors (14), which would clearly suggest the strong possibility of a synergistic
effect of insulin when combined with steroids. Most people also think that insulin has
some anabolic synergy when combined with growth hormone, and certainly there is
a lot of anecdotal evidence for this as well. In addition to anecdotal research, it's
important to note that insulin is actually so anabolic that some researchers have
310
speculated that Growth Hormone’s (GH) ability to stimulate protein synthesis may
actually be, in part, due to GH’s ability to increase insulin sensitivity (12). Certainly
the complex relationship between insulin, IGF, and GH is very synergistic
(13)(15)(16)(17). Using all three of them plus anabolic steroids and a fat-burner is
the most potent muscle-building & fat -burning cycle possible. Of course, when
something seems too good to be true, it usually is…
Unfortunately, the bad news is that insulin can easily stimulate adipose (fat) storage.
Generally, though, most bodybuilders take insulin with a fat burner or two (thyroid
meds are the most popular choice), as well as anabolic steroids and sometimes even
GH and IGF, for reasons previously explained. All of this adds up to decreasing the
chance that fat is stored, and greatly increases the amount of muscle that will be
gained.
Anyway, as you probably guessed, endogenous insulin (the stuff naturally found in
your body) operates on feedback from within your body. When your glucose levels
get high, which is what happens when you eat a sugary snack, insulin is then
released from your beta cells. When glucose is low, insulin is, of course, low. In fact,
simply adding liquid glucose to a liquid amino-acid meal (thereby raising insulin
levels) will increase the absorption of the ingested amino acids by roughly 50%! (7)
Now, think about this: If a natural insulin response to ingested glucose can give you
50% better absorption of protein, how much protein absorption injecting it will give
you?
So, now that we have some kind of understanding as to what endogenous insulin
does, let’s try to figure out exactly what exogenous insulin can do (that’s the kind
you get from a bottle). Medically, of course, insulin is used to treat diabetes, thus
becoming diabetic is a real risk with improper insulin usage.
First, I’m going to give you some clinical examples of how insulin has been used as
an anti-catabolic agent. In the first study I read, insulin levels were increased 15-fold
in infants suffering extreme catabolism. This level of insulin administration produced
a 32% reduction in protein breakdown (4). In the second study, exogenous insulin
impeded muscle protein loss in burn victims (5). It’s important to note that you
MUST have enough amino acids (protein) in your body for insulin to exert an
anabolic effect. If there are not enough amino acids floating around in your body
from your last few meals, insulin will not be anabolic at all. On the other hand, If
amino acid concentrations are maintained at normal or high levels as they would be
in a typical athlete or bodybuilder’s diet, a net protein deposition in muscle will occur
(more protein deposited in your muscle = more mucle gained). This effect—insulin
depositing protein in your muscles—is primarily because of an actual stimulation of
protein synthesis and also owes to an inhibition of protein breakdown (10). The
lesson here is that even with insulin, diet is the key to it all. You need to have
enough protein in order to build muscle, regardless of how much insulin you take.
Lets quantify this a bit. What about the anabolic and anti-catabolic properties of
insulin? Can we put some solid numbers on any of this?
Sure.
From the following chart, you can see that insulin puts your protein balance into a
much more beneficial state, and concomitantly lowers protein degradation by
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inhibition of the lysosomal pathway (this is its anti-catabolic effect) (11) and raises
protein synthesis (this is its anabolic effect).
Protein kinetics. Protein balance, degradation, and synthesis rates are shown
(measured in nmol phenylalanine • min 1 • 100 ml 1). Values represent means ± SE
for the basal (open bars) and last 30 min of the insulin infusion (filled bars) periods
with the 3 different rates of amino acid infusion (in ml • min 1 • kg 1) (* P < 0.05
and ** P < 0.01 for basal vs. infusion period).(5)
What this chart tells me is that insulin can effeciently utilize a great deal of protein
above and beyond what your body normally could, and that if you should decide to
use insulin, you should be taking in at least 2.2g/kg of bodyweight, and preferably 3
4.5g/kg of bodyweight.
So now we know how and why insulin works, and how well it works. Ok, let’s figure
out how to use it. I’ll give you two basic ideas on how to safely use insulin, as well as
a third “hybrid idea,” and a dirty little trick on how to use insulin with a cyclic
ketogenic diet, to get into ketosis earlier.
Whichever way you decide to use, remember, insulin has the ability to stimulate fat
storage, so you want to make sure you are using anabolic steroids with it, as they
will preferentially drive protein and nutrients towards being used for the
accumulation of lean body mass over adipose tissue (fat). Personally, I also like to
use a thyroid medication (Synthroid) to further insure none of my injectable insulin is
going to put any fat on me. If you've been paying attention up until now, I'm sure I
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don't have to tell you that GH and IGF are also very potent (and expensive) additions
to any stack containing insulin. If all of that didn't whet your appetite, then consider
the fact that insulin, GH, and IGF are undetectable on drug tests! Currently, there
are speculative ways to test for them, but nothing consistent has been established. I
suspect that insulin, GH, and IGF have helped out many a top-level “natural”
bodybuilder.
So now that we know something about insulin, let’s see what kind is most
appropriate for bodybuilding or athletic purposes, as there are several types of
insulin available, and choosing the correct type is of utmost imiportance. Basically
there are 5 different types of insulin we'll look at, and from them, we'll pick the type
which will best suit our purposes of building muscle: -Humalog (Insulin lispro inj.) is the fastest acting insulin available -Humulin-R (Regular Insulin) has a short duration of effect -Humulin-N (Insulin Isophane) is intermediate length insulin -Humulin-U(Medium Zinc Suspension) is another intermediate length insulin -Humulin-U, utalente (Prolonged Zinc Suspension) is long acting insulin
(*there are also blends available of two or more of these types of insulin, in varying
ratios of long:short or anything in-between)
Of these 6 possible choices, the first would appear to be the best and safest, but that
particular type of insulin is (unfortunately) only available with a prescription, and
getting it through a typical steroid source (which usually means through the mail) is
not advisable, since you can not be sure it has been properly stored and refrigerated
throughout shipping and handling. Needless to say, attempting to forge a
prescription for this stuff is an exceptionally poor idea.
Our next best choice for injectable insulin is Humulin-R, so that's what we're going to
be using. Humulin R is available without a prescription, from any pharmacy. This
stuff has a fairly rapid onset and peak, ergo it is much easier to deal with than the
other forms of insulin available…some last very long, or have varying peaks and
spikes throughout their duration, and as such are just too difficult to monitor and
control.
The first and most obvious way to utilize insulin for its anabolic effect is to take a
little bit with each meal, possibly 1-2iu’s up to 5-6x a day (insulin is measured in
international units, not mgs as is common with anabolic steroids). This way you’d be
getting the greatest benefit of insulin possible with each meal, and the least risk of
using too much and going into shock. Of course some bodybuilders have reported
using up to 20-40iu/day, but I wouldn’t recommend this unless you are very
experienced, and have your diet in perfect order. You’ll want to take in a tiny bit of
essential fats, a decent amount of mixed carbs (i.e. carbs of varying glycemic
indexes), and at least 40g of protein with each meal, when using this method.
Clearly, you’ll also want to work up to this amount of insulin, perhaps adding 1iu per
day until you reach a level you are comfortable with. This holds true for either
method of insulin use I’m presenting.
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The second way you can use it is to take 1iu of insulin with your post workout meal,
eventually working up to 1iu/10kgs of bodyweight. When using this method, you’ll
want a post workout shake consisting of roughly 100-200g of mixed carbs and 40-50
grams of protein...and don’t forget a small amount of essential fats with your shake.
I have used insulin this way, along with anabolic steroids and a thyroid med, and
have found it to enhance the gains from my cycle by around 15-20% as compared
with a similar cycle that did not include insulin.
The final method is to use the first method as well as the second, so you’d be taking
in 1-2ius with each regular meal and up to 1iu/10kgs of bodyweight with your post
workout meal. This would ensure maximum efficiency from each bite of food you
eat…but this way is also the most dangerous, and you need to monitor your blood
sugar. If you get tired after a shot you’ll need to get some mixed carbs into you
quickly (Gatoraid and a few granola and/or candy bars). It’s a good idea to carry
those kinds of things around with you as insurance that your blood sugar doesn’t go
too low. You also don’t want to take this stuff at night before bed, because you won’t
know if your blood sugar is going low and that's making you drowsy (meaning you
could be facing hypoglycemia, and be about to go into a coma) or you are just tired
because it’s your normal bedtime.
And as for that dirty little trick I was telling you about: A small amount of insulin
may be taken when starting a cyclic ketogenic diet, with your first meal on the day
you begin. This meal would be fats and proteins, without carbs, and only 2-4iu of
insulin would be taken. At the following meal, you can use half the dose of insulin as
you did at your first meal.The result would be that you could be in ketosis before the
end of that first day, whereas usually it would take 2 or even up to 3 days to
accomplish this. Using insulin in this manner is very dangerous, and was even called
"Death Wish Dieting" by Dan Duchaine.
Whichever method you use, remember to keep your insulin refrigerated, as it will
degrade very quickly outside of a cool environment. Don't leave this stuff out of the
fridge too long, either.
The other thing you don’t want to do is use regular needles to inject insulin. You
NEED insulin pins to accurately dose this stuff; remember, too much can be deadly,
and the syringes you would use to inject steroids are too big to measure out units of
insulin. Insulin is given via a subcutaneous injection (below the skin but above the
muscle), and regular needles are just too big to do that.
Insulin (or at least Humulin-R) is currently not a controlled substance, and you
should be able to buy it at your local drug store pretty cheaply: a 10cc multi-use vial
dosed at 100iu/cc will cost you around $50.
References:
1. Human Anatomy and Physiology, 6th Edition, John W. Hole
2. hyperinsulinemia unmasks insulin's effect to stimulate protein synthesis in human
forearm.Am. J. Physiol. 274 (Endocrinol. Metab. 37): E1067-E1074, 1999
3. Impaired anabolic response of muscle protein synthesis is associated with S6K1
314
dysregulation in elderly humans. FASEB J. 2004 Oct;18(13):1586-7. Epub 2004 Aug
19.
4. Intravenous insulin decreases protein breakdown in infants on extracorporeal
membrane oxygenation.J Pediatr Surg. 2004 Jun;39(6):839-44; discussion 839-44.
5. Extremity hyperinsulinemia stimulates muscle protein synthesis in severely injured
patients Am J Physiol Endocrinol Metab. 2004 Apr;286(4):E529-34. Epub 2003 Dec
9.
6. Insulin: the other anabolic hormone of puberty. Acta Paediatr Suppl. 1999
Dec;88(433):84-7. Review.
7. Contribution of amino acids and insulin to protein anabolism during meal
absorption.
Diabetes. 1996 Sep;45(9):1245-52.
8. Anabolic effects of insulin on bone suggest a role for chromium picolinate in
preservation of bone density.Med Hypotheses. 1995 Sep;45(3):241-6. Review.
9. Physiologic hyperinsulinemia stimulates protein synthesis and enhances transport
of selected amino acids in human skeletal muscle. J Clin Invest. 1995
Feb;95(2):811-9.
10. Insulin action on protein metabolism.Baillieres Clin Endocrinol Metab. 1993
Oct;7(4):989-1005. Review.
11. Effects of chronic hyperandrogenism and/or administered central nervous system
insulin on ovarian manifestation and gonadotropin and steroid secretion. Fertil Steril.
2005 Apr;83 Suppl 4:1319-26.
12. Metabolic effects of growth hormone in humans. Metabolism. 1995 Oct;44(10
Suppl 4):33-6.
13. Clinical uses of insulin-like growth factor I. Ann Intern Med. 1994 Apr
1;120(7):593-601.
14. Binding of methyltrienolone to androgen receptors in human skin fibroblasts is
enhanced by insulin.J Androl. 1992 May-Jun;13(3):242-8.
15. Are the metabolic effects of GH and IGF-I separable?Growth Horm IGF Res. 2005
Feb;15(1):19-27
16. IGF-1 and insulin as growth hormones.Novartis Found Symp. 2004;262:56-77;
discussion 77-83, 265-8. Review
17. Divergent effect of endogenous and exogenous sex steroids on the insulin-like
growth factor I response to growth hormone in short normal adolescents.J Clin
Endocrinol Metab. 2004 Dec;89(12):6185-92
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Chapter 14
NUTRITION
(How to eat on a cycle to gain & how to eat off a cycle to
maintain)
In truth, this should have been the first chapter, because your diet while you are on
a cycle will greatly determine your gains. Honestly, though, this book was originally
intended as a book strictly about Anabolics, but then Brian (the other person
involved with the writing of this book) contacted me and told me that he’d been
swamped with e-mails asking about the book and if it would cover diet as well.
Really, diet can be the limiting factor in how much you gain on a cycle, and how
much you keep when you go off. Dietary intake has actually been used to develop a
model for predicting race performance in IronMan Triathalons (1)(2). What the
researchers found was that if you don’t eat right, you don’t place well, and
surprisingly, that Carbs and total calorie intake were the most important factors.
Table 1: Rates of water, energy, carbohydrate and sodium
intakes of 59 Ironman triathletes during the event, and
correlations of the intakes with finish time.
Intake Correlation with
finish time
Carbohydrate (g·kg-1·h-1) 0.96 ± 0.40 -0.59 (-0.74 to -0.39)
Energy (kJ·kg-1·h-1) 16 ± 7 -0.56 (-0.71 to -0.35)
Water (ml·kg-1·h-1) 12 ± 5 -0.45 (-0.63 to -0.22)
Sodium (mg·kg-1·h-1) 4.0 ± 4.8 -0.12 (-0.36 to 0.14)
aMean ± standard deviation
bObserved value of Pearson correlation between dietary
variable and log-transformed finish time; 95% likely range of
true correlation in parentheses.* Chart From SportSci.org,
and (1)(2)
I suppose I don’t even need to tell you that the same is true for bodybuilding
contests, right? The difference between first and fifth place is usually a simple matter
of diet, in contests below the National and Olympia-Level. At the Olympia Level, it’s
a whole ‘nother ballgame, that for the average reader of this book is just not
relevant. If you don’t eat properly, and you’re training hard, you’ll have a vastly
compromised immune system (18), and you’ll get sick much more often. You can’t
make gains when you’re lying in bed, right?
So here we are, two weeks after the book has gone to the editor for final revisions,
and I’m writing the final chapter, which should actually have been the first one.
316
So to make this easy, let’s assume that you are not currently gaining nor losing
weight. What you’re going to have to do is chart your calorie intake for a week, and
figure out how much you are eating, calorie-wise. Once you’ve done that, you’ll
have a good starting point to figure out how the rest of this chapter applies to you.
Once you know that, you know that you’ll have to increase your calories to gain
weight and lower them (yuck) to lose weight. This, of course, is not rocket science,
but it requires accurate record-keeping. For me, I need around 2,800 calories every
day to maintain my weight. I personally move my caloric intake about 500 calories
either way to basically lose or gain a lb every week (given no change in energy
requirements). Of course it’s more complicated than that unless everyone reading
this book is a 210lb guy who stands 5’7”, with 8-9% body fat….but I think those
numbers will give you an idea of where to start. Try moving your calorie intake 10%
either way for a few days, and chart your results, weight-wise to find out where you
need to be personally to lose or gain the weight you desire.
Next, we need to take a look at the three primary macronutrients we’re going to be
working with (protein, carbs, and fat) and the ratios we will want to consume them
in, then some micronutrients (vitamins, minerals, and other fun stuff), and finally
how to manipulate our intake of them to get the most out of our cycles, and
maintain our gains off of them.
Here’s some not-so-quick definitions of the macronutrients involved, their role in
your body, and my recommendations of the percentage of your daily caloric intake
that they should comprise respectively:
Protein is the building block of your muscle. You need to realize that anabolism in
the absence of protein is almost impossible, regardless of what exotic steroids you
are putting into your body. However, humans can synthesize only about 50% of the
necessary amino acids that make up the proteins in our bodies. If the remaining
amino acids (cleverly known as “essential amino acids”) are not consumed in
sufficient quantities, protein production will suffer. What we need to remember, as
athletes or bodybuilders interested in building muscle is that the quality of protein in
a food is vastly differing, and of utmost importance. The quality of a protein is
determined by its essential amino acid content (16). A select few foods (called
complete proteins) contain all of these essential amino acids, and they are contained
in amounts sufficient to maintain and promote protein synthesis through maintaining
a positive nitrogen balance. Let’s look at how nitrogen balance differs in people who
are undergoing strength training, with differing protein intakes:
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Comparison of nitrogen balance (protein requirements) in individuals who
are strength training with differing protein intakes.
Clearly you need to take in more (and higher quality) protein if you’re strength
training, and this would include mostly complete protein foods, optimally. Other
foods simply lack one or two amino acids, and those foods can be combined in a
meal to make sure you get all of your essential amino acids. The foods with all of the
essential amino acids are called complete protein foods, and you can probably guess
what they are. They’ve been on the athletes’ training table for the last two-thousand
years, since ancient Olympians found their benefits. They include stuff like dairy
products, eggs, meat and fish. Incomplete proteins, as you can also guess, are
foods like grains, vegetables and fruits. It is very possible to obtain sufficient
indispensable amino acids from a diet that excludes complete protein foods entirely
by combining grains, vegetables and fruits, this requires some esoteric knowledge of
which foods to combine, by looking at which have amino acids that others lack.
Vegetarians, especially those who exclude eggs and dairy products (Vegans), are
therefore at great risk for insufficient dietary protein intake. I know there aren’t
many vegetarian bodybuilders (Bill Pearl aside), but in one particular study I read,
59 to 69 year-old men, strength training produced greater muscle mass gains with a
meat-containing diet in comparison to a lacto-ovo-vegetarian diet (15). However, in
younger strength and speed athletes there has been shown no clear benefit to eating
meat (7). So, eat meat for your protein if you like it, or because you want to fulfill
some kind of psychological need for a steak, or whatever, but realize it’s not
necessary. It is of note that the latter study concerned athletes who had protein
supplements like (whey powder) available to them. This data strongly suggests that
the type of protein may play an extremely important role in muscle growth when
ingested in conjunction with strength training. The ideal protein for this is, of course,
whey protein. This type of protein, especially whey protein isolates or hydrolyzed
whey peptides, has taken off in the world of strength training and bodybuilding in the
last decade. It’s widely touted by strength athletes as being the highest quality
protein commercially available. This contention is typically (and correctly) based
both on whey’s extremely high bioavailability as well as its content of glutamine,
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leucine, isoleucine and valine. Exercise reduces glutamine levels in the body, which
can cause immunosuppression (20) and when glutamine/glutamate levels dip too
low, there is a high correlation with overtraining (21). Those last three amino acids
(Leucine, isoleucine and valine) are the branched-chain amino acids (BCAAs), and
make up about one-third of muscle protein. When you train, you experience
decreases in all three of those highly important amino acids (18). Of great
importance is that significant decreases in plasma or serum levels of leucine occur
following both aerobic (11 - 33%) as well as anaerobic lactic (5 - 8%) and strength
exercise (30%) sessions. There is also a huge decrease in leucine level in skeletal
muscle and a concurrent reduction in glycogen stores during exhaustive aerobic
exercise. Leucine levels decrease by 1/5th during 5 weeks of speed and strength
training in power-trained athletes who were fed a relatively high daily protein intake
of 1.26 g/kg bodyweight. And this reduction still occurred! This could be due in part
to the relative low concentrations of leucine and other BCAAs in regular whole foods.
As a general rule, the leucine content of protein varies between 5 and 10%. There
are some sports nutritionists and scientists who suggest that the current
recommended dietary intake of leucine for athletes be increased from 14 to 45
grams/day for a 100kg athlete. This would mean that our hypothetical 100kg
bodybuilder has to ingest quite a bit of protein (450-900grams/day!) if it comes
mostly from poor sources. However, to avoid this type of deficiency in total protein
or in specific essential amino acids, athletes ought to consume 2.2 grams of protein
per kg of bodyweight (1g/lb), from high quality protein sources. If you are 100kgs,
and taking in 100grams of whey protein every day, and 100 grams from other
reasonably high quality sources, you’ll have no problem meeting your BCAA and total
protein requirements. Consumption of BCAAs (or roughly 30 to 35% leucine in a
protein supplement like whey) before or during endurance exercise clearly prevents
or greatly decreases the net rate of protein degradation, and in addition may
improve both mental and physical performance (17). Obviously this is of great
interest to athletes because in addition, it may even have a potentially sparing effect
on muscle glycogen degradation and depletion of muscle glycogen store (17).
Legendary strength coach Charles Poliquin recommends 20-40 grams of BCAA’s
before and after training, with perhaps a Carb/BCAA drink during training, as one of
his tricks to adding LBM quickly. This is, of course, a great idea, and can be counted
towards your daily efforts at getting in enough protein. I take some aminos before
training. Typically whey protein is used just following training, since it enters the
blood stream following ingestion faster than casein (the major milk protein), which is
well known to produce a significantly lower but more prolonged increase in blood
amino acids (14). Casein, therefore, and other proteins with a slower absorbtion
rate (albumin, etc) would be more appropriate to use prior to training, when you
want to have amino acids available for an extended amount of time. After a
workout, you want them available and in your body as quickly as possible, to begin
muscle repair. You’re going to need whey protein for that.
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Effect of a strength training session on muscle protein synthesis
Increasing exercise intensity and duration, at least with aerobic exercise (and I know
you aren’t going to skip cardio), causes an increased use of protein, apparently as an
auxiliary fuel (8)(9)(10)(11). What this means is that before you can even start
thinking about how much protein you need to start building muscle, you need to
know how much you’re using as energy, right? Well, nitrogen balance experiments (a
measure of protein excretion vs/ intake) have shown that just doing some
reasonably intense cardio results in an increased daily protein need of around 50% to
75% (1.2–1.4 vs. 0.8 g/kg)! In addition, heavy resistance (strength) exercise
appears to increase protein need by about 100%, again based on nitrogen balance
experiments. Not only does this mean that you are using more protein for fuel but,
also, isotope tracer studies have revealed that the underlying mechanism is not
simply increased fuel use. Rather, your body undergoes changes in muscle protein
synthetic rate (12) resulting from your newfound need to maintain a greater overall
muscle mass (13) caused by the gains you’ve made through your weight training.
Here’s an idea of what I’m talking about:
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Effect of increasing protein intake on protein synthesis in strength athletes
vs. controls
So let’s recap my recommendations on Protein, which are the same on a cycle as off:
Ingest 1g/lb of bodyweight of quality protein (2.2g/kg)
Take in at least half of your protein from whey, and at least half of that
needs to be in a post-workout meal
All of protein which you “count” towards your daily intake should be
“complete” proteins, containing all necessary amino acids
So, with a gram per pound of bodyweight, that means I take in 210grams of protein
every day, or 840 calories…around a third of my calories.
Although Protein is probably the easiest of the three macro-nutrients to determine
your requirements for, moderate exercise will deplete you of protein pretty quickly,
even if you have adequate carbohydrate (solid bars), but even more so when you
have an inadequate amount of carbs (open bars).
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Nitrogen excretion increases with prolonged, moderately intense exercise
and especially so when carbohydrate stores are low (6)
It’s clear that we need to consume protein, but now it’s clear that carbohydrates also
play an important role in preserving protein. And carbs are either simple (released
into your body immediately) or complex (released slowly). Briefly, complex carbs
provide sustained energy, and simple carbs provide a quick (though temporary)
surge in energy. I’m relatively amoral concerning carbs, and I actually ingest a lot of
simple ones…but that’s always post workout. Now, remember how I said you need
to take in enough protein? Well, of course, you need to combine it with
carbohydrates in order to get the most out of the protein you ingest, and not have it
excreted excessively or used as energy during exercise due to a lack of glucose.
This excess excretion of protein will have the exact opposite of stimulating muscle
growth; it will grind new muscle growth to a halt, anabolics or not. If you are
excreting too much protein, and not getting enough in, muscle growth will not be
possible. On the other hand, it is highly possible to stimulate muscle growth (either
by minimizing degradation or possibly maximizing synthesis) via carbohydrate/amino
acid ingestion following a strength exercise session (27)(28). This combination is
probably so effective due to insulin-stimulated (22)(23) changes in muscle amino
acid uptake as well as enhanced protein synthesis (22). Unfortunately, carbs are the
first things we need to cut out when dieting, because proteins and fats are too
important. In fact, remember when I told you that essential amino acids are the key
here? Well it actually appears that the nonessential (dispensable) amino acids are
almost unnecessary (22). So you’ll need to be stocking up on whey protein, if you
want maximum results from your anabolics, and maximum retention of your gains
when you go off. Without maximizing protein synthesis, you’re leaving 5-10lbs on
the training table with every cycle, since a strength training session affects both
muscle protein degradation and synthesis (24)(25).
Carbohydrate intake immediately following exercise can easily enhance muscle
glycogen resynthesis when compared to the same exact intake several hours later
(21). So clearly, post workout, the addition of simple carbs into your whey protein
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shake will speed carbohydrate absorption and aid glycogen recompensation in your
hard-trained muscles, and it has been proven by results in countless athletes that a
carb + protein beverage immediately after exercise is superior to taking either one
alone. Personally, I take 50g of whey protein (I use Solid Muscle Whey Protein) along
with 100 grams or so of (liquid) simple carbs. When combined with simple carbs, a
mere 6 grams of essential amino acids can increase muscle protein synthesis and
insulin release by an astonishing rate. I don’t ever forgo my post-workout shake,
and I think after you see these charts, you won’t either:
Effect on indispensable amino acid intake following strength exercise on
protein synthesis.
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Effect of indispensable amino acid intake following strength exercise on
insulin release.
In addition to your post workout shake, I recommend that you take in enough
carbohydrates to get you comfortably through your workouts and/or athletic training,
and not too much more. I take in 50% of my daily carbohydrates in my post workout
meal and shake. Why? Because that’s when they are most likely to be used for what
I want them to be used for….building muscle. Other than that, I eat relatively low
carbohydrate meals for my other 5 daily meals (10% of my daily carbohydrates at
each meal…which amounts to some veggies, or some other complex carbohydrates
at each meal).
Lets go over my carbohydrate recommendations;
Eat enough to comfortably get through your workouts and training
Complex carbs are eaten all day, except for post workout
Simple carbs should be eaten post workout, which can be up to 50% of
your daily carb intake
If you are trying to lose weight (fat), carbs are the first things to cut out of
your diet to create a caloric deficit
So basically, I have about 200+ grams of carbs every day, or around a third of my
calories.
I’ve left fats for the end of this chapter because they are just, to be simple,
agonizingly complex. I’m going to try to make this relatively painless, though. Let’s
take a look at some different types of fat first.
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You should avoide saturated fats—especially when messing around with steroids—
because of possible heart problems (29), and because they lower insulin sensitivity
(30)(31) and are highly correlated with obesity. They are to be seen as a source of
calories, but not much more, while some of the more interesting fats can actually
have ergogenic (performance enhancing) effects. On the other hand, I love saturated
fats like French fries, eggs, and cheese. No, not all at once. Well, maybe all at once
on special occasions…
After saturated fats, there are unsaturated fats, like those found in linoleic oil,
avacados and nuts. These can actually be beneficial, as they are positively correlated
with lean mass accrual and fat loss (32)(33)(34). If you are going to eat fats, you
should eschew saturated fats, and go for stuff unsaturated fats. Of course, poly and
mono unsaturated fats are simply different types of fats, with poly-unsaturated being
moderately healthier. As you can guess, a saturated fat has all of its positions
“saturated” with hydrogen, while a mono has one position lacking a hydrogen, and
the poly variety is missing more than one. Safflower oil is a very popular unsaturated
fat, and if you add it to any protein shake especially with a mix of proteins and
complex carbs, it will slow absorbtion greatly and give you a nice steady release of
protein over a couple of hours. Fish oil can also be used in that capacity, which has
the added benefits of Omega-3 fatty acids, but a fish and dutch chocolate protein
shake is, well, less than appealing to me, personally. I usually have a small salad
with all of my non-post-workout meals, and put some safflower or olive oil on it. If I
have a protein shake late in the day, it usually has non-hydrogenated (remember,
there’s a hydrogen lacking in unsaturated fats, so hydrogenation makes them
saturated by adding the missing hydrogen) peanut butter in it, or something similar,
to add the fats I need in my diet. Clearly, since protein is 1/3rd of my diet and so are
carbohydrates, fat takes up the last third.
Here’s my final recommendations on fat, for this chapter:
Avoid saturated fats
Favor unsaturated fats, especially polyunsaturated fats
Avoid hydrogenated fats
I’ve tried to make this chapter as painless as possible, since I know most of the
people reading this book will want to know what to put in their syringe, and where
and when they can start shooting it. Hopefully, even though I wrote this chapter last,
you won’t read it last…because it’s probably the most important chapter in the book.
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Chapter 15
Legal Interview:
The Final Chapter, but not the Final Word
The following is an interview conducted with a lawyer who has been involved in
anabolic steroids for almost a decade. His identity will, however, necessarily be
hidden.
BC: Internet message boards… are they safe or unsafe?
Lawyer X: The inherent problem with internet anabolic discussion boards is that in
many cases they are people’s sole source for obtaining anabolic steroids, and this is
in stark contrast to most other controlled substances: heroin, cocaine, etc…. In
general, people look to the Internet Anabolic Steroid message boards (like
Steroid.com) to share their experiences with anabolics, and also obtain information
about the usage of anabolic steroids …typically, there will also be several other
forums where people can engage in conversation about working out, bodybuilding,
powerlifting nutrition, and related issues; those are the legitimate uses of internet
discussion boards and are totally protected under the First Amendment. Steroid.com
for example, operates solely for the exchange of information and is doing the online
steroid community a huge service, by keeping it members and anyone who views it
“safe” in terms of steroid usage, since (except for this book, and the too few like it)
there is simply so much disinformation about steroids these days. Unfortunately,
there are many, many boards nowadays, and the amount of staff required to run
that many means that people are usually engaged in running several boards, or that
they are woefully under-qualified to do so at all (in the vast majority of cases). But
in answer to your question, yes, providing information on steroids and such is totally
legal.
BC: SO did I hear you right? This kind of thing is protected the first Amendment?
It’s just freedom of speech, right?
LX: Right. The conversations that are protected by the first amendment include
training, diet, and stuff like that…but also steroid usage, dosages. In no way is
advocacy of illegal conduct protected via First Amendment speech, nor is
damaging/dangerous conduct (yelling fire in a crowded movie theatre is the most
common example they give at law school). SO yes, for the most part, typical
posting and replying that the average member engages in on Steroid.com in on the
message boards falls under the protection of free speech and can not be prosecuted.
The lesson to be learnt here is that, generally speaking, the Internet message boards
are safe for people to post and gather information. That’s a vast oversimplification,
and of course there are some message boards that violate those boundries walk a
fine line, and get much closer into clearly illegal activities and we should talk about
them for a minute.
BC: SO what can we look for? What kinds of boards are “safe”?
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LX: Of course Steroid.com is safe. I’m sure you already knew that though. Members
there share steroid experiences, engage in steroid conversation, or discuss training
and diet tips. There is no discussion of how to obtain anabolic steroids that people
are talking about, and anything posted on that is not intended to do so. Both the
website, the owner and the staff should feel comfortable there, as should everyone
else. Possible interest to law enforcement officials is, ergo, virtually non-existent and
this kind of website that is very safe, keeps people informed, and is representing the
online community the best.
BC: What about boards with a “Classifieds” forum, where there may (or may not) be
sources of anabolic steroids advertising their wares?
LX: That’s a good question, and like many legal questions, falls into many grey
areas. Certain boards can have what is called a private classified section where
people typically engage in the sales of anabolic steroids; but if it’s not monitored and
the board, the owner, and/or the all derive no clear material benefit from the sale of
those illegal substances, then it is safe, though still rather suspect, and certainly not
in the class of the first type of board I spoke of. As I said, like most legal questions,
there is no really clear-cut answer.
BC: How about totally unsafe boards? What type of board should we avoid?
LX: Well…do you mean legally or philosophically?
BC: I suppose I meant legally, but how about you include philosophically too?
LX: I would personally avoid any kind of “invite board,” “vet board” (also called a
“private board” sometimes)… or basically anything that is not open to the public. As
a rule, which I have not really ever seen broken (and I have seen every such forum
on the internet at the time of this writing), the anabolic advice given in them is
mediocre at best. They basically exist as a gossip forum and a steroid source forum.
If you will allow me a colloquialism, Lots Of Idiots hang out in invite/vet boards, the
information in them is average at best, intellectualism is stifled, and they are
wrought with elitism of the worst kind. For the most part, they are not even a
legitimate source for information concerning anabolics. They should be shunned by
every reader of this book, even if only for the fact that they are basically populated
and staffed by steroid dealers as a rule. The first amendment does not protect this
kind of board, and they are rife with law enforcement officials making easy busts.
Also, as another general rule any kind of “open source” message board that explicitly
allows the open and uncontrolled posting of steroid price lists by steroid dealers
(sources), whether they are so-called international or domestic suppliers, is a
website that should be left alone at all costs. So my public service announcement for
the day is to shun and scorn both invite/vet/private boards as well as open-source
boards (especially when owned by a source!). Lecture over.
Finally, I’d like to add that most boards are safe, at least relatively. You should go to
one where there is no discussion of how to get anabolics, and you will probably be
alright. Another good gague, information-wise, is to check the Anabolic Steroid
Profile information and Educational information available on sites. If the information
on them is well researched and referenced, and written by a current staff member,
or person affiliated with the site, then it’s a good choice. If they are all copied from
another site, then you should simply visit the site they were originally found on. Why
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not go directly to the original source for information? The next thing you should do
is check the temperament of the staff. Are they cursing and acting immaturely? If so
then leave. If they are condescending to members or demeaning in some way, then I
suggest you go elsewhere. Remember, anyone with $50 to spend per month can
operate a board…and these days it would seem that’s the case with most boards.
Remember, the quality of information on discussion boards is not regulated by any
agency…and there are so many now-a-days, that there are not nearly enough
knowledgable people to go around. Sadly, this is the state of affairs we are coping
with…people who mostly say “bro” and “lol” on discussion boards, and provide very
little useful or original anabolic steroid information.
BC: I have to say, you present a pretty bleak picture there, but I can’t disagree with
anything you said. I certainly agree with your comment about invite boards having
“Lots Of Idiots”, even if it’s rude. I’ve always personally wondered why people would
hang out on a board like that, which is private/vet/invite-only…Ok…moving right
along, I’m sure you’re familiar with the term “source check.” But I’d like to define it
for some of our readers, then ask you a question about it. As you know, on various
Internet discussion boards there is a Private Messaging system where you can
contact other members or staff. It has become common practice to send a message
to the staff of such boards asking if a source for anabolic steroids is legitimate or
simply a scam. This is, as you know, called a “source check.” So I guess the
question I’m asking is: are source checks legal or illegal?
LX: A source-check is when somebody gets the e-mail address of a source of
steroids and then address the moderators or veterans of a board with a question as
to that source’s validity. Generaly, the moderators or veterans of a message board
will probably know which sources are trustworthy or not. You should, however, shun
any moderator who attempts to give you the address of a source and dissuade yhou
from using the one you approach them with. Clearly, they are on the source’s payroll
99% of the time. And of course you ought to never ask for a source either openly or
privately. Now; are source checks safe? Not really. Quite frankly, if you freely give
out information to someone about getting their hands on steroids or any controlled
substance, you may get inadvertently involved in a conspiracy. Conspiracy is just a
very vague law, and you’ll probably be shocked to know that a person can actually
be convicted of conspiracy without ever committing a crime! The bizarre part about
all of this is that conspiracy involves a crime that need only be mental, because it
involves both a meeting of the minds as well as intent…but no actual physical crime!
The easy and predictable argument from the person who givesout the source check
to a person who asks, is that they are not dispensing information as such; they are
conforming or denying information that has been presented to them. Ergo, “is
JoeBloe still a good source” is a source check, and in simply answering it, no real
passage of knowledge on obtaining steroids ever happened. But if you want to
maximize your personal safety, then you ought not be engaging in the answering of
questions like the one just discussed.
BC: Recently, a lot of Internet message boards have begun using off-shore servers
(an Internet service provider which is located outside of the United States). Those
boards then typically engage in illegal activity, without fear of prosecution. Are
these types of Internet message boards safer?
LX: I don’t care where your server is, if your ASS is in the UNITED STATES! Off
shore servers are incorrectly and egregiously perceived as being safer because the
server, and ergo the information on the server, is actually offshore. They are neither
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safer for the members, nor the owners and staff. This is a complete and utter fallacy
for the most part. If you live in New Jersey, and own LotsOfIdiots.com and you
seek out an offshore server to protect yourself from facing legal reprocussions from
operating a board in an illegal manner, your server location is basically irrelevant,
and you are totally subject to US law. Having your name hidden from “Who is”
searches or using an IP anonymizer will also not help in cases of such sheer
stupidity. And, in addition, an overseas subpoena can be sent out by the Feds,
simply requesting your hosting company give them all the information- and most
will. Most of the silly things people do to avoid persecution are just that…silly.
I suppose, in theory, an offshore server could work is if BOTH the person who owns
the website and the server is offshore and violating no current laws of their
country…then you clearly have a situation where that website is not under the
jurisdiction of US law and is also therefore immune from US interfearance as well as
prosecution. Several boards exist that fit this description, and would not hesitate to
visit them, for the most part. This situation becomes even better if board owner
actually owns the server that is located offshore as well. It is hard to believe he/she
would comply with a Federal subpoena. This would be a very good route to go, and
many board owners have done this already.
BC: I know you are familiar with the term “research chemical.” This is basically a
chemical bought and sold on the Internet, for research purposes. These chemicals
are almost always simply liquid forms of bodybuilding drugs--ancillaries, clen, etc.—
labeled “not for human consumption.” Is this legal?
LX: In this case, we tend to say they arrest the hookers* and not the Johns. The
client (the customer) has a liability that is nonexistent I believe. This may not be the
case for the research company’s liability however. If you are a the customer, you are
going to be alright, but the companies may ned to worry bit in the future.
(*clearly a terrible inside joke)
BC: Since this is a book about Anabolic Steroids, primarily, let’s talk about them?
How are they classified legally? Are they simply controlled substances? How about a
list or something?
LX: Well, they (steroids) are schedule III drugs for all classification purposes, so
let’s look at that list you asked for as well as the statute it concerns ( which now
interestingly has been updated to proscribe pro-hormons);remember those? This is
the current definition of an anabolic steroid as defined under 21 U.S.C.A.
§802(41)(A):
(41)(A) The term "anabolic steroid" means any drug or hormonal substance,
chemically and pharmacologically related to testosterone (other than estrogens,
progestins, corticosteroids, and dehydroepiandrosterone), and includes
(i) androstanediol--
(I) 3<<beta>>,17<<beta>>-dihydroxy-5<<beta>>- androstane; and
(II) 3α,17α-dihydroxy-5α- androstane;
(ii) androstanedione (5α-androstan-3,17-dione);
(iii) androstenediol--
(I) 1-androstenediol (3<<beta>>,17<<beta>>-dihydroxy-5<<beta>>-androst
1-ene);
(II) 1-androstenediol (3α,17α-dihydroxy-5α-androst-1-ene);
(III) 4-androstenediol (3<<beta>>,17<<beta>>-dihydroxy-androst-4-ene); and
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(IV) 5-androstenediol (3<<beta>>,17<<beta>>-dihydroxy-androst-5-ene);
(iv) androstenedione--
(I) 1-androstenedione ([5α]-androst-1-en-3,17-dione);
(II) 4-androstenedione (androst-4-en-3,17-dione); and
(III) 5-androstenedione (androst-5-en-3,17-dione);
(v) bolasterone (7α,17α- dimethyl-17α-hydroxyandrost-4-en-3-one);
(vi) boldenone (17<<beta>>-hydroxyandrost-1,4,-diene-3-one);
(vii) calusterone (7<<beta>>, 17<<beta>>-dimethyl-17<<beta>>
hydroxyandrost-4- en-3-one);
(viii) clostebol (4-chloro-17<<beta>>-hydroxyandrost-4-en-3-one);
(ix) dehydrochloromethyltestosterone (4-chloro-17<<beta>>-hydroxy
17<<beta>>- methyl-androst-1, 4-dien-3-one);
(x) Δ 1-dihydrotestosterone (a.k.a. "1-testosterone") (17Δ-hydroxy-5Δ-androst-1
en-3-one);
(xi) 4-dihydrotestosterone (17<<beta>>-hydroxy-androstan-3-one);
(xii) drostanolone (17<<beta>>-hydroxy-2<<beta>>- methyl-5<<beta>>
androstan-3- one);
(xiii) ethylestrenol (17α-ethyl-17α-hydroxyestr-4-ene);
(xiv) fluoxymesterone (9-fluoro-17α-methyl-11α, 17α-dihydroxyandrost-4-en-3-
one);
(xv) formebolone (2-formyl-17α-methyl-11α, 17α-dihydroxyandrost-1,4-dien-3-
one);
(xvi) furazabol (17α-methyl-17α-hydroxyandrostano[2,3-c]-furazan);
(xvii) 13<<beta>>-ethyl-17<<beta>>-hydroxygon-4-en-3-one;
(xviii) 4-hydroxytestosterone (4,17<<beta>>-dihydroxy-androst-4-en-3-one);
(xix) 4-hydroxy-19-nortestosterone (4,17<<beta>>-dihydroxy-estr-4-en-3-one);
(xx) mestanolone (17α-methyl- 17α-hydroxy-5α-androstan-3-one);
(xxi) mesterolone (1α-methyl-17α-hydroxy-[5α] -androstan-3-one);
(xxii) methandienone (17α-methyl-17α-hydroxyandrost-1,4-dien-3-one);
(xxiii) methandriol (17α-methyl- 3α,17α-dihydroxyandrost-5-ene);
(xxiv) methenolone (1-methyl-17<<beta>>-hydroxy-5<<beta>>-androst-1-en-3
one);
(xxv) 17α-methyl-3α, 17α-dihydroxy-5α-androstane;
(xxvi) 17α-methyl-3α, 17α-dihydroxy-5α-androstane;
(xxvii) 17α-methyl-3α, 17α-dihydroxyandrost-4-ene.
(xxviii) 17α-methyl-4-hydroxynandrolone (17α-methyl-4-hydroxy-17α-hydroxyestr
4-en-3-one);
(xxix) methyldienolone (17α-methyl-17α-hydroxyestra-4,9(10)-dien-3-one);
(xxx) methyltrienolone (17α-methyl-17α-hydroxyestra-4,9-11-trien-3-one);
(xxxi) methyltestosterone (17α-methyl-17α-hydroxyandrost-4-en-3-one);
(xxxii) mibolerone (7α, 17α-dimethyl-17α-hydroxyestr-4-en-3-one);
(xxxiii) 17α-methyl-α 1-dihydrotestosterone (17α-hydroxy-17α-methyl-5α-androst
1-en-3-one) (a.k.a. "17-α-methyl-1-testosterone");
(xxxiv) nandrolone (17<<beta>>-hydroxyestr-4-en-3-one);
(xxxv) norandrostenediol--
(I) 19-nor-4-androstenediol (3<<beta>>, 17<<beta>>-dihydroxyestr-4-ene);
(II) 19-nor-4-androstenediol (3α, 17α-dihydroxyestr-4-ene);
(III) 19-nor-5-androstenediol (3<<beta>>, 17<<beta>>-dihydroxyestr-5-ene);
and
(IV) 19-nor-5-androstenediol (3α, 17α-dihydroxyestr-5-ene);
(xxxvi) norandrostenedione--
(I) 19-nor-4-androstenedione (estr-4-en-3,17-dione); and
(II) 19-nor-5-androstenedione (estr-5-en-3,17-dione;
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(xxxvii) norbolethone (13<<beta>>, 17<<beta>>-diethyl-17<<beta>>
hydroxygon-4- en-3-one);
(xxxviii) norclostebol (4-chloro-17<<beta>>-hydroxyestr-4-en-3-one);
(xxxix) norethandrolone (17α-ethyl-17α-hydroxyestr-4-en-3-one);
(xl) normethandrolone (17α-methyl-17α-hydroxyestr-4-en-3-one);
(xli) oxandrolone (17α-methyl-17α-hydroxy-2-oxa-[5α]- androstan-3-one);
(xlii) oxymesterone (17α-methyl-4,17α-dihydroxyandrost-4-en-3-one);
(xliii) oxymetholone (17α-methyl-2-hydroxymethylene-17α-hydroxy- [5α]
androstan-3-one);
(xliv) stanozolol (17α-methyl- 17α-hydroxy-[5α]-androst-2-eno[3,2-c]-pyrazole);
(xlv) stenbolone (17<<beta>>-hydroxy-2-methyl-[5<<beta>>] -androst-1-en-3
one);
(xlvi) testolactone (13-hydroxy-3-oxo-13,17-secoandrosta-1,4-dien-17-oic acid
lactone);
(xlvii) testosterone (17<<beta>>-hydroxyandrost-4-en-3-one);
(xlviii) tetrahydrogestrinone (13<<beta>>,17<<beta>>-diethyl-17<<beta>>-
hydroxygon-4,9, 11-trien-3-one);
(xlix) trenbolone (17<<beta>>-hydroxyestr-4,9,11-trien-3-one); and
(xlx) any salt, ester, or ether of a drug or substance described in this paragraph.
The substances excluded under this subparagraph may at any time be scheduled by
the Attorney General in accordance with the authority and requirements of
subsections (a) through (c) of section 811 of this title.
You will however, note that it reads:
Except as provided in clause (ii), such term does not include an anabolic steroid
which is expressly intended for administration through implants to cattle or other
nonhuman species and which has been approved by the Secretary of Health and
Human Services for such administration.
Hmm…perhaps that’s why purchasing finaplex pellets is still legal…though making
your own Trenbolone product is (easy but) illegal.
BC: Damn! That’s all the fun stuff! All of the cool stuff is illegal! Why would they do
that?
LX: Political discussion is perhaps better left for another day, but I feel it necessary
to note that Congress did not determine that steroids were a danger, but rather that
they needed to protect professional sports organizations. As for myself, I can not
remember that being a hot issue around last election time…Apparently, it’s their job
now, and hence passed the Anabolic Steroid Control Act of 1990 - making anabolic
steroids Schedule III substances in the class with opiate painkillers like Vicodin, as
well as barbiturates, ketamine, and various other substances.
BC: Well, let’s talk about importing controlled substances, like steroids. When can
packages be opened? Are there different applicable laws when the package is sent
domestic vs. internationally?
LX: Whoa, slow down. Let’s take those questions one at a time. First of all, any
package coming from an international venue CAN be opened AT WILL. It is very
important to note that absolutely no probable cause or even reasonable suspicion of
331
any type of wrongdoing is necessary. If your package is coming from an overseas
location then it can be opened and inspected for any reason. Any.
As regards domestic mail, first class mail, priority mail, and express mail all require a
search warrant that can only be obtained with what is known as probable cause, a
measurably higher standard than simply reasonable suspicion. This makes it
commeasurately less likely that your domestically mailed package will be randomly
inspected or even deemed to be in the category of packages which can be, but
clearly if the package is leaking oil, bears an invalid return address, the return
address is flagged due to an ongoing investigation, or if unluckily your package
happens to break open—it can be searched and you may be receiving a visit from
the authorities. Also, if the return address is “Illegal Steroids, 69 Steroid Lane,
Steroid Land USA, then it will be opened. In the end, just because you are receiving
a domestic package does not mean you are immune from having your package
searced or from prosecution.
BC: What if I use a P.O. box? Does that afford me any further protection versus
simply using my home address if I were getting something illegal sent to me through
the mail?
LX: The P.O. Box is a viably safer route many people utilize to safeguard themselves
from arrest. I think it’s a great idea to use a P.O. Box or UPS Store for any and all
anabolic steroid deliveries. Now this is not a foolproof, but it is harder for law
enforcement to stake out a P.O. Box to get their hands on you receiving a package.
However, it is certainly doable and the many who have been arrested at a Private
Mail Box (PMB) can attest to this fact with some vigor. It should be noted that using
a PMB reduces the link to search your home because it reduces the nexus between
your home and the illegal substances. Clearly a judge will have to decide that your
receipt of a package at a PMB is sufficient to be deemed probable cause that you also
have steroids in your home; judges tend to use that rationale all the time. Although
it may be slight, it is worth the chance that a judge may not conclude that law
enforcement has established a link between your home and the PMB. Also, we know
that you wonldn’t be so stupid as to have steroids in your home while awaiting a
package of them right? Be aware though that law enforcement will certainly have a
record of all shipments made to your PMB, especially shipments that require a
signature, so if you have received 153 items from China in the last week, its likely
that a judge will conclude that there is clearly probable cause to also search your
home. I still personally use a PMB, and definitely recommend that if you were to
order anabolic steroids you ought NEVER to use your home to receive a shipment.
I also never open my package until I get home, because if I am stopped for a traffic
violation and subject to a search (which if asked, I would say no, whenever possible
to a voluntary search), the package may not be subject to opening without a
warrant. SO if you get pulled over for some reason with an open package of
anabolics in plain view that package is subject to search and seizure law. On the
other hand, if the package is still sealed, it will require a search warrant necessarily
based upon probable cause to open.
BC: Ever hear of “The knock and talk”? Wanna explain to my readers what it is?
LX: Of course, yeah, that’s a very good question. You see, if the police lack probable
cause to search your home, or open a package they may decide to engage you in a
typical practice known as the knock and talk. Everyone…the police, postal
332
inspectors, or even customs agents, can knock on your door and give you an
invitation to chat of sorts. Often they will also request entry into your home which
seems logical, as you need somewhere to chat, but remember law enforcement is
scanning your home visually for evidence which may then allow them to obtain
probable cause to search your home. Once law enforcement is in your home they
may look for anything in plain view that will give rise to probable cause being
merited. The used pin on your counter, the vial crimper on your desk, or the empty
vial are all probable cause to search. The Western Union receipt to China, or
anything else in “plain view” may also be deemed as this. Your mouth may also
give rise to probable cause. We’ve all seen “Cops” and a million cop movies, and we
know that simply stated ANYTHING you say can and may be used against you. If
approached for a knock and talk it is best to have temporary amnesia, meaning you
don’t know anything. In addition, please talk to law enforcement outside, you DO
NOT ever have to allow them into your home without a warrant. In this way, cops
are basically like vampires…you are powerless once you invite them into your home.
BC: My personal policy is to always tell police or anyone of their kind that I would
like a lawyer present if they wish to ask me anything. Not because I have anything
to hide, but because a lawyer may help to avoid any miscommunication or
misunderstanding during such a dialogue. Admittedly, I’ve never been taken up on
that offer by any government agent trying to ask me questions.
LX: Ha ha…I suspect you wouldn’t be taken up on that offer!
BC: Let’s talk about Possession versus Distribution. What can you tell me about
that?
LX: Penalties for simple possession are often much less substantial than penalties for
distribution of a controlled substance, as you may suspect. However, various states
are given the levity to enact their own various rules and guidelines regarding
controlled substances. Generally the Federal Statute is followed, however, there are
many odd variances. For example, in Alaska and Vermont, anabolic steroids are not
scheduled! Is anyone moving?
BC: I’m packing my bags after this interview!
LX: Right, well the main idea here is that what is possession in one particular state
may actually be distribution in another. The differences if you are charged for
possession versus distribution can be highly significant, meaning jail versus no jail,
so it is worthy getting very familiar with your state’s laws to understand how they
classify distribution versus possession. Usually a prosecutor or law enforcement
agent will testify as to what they believe is possession versus distribution, usually
not a good idea for the end user, since 1000 tabs of dianabol is a common place
order on the Internet (a case, usually) , but in almost all legal situations will be
considered possession with intent to distribute.
BC: So I’m on the Internet, and seeing all these Anti-ageing Clinics offering doctors
prescriptions for lots of goodies: testosterone, growth hormone, etc. Is this legal?
LX: Anabolic steroids are clearly controlled substances as we saw in an earlier
question. However, the fact that these hormones are controlled substances does not
automatically make them proscribed for what constitutes a “legitimate medical
purpose.” In fact, most states have enacted statutes regarding what constitutes a
333
legitimate medical purpose. Most people will seek out a prescription for low
testosterone levels, often called HRT (or hormone replacement therapy) and
depending on the practitioner it may or may not be granted. Most of the online
ageing clinics will probably afford a degree laxness with the dispensing of anabolic
steroids for perceived medical purposes, but your general health practitioner will in
probably not find it “ethical” to prescribe anabolic steroids to a 25 year-old male who
perceives his testosterone to be low because its only mid-range. There have been
various prosecutions of doctors who have prescribed anabolic steroids for what is
perceived as being outside the bounds of medical usage, so the need for a physician
to be leery to dispense anabolic steroids is understandable. Some of these cases
even involve doctors prescribing them for wasting conditions, before that was
recognizd that they could be useful for that.
Now online doctors may seem quite cavalier in dispensing a prescription for anabolic
steroids, and in some cases you even get the medications directly from them!
However, these online clinics operate at great risk usually, and this is due to the lack
of physical contact between the physician and patient. Both the AMA and DEA have
viewed this type of patient-physician relationship as invalid and subject to
prosecution.
Of course this can be a valid way to obtain steroids, but just keep all of the
preceeding in mind.
BC: So let’s say I am getting some steroids sent to me in the mail (because I’m just
that type of bad-person who does such things, hypothetically). What should I look
out for? What’s this “Controlled Delivery” I’ve heard so much about?
LX: Well, this is a long and difficult topic, but let us make it abbreviated and as
simplistic as possible.
BC: Thanks…I’m a simple guy…
LX: Well, The bottom line of a controlled delivery is that the government agency
seeking to prosecute you, be it the Postal Inspectors, DEA, FBI, or local law
enforcement, want you to accept the package and in doing so thereby retain
possession of the package. This is why you are asked to sign for the package in
most instances, as it gives them some physical evidence of your having accepted it.
Your signature leads to the presumption that you have now accepted possession and
clearly there exists probable cause to believe you have in fact committed a crime.
Now comes the fun part; often after you accept the package the government agency
usually has already had in its hands what is known as a conditional warrant, which
makes it conditional upon your acceptance that your home can now be searched, but
I prefer the word raided or ransacked. Although you do not always have to sign for
the package, accepting the package affords the same effect to the conditional
warrant as signing it does.
BC: So what could I do, in this hypothetical case?
LX: Obviously you should not sign for any package, or signal acceptance of a
package if you were not expecting to have to sign for the package or have it hand
delivered. This does not get you off the proverbial hook; there have been many
334
instances where law enforcement has used electronic beacons to signal when a
package is open that has been left on someone’s door. So you are sitting at home
glad to have just received your package in the mail, and get your cycle going, and
you did not have to sign for it, nor did you get a hand delivered package, so
everything seems great, but then once you open that package, expect a visitor, and
not the friendly type…the type with a badge is likely to be showing up. There are a
number of nuances here that lead to a longer discussion, such as writing return to
sender on the package (which doesn’t really work anymore), but this discussion will
merit a lot more space and time, and since now you know what a controlled delivery
is, and have some information on how it is executed—just avoid it.
BC: Ok, I think we’ve given everyone a pretty good idea of all of this stuff from a
legal perspective. Can I bother you for your personal predictions regarding anabolic
steroid usage in the United States from a legal perspective?
LX: Well, it would be my wish to end with good news on this topic. But I
feel that the government will continue its ways on outlawing comnpounds that ought
to be legal, and making it difficult to obtain anabolics. The bright becon we have is
that customs is not able to stop everything, and just like the war on drugs from the
80’s, steroids are now (thanks to the government) cheap and easily available. If you
get caught with them, you are kind of screwed, but just as the war on drugs did for
cocaine in the 80’s, the war on steroids has made them cheap, of higher purity, and
readily available.
BC: Thanks for your time, LX. I hope we can get together and do this again in the
future.
335
Steroid Listings
By
Generic Name
336
Generic Name Trade Name Dosage Packaging Country Company Status Vet
boldenone (blend) Equilon 100 100 mg/ml 6 ml vial Myanmar/Burma WDV VET
boldenone undecylenate Ana-Bolde 50 mg/ml 10 ml vial Argentina Fort VET
boldenone undecylenate Anabolic BD 50 mg/ml 10 ml vial Australia SYD Group VET
boldenone undecylenate Anabolic BD 100, 200 mg/ml 10 ml vial Mexico SYD Group VET
boldenone undecylenate Anabolic-BD 100 mg/ml 10 ml vial Mexico Grupo Tarasco [NLM] VET
boldenone undecylenate Bold QV 200 200 mg/ml 10 ml vial Mexico Quality Vet VET
boldenone undecylenate Boldabol 200 mg/ml 10 ml vial Thailand British Dragon
boldenone undecylenate Boldebal-H 50 mg/ml 10 ml vial Australia Ilium/Troy VET
boldenone undecylenate Boldenol 25 25 mg/ml 10, 50,100, 250ml vial Columbia Comandina VET
boldenone undecylenate BoldenoI R 50 mg/ml 10, 50, 100, 250ml vial Columbia Comandina VET
boldenone undecylenate Boldenon 200 mg/ml 10 ml vial Mexico Ttokkyo VET
boldenone undecylenate Boldenona 50mg/ml 10,20,100 ml vial Columbia Biogen VET
boldenone undecylenate Boldenona 50 mg/ml 10, 50,100, 250ml vial Columbia Vecol VET
boldenone undecylenate Boldenona 50 50 mg/ml 10, 50, 100, 250ml vial Columbia Servinsumos VET
boldenone undecylenate Boldenona 50 Gen-Far 50 mg/ml 10, 50,100,250ml vial Bolivia Gen-Far VET
boldenone undecylenate Boldenona 50 Gen-Far 50 mg/ml 10, 50,100, 250ml vial Columbia Gen-Far VET
boldenone undecylenate Boldenona 50 Gen-Far 50 mg/ml 10, 50,100, 250ml vial Costa Rica Gen-Far VET
boldenone undecylenate Boldenona 50 Gen-Far 50 mg/ml 10, 50, 100, 250ml vial Dom. Republic Gen-Far VET
boldenone undecylenate Boldenona 50 Gen-Far 50 mg/ml 10,50,100,250ml vial Ecuador Gen-Far VET
boldenone undecylenate Boldenona 50 Gen-Far 50 mg/ml 10, 50,100, 250ml vial El Salvador Gen-Far VET
boldenone undecylenate Boldenona 50 Gen-Far 50 mg/ml 10,50,100,250ml vial Guatemala Gen-Far VET
boldenone undecylenate Boldenona 50 Gen-Far 50 mg/ml 10,50,100, 250ml vial Honduras Gen-Far VET
boldenone undecylenate Boldenona 50 Gen-Far 50 mg/ml 10, 50,100,250ml vial Nicaragua Gen-Far VET
boldenone undecylenate Boldenona 50 Gen-Far 50 mg/ml 10, 50,100,250ml vial Panama Gen-Far VET
boldenone undecylenate Boldenona 50 Gen-Far 50 mg/ml 10,50,100,250ml vial Peru Gen-Far VET
boldenone undecylenate Boldenone - 50 50 mg/ml 10 ml vial Australia Jurox [NLM] VET
boldenone undecylenate Cebulin 50 50 mg/ml 10, 50, 250 ml vial Columbia Provet VET
boldenone undecylenate Crecibol 50 25 mg/ml 10, 30 ml vial Mexico Unimed VET
boldenone undecylenate Dynabolin 50 50 mg/ml 10, 50,100,250ml vial Columbia Kryovet VET
boldenone undecylenate Equifort 50 mg/ml 10, 50 ml vial Brazil Purina VET
boldenone undecylenate Equi-gan 50 mg/ml 10, 50,100,250 ml vial Mexico Tomel VET
boldenone undecylenate Equipoise® 50 mg/ml 10, 50 ml vial Mexico Fort Dodge VET
boldenone undecylenate Equipoise® 50 mg/ml 50 ml vial U.S. Fort Dodge VET
boldenone undecylenate Equipoise® 25,50 mg/ml 50 ml vial Canada Ciba-Geigy [NLM] VET
boldenone undecylenate Equipoise® 25, 50 mg/ml 50 ml vial Canada Squibb [NLM] VET
boldenone undecylenate Equipoise® 50 mg/ml 50 ml vial Canada Wyeth VET
boldenone undecylenate Equipoise® 25, 50 mg/ml 50 ml vial Mexico Solvay [NLM] VET
boldenone undecylenate Equipoise® 25, 50 mg/ml 50 ml vial Mexico Squibb [NLM] VET
boldenone undecylenate Equipoise® 25. 50 mg/ml 50 ml vial U.S. Squibb [NLM] VET
boldenone undecylenate Ex-Pois 50 mg/ml 10 ml vial Argentina Agofarma VET
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial Bolivia Laboratorios VM VET
boldenone undecylenate Ganabol 25, 50 mg/ml 10, 50,100, 250ml vial Bolivia Laboratories VM VET
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial Chile Laboratorios VM VET
boldenone undecylenate Ganabol 25, 50 mg/ml 10,50, 100, 250ml vial Chile Laboratorios VM VET
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial Columbia Laboratorios VM VET
boldenone undecylenate Ganabol 25, 50 mg/ml 10, 50, 100, 250ml vial Columbia Laboratorios VM VET
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial Dom. Republic Laboratorios VM VET
boldenone undecylenate Ganabol 25, 50 mg/ml 10, 50, 100. 250ml vial Dom. Republic Laboratorios VM VET
Steroid.com
337
Steroid Listings By Generic Name
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial Ecuador Laboratorios VM VET
boldenone undecylenate Ganabol 25, 50 mg/ml 10, 50, 100, 250ml vial Ecuador Laboratorios VM VET
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial El Salvador Laboratorios VM VET
boldenone undecylenate Ganabol 25. 50 mg/ml 10,50, 100, 250ml vial El Salvador Laboratorios VM VET
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial Guatemala Laboratorios VM VET
boldenone undecylenate Ganabol 25, 50 mg/ml 10,50, 100, 250ml vial Guatemala Laboratories VM VET
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial Honduras Laboratories VM VET
boldenone undecylenate Ganabol 25, 50 mg/ml 10, 50,100, 250ml vial Honduras Laboratories VM VET
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial Panama Laboratories VM VET
boldenone undecylenate Ganabol 25, 50 mg/ml 10,50,100. 250ml vial Panama Laboratories VM VET
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial Paraguay Laboratories VM VET
boldenone undecylenate Ganabol 25, 50 mg/ml 10, 50,100, 250ml vial Paraguay Laboratories VM VET
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial Peru Laboratories VM VET
boldenone undecylenate Ganabol 25, 50 mg/ml 10, 50,100, 250ml vial Peru Laboratories VM VET
boldenone undecylenate Ganabol 50 mg/ml 500 ml vial Venezuela Laboratories VM VET
boldenone undecylenate Ganabol 25, 50 mg/ml 10, 50,100, 250ml vial Venezuela Laboratories VM VET
boldenone undecylenate Maxigan 50 mg/ml 10, 50 ml vial Mexico Inpei VET
boldenone undecylenate Mitgan 50 50 mg/ml 50 ml vial Columbia California VET
boldenone undecylenate Porkybol 1% 10 mg/ml 10, 50,100 ml vial Columbia Compania California VET
boldenone undecylenate Sybolin 25 mg/ml 10 ml vial Australia Ranvet VET
boldenone undecylenate Ultragan 100 mg/ml 10 ml vial Mexico Denkall VET
boldenone undecylenate Uttragan 50 mg/ml 50 ml vial Mexico Denkall VET
boldenone undecylenate Vebonol 25 mg/ml 10 ml vial Australia Ciba-Geigy [NLM] VET
boldenone undecylenate Vebonol 25 mg/ml 10 ml vial Germany Ciba-Geigy VET
boldenone undecylenate Vebonol 25 mg/ml 10 ml vial Switzerland Ciba-Geigy [NLM] VET
dostebol acetate Alfa-Trofodermin .5% gel n/a Italy Farmitalia [NLM]
clostebol acetate Alfa-Trofbdermin .5% gel n/a Italy Pharmacia & Upjohn
clostebol acetate Megagrisevit-Mono 15 mg dragee 30 dragee box Germany Pharmacia [NLM]
clostebol acetate Megagrisevit-Mono 10mg/1.5ml 1.5 ml vial Germany Pharmacia [NLM]
clostebol acetate Steranabol 20 mg/ml 2 ml ampule Italy Farmitalia [NLM]
clostebol acetate Trofbdermin Crema cream 30 gram tube Italy Carlo Erba OTC
clostebol acetate Trofbdermin Spray n/a 30 ml spray Italy Carto Erba OTC
dihydrotestosterone Andractim 25mg/g 80 gram gel Belgium Piette
dihydrotestosterone Andractim 25mg/g 100 gram gel France Besins-lscovesco
dihydrotestosterone Andractim 25mg/g 100 gram gel India Chemec
dihydrotestosterone Andractim 25mg/g 80 gram gel Korea n/a
dihydrotestosterone Andractim 25mg/g 80 gram gel Uruguay Servimedic
drostanolone Dromostan 50 mg/ml 5 ml vial Philippines Xelox (export)
drostanolone propionate Drolban 50mg/1ml 1 ml vial U.S. Lilly [NLM]
drostanolone propionate Masterid 100 mg/2ml 2 ml amp Germany Gruenthal [NLM]
drostanolone propionate Masteril 100 mg/2ml 2 ml ampule Bulgaria Syntex [NLM]
drostanolone propionate Masteril 100 mg/2ml 2 ml amp United Kingdom Syntex [NLM]
drostanolone propionate Masteron 100 mg/2ml 2 ml amp Belgium Sarva-Syntex [NLM]
drostanolone propionate Masteron 100 mg/2ml 2 ml amp Portugal Cilag [NLM]
drostanolone propionate Mastisol 5% injection sol. n/a Japan Shionogi [NLM]
drostanolone propionate Metormon 100 mg/2ml 2 ml amp Spain Syntex [NLM]
drostanolone propionate Permastril 100 mg/2ml 2 ml ampule France Cassenne [NLM]
ethylestrenol Maxibolin 2 mg tablet n/a U.S. Organon [NLM]
ethylestrenol Maxibolin Elixir 2mg/5ml n/a U.S. Organon [NLM]
Steroid.com
338
Steroid Listings By Generic Name
ethylestrenol Nandoral .5 mg tablet 100, 500 tablet bottle Australia Intervet VET
ethylestrenol Nitrotain 15mg/4gram 60, 250,1000 gram tube Australia Nature-Vet VET
ethylestrenol Orabol-H 100 mg/5g paste 30 ml plastic tube Australia Vetsearch [NLM] VET
ethylestrenol Orabolin® 2 mg tablet n/a Belgium Organon [NLM]
ethylestrenol Orabolin® 2 mg tablet 10 tablet box India Infar
ethylestrenol Orabolin® 2 mg tablet 100 tablet box Pakistan Organon
ethylestrenol Orabolin® 2 mg tablet n/a South Africa Donmed/Organon [NLM]
ethylestrenol Orabolin® 2 mg tablet n/a United Kingdom Organon [NLM]
ethylestrenol Orgabolin 2 mg tablet n/a Indonesia Organon
ethytestrenol Orgabolin 2 mg tablet n/a Netherlands Organon [NLM]
ethytestrenol Orgabolin 2 mg tablet n/a Turkey Santa [NLM]
ethytestrenol Orgabolin Drops 2mg n/a Turkey Santa [NLM]
ethytestrenol Silabolin 25. 50 mg/ml 1 ml ampule Russia Farmadon [NLM]
fluoxymesterone Android-F 10mg tablet 100 tablet bottle U.S. Brown [NLM]
fluoxymesterone Baojen 5 mg capsule n/a Taiwan Ta Fong
fluoxymesterone Chinglicosan 5 mg capsule n/a Taiwan Ciiphar
fluoxymesterone Ferona 1 mg tablet 30 tablet box Argentina Sidus
fluoxymesterone Fluoxymesterone cap 5 mg capsule n/a Taiwan Yuan Chou
fluoxymesterone Floxymesterone 5 mg capsule n/a Taiwan Chen Ho
fluoxymesterone Fluoxymesterone 10mg tablet 100 tablet bottle U.S. Rosemont
fluoxymesterone Fosteron 5 mg capsule n/a Taiwan Health Chemical
fluoxymesterone Fu Lao Shu 10 mg capsule n/a Taiwan Ming Ta
fluoxymesterone Fuloan 11 mg capsule n/a Taiwan New Chem & Pharm
fluoxymesterone Halotestin® 5 mg tablet 50 tablet bottle Canada Pharmacia
fluoxymesterone Halotestin® 5 mg tablet n/a Denmark Upjohn [NLM]
fluoxymesterone Halotestin® 5 mg tablet n/a Finland Upjohn
fluoxymesterone Halotestin® 5 mg tablet n/a France Pharmacia-Upjohn [NLM]
fluoxymesterone Halotestin® 5 mg tablet 20 tablet box Greece Upjohn
fluoxymesterone Halotestin® 5 mg tablet 20 tablet box Italy Upjohn [NLM]
fluoxymesterone Halotestin® 2, 5 mg tablet n/a Japan n/a
fluoxymesterone Halotestin® 5 mg tablet n/a Netherlands Upjohn [NLM]
fluoxymesterone Halotestin® 5 mg tablet n/a Norway Upjohn [NLM]
fluoxymesterone Halotestin® 5 mg tablet n/a Philippines Pharmacia & Upjohn
fluoxymesterone Halotestin® 5 mg tablet n/a Sweden Upjohn [NLM]
fluoxymesterone Halotestin® 5 mg tablet 100 tablet bottle Thailand Pharmacia
fluoxymesterone Halotestin® 2,5,10 mg tablet 100 tablet bottle U.S. Pharmacia & Upjohn
fluoxymesterone Halotestin® 10mg tablet 100 tablet bottle U.S. Wamer-Chilcott [NLM]
fluoxymesterone Halotestin® 5 mg tablet n/a YugoslaviaFRMRGalenika [NLM]
fluoxymesterone Hysterone 20 mg tablet 100 tablet bottle U.S. Major [NLM]
fluoxymesterone Lipaw 10 mg capsule n/a Taiwan Long Der
fluoxymesterone Long 10mg capsule n/a Taiwan Century
fluoxymesterone ODK 5 mg capsule n/a Taiwan Winston
fluoxymesterone Oralsterone 5 mg capsule n/a Taiwan Long Der
fluoxymesterone Ora-Testryl 5 mg tablet 100 tablet bottle U.S. Squibb Mark [NLM]
fluoxymesterone Sidomon 5 mg capsule n/a Taiwan n/a
fluoxymesterone Stenox 2.5 mg tablet 20 tablet box Mexico Atlantis
fluoxymesterone Tealigen 5 mg capsule n/a Taiwan Ming ta
fluoxymesterone Ton Lin 10mg capsule n/a Taiwan Chin Teng
fluoxymesterone Ultandren 1,5 mg tablet n/a United Kingdom Ciba [NLM]
Steroid.com
339
Steroid Listings By Generic Name
fluoxymesterone Vewon 5 mg tablet n/a Taiwan Yung Shin
fluoxymesterone Vi Jane 10mg capsule n/a Taiwan Shyh Sar
fluoxymesterone Waromom 5 mg tablet n/a Taiwan Washington
formebolone Esiclene 1 mg drops n/a Italy LPB [NLM]
formebolone Esiclene 2 mg/ml 2 ml ampule Italy LPB [NLM]
formebolone Esiclene 5 mg tablet n/a Italy LPB [NLM]
formebolone Esiclene 1 mg drops n/a Portugal Biofarma [NLM]
formebolone Esiclene 5 mg tablet n/a Portugal Biofarma [NLM]
formebolone Hubernol 5 mg dragee n/a Spain ICN Hubber [NLM]
formebolone Hubernol 1 mg drops n/a Spain ICN Hubber [NLM]
furazabol Miotolan 1 mg tablet n/a Japan Daiichi Seiyaku [NLM]
mesterolone Mesterolon 25 mg tablet n/a Philippines Brown & Burk
mesterolone Mesterolon 25 mg tablet n/a Sweden Schering [NLM]
mesterolone Mestoranum 25 mg tablet n/a Denmark Schering
mesterolone Mestoranum 25 mg tablet n/a Norway Sobering [NLM]
mesterolone Pluriviron 25 mg dragee 30 dragee box Germany Asche [NLM]
mesterolone Proviron 25 mg tablet 20 tablet box Algeria Schering
mesterolone Proviron 25 mg tablet 50 tablet box Taiwan Schering
mesterolone Proviron 25 mg tablet 20 tablet box Turkey Schering
mesterolone Proviron® 25 mg tablet n/a Argentina Schering
mesterolone Proviron® 25, 50 mg tablet n/a Australia Schering
mesterolone Proviron® 25 mg tablet 50 tablet bottle Austria Schering
mesterolone Proviron® 25 mg tablet 50 tablet bottle Belgium Schering
mesterolone Proviron® 25 mg tablet 20 tablet box Brazil Schering
mesterolone Proviron® 25 mg tablet 20, 50 tablet box Bulgaria Schering
mesterolone Proviron® 25 mg tablet 20 tablet box Colombia Schering
mesterolone Proviron® 25 mg tablet n/a Costa Rica Schering
mesterolone Proviron® 25 mg tablet 20 tablet box Croatia Schering
mesterolone Proviron® 25 mg tablet 20, 50 tablet box Czech. Rep. Schering
mesterolone Proviron® 25 mg tablet 20 tablet bottle Dom. Rep. Schering
mesterolone Proviron® 25 mg tablet 20 tablet box Egypt Schering/CID [NLM]
mesterolone Proviron® 25 mg tablet n/a El Salvador Schering
mesterolone Proviron® 25 mg tablet 20 tablet box Estonia Schering [NLM]
mesterolone Proviron® 25 mg tablet n/a Finland Leiras
mesterolone Proviron® 25 mg tablet n/a France Schering [NLM]
mesterolone Proviron® 25 mg tablet 50 tablet bottle Germany Schering [NLM]
mesterolone Proviron® 25 mg tablet 20 tablet bottle Greece Schering
mesterolone Proviron® 25 mg tablet n/a Guatemala Schering
mesterolone Proviron® 25 mg tablet n/a Honduras Schering
mesterolone Proviron® 25 mg tablet 10, 15, 20, 50, 100, 150 tab bottle Hungary Schering
mesterolone Proviron® 25 mg tablet 30 tablet box India Schering
mesterolone Proviron® 25 mg tablet n/a Indonesia Schering
mesterolone Proviron® 25 mg tablet 20, 50 tablet box Israel Schering
mesterolone Proviron® 25 mg tablet 20 tablet box Italy Schering
mesterolone Proviron® 25 mg tablet 20 tablet box Latvia Schering [NLM]
mesterolone Proviron® 25 mg tablet 20 tablet box Lithuania Schering [NLM]
mesterolone Proviron® 25 mg tablet 10 tablet box Mexico Schering
mesterolone Proviron® 25 mg tablet 50 tablet bottle Netherlands Schering
mesterolone Proviron® 25 mg tablet n/a Nicaragua Schering
Steroid.com
340
Steroid Listings By Generic Name
mesterolone Proviron® 25 mg tablet n/a Panama Schering
mesterolone Proviron® 25 mg tablet 20 tablet box Paraguay Schering
mesterolone Proviron® 25 mg tablet 20 tablet box Poland Schering
mesterolone Proviron® 25 mg tablet 20 tablet box Portugal Schering
mesterolone Proviron® 25 mg tablet 20 tablet bottle Russia Schering
mesterolone Proviron® 25 mg tablet 20, 50 tablet bottle Slovakia Schering
mesterolone Proviron® 25 mg tablet 20, 100 tablet bottle South Africa Schering/Beriimed
mesterolone Proviron® 25 mg tablet 20 tablet box Spain Schering
mesterolone Proviron® 25 mg tablet n/a Switzerland Schering [NLM]
mesterolone Proviron® 25 mg tablet 20 tablet box Ukraine Schering
mesterolone Proviron® 25 mg tablet 30 tablet box United Kingdom Schering
mesterolone Proviron® 25 mg tablet n/a Uruguay Schering
mesterolone Proviron® 25 mg tablet 15 tablet box Venezuela Schering
mesterolone Proviron® 25 mg tablet n/a Yugoslavia FRMRAlkoid
mesterolone Provironum 25 mg tablet 50 tablet box Singapore Organon
mesterolone Provironum 25 mg tablet 150 tablet box Thailand Schering
mesterolone Restore 25 mg tablet 20 tablet box India Brown & Burk
mesterolone Vistimon 25 mg tablet 20 tablet box Germany Jenapharm [NLM]
mesterolone Vistimon 25 mg tablet n/a Korea n/a
mesterolone Vistimon 25 mg tablet 30 tablet box Taiwan Jenapharm
methandrostenolone Ammipire 5 mg tablet 1000 tablet bottle Thailand Ammipire
methandrostenolone Anabol 50 mg tablet n/a Thailand British Dragon [NLM]
methandrostenolone Anabol Tablets 5 mg tablet 1000 tablet bottte Thailand British Dispensary
methandrostenolone Anabol Tablets 5 mg tablet 1000 tablet bottle Thailand L.P Standard [NLM]
methandrostenolone Anabolex 3 mg tablet 100 tablet box Dom. Rep. Ethical
methandrostenolone Anabolikum 2.5% 25mg/ml 50 ml vial Germany Meca G [NLM] VET
methandrostenolone Anabolin 5 mg tablet n/a Finland Leiras [NLM]
methandrostenolone Anabolin 0.5% cream n/a Finland Leiras [NLM]
methandrostenolone Anabol-Jet 25mg/ml 30,100, 250 ml vial Mexico Norvet VET
methandrostenolone Anabol-Jet ADE 30mg/ml 100,250 ml vial Mexico Norvet VET
methandrostenolone Anabol-Pets 10.25 mg tablet 200 tablet bottle Mexico Norvet VET
methandrostenolone Andoredan 5 mg tablet n/a Japan Takeshima-Kodama [NLM]
methandrostenolone Bionabol 2, 5 mg tab 40 tablet box Bulgaria Balkanpharma
methandrostenolone Bionabol 2 mg tablet 40 tablet bottle Bulgaria Pharmacia [NLM]
methandrostenolone Bionabol 5mg tab 40 tablet bottle Bulgaria Pharmacia [NLM]
methandrostenolone Chinlipan Tab 2 mg tablet n/a Taiwan Chin Tien
methandrostenolone Danabol OS 10mg tablet 500 tablet bottle Thailand Body Research
methandrostenolone D-Bol 10mg tablet 100 tablet bottle Mexico Denkall VET
methandrostenolone D-Bol 10mg capsule 96 capsule box Mexico Denkall VET
methandrostenolone D-Bol 10mg capsule 300 capsule bottle Mexico Denkall VET
methandrostenolone D-Bol 25mg/ml 10 ml vial Mexico Denkall VET
methandrostenolone Dialone 5 mg tablet 100 tablet bottle U.S. Major [NLM]
methandrostenolone Dianabol 10mg tablet 100 tablet bottle Mexico Salud VET
methandrostenolone Dianabol 25 mg/ml 10,50,100 ml vial Mexico Salud VET
methandrostenolone Dianabol 25 mg tablet 30 tablet bottle Belize Planet Pharmacy
methandrostenolone Dianabol 5 mg tablet 100 tablet bottle Germany Ciba [NLM]
methandrostenolone Dianabol 5 mg tablet 100 tablet bottle U.S. Ciba [NLM]
methandrostenolone Dianabol 5 mg tablet 100 tablet bottle United Kingdom Ciba [NLM]
methandrostenolone Encephan 5 mg tablet n/a Japan Sato [NLM]
Steroid.com
341
Steroid Listings By Generic Name
methandrostenolone Ganabol 25 mg/ml 50 ml vial Mexico Salud [NLM] VET
methandrostenolone Melic 5 mg tablet 1000 tablet box, bottle Thailand Phanmasant
methandrostenolone Metaboline 2 mg tablet 60, 500 tablet bottle Canada Desbergers [NLM]
methandrostenolone Metanabol 5 mg tablet 20 tablet box Poland Jelfa
methandrostenolone Metanabol 5 mg tablet 20 tablet box Poland Polfa [NLM]
methandrostenolone Metanabol I mg tablet 20 tablet box Poland Polfa [NLM]
methandrostenolone Metanabol 0.5% cream n/a Poland Polfa [NLM]
methandrostenolone Metandiabol 25 mg/ml 50 ml vial Mexico Quimper VET
methandrostenolone Metandienon 5 mg tablet 100 tablet box Russia Bioreaktor
methandrostenolone Metandrol 10 10mg tablet 500 tablet bottle Mexico Bratis Labs VET
methandrostenolone Metandrostenolon 5 mg tablet 100 tablet box Russia Akrihin [NLM]
methandrostenolone Metandrostenolon 5 mg tablet 100 tablet box Russia Akrikhin
methandrostenolone Metandrostenolon 5 mg tablet 100 tablet box Russia Bioreaktor [NLM]
methandrostenolone Methanabol 5 mg tablet 500 tablet pouch Thailand British Dragon
methandrostenolone Methanabol 50 mg tablet 100 tablet pouch Thailand British Dragon
methandrostenolone Methandienone 5, 10mg tablet 100,1000 tablet bottle Mexico Ttokkyo VET
methandrostenolone Methandon 5 mg tablet 1000 tablet bottle Thailand Acdhon Co.
methandrostenolone Naposim 5 mg tablet 20 tablet box Rumania Terapia
methandrostenolone Neo-Anabolene 5 mg tablet 10 tablet strip Indonesia Haurus
methandrostenolone Nerobol 5 mg tablet 20 tablet box Bulgaria Gedeon Richter [NLM]
methandrostenolone Nerobol 5 mg tablet 20 tablet box Hungary Gedeon Richter [NLM]
methandrostenolone Nerobol 5 mg tablet 20 tablet box Yugoslavia/FRMRGalenika [NLM]
methandrostenolone Pronabol-5 5 mg tablet 100 tablet box India P&B Labs [NLM]
methandrostenolone Reforvit 25 mg tab 100, 300 tablet bottle Mexico Loeffler VET
methandrostenolone Reforvit-B 25mg/ml 10, 50ml Mexico Loeffler VET
methandrostenolone Restauvit 2 mg tablet n/a Mexico Ciba, Rugby [NLM]
methandrostenolone Stenolon 5 mg tablet 20 tablet box Czech. Rep. Leciva [NLM]
methandrostenolone Stenolon 1 mg tablet 20 tablet box Czech. Rep. Leciva [NLM]
methandrostenolone Trinergic 5 mg capsule n/a India Unimed [NLM]
methandrostenolone/stanozolol Diosterol 50 mg tablet 30 tablet bottle Belize Planet Pharmacy
methenolone acetate Metabolon 25 25 mg tablet 100 tablet bottle Mexico Bratis Labs VET
methenolone acetate Primobolan® 5 mg tablet n/a Austria Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a Belgium Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a Bolivia Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a Costa Rica Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a Dom. Rep. Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a Ecuador Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a El Salvador Schering [NLM]
methenolone acetate Primobolan® 50 mg tablet n/a France Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a Germany Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a Guatemala Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a Honduras Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet 100,1000 tablet box Japan Schering
methenolone acetate Primobolan® 5 mg tablet n/a Mexico Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a Nicaragua Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a Panama Schering [NLM]
methenolone acetate Primobolan® 5 mg tablet n/a South Africa Schering/Berlimed [NLM]
methenolone acetate Primobolan® Acetate 25 mg/ml 1 ml ampule Germany Schering [NLM]
methenolone acetate Primobolan® S 25 mg tablet n/a Finland Leiras [NLM]
Steroid.com
342
Steroid Listings By Generic Name
methenolone acetate Primobolan® S 25 mg tablet n/a Germany Schering [NLM]
methenolone acetate Primobolan® S 25 mg tablet n/a Netherlands Schering [NLM]
methenolone acetate Primobolan® S 25 mg tablet 50 tablet bottle South Africa Schering/Berlimed
methenolone acetate Primobolan® S 25 mg tablet n/a Thailand Schering [NLM]
methenolone acetate Primo-Plus 50 50 mg tablet 100 tablet bottle Mexico Ttokkyo VET
methenolone enanthate Primobolan Depot 100 mg/ml 1 ml ampule Egypt Schering/CID [NLM]
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Austria Schering [NLM]
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Belgium Schering [NLM]
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Czech. Rep. Schering [NLM]
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Ecuador Schering
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule France Schering [NLM]
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Germany Schering [NLM]
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Greece Schering [NLM]
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Guatemala Schering
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Italy Schering [NLM]
methenolone enanthate Primobolan® Depot 50 mg/ml 1 ml ampule Japan Schering [NLM]
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Japan Schering
methenolone enanthate Primobolan® Depot 50 mg/ml 1 ml ampule Mexico Schering
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Paraguay Schering
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Portugal Schering [NLM]
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule South Africa Schering/Berlimed [NLM]
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Spain Schering
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Switzerland Schering [NLM]
methenolone enanthate Primobolan® Depot 100 mg/ml 1 ml ampule Turkey Schering
methenolone enanthate Primobolan® Depot mite 50 mg/ml 1 ml ampule Germany Schering [NLM]
methyltestosterone Oreton Methyl 10 mg sub. tablet n/a U.S. Schering [NLM]
methyltestosterone T. Lingvalete 5 mg sub. dragee n/a YugoslaviaFRMRGatenika [NLM]
methyltestosterone Testo Tab 25 mg tablet n/a Korea Samil
methyltestosterone Teston 25 mg tablet 30 tablet box Greece Remek
methyltestosterone Testopropon 25 mg tablet n/a Malaysia Scanpharm
methyltestosterone Testormon 10mg tablet n/a Portugal Unitas
methyltestosterone Testosteron 5 mg tablet n/a Germany Berco [NLM]
methyltestosterone Testosure n/a n/a Hong Kong Europharm
methyltestosterone Testovis 10mg tablet n/a Italy SIT
methyltestosterone Testoyohim 25 mg dragee 30 dragee box Germany Paul Mehner [NLM]
methyltestosterone Testred 10mg capsule 100 capsule bottle U.S. ICN
methyltestosterone TP Men Hormone 10mg capsule 24 tablets Thailand TP Drugs
methyltestosterone Virilon (time released) 10 mg capsule 100,1000 capsule bottle U.S. Star
mibolerone Cheque Drops 100 meg/ml 55 mg bottle U.S. Upjohn [NLM] VET
mibolerone mibolerone drops 100 meg/ml 55 mg bottle U.S. Wedgewood VET
nandrolone (blend) Dinandrol 100mg/ml 2 ml vial Philippines Xelox (export)
nandrolone cyclohexylpropionate Sanabolicum 25, 50 mg/ml 1 ml ampule Egypt Biochemie/Nile
nandrolone cyclohexylpropionate Sanabolicum-Vet 50mg/ml 10 ml vial Austria Werfft-Chemie VET
nandrolone cypionate Anabolic DN 50 mg/ml 10 ml vial Australia SYD Group VET
nandrolone cypionate Anabolic DN 50, 300 mg/ml 10 ml vial Mexico SYD Group VET
nandrolone cypionate Anabolic-DN 50 mg/ml 10 ml vial Mexico Grupo Tarasco [NLM] VET
nandrolone cypionate Dynabol 50 mg/ml 10ml vial Australia Jurox [NLM] VET
nandrolone decanoate Anabolicum 25 mg/ml 10, 50 ml vial Germany Bela-Pharm VET
nandrolone decanoate Anabolin Forte 50 mg/ml 10 ml vial Netherlands Alfasan VET
Steroid.com
343
Steroid Listings By Generic Name
nandrolone decanoate Anabolin Forte 50 mg/ml 10 ml vial Rumania Alfasan VET
nandrolone decanoate Anabolin Forte 50 mg/ml 10,50 ml vial Spain Alfasan VET
nandrolone decanoate Anaboline Depot 50 mg/ml 1 ml Greece Adeteo
nandrolone decanoate Anaprolina 25, 50 mg/ml 1 ml ampule Chile Silesia
nandrolone decanoate Androlone-D 200 200 mg/ml 1 ml U.S. Keene [NLM]
nandrolone decanoate Canoate Inj 25, 50 mg/ml n/a Korea n/a
nandrolone decanoate Deca QV 200 200 mg/ml 10, 50 ml vial Mexico Quality Vet VET
nandrolone decanoate Deca QV 300 300 mg/ml 10 ml vial Mexico Quality Vet VET
nandrolone decanoate Deca-Dubol-100 100 mg/ml 2 ml vial India BM Pharmaceuticals
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml Argentina Organon
nandrolone decanoate Deca-Durabolin® 50 mg/ml 2ml Argentina Organon
nandrolone decanoate Deca-Durabolin® 25 mg/ml 1 ml Austria Organon [NLM]
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule, syringe Belgium Organon
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule Brazil Organon
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule Bulgaria Organon
nandrolone decanoate Deca-Durabolin® 50 mg/ml 2ml Canada Organon [NLM]
nandrolone decanoate Deca-Durabolin® 100 mg/ml 2ml Canada Organon
nandrolone decanoate Deca-Durabolin® 25, 50,100 mg/ml 1 ml ampule Chile Organon
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule Colombia Organon
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml Denmark Organon [NLM]
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule Egypt Organon/Nile
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml Finland Organon
nandrolone decanoate Deca-Durabolin® 100 mg/ml 1, 2ml Finland Organon
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml France Organon [NLM]
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml Germany Organon [NLM]
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml vial Greece Organon
nandrolone decanoate Deca-Durabolin® 100 mg/ml 2 ml vial Greece Organon
nandrolone decanoate Deca-Durabolin® 100 mg/ml 2 ml vial Greece Organon
nandrolone decanoate Deca-Durabolin® 25,50, 100 mg/ml 1 ml ampule India Infar
methenolone enanthate Primo-Plus 100 100mg/ml 1 ml ampule Mexico Ttokkyo VET
methylandrostenediol Andris 10mg tablet n/a Greece Chifar [NLM]
methylandrostenediol Methyldiol 2 mg tablet n/a U.S. Vortech [NLM]
methylandrostenediol Methyldiol Aqueous 50mg/ml n/a U.S. Vortech [NLM]
methylandrostenediol Metyandrostendiol 10, 25 mg tablet n/a Poland Jelfa [NLM]
methylandrostenediol Novandrol 10, 25 mg dragee n/a Yugoslavia/FRMRGalenika [NLM]
methylandrostenediol (blend) Anabolic NA 75mg/ml 10 ml vial Australia SYD Group VET
methylandrostenediol (blend) Anabolic NA 75mg/ml 10 ml vial Mexico SYD Group VET
methylandrostenediol (blend) Anabolic-NA 75 mg/ml 10 ml vial Mexico Grupo Tarasco [NLM] VET
methylandrostenediol (blend) Drive 55mg/ml 10 ml vial Australia RWR VET
methylandrostenediol (blend) Filybol 70 mg/ml 10, 20 ml vial Australia Ranvet VET
methylandrostenediol (blend) libriol 75 mg/ml 10, 20 ml vial Australia RWR VET
methylandrostenediol (blend) Spectriol 65 mg/ml 10 ml vial Australia RWR VET
methylandrostenediol (blend) Tribolin 75 mg/ml 10, 20 ml vial Australia Ranvet VET
Methandriol Dipropionate Methandriol Dipropionate 75mg/ml 10ml vial Thailand British Dragon
methylandrostenediol dipropionate Anadiol 5mg tab 10, 100 tablet bottle Australia Ilium/Troy VET
methylandrostenediol dipropionate Anadiol Depot 75 mg/ml 10 ml vial Australia Ilium/Troy VET
methylandrostenediol dipropionate Arbolic 50 mg/ml n/a U.S. Burgin Arden [NLM]
methylandrostenediol dipropionate Crestabolic 50 mg/ml n/a U.S. Nutrition [NLM]
methylandrostenediol dipropionate Denkadiol 75 mg/ml 10 ml vial Mexico Denkall VET
Steroid.com
344
Steroid Listings By Generic Name
methylandrostenediol dipropionate Durandrol 50 mg/ml n/a U.S. Pharmex [NLM]
methylandrostenediol dipropionate Hybolin 50 mg/ml n/a U.S. Hyrex [NLM]
methylandrostenediol dipropionate Methandriol 75 mg/ml 10 ml vial Australia Ilium/Troy [NLM] VET
methylandrostenediol dipropionate Methasus 50 50 mg/ml 20 ml vial Australia Jurox [NLM] VET
methylandrostenediol dipropionate Protabol 75 mg/ml 10 ml vial Australia Protabol VET
methylandrostenediol dipropionate Superbolin 75 mg/ml 10 ml vial Australia Vetsearch VET
methyltestosterone Afro 25 mg tablet 40 tablet box Turkey Casel
methyltestosterone Agovirin 10 mg dragee 100 dragee bottle Czech. Rep. Leciva [NLM]
methyltestosterone Android 5, 10,25 mg tablet 60 tablet bottle U.S. ICN Pharm
methyltestosterone Android 5, 10, 25 mg tablet n/a U.S. Brown [NLM]
methyltestosterone Androral 10mg tablet n/a Hungary Gedeon Richter
methyltestosterone Arcosterone 10 mg n/a U.S. Acrum [NLM]
methyltestosterone Arcosterone 10, 25 mg tablet n/a U.S. Acrum [NLM]
methyltestosterone Debosteron n/a n/a Korea n/a
methyltestosterone Gen Tabs 2 mg tablet 50, 200 tablet bottle Canada Vetcom VET
methyltestosterone Glando Stridox 10mg tablet 20 tablet box Uruguay Ion
methyltestosterone Hormobin 5 mg tablet 40 tablet box Turkey Munrin Sahin
methyltestosterone KangJungBing n/a n/a Korea n/a
methyltestosterone Longivol (plus estrogen) 1 mg tablet n/a Spain Medical S.A.
methyltestosterone Mediatric 10mg tablet n/a U.S. Wyeth-Ayerst [NLM]
methyltestosterone Mesteron 10mg tablet n/a Poland Jelfa [NLM]
methyltestosterone Metandren 5 mg sub. dragee n/a U.S. Ciba [NLM]
methyltestosterone Metandren 10, 25 mg tablet n/a U.S. Ciba [NLM]
methyltestosterone Metandren 10, 25 mg tablet 100 tablet bottle U.S. Novartis [NLM]
methyltestosterone Metesto 25 mg tablet 100 tablet bottle Thailand Acdhon
methyltestosterone Methyltestosterone 10 mg tablet n/a U.S. Goldline [NLM]
methyltestosterone Methyltestosterone 10mg tablet n/a U.S. Global
methyltestosterone Metil Testosteron 10mg tablet 50 tablet box Rumania Terapia
methyltestosterone Metil Thomsina S 10 mg tablet 20 tablet box Uruguay Celsius
methyltestosterone Metil-Test 50 mg tablet 100 tablet bottle Mexico Brovel VET
methyltestosterone Metiltestosterona n/a n/a Paraguay Botica
methyltestosterone Neo Aphro 5 mg tablet 30 tablet Egypt Misr
methyltestosterone Oreton n/a n/a Venezuela n/a
methyltestosterone Oreton Methyl 10mg tablet n/a U.S. Schering [NLM]
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule Indonesia Organon
nandrolone decanoate Deca-Durabolin® n/a n/a Ireland Organon
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule Italy Organon
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule Korea Organon
nandrolone decanoate Deca-Durabolin® 25 mg/ml 1 ml ampule Malaysia Organon
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule Netherlands Organon
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml ampule New Zealand Organon
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml ampule Norway Organon
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml ampule Peru Organon
nandrolone decanoate Deca-Durabolin® 25 mg/ml 1 ml ampule Poland Organon [NLM]
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml ampule Poland Organon
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml ampule Rumania Organon
nandrolone decanoate Deca-Durabolin® 25 mg/ml 1 ml ampule Singapore Organon
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule South Africa Donmed / Organon
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule Spain Organon
Steroid.com
345
Steroid Listings By Generic Name
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml ampule Sweden Organon
nandrolone decanoate Deca-Durabolin® 25, 100 mg/ml 1, 2ml Sweden Organon [NLM]
nandrolone decanoate Deca-Durabolin® 25 mg/ml 1 ml ampule Switzerland Organon [NLM]
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml ampule Switzerland Organon
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml ampule Taiwan Organon
nandrolone decanoate Deca-Durabolin® 25, 50 mg/ml 1 ml ampule Thailand Organon
nandrolone decanoate Deca-Durabolin® 100 mg/ml 1 , 2 ml vial U.S. Organon [NLM]
nandrolone decanoate Deca-Durabolin® 200 mg/ml 1 ml vial U.S. Organon [NLM]
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml ampule United Kingdom Organon
nandrolone decanoate Deca-Durabolin® 100 mg/ml 1 , 2 ml ampule United Kingdom Organon [NLM]
nandrolone decanoate Deca-Durabolin® 25 mg/ml 1 ml ampule Venezuela Organon
nandrolone decanoate Deca-Durabolin® 50 mg/ml 1 ml syringe Venezuela Organon
nandrolone decanoate Deca-Durabolin® 100 mg/ml 2 ml vial Netherlands Organon
nandrolone decanoate Deca-Evabolin 25 mg/ml 1 ml ampule India Concept
nandrolone decanoate Decagic 100 mg/ml 10 ml vial India Unichem [NLM]
nandrolone decanoate Decanandrolen 200mg/ml 10 ml vial Mexico Denkall VET
nandrolone decanoate Decaneurabol 25, 50 mg/ml 1 ml ampule India Cadila
nandrolone decanoate Decaneurophen 25, 50 mg/ml 1 ml ampule India Ind-Swift
nandrolone decanoate Decanoato de Nandrobna 200 mg/ml 10ml vial Mexico Tomel VET
nandrolone decanoate Decanoato Nandrolona 25, 50 mg/ml 1 ml ampule Chile Astorga
nandrolone decanoate Decanoato Nandrolona 50 mg/ml 1 ml ampule Chile Biosano
nandrolone decanoate Decanofort 25 mg/ml 1 ml ampule Rumania Terapia
nandrolone decanoate Deca-Pronabol 100 mg/ml 2 ml ampule India P & B Labs [NLM]
nandrolone decanoate Decatron250 250 mg/ml 10 ml vial Mexico Brovel VET
nandrolone decanoate Dimetabol 50 mg/ml 50 ml vial Dom. Rep. Bremer Pharma [NLM] VET
nandrolone decanoate Dimetabol ADE 25 mg/ml 50, 100 ml vial Mexico Lapisa VET
nandrolone decanoate Dynabolon Inj 40 mg/.5 ml 1 ml ampule Korea n/a
nandrolone decanoate Elpihormo 50 mg/ml 1 ml Greece Chemica [NLM]
nandrolone decanoate Extraboline 50 mg/ml 2 ml vial Greece Genepharm
nandrolone decanoate Gerabolin 25 mg/ml 1 ml ampule Egypt Nile
nandrolone decanoate Hybolin Decanoate 50, 100 mg/ml 1, 2 ml vial U.S. Hyrex
nandrolone decanoate Jebolan 50 mg/ml 1 ml ampule Turkey Etem [NLM]
nandrolone decanoate Metadec 25, 50 mg/ml 1 ml ampule India Jagsonpal
nandrolone decanoate Myobolin 25 mg/ml 1 ml ampule India Troikaa
nandrolone decanoate Nandrobolic L.A. 100 mg/ml 1 , 2 ml vial U.S. Forest [NLM]
nandrolone decanoate Nandrolona 300 L.A. 300mg/ml 10ml vial Mexico Ttokkyo VET
nandrolone decanoate nandrolona decanoato 50 mg/ml 1 ml ampule Chile Chile
nandrolone decanoate nandrolone decanoate 200 mg/2ml 2 ml vial Greece Norma Hellas
nandrolone decanoate nandrolone decanoate 100mg/ml 1,2 ml vial U.S. Lyphomed [NLM]
nandrolone decanoate nandrolone decanoate I00mg/ml 1, 2 ml vial U.S. Quad [NLM]
nandrolone decanoate nandrolone decanoate 50, 100, 200 mg/ml 1, 2 ml vial U.S. Steris [NLM]
nandrolone decanoate Nandrolone Decanoate Inj 100 mg/ml 2 ml vial U.S. Watson Pharma
nandrolone decanoate Nandrolone Decanoate Inj 200 mg/ml 1 ml vial U.S. Watson Pharma
nandrolone decanoate Nandrosande 25.50, 100 mg/ml 1 ml ampule Chile Sanderson
nandrolone decanoate Neo-Durabolic 100, 200 mg/ml 1, 2 ml vial U.S. Hauck [NLM]
nandrolone decanoate Norandren 50, 200 mg/ml 10, 50ml vial Mexico Brovel VET
nandrolone decanoate Nurezan 50 mg/ml 1 ml ampule Greece Rafarm
nandrolone decanoate Retabolil 25, 50 mg/ml 1 ml ampule Bulgaria Gedeon Richter [NLM]
nandrolone decanoate Retabolil 50 mg/ml 1 ml ampule Egypt Medimpex/Alxndria
Steroid.com
346
Steroid Listings By Generic Name
nandrolone decanoate Retabolil 50 mg/ml 1 ml ampule Estonia Gedeon Richter
nandrolone decanoate Retabolil 25, 50 mg/ml 1 ml ampule Hungary Gedeon Richter
nandrolone decanoate Retabolil 25, 50 mg/ml 1 ml ampule Malaysia Gedeon Richter
nandrolone decanoate Retabolin 50 mg/ml 1 ml ampule Russia Medexport Russia [NLM]
nandrolone decanoate RWR Deca 50 50 mg/ml 10 ml vial Australia RWR VET
nandrolone decanoate Sterobolin 50 mg/ml 1 ml ampule Finland Orion [NLM]
nandrolone decanoate Turinabol Depot 50 mg/ml 1 ml ampule Bulgaria Jenapharm [NLM]
nandrolone decanoate Turinabol Depot 50 mg/ml 1 ml ampule Czech. Rep. Jenapharm [NLM]
nandrolone decanoate Turinabol Depot 50 ma/ ml 1 ml ampule Germany Jenapharm [NLM]
nandrolone decanoate Ziremilon 50 mg/ml 1 ml ampule Greece Demo
nandrolone hexyloxyphenylpropionate Anador 25 mg/ml 2 ml ampule France Pharmacia-Upjohn [NLM]
nandrolone hexyloxyphenylpropionate Anadur 25, 50 mg/ml 1, 2 ml ampule Austria Kabi Pharmacia [NLM]
nandrolone hexyloxyphenylpropionate Anadur 25, 50 mg/ml 1 , 2 ml ampule Belgium Pharmacia [NLM]
nandrolone hexyloxyphenylpropionate Anadur 25, 50 mg/ml 1 , 2 ml ampule Czech. Rep. Pharmacia [NLM]
nandrolone hexyloxyphenylpropionate Anadur 25 mg/ml 2 ml ampule Denmark Lundbeck [NLM]
nandrolone hexyloxyphenylpropionate Anadur 25, 50 mg/ml 1 , 2 ml ampule Finland Pharmacia [NLM]
nandrolone hexyloxyphenylpropionate Anadur 25, 50 mg/ml 1 , 2 ml ampule Germany Kabi Pharmacia [NLM]
nandrolone hexyloxyphenylpropionate Anadur 25, 50 mg/ml 1 , 2 ml ampule Netherlands Pharmacia [NLM]
nandrolone hexyloxyphenylpropionate Anadur 25, 50 mg/ml 1 , 2 ml ampule Norway Kabi Pharmacia [NLM]
nandrolone hexyloxyphenylpropionate Anadur 25 mg/ml 2 ml ampule Spain Leo [NLM]
nandrolone hexyloxyphenylpropionate Anadur 25, 50 mg/ml 1 , 2 ml ampule Switzerland Kabi Pharmacia [NLM]
nandrolone hexyloxyphenylpropionate Anadur 25 mg/ml 2 ml ampule Turkey Eczacibasi [NLM]
nandrolone hexyloxyphenylpropionate Anadurin 50 mg/ml 1 ml ampule Greece Xponei [NLM]
nandrolone laurate Fortabol 20 mg/ml 10, 50 ml vial Mexico Parfam VET
nandrolone laurate Fortadex 25, 50 mg/ml n/a Germany Hydro VET
nandrolone laurate Laudrol LA 250 mg/ml 10 ml vial Mexico Loeffler VET
nandrolone laurate Laura bolin 25, 50 mg/ml 10ml vial Australia Intervet VET
nandrolone laurate Laura bolin 50 mg/ml n/a Austria Werffi-Chemie VET
nandrolone laurate Laura bolin 50 mg/ml 10, 50 ml Columbia Intervet VET
nandrolone laurate Laurabolin 25, 50 mg/ml 5, 10,50ml Germany Vemie VET
nandrolone laurate Laura bolin 20, 50 mg/ml 10, 50 ml vial Mexico Intervet VET
nandrolone laurate Laurabolin V 50 mg/ml 10, 50 ml Netherlands Intervet VET
nandrolone phenylpropionate Activin 10 mg/ml n/a Spain Aristegvi [NLM]
nandrolone phenylpropionate Anabolin 50 mg/ml n/a U.S. Alto [NLM]
nandrolone phenylpropionate Anabolin-IM 50 mg/ml n/a U.S. Alto [NLM]
nandrolone phenylpropionate Anabolin-LA 1 00 mg/ml n/a U.S. Alto [NLM]
nandrolone phenylpropionate Androlone 50 mg/ml n/a U.S. Keene [NLM]
nandrolone phenylpropionate Daily Reborn Inj 25 mg/ml n/a Taiwan Shiteh
nandrolone phenylpropionate Dubol-100 100 mg/ml 2 ml vial India BM Pharmaceuticals
nandrolone phenylpropionate Dubol-50 50 mg/ml 1 ml ampule India BM Pharmaceuticals
nandrolone phenylpropionate Durabol 100 mg/ml 10ml vial Thailand British Dragon
nandrolone phenylpropionate Durabolin® 25 mg/ml n/a Belgium Organon [NLM]
nandrolone phenylpropionate Durabolin® 25,50 mg/ml n/a Canada Organon [NLM]
nandrolone phenylpropionate Durabolin® 25mg/ml n/a Finland Organon
nandrolone phenylpropionate Durabolin® 25 mg/ml 1 ml ampule Greece Organon [NLM]
nandrolone phenylpropionate Durabolin® 25 mg/ml 1 ml ampule India Infar
nandrolone phenylpropionate Durabolin® 12.5 mg/ml 2 ml ampule Indonesia Organon
nandrolone phenylpropionate Durabolin® 25 mg/ml 1 ml ampule Malaysia Organon
nandrolone phenylpropionate Durabolin® 25 mg/ml 1 ml ampule Netherlands Organon
Steroid.com
347
Steroid Listings By Generic Name
nandrolone phenylpropionate Durabolin® 50 mg/ml n/a Portugal Organon
nandrolone phenylpropionate Durabolin® 25 mg/ml 1 ml ampule Spain Organon [NLM]
nandrolone phenylpropionate Durabolin® 25 mg/ml n/a Switzerland Opopharma [NLM]
nandrolone phenylpropionate Durabolin® 25 mg/ml 2 ml vial Taiwan Organon
nandrolone phenylpropionate Durabolin® 25, 50 mg/ml n/a U.S. Organon [NLM]
nandrolone phenylpropionate Durabolin® 50 mg/ml 1 ml ampule United Kingdom Organon [NLM]
nandrolone phenylpropionate Durabolin® 50 mg/ml n/a Yugoslavia/FRMROrganon
nandrolone phenylpropionate Equibolin-50 50 mg/ml n/a U.S. Vortech [NLM]
nandrolone phenylpropionate Estigor 10 mg/ml 250ml Argentina Bumet VET
nandrolone phenylpropionate Evabolin 25 mg/ml 1 ml ampule India Concept
nandrolone phenylpropionate Fenobolin 20 mg/ml n/a Russia Medexport Russia [NLM]
nandrolone phenylpropionate Fherbolico 50 mg/ml n/a Spain Fher [NLM]
nandrolone phenylpropionate Ganekyl 50 mg/ml 10,100 ml vial Argentina Over Labs VET
nandrolone phenylpropionate Hybolin 25,50 mg/ml n/a U.S. Hyrex [NLM]
nandrolone phenylpropionate Macrabone 25 mg/ml n/a Taiwan Ta Fong
nandrolone phenylpropionate Menabolin 25 mg/ml 1 ml ampule Egypt Theramex / Memphis
nandrolone phenylpropionate Metabol 25 mg/ml 1 ml ampule India Jagsonpal
nandrolone phenylpropionate Metabolin 25 mg/ml n/a Taiwan Metro
nandrolone phenylpropionate Nandrobolic 25 mg/ml n/a U.S. Forest [NLM]
nandrolone phenylpropionate Nandrolin 50 mg/ml 25 ml vial Australia Intervet VET
nandrolone phenylpropionate Nandrolin 25 mg/ml 10 ml vial Australia Intervet VET
nandrolone phenylpropionate nandrolone phenylpropionate 50,100mg/ml 2 ml vial India Hayrian Biotogicals [NLM]
nandrolone phenylpropionate nandrolone phenylpropionate 50 mg/ml n/a U.S. Quad [NLM]
nandrolone phenylpropionate Nerobolil 25 mg/ml 1 ml ampule Bulgaria Godeon Richter [NLM]
nandrolone phenylpropionate Nerobolil 25 mg/ml n/a Hungary Godeon Richter [NLM]
nandrolone phenylpropionate Neurabol Inj 25 mg/ml 1 ml ampule India Cadila
nandrolone phenylpropionate Neurophen 25 mg/ml 1 ml ampule India Ind-Swift
nandrolone phenylpropionate Norabon 25 mg/ml 1 ml ampule Thailand Phihalab
nandrolone phenylpropionate Nu-Bolic 25 mg/ml n/a U.S. Seatrace [NLM]
nandrolone phenylpropionate Protosin Inj 25 mg/ml n/a Taiwan Astar
nandrolone phenylpropionate Rubolin 25 mg/ml n/a Taiwan Ying Yuan
nandrolone phenylpropionate Sinbolin 25 mg/ml n/a Taiwan Sinton
nandrolone phenylpropionate Superanabolon 25 mg/ml 1 ml ampule Czech. Rep. Spofa
nandrolone phenylpropionate Turinabol 25 mg/ml n/a Bulgaria Jenapharm [NLM]
nandrolone phenylpropionate Turinabol 25 mg/ml n/a Czech. Rep. Germed [NLM]
nandrolone phenylpropionate Turinabol 25 mg/ml n/a Germany Jenapharm [NLM]
nandrolone undecanoate Dynabolon 80.5 mg/ml 1 ml ampule France Theramex [NLM]
nandrolone undecanoate Dynabolon 80.5 mg/ml 1 ml ampule Italy Farmasister [NLM]
nandrolone undecanoate Dynabolon 80.5 mg/ml 1 ml ampule Italy Foumier
nandrolone undecanoate Psychobolan 80.5 mg/ml 1 ml ampule Greece Theramex [NLM]
norethandrolone Anaptex 5 mg tablet 100 tablet bottle Australia Jurox VET
norethandrolone Nilevar 10mg tablet 30 tablet bottle France Searle
norethandrolone Nilevar 10mg tablet 30 tablet bottle Switzerland Searie [NLM]
norethandrolone Nilevar 10 mg tablet 100 tablet bottle U.S. Searle
Omnadren (testosterone blend) Omnadren 250 mg/ml 1 ml ampule Poland Jelfa
Omnadren (testosterone blend) Omnadren 250 mg/ml 1ml ampule Poland Polfa [NLM]
Omnadren (testosterone blend) Omnadren 250 250mg/ml 1 ml ampule Bulgaria Jelfa
oxabolone cypionate Steranabol Ritardo 12.5 mg/ml 2 ml ampule Italy Pharmacia & Upjohn [NLM]
oxandrolone Anatrophill 2.5 mg tablet n/a France Searle [NLM]
Steroid.com
348
Steroid Listings By Generic Name
oxandrolone Anavar 5 mg tablet 30 tablet strip China Hubei Huangshi
oxandrolone Anavar 2.5 mg tablet 100 tablet bottle U.S. Searle [NLM]
oxandrolone Bonavar 2.5 mg tablet 10 tablet strip Thailand Body Research
oxandrolone Kicker Tab 2.5 mg tablet n/a Korea n/a
oxandrolone Lipidex 2.5 mg tablet n/a Brazil Searle [NLM]
oxandrolone Lonavar 2.5 mg tablet 100 tablet bottle Israel BTG
oxandrolone Lonavar 2 mg tablet n/a Japan Dainippon [NLM]
oxandrolone Lonavar 2.5 mg tablet n/a Argentina Searle [NLM]
oxandrolone Oxafort 5 mg tablet 100 tablet bottle Mexico Loeffler VET
oxandrolone Oxanabol 5 mg tablet 100 tablet pouch Thailand British Dragon
oxandrolone Oxandrin® 2.5,10 mg tablet 100 tablet bottle U.S. BTG
oxandrolone Oxandrolone 10 10 mg tablet 100 tablet bottle Mexico Bratis Labs VET
oxandrolone Oxandrolone 5 mg tablet 30 tablet bottle Belize Planet Pharmacy
oxandrolone Oxandrolone 2.5 tablet 100 tablet bottle Mexico Ttokkyo [NLM] VET
oxandrolone Oxandrolone 5 mg tablet 100 tablet bottle Mexico Ttokkyo VET
oxandrolone Oxandrolone SPA 2.5 mg tablet 30 tablet box Italy SPA [NLM]
oxandrolone Oxandrolone SPA (Export) 2.5 mg tablet 30 tablet box Italy SPA
oxandrolone Oxandrovet 5 mg tablet 100 tablet bottle Mexico Denkall VET
oxandrolone Vasorome 0.5 mg tablet n/a Japan Kowa [NLM]
oxandrolone Vasorome 2 mg tablet n/a Japan Kowa [NLM]
oxymetholone Anabrol 50 mg tablet 100 tablet bottle Mexico Brovel VET
oxymetholone Anadrol 5 mg tablet n/a Japan n/a
oxymetholone Anadrol 50® 50 mg tablet 100 tablet bottle U.S. Unimed
oxymetholone Anadrol 50® 50 mg tablet 100 tablet bottle Canada Syntex [NLM]
oxymetholone Anadrol 50® 50 mg tablet 100 tablet bottle U.S. Syntex [NLM]
oxymetholone Anapolon 50 mg tablet n/a Bulgaria Syntex [NLM]
oxymetholone Anapolon 50 mg tablet 20 tablet box Turkey Ibrahim
oxymetholone Anapolon 2.5, 5 mg tablet 20 tablet box Turkey Ibrahim [NLM]
oxymetholone Anapolan 50 50 mg tablet 100 tablet bottle Malaysia Syntex [NLM]
oxymetholone Anapolan 50 50 mg tablet 20 tablet strip Mexico Syntex [NLM]
oxymetholone Anapolan 50 50 mg tablet 100 tablet bottle United Kingdom Syntex [NLM]
oxymetholone Anapolan 50 50 mg tablet 100 tablet bottle Canada Hoffman-La Rouche [NLM]
oxymetholone Anasteron 25 mg tablet 60 tablet bottle Greece Farmaprod
oxymetholone Anasteron 50 mg tablet n/a Greece Syntex [NLM]
oxymetholone Anasteron 50 mg tablet n/a Sweden Syntex [NLM]
oxymetholone Androlic 50 mg tablet 100 tablet bottle, pouch Thailand British Dispensary
oxymetholone Androlic (Export) 50 mg tablet 20 tablet pouch Thailand British Dragon
oxymetholone Androyd 5 mg tablet 100 tablet India Parke Davis
oxymetholone Bonalone 50 mg tablet 100 tablet bottle Thailand Body Research
oxymetholone Dynasten 50 mg tablet n/a Portugal Cilag [NLM]
oxymetholone Hemogenin 50 mg tablet 10 tablet box Brazil Syntex [NLM]
oxymetholone Hemogenin 50 mg tablet n/a Brazil Aventis
oxymetholone Hemogenin 50 mg tablet 10 tablet box Brazil Sarsa [NLM]
oxymetholone Kanestron 50 mg tablet 100 tablet bottle Mexico Loeffler VET
oxymetholone Oximetalon 75 mg tablet 100 tablet bottle Mexico Denkall VET
oxymetholone Oxitosona 5O 50 mg tablet 100 tablet box Spain Syntex [NLM]
oxymetholone Oxitron 5O 50 mg tablet 100 tablet bottte Mexico Bratis Labs VET
oxymetholone Oxybolone 50 mg tablet 20 tablet box Greece Genapharm
oxymetholone Oxydrol 100 mg tablet 50 tablet pouch Thailand British Dragon
Steroid.com
349
Steroid Listings By Generic Name
oxymetholone Oxylone 50 mg tablet 100 tablet bottle Malaysia Duopharma
oxymetholone Oxymetholone 50 mg tablet 30 tablet bottle Belize Planet Pharmacy
oxymetholone Oxymetholone 50 mg tablet n/a Malaysia Sime Darby
oxymetholone Oxymetholone 50 mg tablet 100 tablet pouch Thailand British Dispensary
oxymetholone Oxymetholone Dongindang n/a n/a Korea Dongindang
oxymetholone Oxymetholone HanBul 50 mg tablet n/a Korea HanBul
oxymetholone Oxymetholone HanSeo 50 mg tablet 100 tablet bottle Korea HanSeo
oxymetholone Oxymetholone Korea United 50 mg tablet n/a Korea Korea United
oxymetholone Oxymetholone Miverva 50 mg tablet 100 tablet Greece Minerva [NLM]
oxymetholone Oxymetolona 50 50 mg tablet 100 tablet bottle Mexico Ttokkyo VET
oxymetholone Oxytone 50 50 mg tablet 100 tablet bottle Thailand SB Laboratories
oxymetholone Ptenastril 50 mg tablet n/a Austria Grunenthal [NLM]
oxymetholone Plenastril 50 mg tablet n/a Switzerland Proto chemie [NLM]
oxymetholone Roboral 50 mg tablet 100 tablets Israel Abic/Ramat-Gan [NLM]
oxymetholone Synasteron 50 mg tablet 50 tablet bottle Belgium Sarva [NLM]
quinbolone Anabolicum Vister 10 mg capsule 30 capsule bottte Italy Parke Davis [NLM]
quinbolone Anabolicum Vister oral drops n/a Italy Parke Davis [NLM]
stanozolol (inj) Anabolic ST 50mg/ml 20 ml vial Australia SYD Group VET
stanozolol (inj) Anabolic ST 50mg/ml 20 ml vial Mexico SYD Group VET
stanozolol (inj) Anabolico Cimol 60mg/ml 5 ml vial Argentina Cimol VET
stanozolol (inj) Anabolico Produvet 10mg/ml 25 ml vial Argentina Cimol VET
stanozolol (inj) Anabolic-ST 50mg/ml 20 ml vial Mexico Grupo Tarasco [NLM] VET
stanozolol (inj) Estrombol 25mg/ml 10 ml vial Argentina Fundacion VET
stanozolol (inj) Nabolic 2mg/ml 50 ml vial Argentina Chinfield Ind. VET
stanozolol (inj) Nabolic Strong 25mg/ml 50 ml vial Argentina Chinfield Ind. VET
stanozolol (inj) Stan QV 100 100mg/ml 20 ml vial Mexico Quality Vet VET
stanozolol (inj) Stan QV 50 50mg/ml 20 ml vial Mexico Quality Vet VET
stanozolol (inj) Stanabolic 50mg/ml 20 ml vial Australia Ilium/Troy VET
stanozolol (inj) Stanazol 50mg/ml 20, 50 ml vial Australia RWR [NLM] VET
stanozolol (inj) Stanazolic 50, 100mg/ml 20ml, 10ml vial Mexico Denkall VET
stanozolol (inj) Stanol 50 50mg/ml 20 ml vial Mexico BratisLabs VET
stanozolol (inj) Stand-V 50, 100 mg/ml 20 ml vial Mexico Ttokkyo VET
stanozolol (inj) Stanosus 50mg/ml 20 ml vial Australia Jurox [NLM] VET
stanozolol (inj) Stromba 50 mg/ml n/a United Kingdom Sterling Research [NLM]
stanozolol (inj) Stromba 50 mg/ml n/a Sweden Sterling- Winthrop [NLM]
stanozolol (inj) Stromba 50 mg/ml n/a Sweden Winthrop [NLM]
stanozolol (inj) Strombaject 50 mg/ml n/a Belgium Winthrop [NLM]
stanozolol (inj) Strombaject 50 mg/ml n/a Germany Winthrop [NLM]
stanozolol (inj) Tanoxol 25 mg/ml 10 ml vial Argentina Bumet VET
stanozolol (inj) Vitabolic 20 mg/ml 10. 100 ml vial Argentina Over Labs VET
stanozolol (inj) Winstrol® 50 mg/ml n/a Greece Winthrop [NLM]
stanozolol (inj) Winstrol® Depot 50 mg/ml 1 ml vial Italy Zambon [NLM]
stanozolol (inj) Winstrol® Depot 50 mg/ml 1 ml ampule Spain Zambon
stanozolol (inj) Winstrol® V 50 mg/ml 10, 30ml vial Canada Pharmacia VET
stanozolol (inj) Winstrol® V 50 mg/ml 10, 30ml vial U.S. Pharmacia & Upjohn VET
stanozolol (inj) Winstrol® V 50 mg/ml 10, 30ml vial U.S. Winthrop [NLM] VET
stanozolol (oral) Anazol 2 mg tablet 100 tablet box Philippines Xetox (export)
stanozolol (oral) Anazol 2 mg tablet 100, 1000 tablet bottle Philippines Xetox (export)
stanozolol (oral) Apetil 4 mg/ml 10 ml dropper bottle Argentina Holliday VET
Steroid.com
350
Steroid Listings By Generic Name
stanozolol (oral) Cetabon 2 mg tablet 10 tablet strip Thailand Therapharma
stanozolol (oral) Estano-Pets 10, 25 mg tablet 100 tablet bottle Mexico Norvet VET
stanozolol (oral) Menabol 5 mg tablet 100 tablet box India n/a
stanozolol (oral) Neurabol 2 mg capsule 10 capsule box India Cadila
stanozolol (oral) Seidon 2 mg tablet 100 tablet box Korea Seoul Pharm
stanozolol (oral) Stabon 2 mg tablet n/a Korea n/a
stanozolol (oral) Stanabol 5 mg tablet 250 tablet pouch Thailand British Dragon
stanozolol (oral) Stanabol 5 mg tablet 200,1000 tablet bottle Thailand British Dragon
stanozolol (oral) Stanabol 5 mg tablet 200 tablet pouch Thailand British Dragon
stanozolol (oral) Stanabol 50 mg tablet 100 tablet pouch Thailand British Dragon
stanozolol (oral) Stanazolic 6mgcap 300 capsule bottle Mexico Denkall VET
stanozolol (oral) Stanazolic 10 mg tablet 100 tablet bottle Mexico Denkall VET
stanozolol (oral) Stanol 2 mg tablet n/a Taiwan Hua Shin
stanozolol (oral) Stanol 5 mg tablet 200 tablet bottle Thailand Body Research
stanozolol (oral) Stanol 10 10mg tablet 250 tablet bottle Mexico BratisLabs VET
stanozolol (oral) Stanol-V 10 mg tablet 100,500 tablet bottte Mexico Ttokkyo VET
stanozolol (oral) Stanozodon 2 mg tablet 1000 tablet bottte Thailand AcdhonCo.
stanozolol (oral) stanozolol 25 mg tablet 30 tablet bottle Belize Planet Pharmacy
stanozolol (oral) stanozolol Tab 5 mg tablet 30 tablet box Greece Genepharm
stanozolol (oral) stanozolol 2 mg tablet n/a Taiwan Chen Ho
stanozolol (oral) Stanzol 5 mg tablet 200 tablet bottle Thailand SB Laboratories
stanozolol (oral) Stromba 5 mg tablet 10 tablet box Belgium Winthrop [NLM]
stanozolol (oral) Stromba 5 mg tablet 56 tablet box Greece n/a
stanozolol (oral) Stromba 5 mg tablet n/a Hungary Sterling-Health
stanozolol (oral) Stromba 5 mg tablet n/a Austria Berger [NLM]
stanozolol (oral) Stromba 5 mg tablet n/a Czech. Rep. Sterling-Health [NLM]
stanozolol (oral) Stromba 5 mg tablet n/a Denmark Winthrop [NLM]
stanozolol (oral) Stromba 5 mg tablet n/a Germany Winthrop [NLM]
stanozolol (oral) Stromba 5 mg tablet 100 tablet box Netherlands Sanofi
stanozolol (oral) Stromba 5 mg tablet n/a Netherlands Winthrop [NLM]
stanozolol (oral) Stromba 5 mg tablet n/a Sweden Winthrop [NLM]
stanozolol (oral) Stromba 5 mg tablet n/a Switzerland Winthrop [NLM]
stanozolol (oral) Stromba 5 mg tablet n/a United Kingdom Sanofi [NLM]
stanozolol (oral) Stromba 5 mg tablet n/a United Kingdom Sterling [NLM]
stanozolol (oral) Terabon 2 mg tablet 10 tablet strip Korea Jin Yang
stanozolol (oral) Winstrol 2 mg tablet n/a Japan n/a
stanozolol (oral) Winstrol® 2 mg tablet 20 tablet box Italy Zambon [NLM]
stanozolol (oral) Winstrol® 2 mg tablet 20 tablet box Spain Zambon
stanozolol (oral) Winstrol® 2 mg tablet 100 tablet bottle U.S. Sanofi
stanozolol (oral) Winstrol® 2 mg tablet 100 tablet bottle U.S. Upjohn [NLM]
stanozolol (oral) Winstrol® 2 mg tablet 100 tablet bottle U.S. Winthrop [NLM]
stanozolol (oral) Winstrol® 2 mg tablet n/a Greece Winthrop [NLM]
stanozolol (oral) Winstrol® 2 mg tablet n/a Portugal Winthrop [NLM]
stanozolol (oral) Winstrol-V® 2 mg tablet 100 tablet bottle Canada Pharmacia VET
stanozolol (oral) Wmstrol-V® 2 mg tablet 100 tablet bottle U.S. Pharmacia & Upjohn VET
stanozolol (oral) Winstrol-V® 2 mg chewable tab 100 tablet bottle U.S. Pharmacia & Upjohn VET
Sten (testosterone blend) Sten 50mg/ml 2 ml ampule Mexico Atlantis
Sustanon 100 (testosterone blend) Sustanon (Cyctahoh) 100mg/ml 1 ml ampule India Infer
Sustanon 100 (testosterone blend) Sustanon 100 100 mg/ml 1 ml ampule Germany Organon [NLM]
Steroid.com
351
Steroid Listings By Generic Name
Sustanon 100 (testosterone blend) Sustanon '100'® 100mg/ml 1 ml ampule Egypt Organon/Nile
Sustanon 100 (testosterone blend) Sustanon '100'® 100 mg/ml 1 ml ampule Netherlands Organon
Sustanon 100 (testosterone blend) Sustanon '100'® 100 mg/ml 1 ml ampule United Kingdom Organon
Sustanon 100 (testosterone blend) Testonon'1001® 100 mg/ml 1 ml ampule Egypt Nile
Sustanon 250 (testosterone blend) Durandron 250 mg/ml 1 ml ampule Spain Organon [NLM]
Sustanon 250 (testosterone blend) Durateston 250 mg/ml 5 ml vial Australia Intervet VET
Sustanon 250 (testosterone blend) Durateston 250® 250 mg/ml 1 ml ampule Bolivia Organon
Sustanon 250 (testosterone blend) Durateston 250® 250 mg/ml 1 ml ampule Brazil Organon
Sustanon 250 (testosterone blend) Polysteron 250 250 mg/ml 1 ml ampule Venezuela Organon
Sustanon 250 (testosterone blend) Sostenon 250® 250 mg/ml 1 ml ampule Mexico Organon
Sustanon 250 (testosterone blend) Sostenon 250® 250 mg/ml 1 ml ampule Spain Organon [NLM]
Sustanon 250 (testosterone blend) Super Test-250 250 mg/ml 5,10 ml vial Mexico Tomel VET
Sustanon 250 (testosterone blend) Sustanon 250 mg/ml 1 ml ampule Ireland Organon
Sustanon 250 (testosterone blend) Sustanon 250 mg/ml 1 ml ampule Israel Organon
Sustanon 250 (testosterone blend) Sustanon 250 mg/ml 1 ml ampule Slovakia Organon
Sustanon 250 (testosterone blend) Sustanon "250" 250 mg/ml 1 ml ampule Argentina Organon
Sustanon 250 (testosterone blend) Sustanon "250" 250 mg/ml 1 ml ampule Indonesia Organon
Sustanon 250 (testosterone blend) Sustanon "250" 250 mg/ml 1 ml ampule Singapore Organon
Sustanon 250 (testosterone blend) Sustanon "250" 250 mg/ml 1 ml ampule Vietnam Organon
Sustanon 250 (testosterone blend) Sustanon (Cyctahoh 250) 250 mg/ml 1 ml ampule Russia Organon
Sustanon 250 (testosterone blend) Sustanon 250 250 mg/ml 1 ml ampule Czech. Rep. Organon
Sustanon 250 (testosterone blend) Sustanon 250 250 mg/ml 1 ml ampule Germany Organon [NLM]
Sustanon 250 (testosterone blend) Sustanon 250 250 mg/ml 1 ml ampule New Zealand Organon
Sustanon 250 (testosterone blend) Sustanon 250 250 mg/ml 1 ml ampule Taiwan Organon
Sustanon 250 (testosterone blend) Sustanon 250 (Cyctahon) 250 mg/ml 1 ml ampule India Infar
Sustanon 250 (testosterone blend) Sustanon 250® 250 mg/ml 1 ml ampule Belgium Organon
Sustanon 250 (testosterone blend) Sustanon 250® 250 mg/ml 1 ml ampule Estonia Organon
Sustanon 250 (testosterone blend) Sustanon 250® 250 mg/ml 1 ml ampule Finland Organon
Sustanon 250 (testosterone blend) Sustanon 250® 250 mg/ml 1 ml ampule Netherlands Organon
Sustanon 250 (testosterone blend) Sustanon 250® 250 mg/ml 1 ml ampule Turkey Organon
Sustanon 250 (testosterone blend) Sustanon '250'® 250 mg/ml 1 ml ampule Egypt Organon/Nile
Sustanon 250 (testosterone blend) Sustanon '250'® 250 mg/ml 1 ml ampule Malaysia Organon
Sustanon 250 (testosterone blend) Sustanon '250'® 250 mg/ml 1 ml ampule Pakistan Organon
Sustanon 250 (testosterone blend) Sustanon '250'® 250 mg/ml 1 ml ampule South Africa Donmed/Organon
Sustanon 250 (testosterone blend) Sustanon '250'® 250 mg/ml 1 ml ampule Thailand Organon
Sustanon 250 (testosterone blend) Sustanon '250'® 250 mg/ml 1 ml ampule United Kingdom Organon
Sustanon 250 (testosterone blend) Sustanon® 250 mg/ml 1 ml ampule Italy Organon
Sustanon 250 (testosterone blend) Sustaretard 250 250 mg/ml 1 ml ampule India BM Pharmaceuticals
Sustanon 250 (testosterone blend) Sustenan 250 250 mg/ml 1 ml ampule Chile Organon
Sustanon 250 (testosterone blend) Sustenon 250® 250 mg/ml 1 ml ampule Portugal Organon
Sustanon 250 (testosterone blend) Testenon 250 250 mg/ml 5 ml vial Mexico Ttokkyo VET
Sustanon 250 (testosterone blend) Testo-Jet L.A. 250 mg/ml 10 ml vial Mexico Norvet VET
Sustanon 250 (testosterone blend) Testonon '250'® 250 mg/ml 1 ml ampule Egypt Nile
Sustanon 250 (testosterone blend) Testosteron 250 250 mg/ml 1 ml ampule Germany Rotex Medica [NLM]
Sustanon 250 (testosterone blend) Testosterone 250 250 mg/ml 10ml vial Costa Rica Qualityvet VET
Sustanon 250 (testosterone blend) Testosterona IV L/A 250 mg/ml 10 ml vial Mexico Loeffler VET
Sustanon 250 (testosterone blend) Testron 4 250 250 mg/ml 10 ml via! Mexico Bratis Labs VET
Test 400 (testosterone blend) Test 400 400 mg/ml 10 ml vial Mexico Denkall VET
testosterone (gel) Androge! 25, 50 mg single dose packet Canada Solvay
Steroid.com
352
Steroid Listings By Generic Name
testosterone (gel) Androgel 25, 50 mg single dose packet Netherlands Besins
testosterone (gel) Androgel 25, 50 mg single dose packet Sweden Besins
testosterone (gel) Androgel 50, 75, 100 mg single dose packet U.S. Unimed
testosterone (gel) Androtop Gel 50 mg single dose packet Germany Kade/Besins
testosterone (gel) Testogel 25, 50 mg single dose packet Australia Schering
testosterone (gel) Testogel 50 mg single dose packet Austria Schering
testosterone (gel) Testogel 25, 50 mg single dose packet Germany Jenapharm
testosterone (gel) Testogel 25, 50 mg single dose packet Netherlands Besins
testosterone (gel) Testogel 25, 50 mg single dose packet Sweden Besins
testosterone (implant) Ropel Testosterone Pellets 23.5 mg pellet 450,600 pellet bottle Australia Jurox VET
testosterone (patch) Androderm® 12.2 mg patch. 30 patches/box Canada Pharmascience
testosterone (patch) Androderm® 12.2 mg patch. 10, 30, 60 patches/box Germany AstraZenica
testosterone (patch) Androderm® 12.2 mg patch. n/a Italy Schwarz Pharma
testosterone (patch) Androderm® 12.2 mg patch. n/a Korea n/a
testosterone (patch) Androderm® 2.5 mg patch 30, 60 patch box Spain Schwarz Pharma
testosterone (patch) Androderm® 5 mg patch 30 patch box Spain Schwarz Pharma
testosterone (patch) Androderm® 12.2 mg patch n/a Switzerland Astrazenica
testosterone (patch) Androderm® 1 2.2 mg patch 60 patches/box U.S. Smith Kline Beecham [NLM]
testosterone (patch) Androderm® 12.2, 24.3 mg patch 60 patches/box U.S. Watson Pharma
testosterone (patch) Andropatch 12.2 mg patch 30, 60 patch box Netherlands Schwarz Pharma
testosterone (patch) Andropatch 2.5 mg patch 60 patches/box United Kingdom GSK
testosterone (patch) Andropatch 5 mg patch 30 patches/box United Kingdom GSK
testosterone (patch) Atmos 5 mg patch 30 patch box Norway Astra Zenica
testosterone (patch) Atmos 5 mg patch n/a Sweden Astra
testosterone (patch) Testoderm 15mgpatch n/a Malaysia Alza
testosterone (patch) Testoderm 6 mg patch 10, 30 patch box Spain Esteve
testosterone (patch) Testoderm 4 mg patch 10 patch box Spain Esteve
testosterone blend (misc) Deposterona 60mg/ml 10 ml vial Mexico Fort Dodge VET
testosterone blend (misc) Deposterona 60mg/ml 10 ml vial Mexico Syntex [NLM] VET
testosterone blend (misc) Equitest 200 200 mg/ml 6 ml vial Myanmar/Burma WDV VET
testosterone blend (misc) Triolandren 250 mg/ml 1 ml ampule Egypt Novartis
testosterone blend (misc) Triolandren 250 mg/ml 1 ml ampule Taiwan Novartis
testosterone cyclohexylpropionate Testosterone CHP Theramex 296, 148, 37 mg/ml 1 ml ampule France Theramex [NLM]
testosterone cypionate Anabolic TL 100 mg/ml 10ml vial Australia SYD Group VET
testosterone cypionate Anabolic TL 200 mg/ml 10ml vial Mexico SYD Group VET
testosterone cypionate Andro-Cyp 100, 200 mg/ml 10 ml vial U.S. Brown [NLM]
testosterone cypionate Andro-Cyp 100, 200 mg/ml 10 ml vial U.S. Keene [NLM]
testosterone cypionate Andronaq LA 100, 200 mg/ml 10 ml vial U.S. Central [NLM]
testosterone cypionate Andronate 100, 200 mg/ml 10 ml vial U.S. Pasadena [NLM]
testosterone cypionate Banrot 75 mg/ml 200 ml bladder Australia Coopers [NLM] VET
testosterone cypionate Biselmon Depot 50 mg/ml n/a Taiwan Ta Fong
testosterone cypionate Cyclo-Testosterone Depot 130 mg/ml n/a Taiwan Astar
testosterone cypionate Cypionax 100 mg/ml 2 ml ampule Thailand Body Research
testosterone cypionate CypioTest 250 250 mg/ml 10 ml vial Mexico Denkall VET
testosterone cypionate Cypriotest L/A 250 mg/ml 10ml vial Mexico Loeffler VET
testosterone cypionate Dep Andro-100-200 100, 200 mg/ml 10 ml vial U.S. Forest [NLM]
testosterone cypionate Deposteron 100 mg/ml 2 ml ampule Brazil Novaquimica/Sigma
testosterone cypionate Depot-Bifuron 50 mg/ml n/a Taiwan Gentle
testosterone cypionate Depo-TCP 200mg/ml n/a Korea n/a
Steroid.com
353
Steroid Listings By Generic Name
testosterone cypionate Depotest 100, 200 mg/ml 10ml vial U.S. Hyrex [NLM]
testosterone cypionate Depotest 100, 200 mg/ml 10 ml vial U.S. Kay [NLM]
testosterone cypionate Depo-Testermon 200 mg/ml n/a Taiwan CCPC
testosterone cypionate Depo-Testerone 200 mg/ml n/a Taiwan Metro
testosterone cypionate Depo-Testomon 100 mg/ml n/a Taiwan LiTa
testosterone cypionate Depo-Testosterone 100 mg/ml 10 ml vial South Africa Pharmacia & Upjohn
testosterone cypionate Depo-Testosterone CPP 100 mg/ml n/a Taiwan Metro
testosterone cypionate Depo-Testosterone® 100 mg/ml 10 ml vial Canada Pharmacia
testosterone cypionate Depo-Testosterone® 100 mg/ml n/a Malaysia Pharmacia
testosterone cypionate Depo-Testosterone® 10 mg/ml 10 ml vial New Zealand Pharmacia & Upjohn
testosterone cypionate Depo-Testosterone® 100 mg/ml 10 ml vial Singapore Pharmacia & Upjohn
testosterone cypionate Depo-Testosterone® 100, 200 mg/ml 10 ml vial U.S. Pharmacia & Upjohn
testosterone cypionate Depo-Testosterone® 200 mg/ml 1 ml vial U.S. Pharmacia & Upjohn
testosterone cypionate Depot-Hormon MF 50 mg/ml n/a Taiwan Sintong
testosterone cypionate Depotrone 100 mg/ml 2 ml ampule South Africa Propan-Zurich
testosterone cypionate Depovirin Inj 125 mg/ml 2ml Korea n/a
testosterone cypionate Dep-Test 100 mg/ml 10 ml vial U.S. Rocky Mountain [NLM]
testosterone cypionate D-Test 100/200 100,200 mg/ml 10 ml vial U.S. Sig [NLM]
testosterone cypionate Duratest-100-200 100,200mg/ml 10 ml vial U.S. Roberts [NLM]
testosterone cypionate Duratest-100-200 100,200 mg/ml 10 ml vial U.S. Hauck [NLM]
testosterone cypionate Malogen Cyp 100,200 mg/ml 10 ml vial U.S. Forest [NLM]
testosterone cypionate Miro Depo 125 mg/ml 2 ml vial Korea Hanil Pharm
testosterone cypionate Nannismon Depot 50,100 mg/ml n/a Taiwan Chi Sheng
testosterone cypionate Ridrot Testosterone Inj. 75 mg/ml 250 ml vial Australia Troy VET
testosterone cypionate Scheinpharma Testone-Cyp 100 mg/ml 10 ml vial Canada Schein
testosterone cypionate Testabot Depot 200 mg/ml 10 ml vial Thailand British Dragon
testosterone cypionate Testa-C 200 mg/ml 10 ml vial U.S. Vortech [NLM]
testosterone cypionate Testacyp 100 mg/ml 2 ml vial India BM Pharmaceuticals
testosterone cypionate Testadiate-Depo 200 mg/ml 10 ml vial U.S. Kay [NLM]
testosterone cypionate Testex Leo prolongatum 50,125 mg/ml 2 ml ampule Spain Altana Pharma
testosterone cypionate Testex Leo prolongatum 50,125 mg/ml 2 ml ampule Spain Leo [NLM]
testosterone cypionate Testo LA 100 mg/ml 10 ml vial Australia Jurox [NLM] VET
testosterone cypionate Testoject 100 mg/ml n/a U.S. Mayrand [NLM]
testosterone cypionate Testoject 50 50 mg/ml n/a U.S. Mayrand [NLM]
testosterone cypionate Testoject-LA 200 mg/ml n/a U.S. Mayrand [NLM]
testosterone cypionate Teston QV 200 200 mg/ml 10 ml vial Mexico Quality Vet VET
testosterone cypionate Testorone Depot 100 mg/ml n/a Taiwan Gentle
testosterone cypionate Testosterona Ultra Lenta 100 mg/ml 20 ml vial Uruguay Dispert Labs. VET
testosterone cypionate Testosterona Ultra Lenta Fuerte 200 mg/ml 5 ml ampule Uruguay Dispert Labs. VET
testosterone cypionate Testosterona Ultra Lenta Fuerte 200 mg/ml 20 ml vial Uruguay Dispert Labs. VET
testosterone cypionate testosterone cypionate 100 mg/ml 10 ml vial U.S. Geneva Geriatrics [NLM]
testosterone cypionate testosterone cypionate 100, 200 mg/ml 10 ml vial U.S. Goldline [NLM]
testosterone cypionate testosterone cypionate 50,100, 200 mg/ml 10 ml vial U.S. Huffman [NLM]
testosterone cypionate testosterone cypionate 200 mg/ml 10 ml vial U.S. Legere [NLM]
testosterone cypionate testosterone cypionate 100, 200 mg/ml 10 ml vial U.S. Schein [NLM]
testosterone cypionate testosterone cypionate 100,200 mg/ml 10ml vial U.S. Steris [NLM]
testosterone cypionate Testosterone Cypionate 200 200 mg/ml 10ml vial Mexico Ttokkyo VET
testosterone cypionate Testosterone Cypionate Inj 200 mg/ml n/a Hong Kong Charmaine
testosterone cypionate Testosterone Cypionate Inj 200 mg/ml n/a Taiwan Gwo Chyang
Steroid.com
354
Steroid Listings By Generic Name
testosterone cypionate Testosterone Cypionate Inj 200 mg/ml n/a Taiwan Tai Yu
testosterone cypionate Testosterone Cypionate Inj. 100 mg/ml 2 ml vial Canada Cytex
testosterone cypionate Testosterone Cypionate Inj. 200 mg/ml 10 ml vial Canada Sabex
testosterone cypionate Testosterone Cypionate LA 100 mg/ml 10ml vial Mexico Ttokkyo [NLM] VET
testosterone cypionate Testosterone Depositum n/a n/a Italy SPA
testosterone cypionate Testred Cypionate 200 mg/ml 10 ml vial U.S. INC [NLM]
testosterone cypionate Vironate 200 mg/ml 5 ml vial Philippines Xelox (export)
testosterone decanoate Neotest 250 250 mg/ml 10 ml bottle Mexico Loeffler
testosterone enanthate Anderone 100/200 100,200 mg/ml 10ml vial U.S. Burgin-Arden [NLM]
testosterone enanthate Andro 100 100 mg/ml 10ml vial U.S. Forest [NLM]
testosterone enanthate Andro LA 200 200 mg/ml 10 ml vial U.S. Forest [NLM]
testosterone enanthate Andropository 200 mg/ml 10ml vial U.S. Rugby [NLM]
testosterone enanthate Androtardyl® 250 mg/ml 1 ml ampule Algeria Schering
testosterone enanthate Androtardyl® 250 mg/ml 1 ml ampule France Schering
testosterone enanthate Androtardyl® 250 mg/ml 1 ml ampule Morocco Schering
testosterone enanthate Androtardyl® 250 mg/ml 1 ml ampule Tunisia Schering
testosterone enanthate Andryl 200 200 mg/ml 10 ml vial U.S. Keene [NLM]
testosterone enanthate Delatest 100/mg/ml 10 ml vial U.S. Dunhall [NLM]
testosterone enanthate Delatestryl 200 mg/ml 5 ml vial Canada Theramed
testosterone enanthate Delatestryl 200 mg/ml 10 ml vial Mexico Brovel [NLM] VET
testosterone enanthate Delatestryl 200 mg/ml 1 ml syringe U.S. BTG
testosterone enanthate Delatestryl 200mg/ml 5 ml vial U.S. BTG
testosterone enanthate Delatestryt 200 mg/ml 10 ml vial U.S. Mead Johnson [NLM]
testosterone enanthate DepoTestmon Inj 65mg/ml n/a Taiwan CCPC
testosterone enanthate Dura-Testosterone 200 mg/ml 10 ml vial U.S. Pharmex [NLM]
testosterone enanthate Durathate-200 Injection 200 mg/ml n/a U.S. Hauck [NLM]
testosterone enanthate Durathate-200 Injection 200 mg/ml n/a U.S. Roberts [NLM]
testosterone enanthate Enantat QV 250 250 mg/ml 10,50 ml vial Mexico Quality Vet Vet
testosterone enanthate Enarmon-Depot 125 mg/ml n/a Japan Teskoku Hormone
testosterone enanthate Everone 100, 200 mg/ml 10 ml vial U.S. Hyrex [NLM]
testosterone enanthate Jenasteron Inj 250 mg/ml n/a Korea n/a
testosterone enanthate Jenasteron Inj 250 mg/ml 1 ml ampule Malaysia Jenahexal
testosterone enanthate Matogen 100/200 L.A. 100,200 mg/ml 10 ml vial U.S. Forest [NLM]
testosterone enanthate Malogex LA200 200 mg/ml 10 ml vial Canada Germiphene [NLM]
testosterone enanthate PMS-Testosterone Enanthate 200 mg/ml 10 ml vial Canada Pharmascience
testosterone enanthate Primoniat®-Depot 250 250 mg/ml 1 ml ampule Chile Schering-Chile [NLM]
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule Egypt Schering/CID
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule Finland Leiras [NLM]
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule Norway Schering
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule United Kingdom Sobering [NLM]
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule Australia Schering Vet
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule Ecuador Schering
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule Guatemala Schering
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule Jordan Schering
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule Kuwait Schering [NLM]
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule Mauritius Schering
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule Mexico Schering
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml syringe New Zealand Schering
testosterone enanthate Primoteston®-Depot 250 mg/ml 1 ml ampule Sudan Schering
Steroid.com
355
Steroid Listings By Generic Name
testosterone enanthate Proviron®-Depot 250 mg/ml 1 ml ampule Venezuela Schering
testosterone enanthate Ropel Liquid Testosterone 75 mg/ml 200 ml vial Australia Jurox
testosterone enanthate Sunamon Depot Inj 130 mg/ml n/a Taiwan Astar
testosterone enanthate Sunamon Inj 250 mg/ml n/a Taiwan Astar
testosterone enanthate Tesone L.A. 200 mg/ml 10 ml vial U.S. Sig [NLM]
testosterone enanthate Testanate No. 1 100 mg/ml n/a U.S. Kenyon [NLM]
testosterone enanthate Testaval 100,200 mg/ml 10 ml vial U.S. Legere [NLM]
testosterone enanthate Testen-250 250 mg/ml 2 ml vial India BM Pharmaceuticals
testosterone enanthate Testenan Depot 250 mg/ml n/a Taiwan Sinton
testosterone enanthate Testermon 25 mg/ml n/a Taiwan CCPC
testosterone enanthate Testinon-Depot n/a n/a Japan n/a
testosterone enanthate Testoenan L/A 250 mg/ml 10 ml vial Mexico Loeffler Vet
testosterone enanthate Testo-Enant 125 mg/ml 2 ml ampule Italy Geymonat
testosterone enanthate Testo-Enant 250 mg/ml 1 ml ampule Italy Geymonat
testosterone enanthate Testosteron Depot 100 mg/ml 1 ml ampule Germany Rotex Medica [NLM]
testosterone enanthate Testosteron Depot 250 mg/ml 1 ml ampule Germany Rotex Medica
testosterone enanthate Testosterona 200 200 mg/ml 10 ml vial Mexico Brovel Vet
testosterone enanthate testosterone enantato 250 mg/ml 1 ml ampule Chile Biosano
testosterone enanthate testosterona enantato 100 mg/ml 1 ml ampule Chile Chile [NLM]
testosterone enanthate testosterona enantato 250 mg/ml 1 ml ampule Chile Chile
testosterone enanthate Testosteron-Depo 100 mg/ml 1 ml ampule YugoslaviaFRMRGalenika [NLM]
testosterone enanthate Testosteron-Depo 250 mg/ml 1 ml ampule YugoslaviaFRMRGalenika
testosterone enanthate Testosteron-Depo 100, 250 mg/ml 1 ml ampule YugoslaviaFRMRHemofarm [NLM]
testosterone enanthate Testosteron-Depot 250 mg/ml 1 ml ampule Germany Eifelfango
testosterone enanthate Testosteron-Depot 250 mg/ml 1 ml ampule Bulgaria Jenapharm
testosterone enanthate Testosteron-Depot 250mg/ml 1 ml ampule Germany Jenapharm
testosterone enanthate Testosterone 200 Depot 200mg/ml 10 ml vial Mexico Tomel vet
testosterone enanthate testosterone enanthate 100,200mg/ml 10 ml vial U.S. Geneva Geriatrics [NLM]
testosterone enanthate testosterone enanthate 100,200 mg/ml 10 ml vial U.S. Goldlline [NLM]
testosterone enanthate testosterone enanthate 100,200mg/ml 10 ml vial U.S. Quad [NLM]
testosterone enanthate testosterone enanthate 100,200 mg/ml 10 ml vial U.S. Schein [NLM]
testosterone enanthate testosterone enanthate 100,200 mg/ml 10 ml vial U.S. Steris [NLM]
testosterone enanthate Testosterone Enanthate 250 250 mg/ml 1 ml ampule Iran Aburaihan
testosterone enanthate Testosterone Enanthate Dalim 250 mg/ml n/a Korea Dalim
testosterone enanthate Testosterone Enanthate Inj 200 mg/ml 10 ml vial Canada Taro [NLM]
testosterone enanthate Testosterone Heptytate 50,100,250 mg/ml 1 ml ampule France Theramex
testosterone enanthate Testosteronum Prolongatum 100 mg/ml 1 ml ampule Belgium Polfa [NLM]
testosterone enanthate Testosteronum Prolongatum 100 mg/ml 1 ml ampule Bulgaria Jetfa [NLM]
testosterone enanthate Testosteronum Prolongatum 100 mg/ml 1 ml ampule Poland Jelfa
testosterone enanthate Testosteronum Prolongatum 100 mg/ml 1 ml ampule Poland Polfa [NLM]
testosterone enanthate Testoviron Depot 250 mg/ml 1 ml ampule Taiwan Schering
testosterone enanthate Testoviron® Depot 250 mg/ml 1 ml ampule Argentina Schering
testosterone enanthate Testoviron® Depot 250 mg/ml 1 ml ampule Hungary Schering [NLM]
testosterone enanthate Testoviron® Depot 250 mg/ml 1 ml ampule Ireland Schering [NLM]
testosterone enanthate Testoviron® Depot 250 mg/ml 1 ml ampule Peru Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Hong Kong Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Iceland Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Thailand Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Yemen Schering
Steroid.com
356
Steroid Listings By Generic Name
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 mi ampule Austria Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Bahrain Schering [NLM]
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Colombia Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Czech. Rep. Schering [NLM]
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Denmark Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Dom. Rep. Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Ethiopia Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Germany Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Greece Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule India Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Israel Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Italy Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Japan Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Lebanon Schering [NLM]
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Malaysia Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Malta Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Pakistan Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Paraguay Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Portugal Schering
testosterone enanthate Testovjron®-Depot 250 mg/ml 1 ml ampule Qatar Schering [NLM]
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Saudi Arabia Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Spain Schering
testosterone enanthate Testoviron®-Depot 250 mg/m! 1 ml ampule Sri Lanka Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Sweden Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Switzerland Schering
testosterone enanthate Testoviron®-Depot 250 mg/ml 1 ml ampule Uruguay Schering
testosterone enanthate Testrin-PA 200 mg/ml n/a U.S. Pasadena Res. [NLM]
testosterone enanthate Testron Depot 125,250 mg/ml 1 ml vial Japan n/a
testosterone enanthate Weratestone 250 250 mg/ml 1 ml ampule Algeria Weimer Pharma
testosterone enanthate Weratestone 250 250 mg/ml 1 ml ampule Mozambique Weimer Pharma
testosterone enanthate Weratestone 250 250 mg/ml 1 ml ampule Zimbabwe Weimer Pharma
testosterone enanthate Weratestone 250 250 mg/ml 1 ml ampule Zimbabwe Weimer Pharma
testosterone phenylpropionate Testolent 100 mg/ml 1 ml ampule Rumania Sicomed [NLM]
testosterone propionate Agovirin injectable 25 mg/ml n/a Czech. Rep. Leciva [NLM]
testosterone propionate Anatest 100 mg/ml 10 ml vial Canada Rhone [NLM] VET
testosterone propionate Anatest 100 mg/ml 10 ml vial Canada Sterivet [NLM] VET
testosterone propionate Anatest 100 mg/ml 10 ml vial Canada Vetoquinol VET
testosterone propionate Androfort-Richter 10, 25 mg/ml n/a Hungary Gedeon Richter
testosterone propionate Androlan 50, 100 mg/ml n/a U.S. Lannett [NLM]
testosterone propionate Ara-Test 25 mg/ml 10 ml vial Mexico Aranda Laboratories [NLM] VET
testosterone propionate Astrapin 50 mg/ml 1 ml ampule Malaysia Astrapin
testosterone propionate AVP Supertest 50 mg/ml 10 ml vial Australia Vetsearch VET
testosterone propionate Dubol 25 mg/ml 1 ml ampule China n/a
testosterone propionate Facovit 1 mg/ml 10 ml vial Italy Teofarma
testosterone propionate Hybolin Imp. 25, 50 mg/ml n/a U.S. Hyrex [NLM]
testosterone propionate Malogen In Oil 100 mg/ml 10 ml vial Canada Germiphene [NLM]
testosterone propionate Nansmon Depot 25 mg/ml n/a Taiwan Chi Sheng
testosterone propionate Neo-Hombreol 50 mg/ml n/a Netherlands Organon [NLM]
testosterone propionate Oreton 25 mg/ml n/a Mexico Goldline [NLM]
Steroid.com
357
Steroid Listings By Generic Name
testosterone propionate Propionat QV 1OO 100 mg/ml 10 ml vial Mexico Quality Vet VET
testosterone propionate Propionato de Testosterona 25 mg/ml 20 ml vial Argentina Induvet VET
testosterone propionate Tepro Hormone 100 mg/ml 500 ml vial Australia Virbac VET
testosterone propionate Testabol Propionate 100 mg/ml 10 ml vial Thailand British Dragon
testosterone propionate Testex 50, 100 mg/ml n/a U.S. Pasadena [NLM]
testosterone propionate Testex Leo 25 mg/ml 1 ml ampule Spain Altana Pharma
testosterone propionate Testex Leo 25 mg/ml 1 ml ampule Spain Leo [NLM]
testosterone propionate Testo 50 mg/ml 10 ml vial Korea Samil
testosterone propionate Testogan 25 mg/ml 50 ml vial Costa Rica Laguinsa VET
testosterone propionate Testogan 25 mg/ml 50 ml vial Dom. Rep. Laguinsa VET
testosterone propionate Testogan 25 mg/ml 50 ml vial Ecuador Laguinsa VET
testosterone propionate Testogan 25 mg/ml 50 ml vial El Salvador Laguinsa VET
testosterone propionate Testogan 25 mg/ml 50 ml vial Guatemala Laguinsa VET
testosterone propionate Testogan 25 mg/ml 50 ml vial Honduras Laguinsa VET
testosterone propionate Testogan 25 mg/ml 50 ml vial Nicaragua Laguinsa VET
testosterone propionate Testogan 25 mg/ml 50 ml vial Panama Laguinsa VET
testosterone propionate Testolic 50 mg/ml 2 ml ampule Thailand Body Research
testosterone propionate Testone-E 25 mg/ml 1 ml ampule Egypt Misr
testosterone propionate Testopin-100 100 mg/ml 2 ml vial India BM Phanmaceuticals
testosterone propionate Testopin-100 100 mg/ml 1 ml ampule India BM PharmaceutJcals
testosterone propionate Testopro L/A 250 mg/ml 10 ml vial Mexico Loeffler VET
testosterone propionate Testosteron 25 mg/ml 1 ml ampule Rumania Sicomed [NLM]
testosterone propionate Testosteron 50 mg/ml 1 ml ampule Bulgaria Sopharma
testosterone propionate Testosteron 5, 10, 25, 50 mg/ml 1 ml ampule Hungary Hemofarm [NLM]
testosterone propionate Testosteron 50 mg/ml 1 ml ampule Switzerland Streuli & Co. AG [NLM]
testosterone propionate Testosteron 5, 10, 25, 50 mg/ml 1 ml ampule YugoslaviaFRMRGalenika [NLM]
testosterone propionate Testosteron Depot 25 mg/ml n/a Taiwan Gentle
testosterone propionate Testosterona 50, 100 mg/ml 10, 20 ml vial Mexico Brovel VET
testosterone propionate Testosterona Proptonat 50, 100 mg/ml 1 ml ampule Russia Farmadon
testosterone propionate Testosterona Propionato n/a n/a Paraguay Botica
testosterone propionate Testosterone Berco Supp. 40 mg/suppository 1 8 supp. box Germany Funke [NLM]
testosterone propionate Testosterone Jenaphamn 25 mg/ml 1 ml ampule Germany Jenapharm [NLM]
testosterone propionate testosterone propionate 50 mg/ml n/a U.S. Quad & Lilly [NLM]
testosterone propionate testosterone propionate 100 mg/ml 10, 30 ml vial U.S. Rugby [NLM]
testosterone propionate testosterone propionate 100mg/ml 10ml vial U.S. Steris [NLM]
testosterone propionate Testosterone Propionate Inj. 100 mg/ml 1 0 ml vial Canada Cytex
testosterone propionate Testosterone Propionate Inj. 100 mg/ml 10 ml vial Canada Dominion VET
testosterone propionate Testosterone Propionate Inj. 100 mg/ml 10 ml vial Canada Taro [NLM]
testosterone propionate Testosterone Propionate Inj 50 mg/ml 1 ml ampule China n/a
testosterone propionate Testosterone Propionate Inj 25 mg/ml n/a Hong Kong Charmaine
testosterone propionate Testosterone Propionate Inj 50 mg/ml n/a Hong Kong Hong Kong Med
testosterone propionate Testosterone Propionate Inj 25 mg/ml n/a Taiwan Tai Yu
testosterone propionate Testosterone Streuli n/a 5, 10, 25, 50 mg/ml Austria Streuli & Co. AG [NLM]
testosterone propionate Testosterone Vitis n/a 10, 25 mg/ml Germany Neopharma [NLM]
testosterone propionate Testosterone-Prop. Disp. 10, 25 mg/ml 1 ml ampule Austria Disperga [NLM]
testosterone propionate testosteronpropionat 50 mg/ml 1 ml ampule Germany Eifelfango [NLM]
testosterone propionate testosteronpropionat 25 mg/ml 1 ml ampule Germany Eifelfango
testosterone propionate Testosteronum Propionicum 50 mg/ml 1 ml ampule Poland Jelfa
testosterone propionate Testoviron® 10,25, 50 mg/ml 1 ml ampule Greece Sobering
Steroid.com
358
Steroid Listings By Generic Name
testosterone propionate Testoviron® 10, 25 mg/ml 1 ml ampule Italy Schering [NLM]
testosterone propionate Testoviron® 50 mg/ml 2 ml ampule Spain Schering [NLM]
testosterone propionate Testovis 20 mg/ml n/a Italy SIT
testosterone propionate Triolandren 100 mg/ml 10 ml vial Switzerland Ciba Geigy CH [NLM]
testosterone propionate Uni-Test Inj 50, 100 mg/ml 1 ml ampule Canada Univet VET
testosterone propionate Virormone 50 mg/ml 2 ml ampule Thailand Paines
testosterone propionate Virormone 50 mg/ml 2 ml ampule United Kingdom Ferring [NLM]
testosterone propionate Virormone 50 mg/ml 10 ml vial United Kingdom Nordic
testosterone propionate VR Testprop 22 mg/pellet n/a Australia Jurox VET
testosterone propionate (implant) Implus-H 20 mg/pellet n/a U.S. Upjohn
testosterone propionate (implant) Progro-H (plus estradiol) 20 mg/pellet n/a Australia Pro Beef VET
testosterone propionate (implant) Synovex®-H (plus estradiol) 20 mg/pellet n/a Canada Ayerst
testosterone propionate (implant) Synovex®-H (plus estrogen) 25 mg/pellet 80 pellet cartridge Australia Fort Dodge VET
testosterone propionate (implant) Synovex®-H (plus estrogen) 20 mg/pellet n/a Mexico Fort Dodge
testosterone propionate (implant) Synovex®-H (plus estrogen) 20 mg/pellet n/a Mexico Syntex [NLM]
testosterone propionate (implant) Synovex®-H (plus estrogen) 20 mg/pellet n/a U.S. Fort Dodge VET
testosterone propionate (implant) Synovex®-H (plus estrogen) 23.5 mg pellet 450 pellets U.S. Syntex [NLM] VET
testosterone propionate (implant) Virbac Tepro Pellets 100 mg/ml 20 ml vial Australia Virbac VET
testosterone suspension Anabolic TS 100 mg/ml 20 ml vial Australia SYD Group VET
testosterone suspension Anabolic TS 100 mg/ml 20 ml via! Mexico SYD Group VET
testosterone suspension Anabolic-TS 25,50, 100 mg/ml n/a Mexico Grupo Tarasco [NLM] VET
testosterone suspension Androlan Aqueous 100 mg/ml n/a U.S. Lannet [NLM]
testosterone suspension Androlin 50 mg/ml n/a U.S. Lincoln [NLM]
testosterone suspension Andronaq-50 100 mg/ml 10 ml vial U.S. Central [NLM]
testosterone suspension AquaTest 25 mg/ml 1 ml ampule Mexico Denkall VET
testosterone suspension Aquaviron 100 mg/ml n/a India Nicholas
testosterone suspension Histerone Injection 100 mg/ml n/a U.S. Roberts [NLM]
testosterone suspension Histerone Injection 25, 50, 100, mg/ml n/a U.S. Hauck [NLM]
testosterone suspension Malogen 100 mg/ml 10ml vial U.S. Forest [NLM]
testosterone suspension Malogen Aqueous 25, 50 mg/ml n/a Canada Germiphene [NLM]
testosterone suspension Malotrone 100 mg/ml 20 ml vial U.S. Bluco [NLM]
testosterone suspension RWR Suspension 25, 50, 100, mg/ml n/a Australia RWR VET
testosterone suspension Tesamone 25, 50, 100, mg/ml n/a U.S. Dunhall [NLM]
testosterone suspension Testolin 100 mg/ml 10 ml vial U.S. Pasadena [NLM]
testosterone suspension Testos 100 100 mg/ml n/a Canada Vetcom VET
testosterone suspension testosterone suspension 50, 100 mg/ml 10, 30ml vial U.S. Legere [NLM]
testosterone suspension testosterone suspension U.S. Schein [NLM]
testosterone suspension testosterone suspension 50, 100 mg/ml 10, 30ml vial U.S. Steris [NLM]
testosterone suspension Testosus 100 100 mg/ml 20 ml vial Australia Jurox [NLM] VET
testosterone suspension Uni-Test Suspension 100 mg/ml 30 ml vial Canada Univet VET
testosterone suspension Veto-Test Sus 100 mg/ml 30 ml vial Canada Austin VET
testosterone suspension (isobutyrate) Agovirin-Depot 25 mg/ml 2 ml ampule Czech. Rep. Biotika
testosterone undecanoate Andriol 40 mg capsules 60 capsule bottle Algeria Organon
testosterone undecanoate Andriol 40 mg capsules n/a Aruba Organon
testosterone undecanoate Andriol 40 mg capsules 60 capsule bottle Australia Organon
testosterone undecanoate Andriol 40 mg capsules 60 capsule bottle Austria Organon
testosterone undecanoate Andriol 40 mg capsules n/a Bahrain Organon
testosterone undecanoate Andriol 40 mg capsules n/a Bangladesh Organon
testosterone undecanoate Andriol 40 mg capsules n/a Belarus Organon
Steroid.com
359
Steroid Listings By Generic Name
testosterone undecanoate Andriol 40 mg capsules 60 capsule bottle Canada Organon
testosterone undecanoate Andriol 40 mg capsules 16 capsule box China Organon
testosterone undecanoate Andriol 40 mg capsules n/a Cyprus Organon
testosterone undecanoate Andriol 40 mg capsules n/a Dutch Antilles Organon
testosterone undecanoate Andriol 40 mg capsules n/a Ecuador Organon
testosterone undecanoate Andriol 40 mg capsules 20 capsule box Egypt Organon/Sedico
testosterone undecanoate Andriol 40 mg capsules n/a Georgia Organon
testosterone undecanoate Andriol 40 mg capsules 30, 60 capsule bottle Germany Organon
testosterone undecanoate Andriol 40 mg capsules n/a Ghana Organon
testosterone undecanoate Andriol 40 mg capsules n/a Hong-Kong Organon
testosterone undecanoate Andriol 40 mg capsules n/a Hungary Organon
testosterone undecanoate Andriol 40 mg capsules n/a Indonesia Organon
testosterone undecanoate Andriol 40 mg capsules 60 capsule bottle Italy Organon
testosterone undecanoate Andriol 40 mg capsules n/a Jordan Organon
testosterone undecanoate Andriol 40 mg capsules n/a Kenya Organon
testosterone undecanoate Andriol 40 mg capsules n/a Korea Organon
testosterone undecanoate Andriol 40 mg capsules n/a Kuwait Organon
testosterone undecanoate Andriol 40 mg capsules n/a Lebanon Organon
testosterone undecanoate Andriol 40 mg capsules 60 capsule bottle Malaysia Organon
testosterone undecanoate Andriol 40 mg capsules n/a Mauritius Organon
testosterone undecanoate Andriol 40 mg capsules n/a Morocco Organon
testosterone undecanoate Andriol 40 mg capsules n/a Myanmar/Burma Organon VET
testosterone undecanoate Andriol 40 mg capsules n/a Netherlands Organon
testosterone undecanoate Andriol 40 mg capsules n/a Nigeria Organon
testosterone undecanoate Andriol 40 mg capsules n/a Oman Organon
testosterone undecanoate Andriol 40 mg capsules n/a Philippines Organon
testosterone undecanoate Andriol 40 mg capsules n/a Portugal Organon
testosterone undecanoate Andriol 40 mg capsules n/a Qatar Organon
testosterone undecanoate Andriol 40 mg capsules n/a Russia Organon
testosterone undecanoate Andriol 40 mg capsules n/a Saudi Arabia Organon
testosterone undecanoate Andriol 40 mg capsules 60 capsule bottle Singapore Organon
testosterone undecanoate Andriol 40 mg capsules n/a Sri Lanka Organon
testosterone undecanoate Andriol 40 mg capsules n/a Switzerland Organon
testosterone undecanoate Andriol 40 mg capsules 10 capsule strip Thailand Organon
testosterone undecanoate Andriol 40 mg capsules n/a Tunisia Organon
testosterone undecanoate Andriol 40 mg capsules n/a Ukraine Organon
testosterone undecanoate Andriol 40 mg capsules n/a United Arab E Organon
testosterone undecanoate Andriol 40 mg capsules n/a Vietnam Organon
testosterone undecanoate Andriol 40 mg capsules n/a Yemen Organon
testosterone undecanoate Andriol 40 mg capsules n/a YugoslaviaFRMROrganon
testosterone undecanoate Andriol capsulas 40 mg capsules 30 capsule bottle Mexico Organon
testosterone undecanoate Andriol capsulas 40 mg capsules n/a Venezuela Organon
testosterone undecanoate Androxon 40 mg capsules 20 capsule box Brazil Organon
testosterone undecanoate Androxon 40 mg capsules 30 capsule bottle Israel Organon
testosterone undecanoate Androxon 40 mg capsules 60 capsule bottle Norway Organon
testosterone undecanoate Androxon 40 mg capsules n/a Pakistan Organon
testosterone undecanoate Androxon 40 mg capsules 60 capsule bottle South Africa Don med/Organon
testosterone undecanoate Nuvir 40 mg capsules 30 capsule bottle India Organon
testosterone undecanoate Panteston 40 mg capsules 60 capsule bottle Finland Organon
Steroid.com
360
Steroid Listings By Generic Name
testosterone undecanoate Panteston 40 mg capsules n/a Latvia Organon
testosterone undecanoate Panteston 40 mg capsules n/a Lithuania Organon
testosterone undecanoate Panteston 40 mg capsules 30,60 capsule bottle Peru Organon
testosterone undecanoate Panteston capsules 40 mg capsules n/a New Zealand Organon
testosterone undecanoate Pantestone 40 mg capsules 60 capsule bottle Estonia Organon
testosterone undecanoate Pantestone 40 mg capsules 60 capsule bottle France Organon
testosterone undecanoate Restandol 40 mg capsules 60 capsule bottle Denmark Organon
testosterone undecanoate Restandol 40 mg capsules 60 capsule bottle Greece Organon
testosterone undecanoate Restandol 40 mg capsules n/a Taiwan Organon
testosterone undecanoate Restandol 40 mg capsules 28, 56 capsule box United Kingdom Organon
testosterone undecanoate Sustenan Oral 40 mg capsules n/a Chile Organon
testosterone undecanoate Undestor 40 mg capsules n/a Argentina Organon
testosterone undecanoate Undestor 40 mg capsules 60 capsule bottle Belgium Organon
testosterone undecanoate Undestor 40 mg capsules 60 capsule bottle Bulgaria Organon
testosterone undecanoate Undestor 40 mg capsules 60 capsule bottle Czech. Rep. Organon
testosterone undecanoate Undestor 40 mg capsules n/a Luxemburg Organon
testosterone undecanoate Undestor 40 mg capsules 60 capsule bottle Poland Organon
testosterone undecanoate Undestor 40 mg capsules 60 capsule bottle Rumania Organon
testosterone undecanoate Undestor 40 mg capsules n/a Slovakia Organon
testosterone undecanoate Undestor 40 mg capsules n/a Sweden Organon
testosterone undecanoate Virigen 40 mg capsules 30 capsule bottle Turkey Organon
Testosterone Blend Andropen 275 275 mg/ml 10 and 20 ml vial Thailand British Dragon
Testoviron (testosterone blend) Aratest 2500 250 mg/ml 10 ml vial Mexico Aranda VET
Testoviron (testosterone blend) Bi-Testo 60 mg/ml 10 ml vial Argentina Cimol VET
Testoviron (testosterone blend) Primoniat®-Depot 100 135 mg/ml 1 ml ampule Chile Schering-Chile [NLM]
Testoviron (testosterone blend) Primoteston Depot 100 135 mg/ml 1 ml ampule Australia Schering [NLM]
Testoviron (testosterone blend) Primoteston Depot 50 75 mg/ml 1 ml ampule Australia Schering [NLM]
Testoviron (testosterone blend) Primoteston®-Depot 100 135 mg/ml 1 ml ampule Egypt Schering/CID
Testoviron (testosterone blend) Testenat 100 mg/ml 1 ml ampule Russia Farmadon [NLM]
Testoviron (testosterone blend) Testenon 135 mg/ml 2 ml vial India BM Pharmaceuticals
Testoviron (testosterone blend) Testenon 135 mg/ml 1 ml ampule India BM Pharmaceuticals
Testoviron (testosterone blend) Testoprim-D 250 mg/ml 1 ml ampule Mexico Labs. Tocogino
Testoviron (testosterone blend) Testoviron® Depot 135 mg/ml 1 ml ampule Argentina Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 135 mg/ml 1 ml ampule Hungary Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 100 135 mg/ml 1 ml ampule Austria Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 100 135 mg/ml 1 ml ampule Dom. Rep. Schering
Testoviron (testosterone blend) Testoviron® Depot 100 135 mg/ml 1 ml ampule Germany Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 100 135 mg/ml 1 ml ampule Greece Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 100 135 mg/ml 1 ml ampule Italy Schering
Testoviron (testosterone blend) Testoviron® Depot 100 135 mg/ml 1 ml ampule Netherlands Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 100 135 mg/ml 1 ml ampule Portugal Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 100 135 mg/ml 1 ml ampule Spain Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 100 135 mg/ml 1 ml ampule Switzerland Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 135 135 mg/ml 1 ml ampule Denmark Schering
Testoviron (testosterone blend) Testoviron® Depot 135 135 mg/ml 1 ml ampule Sweden Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 50 75 mg/ml 1 ml ampule Austria Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 50 75 mg/ml 1 ml ampule Germany Schering [NLM]
Testoviron (testosterone blend) Testoviron® Depot 50 75 mg/ml 1 ml ampule Italy Sobering [NLM]
Testoviron (testosterone Wend) Testoviron® Depot 50 75 mg/ml 1 ml ampule Spain Schering [NLM]
Steroid.com
361
Steroid Listings By Generic Name
trenbolone acetate Acetrenbo 50 50 mg tablet 20 tablet bottle Mexico Loeffler VET
trenbolone acetate ComponentTE-G® 20 mg pellet 40 pellet cartridge U.S. VetLife VET
trenbolone acetate ComponentTE-S® 20 mg pellet 120 pellet cartridge U.S. VetLife VET
trenbolone acetate ComponentTE-H® 20 mg pellet 200 pellet cartridge U.S. VetLife VET
trenbolone acetate ComponentTE-S® 20 mg pellet 140 pellet cartridge U.S. VetLife VET
trenbolone acetate Finaject 30 mg/ml n/a France Roussel [NLM] VET
trenbolone acetate Finajet 30 mg/ml 50 ml vial U.S. Hoechst [NLM] VET
trenbolone acetate Finajet 30 mg/ml 50 ml vial United Kingdom Hoechst [NLM] VET
trenbolone acetate Finaplix-H® 20 20 mg pellet 100 pellet cartridge U.S. Hoechst-Roussel [NLM] VET
trenbolone acetate Finaplix-H® 20 mg pellet 100 pellet cartridge U.S. Intervet VET
trenbolone acetate Finaplix-H® 20 mg pellet 70,100 pellet cartridge Mexico Roussel [NLM] VET
trenbolone acetate Finaplix-S® 20 mg pellet 70 pellet cartridge U.S. Hoechst-Roussel [NLM] VET
trenbolone acetate Parabolan Tabs (Export) 25 mg tablet 20 tablet pouch Thailand British Dragon
trenbolone acetate Revator-200 (plus estradiol) 20 mg pellet 100 pellet cartridge U.S. Intervet VET
trenbolone acetate Revator-G (plus estradiol) 20 mg pellet 20 pellet cartridge U.S. Intervet VET
trenbolone acetate Revator-H (plus estradiol) 20 mg pellet 70 pellet cartridge Canada Intervet VET
trenbolone acetate Revator-H (plus estradiol) 20 mg pellet 70 pellet cartridge U.S. Hoechst-Roussel [NLM] VET
trenbolone acetate Revator-H (plus estradiol) 20 mg pellet 70 pellet cartridge U.S. Intervet VET
trenbolone acetate Revator-IH (plus estradiol) 20 mg pellet 40 pellet cartridge U.S. Intervet VET
trenbolone acetate Revator-IS (plus estradiol) 20 mg pellet 40 pellet cartridge U.S. Intervet VET
trenbolone acetate Revator-S (plus estradiol) 20 mg pellet 60 pellet cartridge Canada Intervet VET
trenbolone acetate Revator-S (plus estradiol) 20 mg pellet 60 pellet cartridge U.S. Hoechst-Roussel [NLM] VET
trenbolone acetate Revator-S (plus estradiol) 20 mg pellet 60 pellet cartridge U.S. Intervet VET
trenbolone acetate Synovex plus (plus estradiol) 25 mg pellet 80 pellet cartridge Canada Wyeth VET
trenbolone acetate Synovex plus (plus estradiol) 25 mg pellet 80 pellet cartridge Mexico Fort Dodge VET
trenbolone acetate Synovex plus (plus estradiol) 25 mg pellet 80 pellet cartridge U.S. Fort Dodge VET
trenbolone acetate Synovex plus (plus estradiol) 25 mg pellet 80 pellet cartridge U.S. Syntex [NLM] VET
trenbolone acetate Trembolone QV 75 75 mg/ml 10 ml vial Mexico Quality Vet VET
trenbolone acetate Trenabol 75 mg/ml 10 ml vial Thailand British Dragon
trenbolone acetate Trenbol 75 75 mg/ml 20 ml vial Mexico Ttokkyo VET
Trenbolone acetate Trenabol 200 200 mg/ml 10 ml vial Thailand British Dragon
trenbolone acetate Trend 50 50 mg/ml 6 ml vial Myanmar/Burma WDV VET
trenbolone hexahydrobenzytearbonate Parabolan 76 mg/1.5 ml 1.5 ml ampule France Negma [NLM]
Trenbolone Blend Tri-Trenabol 150 150mg/ml 10 ml vial Thailand British Dragon
Steroid.com
362
Steroid Listings By Generic Name
Steroid Listings
By
Trade Name
363
Trade Name Generic Name Dosage Packaging Country Company Status Vet
Acetrenbo 50 trenbolone acetate 50 mg tablet 20 tablet bottle Mexico Loeffler VET
Activin nandrolone phenylpropionate 10 mg/ml n/a Spain Aristegvi [NLM]
Afro methyltestosterone 25 mg tablet 40 tablet box Turkey Casel
Agovirin methyltestosterone 10 mg dragee 100 dragee bottle Czech. Rep. Leciva [NLM]
Agovirin injectable testosterone propionate 25 mg/ml n/a Czech. Rep. Leciva [NLM]
Agovirin-Depot testosterone suspension (isobutyrate) 25 mg/ml 2 ml ampule Czech. Rep. Biotika
Alfa-Trofbdermin clostebol acetate .5% gel n/a Italy Pharmacia & Upjohn
Alfa-Trofodermin dostebol acetate .5% gel n/a Italy Farmitalia [NLM]
Ammipire methandrostenolone 5 mg tablet 1000 tablet bottle Thailand Ammipire
Anabol methandrostenolone 50 mg tablet n/a Thailand British Dragon [NLM]
Anabol Tablets methandrostenolone 5 mg tablet 1000 tablet bottte Thailand British Dispensary
Anabol Tablets methandrostenolone 5 mg tablet 1000 tablet bottle Thailand L.P Standard [NLM]
Ana-Bolde boldenone undecylenate 50 mg/ml 10 ml vial Argentina Fort VET
Anabolex methandrostenolone 3 mg tablet 100 tablet box Dom. Rep. Ethical
Anabolic BD boldenone undecylenate 50 mg/ml 10 ml vial Australia SYD Group VET
Anabolic BD boldenone undecylenate 100, 200 mg/ml 10 ml vial Mexico SYD Group VET
Anabolic DN nandrolone cypionate 50 mg/ml 10 ml vial Australia SYD Group VET
Anabolic DN nandrolone cypionate 50, 300 mg/ml 10 ml vial Mexico SYD Group VET
Anabolic NA methylandrostenediol (blend) 75mg/ml 10 ml vial Australia SYD Group VET
Anabolic NA methylandrostenediol (blend) 75mg/ml 10 ml vial Mexico SYD Group VET
Anabolic ST stanozolol (inj) 50mg/ml 20 ml vial Australia SYD Group VET
Anabolic ST stanozolol (inj) 50mg/ml 20 ml vial Mexico SYD Group VET
Anabolic TL testosterone cypionate 100 mg/ml 10ml vial Australia SYD Group VET
Anabolic TL testosterone cypionate 200 mg/ml 10ml vial Mexico SYD Group VET
Anabolic TS testosterone suspension 100 mg/ml 20 ml vial Australia SYD Group VET
Anabolic TS testosterone suspension 100 mg/ml 20 ml via! Mexico SYD Group VET
Anabolic-BD boldenone undecylenate 100 mg/ml 10 ml vial Mexico Grupo Tarasco [NLM] VET
Anabolic-DN nandrolone cypionate 50 mg/ml 10 ml vial Mexico Grupo Tarasco [NLM] VET
Anabolic-NA methylandrostenediol (blend) 75 mg/ml 10 ml vial Mexico Grupo Tarasco [NLM] VET
Anabolico Cimol stanozolol (inj) 60mg/ml 5 ml vial Argentina Cimol VET
Anabolico Produvet stanozolol (inj) 10mg/ml 25 ml vial Argentina Cimol VET
Anabolic-ST stanozolol (inj) 50mg/ml 20 ml vial Mexico Grupo Tarasco [NLM] VET
Anabolic-TS testosterone suspension 25,50, 100 mg/ml n/a Mexico Grupo Tarasco [NLM] VET
Anabolicum nandrolone decanoate 25 mg/ml 10, 50 ml vial Germany Bela-Pharm VET
Anabolicum Vister quinbolone 10 mg capsule 30 capsule bottte Italy Parke Davis [NLM]
Anabolicum Vister quinbolone oral drops n/a Italy Parke Davis [NLM]
Anabolikum 2.5% methandrostenolone 25mg/ml 50 ml vial Germany Meca G [NLM] VET
Anabolin methandrostenolone 5 mg tablet n/a Finland Leiras [NLM]
Anabolin methandrostenolone 0.5% cream n/a Finland Leiras [NLM]
Anabolin nandrolone phenylpropionate 50 mg/ml n/a U.S. Alto [NLM]
Anabolin Forte nandrolone decanoate 50 mg/ml 10 ml vial Netherlands Alfasan VET
Anabolin Forte nandrolone decanoate 50 mg/ml 10 ml vial Rumania Alfasan VET
Anabolin Forte nandrolone decanoate 50 mg/ml 10,50 ml vial Spain Alfasan VET
Anaboline Depot nandrolone decanoate 50 mg/ml 1 ml Greece Adeteo
Anabolin-IM nandrolone phenylpropionate 50 mg/ml n/a U.S. Alto [NLM]
Anabolin-LA nandrolone phenylpropionate 1 00 mg/ml n/a U.S. Alto [NLM]
Anabol-Jet methandrostenolone 25mg/ml 30,100, 250 ml vial Mexico Norvet VET
Anabol-Jet ADE methandrostenolone 30mg/ml 100,250 ml vial Mexico Norvet VET
Steroid.com
364
Steroid Listings By Trade Name
Anabol-Pets methandrostenolone 10.25 mg tablet 200 tablet bottle Mexico Norvet VET
Anabrol oxymetholone 50 mg tablet 100 tablet bottle Mexico Brovel VET
Anadiol methylandrostenediol dipropionate 5mg tab 10, 100 tablet bottle Australia Ilium/Troy VET
Anadiol Depot methylandrostenediol dipropionate 75 mg/ml 10 ml vial Australia Ilium/Troy VET
Anador nandrolone hexyloxyphenylpropionate 25 mg/ml 2 ml ampule France Pharmacia-Upjohn [NLM]
Anadrol oxymetholone 5 mg tablet n/a Japan n/a
Anadrol 50® oxymetholone 50 mg tablet 100 tablet bottle U.S. Unimed
Anadrol 50® oxymetholone 50 mg tablet 100 tablet bottle Canada Syntex [NLM]
Anadrol 50® oxymetholone 50 mg tablet 100 tablet bottle U.S. Syntex [NLM]
Anadur nandrolone hexyloxyphenylpropionate 25, 50 mg/ml 1, 2 ml ampule Austria Kabi Pharmacia [NLM]
Anadur nandrolone hexyloxyphenylpropionate 25, 50 mg/ml 1 , 2 ml ampule Belgium Pharmacia [NLM]
Anadur nandrolone hexyloxyphenylpropionate 25, 50 mg/ml 1 , 2 ml ampule Czech. Rep. Pharmacia [NLM]
Anadur nandrolone hexyloxyphenylpropionate 25 mg/ml 2 ml ampule Denmark Lundbeck [NLM]
Anadur nandrolone hexyloxyphenylpropionate 25, 50 mg/ml 1 , 2 ml ampule Finland Pharmacia [NLM]
Anadur nandrolone hexyloxyphenylpropionate 25, 50 mg/ml 1 , 2 ml ampule Germany Kabi Pharmacia [NLM]
Anadur nandrolone hexyloxyphenylpropionate 25, 50 mg/ml 1 , 2 ml ampule Netherlands Pharmacia [NLM]
Anadur nandrolone hexyloxyphenylpropionate 25, 50 mg/ml 1 , 2 ml ampule Norway Kabi Pharmacia [NLM]
Anadur nandrolone hexyloxyphenylpropionate 25 mg/ml 2 ml ampule Spain Leo [NLM]
Anadur nandrolone hexyloxyphenylpropionate 25, 50 mg/ml 1 , 2 ml ampule Switzerland Kabi Pharmacia [NLM]
Anadur nandrolone hexyloxyphenylpropionate 25 mg/ml 2 ml ampule Turkey Eczacibasi [NLM]
Anadurin nandrolone hexyloxyphenylpropionate 50 mg/ml 1 ml ampule Greece Xponei [NLM]
Anapolan 50 oxymetholone 50 mg tablet 100 tablet bottle Malaysia Syntex [NLM]
Anapolan 50 oxymetholone 50 mg tablet 20 tablet strip Mexico Syntex [NLM]
Anapolan 50 oxymetholone 50 mg tablet 100 tablet bottle United Kingdom Syntex [NLM]
Anapolan 50 oxymetholone 50 mg tablet 100 tablet bottle Canada Hoffman-La Rouche [NLM]
Anapolon oxymetholone 50 mg tablet n/a Bulgaria Syntex [NLM]
Anapolon oxymetholone 50 mg tablet 20 tablet box Turkey Ibrahim
Anapolon oxymetholone 2.5, 5 mg tablet 20 tablet box Turkey Ibrahim [NLM]
Anaprolina nandrolone decanoate 25, 50 mg/ml 1 ml ampule Chile Silesia
Anaptex norethandrolone 5 mg tablet 100 tablet bottle Australia Jurox VET
Anasteron oxymetholone 25 mg tablet 60 tablet bottle Greece Farmaprod
Anasteron oxymetholone 50 mg tablet n/a Greece Syntex [NLM]
Anasteron oxymetholone 50 mg tablet n/a Sweden Syntex [NLM]
Anatest testosterone propionate 100 mg/ml 10 ml vial Canada Rhone [NLM] VET
Anatest testosterone propionate 100 mg/ml 10 ml vial Canada Sterivet [NLM] VET
Anatest testosterone propionate 100 mg/ml 10 ml vial Canada Vetoquinol VET
Anatrophill oxandrolone 2.5 mg tablet n/a France Searle [NLM]
Anavar oxandrolone 5 mg tablet 30 tablet strip China Hubei Huangshi
Anavar oxandrolone 2.5 mg tablet 100 tablet bottle U.S. Searle [NLM]
Anazol stanozolol (oral) 2 mg tablet 100 tablet box Philippines Xetox (export)
Anazol stanozolol (oral) 2 mg tablet 100, 1000 tablet bottle Philippines Xetox (export)
Anderone 100/200 testosterone enanthate 100,200 mg/ml 10ml vial U.S. Burgin-Arden [NLM]
Andoredan methandrostenolone 5 mg tablet n/a Japan Takeshima-Kodama [NLM]
Andractim dihydrotestosterone 25mg/g 80 gram gel Belgium Piette
Andractim dihydrotestosterone 25mg/g 100 gram gel France Besins-lscovesco
Andractim dihydrotestosterone 25mg/g 100 gram gel India Chemec
Andractim dihydrotestosterone 25mg/g 80 gram gel Korea n/a
Andractim dihydrotestosterone 25mg/g 80 gram gel Uruguay Servimedic
Andriol testosterone undecanoate 40 mg capsules 60 capsule bottle Algeria Organon
Steroid.com
365
Steroid Listings By Trade Name
Andriol testosterone undecanoate 40 mg capsules n/a Aruba Organon
Andriol testosterone undecanoate 40 mg capsules 60 capsule bottle Australia Organon
Andriol testosterone undecanoate 40 mg capsules 60 capsule bottle Austria Organon
Andriol testosterone undecanoate 40 mg capsules n/a Bahrain Organon
Andriol testosterone undecanoate 40 mg capsules n/a Bangladesh Organon
Andriol testosterone undecanoate 40 mg capsules n/a Belarus Organon
Andriol testosterone undecanoate 40 mg capsules 60 capsule bottle Canada Organon
Andriol testosterone undecanoate 40 mg capsules 16 capsule box China Organon
Andriol testosterone undecanoate 40 mg capsules n/a Cyprus Organon
Andriol testosterone undecanoate 40 mg capsules n/a Dutch Antilles Organon
Andriol testosterone undecanoate 40 mg capsules n/a Ecuador Organon
Andriol testosterone undecanoate 40 mg capsules 20 capsule box Egypt Organon/Sedico
Andriol testosterone undecanoate 40 mg capsules n/a Georgia Organon
Andriol testosterone undecanoate 40 mg capsules 30, 60 capsule bottle Germany Organon
Andriol testosterone undecanoate 40 mg capsules n/a Ghana Organon
Andriol testosterone undecanoate 40 mg capsules n/a Hong-Kong Organon
Andriol testosterone undecanoate 40 mg capsules n/a Hungary Organon
Andriol testosterone undecanoate 40 mg capsules n/a Indonesia Organon
Andriol testosterone undecanoate 40 mg capsules 60 capsule bottle Italy Organon
Andriol testosterone undecanoate 40 mg capsules n/a Jordan Organon
Andriol testosterone undecanoate 40 mg capsules n/a Kenya Organon
Andriol testosterone undecanoate 40 mg capsules n/a Korea Organon
Andriol testosterone undecanoate 40 mg capsules n/a Kuwait Organon
Andriol testosterone undecanoate 40 mg capsules n/a Lebanon Organon
Andriol testosterone undecanoate 40 mg capsules 60 capsule bottle Malaysia Organon
Andriol testosterone undecanoate 40 mg capsules n/a Mauritius Organon
Andriol testosterone undecanoate 40 mg capsules n/a Morocco Organon
Andriol testosterone undecanoate 40 mg capsules n/a Myanmar/Burma Organon VET
Andriol testosterone undecanoate 40 mg capsules n/a Netherlands Organon
Andriol testosterone undecanoate 40 mg capsules n/a Nigeria Organon
Andriol testosterone undecanoate 40 mg capsules n/a Oman Organon
Andriol testosterone undecanoate 40 mg capsules n/a Philippines Organon
Andriol testosterone undecanoate 40 mg capsules n/a Portugal Organon
Andriol testosterone undecanoate 40 mg capsules n/a Qatar Organon
Andriol testosterone undecanoate 40 mg capsules n/a Russia Organon
Andriol testosterone undecanoate 40 mg capsules n/a Saudi Arabia Organon
Andriol testosterone undecanoate 40 mg capsules 60 capsule bottle Singapore Organon
Andriol testosterone undecanoate 40 mg capsules n/a Sri Lanka Organon
Andriol testosterone undecanoate 40 mg capsules n/a Switzerland Organon
Andriol testosterone undecanoate 40 mg capsules 10 capsule strip Thailand Organon
Andriol testosterone undecanoate 40 mg capsules n/a Tunisia Organon
Andriol testosterone undecanoate 40 mg capsules n/a Ukraine Organon
Andriol testosterone undecanoate 40 mg capsules n/a United Arab E Organon
Andriol testosterone undecanoate 40 mg capsules n/a Vietnam Organon
Andriol testosterone undecanoate 40 mg capsules n/a Yemen Organon
Andriol testosterone undecanoate 40 mg capsules n/a YugoslaviaFRMROrganon
Andriol capsulas testosterone undecanoate 40 mg capsules 30 capsule bottle Mexico Organon
Andriol capsulas testosterone undecanoate 40 mg capsules n/a Venezuela Organon
Andris methylandrostenediol 10mg tablet n/a Greece Chifar [NLM]
Steroid.com
366
Steroid Listings By Trade Name
Andro 100 testosterone enanthate 100 mg/ml 10ml vial U.S. Forest [NLM]
Andro LA 200 testosterone enanthate 200 mg/ml 10 ml vial U.S. Forest [NLM]
Andro-Cyp testosterone cypionate 100, 200 mg/ml 10 ml vial U.S. Brown [NLM]
Andro-Cyp testosterone cypionate 100, 200 mg/ml 10 ml vial U.S. Keene [NLM]
Androderm® testosterone (patch) 12.2 mg patch. 30 patches/box Canada Pharmascience
Androderm® testosterone (patch) 12.2 mg patch. 10, 30, 60 patches/box Germany AstraZenica
Androderm® testosterone (patch) 12.2 mg patch. n/a Italy Schwarz Pharma
Androderm® testosterone (patch) 12.2 mg patch. n/a Korea n/a
Androderm® testosterone (patch) 2.5 mg patch 30, 60 patch box Spain Schwarz Pharma
Androderm® testosterone (patch) 5 mg patch 30 patch box Spain Schwarz Pharma
Androderm® testosterone (patch) 12.2 mg patch n/a Switzerland Astrazenica
Androderm® testosterone (patch) 1 2.2 mg patch 60 patches/box U.S. Smith Kline Beecham [NLM]
Androderm® testosterone (patch) 12.2, 24.3 mg patch 60 patches/box U.S. Watson Pharma
Androfort-Richter testosterone propionate 10, 25 mg/ml n/a Hungary Gedeon Richter
Androge! testosterone (gel) 25, 50 mg single dose packet Canada Solvay
Androgel testosterone (gel) 25, 50 mg single dose packet Netherlands Besins
Androgel testosterone (gel) 25, 50 mg single dose packet Sweden Besins
Androgel testosterone (gel) 50, 75, 100 mg single dose packet U.S. Unimed
Android methyltestosterone 5, 10,25 mg tablet 60 tablet bottle U.S. ICN Pharm
Android methyltestosterone 5, 10, 25 mg tablet n/a U.S. Brown [NLM]
Android-F fluoxymesterone 10mg tablet 100 tablet bottle U.S. Brown [NLM]
Androlan testosterone propionate 50, 100 mg/ml n/a U.S. Lannett [NLM]
Androlan Aqueous testosterone suspension 100 mg/ml n/a U.S. Lannet [NLM]
Androlic oxymetholone 50 mg tablet 100 tablet bottle, pouch Thailand British Dispensary
Androlic (Export) oxymetholone 50 mg tablet 20 tablet pouch Thailand British Dragon
Androlin testosterone suspension 50 mg/ml n/a U.S. Lincoln [NLM]
Androlone nandrolone phenylpropionate 50 mg/ml n/a U.S. Keene [NLM]
Androlone-D 200 nandrolone decanoate 200 mg/ml 1 ml U.S. Keene [NLM]
Andronaq LA testosterone cypionate 100, 200 mg/ml 10 ml vial U.S. Central [NLM]
Andronaq-50 testosterone suspension 100 mg/ml 10 ml vial U.S. Central [NLM]
Andronate testosterone cypionate 100, 200 mg/ml 10 ml vial U.S. Pasadena [NLM]
Andropatch testosterone (patch) 12.2 mg patch 30, 60 patch box Netherlands Schwarz Pharma
Andropatch testosterone (patch) 2.5 mg patch 60 patches/box United Kingdom GSK
Andropatch testosterone (patch) 5 mg patch 30 patches/box United Kingdom GSK
Andropen 275 Testosterone Blend 275 mg/ml 10 and 20 ml vial Thailand British Dragon
Andropository testosterone enanthate 200 mg/ml 10ml vial U.S. Rugby [NLM]
Androral methyltestosterone 10mg tablet n/a Hungary Gedeon Richter
Androtardyl® testosterone enanthate 250 mg/ml 1 ml ampule Algeria Schering
Androtardyl® testosterone enanthate 250 mg/ml 1 ml ampule France Schering
Androtardyl® testosterone enanthate 250 mg/ml 1 ml ampule Morocco Schering
Androtardyl® testosterone enanthate 250 mg/ml 1 ml ampule Tunisia Schering
Androtop Gel testosterone (gel) 50 mg single dose packet Germany Kade/Besins
Androxon testosterone undecanoate 40 mg capsules 20 capsule box Brazil Organon
Androxon testosterone undecanoate 40 mg capsules 30 capsule bottle Israel Organon
Androxon testosterone undecanoate 40 mg capsules 60 capsule bottle Norway Organon
Androxon testosterone undecanoate 40 mg capsules n/a Pakistan Organon
Androxon testosterone undecanoate 40 mg capsules 60 capsule bottle South Africa Don med/Organon
Androyd oxymetholone 5 mg tablet 100 tablet India Parke Davis
Andryl 200 testosterone enanthate 200 mg/ml 10 ml vial U.S. Keene [NLM]
Steroid.com
367
Steroid Listings By Trade Name
Apetil stanozolol (oral) 4 mg/ml 10 ml dropper bottle Argentina Holliday VET
AquaTest testosterone suspension 25 mg/ml 1 ml ampule Mexico Denkall VET
Aquaviron testosterone suspension 100 mg/ml n/a India Nicholas
Ara-Test testosterone propionate 25 mg/ml 10 ml vial Mexico Aranda Laboratories [NLM] VET
Aratest 2500 Testoviron (testosterone blend) 250 mg/ml 10 ml vial Mexico Aranda VET
Arbolic methylandrostenediol dipropionate 50 mg/ml n/a U.S. Burgin Arden [NLM]
Arcosterone methyltestosterone 10 mg n/a U.S. Acrum [NLM]
Arcosterone methyltestosterone 10, 25 mg tablet n/a U.S. Acrum [NLM]
Astrapin testosterone propionate 50 mg/ml 1 ml ampule Malaysia Astrapin
Atmos testosterone (patch) 5 mg patch 30 patch box Norway Astra Zenica
Atmos testosterone (patch) 5 mg patch n/a Sweden Astra
AVP Supertest testosterone propionate 50 mg/ml 10 ml vial Australia Vetsearch VET
Banrot testosterone cypionate 75 mg/ml 200 ml bladder Australia Coopers [NLM] VET
Baojen fluoxymesterone 5 mg capsule n/a Taiwan Ta Fong
Bionabol methandrostenolone 2, 5 mg tab 40 tablet box Bulgaria Balkanpharma
Bionabol methandrostenolone 2 mg tablet 40 tablet bottle Bulgaria Pharmacia [NLM]
Bionabol methandrostenolone 5mg tab 40 tablet bottle Bulgaria Pharmacia [NLM]
Biselmon Depot testosterone cypionate 50 mg/ml n/a Taiwan Ta Fong
Bi-Testo Testoviron (testosterone blend) 60 mg/ml 10 ml vial Argentina Cimol VET
Bold QV 200 boldenone undecylenate 200 mg/ml 10 ml vial Mexico Quality Vet VET
Boldabol boldenone undecylenate 200 mg/ml 10 ml vial Thailand British Dragon
Boldebal-H boldenone undecylenate 50 mg/ml 10 ml vial Australia Ilium/Troy VET
BoldenoI R boldenone undecylenate 50 mg/ml 10, 50, 100, 250ml vial Columbia Comandina VET
Boldenol 25 boldenone undecylenate 25 mg/ml 10, 50,100, 250ml vial Columbia Comandina VET
Boldenon boldenone undecylenate 200 mg/ml 10 ml vial Mexico Ttokkyo VET
Boldenona boldenone undecylenate 50mg/ml 10,20,100 ml vial Columbia Biogen VET
Boldenona boldenone undecylenate 50 mg/ml 10, 50,100, 250ml vial Columbia Vecol VET
Boldenona 50 boldenone undecylenate 50 mg/ml 10, 50, 100, 250ml vial Columbia Servinsumos VET
Boldenona 50 Gen-Far boldenone undecylenate 50 mg/ml 10, 50,100,250ml vial Bolivia Gen-Far VET
Boldenona 50 Gen-Far boldenone undecylenate 50 mg/ml 10, 50,100, 250ml vial Columbia Gen-Far VET
Boldenona 50 Gen-Far boldenone undecylenate 50 mg/ml 10, 50,100, 250ml vial Costa Rica Gen-Far VET
Boldenona 50 Gen-Far boldenone undecylenate 50 mg/ml 10, 50, 100, 250ml vial Dom. Republic Gen-Far VET
Boldenona 50 Gen-Far boldenone undecylenate 50 mg/ml 10,50,100,250ml vial Ecuador Gen-Far VET
Boldenona 50 Gen-Far boldenone undecylenate 50 mg/ml 10, 50,100, 250ml vial El Salvador Gen-Far VET
Boldenona 50 Gen-Far boldenone undecylenate 50 mg/ml 10,50,100,250ml vial Guatemala Gen-Far VET
Boldenona 50 Gen-Far boldenone undecylenate 50 mg/ml 10,50,100, 250ml vial Honduras Gen-Far VET
Boldenona 50 Gen-Far boldenone undecylenate 50 mg/ml 10, 50,100,250ml vial Nicaragua Gen-Far VET
Boldenona 50 Gen-Far boldenone undecylenate 50 mg/ml 10, 50,100,250ml vial Panama Gen-Far VET
Boldenona 50 Gen-Far boldenone undecylenate 50 mg/ml 10,50,100,250ml vial Peru Gen-Far VET
Boldenone - 50 boldenone undecylenate 50 mg/ml 10 ml vial Australia Jurox [NLM] VET
Bonalone oxymetholone 50 mg tablet 100 tablet bottle Thailand Body Research
Bonavar oxandrolone 2.5 mg tablet 10 tablet strip Thailand Body Research
Canoate Inj nandrolone decanoate 25, 50 mg/ml n/a Korea n/a
Cebulin 50 boldenone undecylenate 50 mg/ml 10, 50, 250 ml vial Columbia Provet VET
Cetabon stanozolol (oral) 2 mg tablet 10 tablet strip Thailand Therapharma
Cheque Drops mibolerone 100 meg/ml 55 mg bottle U.S. Upjohn [NLM] VET
Chinglicosan fluoxymesterone 5 mg capsule n/a Taiwan Ciiphar
Chinlipan Tab methandrostenolone 2 mg tablet n/a Taiwan Chin Tien
ComponentTE-G® trenbolone acetate 20 mg pellet 40 pellet cartridge U.S. VetLife VET
Steroid.com
368
Steroid Listings By Trade Name
ComponentTE-H® trenbolone acetate 20 mg pellet 200 pellet cartridge U.S. VetLife VET
ComponentTE-S® trenbolone acetate 20 mg pellet 120 pellet cartridge U.S. VetLife VET
ComponentTE-S® trenbolone acetate 20 mg pellet 140 pellet cartridge U.S. VetLife VET
Crecibol 50 boldenone undecylenate 25 mg/ml 10, 30 ml vial Mexico Unimed VET
Crestabolic methylandrostenediol dipropionate 50 mg/ml n/a U.S. Nutrition [NLM]
Cyclo-Testosterone Depot testosterone cypionate 130 mg/ml n/a Taiwan Astar
Cypionax testosterone cypionate 100 mg/ml 2 ml ampule Thailand Body Research
CypioTest 250 testosterone cypionate 250 mg/ml 10 ml vial Mexico Denkall VET
Cypriotest L/A testosterone cypionate 250 mg/ml 10ml vial Mexico Loeffler VET
Daily Reborn Inj nandrolone phenylpropionate 25 mg/ml n/a Taiwan Shiteh
Danabol OS methandrostenolone 10mg tablet 500 tablet bottle Thailand Body Research
D-Bol methandrostenolone 10mg tablet 100 tablet bottle Mexico Denkall VET
D-Bol methandrostenolone 10mg capsule 96 capsule box Mexico Denkall VET
D-Bol methandrostenolone 10mg capsule 300 capsule bottle Mexico Denkall VET
D-Bol methandrostenolone 25mg/ml 10 ml vial Mexico Denkall VET
Debosteron methyltestosterone n/a n/a Korea n/a
Deca QV 200 nandrolone decanoate 200 mg/ml 10, 50 ml vial Mexico Quality Vet VET
Deca QV 300 nandrolone decanoate 300 mg/ml 10 ml vial Mexico Quality Vet VET
Deca-Dubol-100 nandrolone decanoate 100 mg/ml 2 ml vial India BM Pharmaceuticals
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml Argentina Organon
Deca-Durabolin® nandrolone decanoate 50 mg/ml 2ml Argentina Organon
Deca-Durabolin® nandrolone decanoate 25 mg/ml 1 ml Austria Organon [NLM]
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule, syringe Belgium Organon
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule Brazil Organon
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule Bulgaria Organon
Deca-Durabolin® nandrolone decanoate 50 mg/ml 2ml Canada Organon [NLM]
Deca-Durabolin® nandrolone decanoate 100 mg/ml 2ml Canada Organon
Deca-Durabolin® nandrolone decanoate 25, 50,100 mg/ml 1 ml ampule Chile Organon
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule Colombia Organon
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml Denmark Organon [NLM]
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule Egypt Organon/Nile
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml Finland Organon
Deca-Durabolin® nandrolone decanoate 100 mg/ml 1, 2ml Finland Organon
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml France Organon [NLM]
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml Germany Organon [NLM]
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml vial Greece Organon
Deca-Durabolin® nandrolone decanoate 100 mg/ml 2 ml vial Greece Organon
Deca-Durabolin® nandrolone decanoate 100 mg/ml 2 ml vial Greece Organon
Deca-Durabolin® nandrolone decanoate 25,50, 100 mg/ml 1 ml ampule India Infar
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule Indonesia Organon
Deca-Durabolin® nandrolone decanoate n/a n/a Ireland Organon
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule Italy Organon
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule Korea Organon
Deca-Durabolin® nandrolone decanoate 25 mg/ml 1 ml ampule Malaysia Organon
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule Netherlands Organon
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml ampule New Zealand Organon
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml ampule Norway Organon
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml ampule Peru Organon
Deca-Durabolin® nandrolone decanoate 25 mg/ml 1 ml ampule Poland Organon [NLM]
Steroid.com
369
Steroid Listings By Trade Name
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml ampule Poland Organon
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml ampule Rumania Organon
Deca-Durabolin® nandrolone decanoate 25 mg/ml 1 ml ampule Singapore Organon
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule South Africa Donmed / Organon
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule Spain Organon
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml ampule Sweden Organon
Deca-Durabolin® nandrolone decanoate 25, 100 mg/ml 1, 2ml Sweden Organon [NLM]
Deca-Durabolin® nandrolone decanoate 25 mg/ml 1 ml ampule Switzerland Organon [NLM]
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml ampule Switzerland Organon
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml ampule Taiwan Organon
Deca-Durabolin® nandrolone decanoate 25, 50 mg/ml 1 ml ampule Thailand Organon
Deca-Durabolin® nandrolone decanoate 100 mg/ml 1 , 2 ml vial U.S. Organon [NLM]
Deca-Durabolin® nandrolone decanoate 200 mg/ml 1 ml vial U.S. Organon [NLM]
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml ampule United Kingdom Organon
Deca-Durabolin® nandrolone decanoate 100 mg/ml 1 , 2 ml ampule United Kingdom Organon [NLM]
Deca-Durabolin® nandrolone decanoate 25 mg/ml 1 ml ampule Venezuela Organon
Deca-Durabolin® nandrolone decanoate 50 mg/ml 1 ml syringe Venezuela Organon
Deca-Durabolin® nandrolone decanoate 100 mg/ml 2 ml vial Netherlands Organon
Deca-Evabolin nandrolone decanoate 25 mg/ml 1 ml ampule India Concept
Decagic nandrolone decanoate 100 mg/ml 10 ml vial India Unichem [NLM]
Decanandrolen nandrolone decanoate 200mg/ml 10 ml vial Mexico Denkall VET
Decaneurabol nandrolone decanoate 25, 50 mg/ml 1 ml ampule India Cadila
Decaneurophen nandrolone decanoate 25, 50 mg/ml 1 ml ampule India Ind-Swift
Decanoato de Nandrobna nandrolone decanoate 200 mg/ml 10ml vial Mexico Tomel VET
Decanoato Nandrolona nandrolone decanoate 25, 50 mg/ml 1 ml ampule Chile Astorga
Decanoato Nandrolona nandrolone decanoate 50 mg/ml 1 ml ampule Chile Biosano
Decanofort nandrolone decanoate 25 mg/ml 1 ml ampule Rumania Terapia
Deca-Pronabol nandrolone decanoate 100 mg/ml 2 ml ampule India P & B Labs [NLM]
Decatron250 nandrolone decanoate 250 mg/ml 10 ml vial Mexico Brovel VET
Delatest testosterone enanthate 100/mg/ml 10 ml vial U.S. Dunhall [NLM]
Delatestryl testosterone enanthate 200 mg/ml 5 ml vial Canada Theramed
Delatestryl testosterone enanthate 200 mg/ml 10 ml vial Mexico Brovel [NLM] VET
Delatestryl testosterone enanthate 200 mg/ml 1 ml syringe U.S. BTG
Delatestryl testosterone enanthate 200mg/ml 5 ml vial U.S. BTG
Delatestryt testosterone enanthate 200 mg/ml 10 ml vial U.S. Mead Johnson [NLM]
Denkadiol methylandrostenediol dipropionate 75 mg/ml 10 ml vial Mexico Denkall VET
Dep Andro-100-200 testosterone cypionate 100, 200 mg/ml 10 ml vial U.S. Forest [NLM]
Deposteron testosterone cypionate 100 mg/ml 2 ml ampule Brazil Novaquimica/Sigma
Deposterona testosterone blend (misc) 60mg/ml 10 ml vial Mexico Fort Dodge VET
Deposterona testosterone blend (misc) 60mg/ml 10 ml vial Mexico Syntex [NLM] VET
Depot-Bifuron testosterone cypionate 50 mg/ml n/a Taiwan Gentle
Depo-TCP testosterone cypionate 200mg/ml n/a Korea n/a
Depotest testosterone cypionate 100, 200 mg/ml 10ml vial U.S. Hyrex [NLM]
Depotest testosterone cypionate 100, 200 mg/ml 10 ml vial U.S. Kay [NLM]
Depo-Testermon testosterone cypionate 200 mg/ml n/a Taiwan CCPC
Depo-Testerone testosterone cypionate 200 mg/ml n/a Taiwan Metro
DepoTestmon Inj testosterone enanthate 65mg/ml n/a Taiwan CCPC
Depo-Testomon testosterone cypionate 100 mg/ml n/a Taiwan LiTa
Depo-Testosterone testosterone cypionate 100 mg/ml 10 ml vial South Africa Pharmacia & Upjohn
Steroid.com
370
Steroid Listings By Trade Name
Depo-Testosterone CPP testosterone cypionate 100 mg/ml n/a Taiwan Metro
Depo-Testosterone® testosterone cypionate 100 mg/ml 10 ml vial Canada Pharmacia
Depo-Testosterone® testosterone cypionate 100 mg/ml n/a Malaysia Pharmacia
Depo-Testosterone® testosterone cypionate 10 mg/ml 10 ml vial New Zealand Pharmacia & Upjohn
Depo-Testosterone® testosterone cypionate 100 mg/ml 10 ml vial Singapore Pharmacia & Upjohn
Depo-Testosterone® testosterone cypionate 100, 200 mg/ml 10 ml vial U.S. Pharmacia & Upjohn
Depo-Testosterone® testosterone cypionate 200 mg/ml 1 ml vial U.S. Pharmacia & Upjohn
Depot-Hormon MF testosterone cypionate 50 mg/ml n/a Taiwan Sintong
Depotrone testosterone cypionate 100 mg/ml 2 ml ampule South Africa Propan-Zurich
Depovirin Inj testosterone cypionate 125 mg/ml 2ml Korea n/a
Dep-Test testosterone cypionate 100 mg/ml 10 ml vial U.S. Rocky Mountain [NLM]
Dialone methandrostenolone 5 mg tablet 100 tablet bottle U.S. Major [NLM]
Dianabol methandrostenolone 10mg tablet 100 tablet bottle Mexico Salud VET
Dianabol methandrostenolone 25 mg/ml 10,50,100 ml vial Mexico Salud VET
Dianabol methandrostenolone 25 mg tablet 30 tablet bottle Belize Planet Pharmacy
Dianabol methandrostenolone 5 mg tablet 100 tablet bottle Germany Ciba [NLM]
Dianabol methandrostenolone 5 mg tablet 100 tablet bottle U.S. Ciba [NLM]
Dianabol methandrostenolone 5 mg tablet 100 tablet bottle United Kingdom Ciba [NLM]
Dimetabol nandrolone decanoate 50 mg/ml 50 ml vial Dom. Rep. Bremer Pharma [NLM] VET
Dimetabol ADE nandrolone decanoate 25 mg/ml 50, 100 ml vial Mexico Lapisa VET
Dinandrol nandrolone (blend) 100mg/ml 2 ml vial Philippines Xelox (export)
Diosterol methandrostenolone/stanozolol 50 mg tablet 30 tablet bottle Belize Planet Pharmacy
Drive methylandrostenediol (blend) 55mg/ml 10 ml vial Australia RWR VET
Drolban drostanolone propionate 50mg/1ml 1 ml vial U.S. Lilly [NLM]
Dromostan drostanolone 50 mg/ml 5 ml vial Philippines Xelox (export)
D-Test 100/200 testosterone cypionate 100,200 mg/ml 10 ml vial U.S. Sig [NLM]
Dubol testosterone propionate 25 mg/ml 1 ml ampule China n/a
Dubol-100 nandrolone phenylpropionate 100 mg/ml 2 ml vial India BM Pharmaceuticals
Dubol-50 nandrolone phenylpropionate 50 mg/ml 1 ml ampule India BM Pharmaceuticals
Durabol nandrolone phenylpropionate 100 mg/ml 10ml vial Thailand British Dragon
Durabolin® nandrolone phenylpropionate 25 mg/ml n/a Belgium Organon [NLM]
Durabolin® nandrolone phenylpropionate 25,50 mg/ml n/a Canada Organon [NLM]
Durabolin® nandrolone phenylpropionate 25mg/ml n/a Finland Organon
Durabolin® nandrolone phenylpropionate 25 mg/ml 1 ml ampule Greece Organon [NLM]
Durabolin® nandrolone phenylpropionate 25 mg/ml 1 ml ampule India Infar
Durabolin® nandrolone phenylpropionate 12.5 mg/ml 2 ml ampule Indonesia Organon
Durabolin® nandrolone phenylpropionate 25 mg/ml 1 ml ampule Malaysia Organon
Durabolin® nandrolone phenylpropionate 25 mg/ml 1 ml ampule Netherlands Organon
Durabolin® nandrolone phenylpropionate 50 mg/ml n/a Portugal Organon
Durabolin® nandrolone phenylpropionate 25 mg/ml 1 ml ampule Spain Organon [NLM]
Durabolin® nandrolone phenylpropionate 25 mg/ml n/a Switzerland Opopharma [NLM]
Durabolin® nandrolone phenylpropionate 25 mg/ml 2 ml vial Taiwan Organon
Durabolin® nandrolone phenylpropionate 25, 50 mg/ml n/a U.S. Organon [NLM]
Durabolin® nandrolone phenylpropionate 50 mg/ml 1 ml ampule United Kingdom Organon [NLM]
Durabolin® nandrolone phenylpropionate 50 mg/ml n/a Yugoslavia/FRMROrganon
Durandrol methylandrostenediol dipropionate 50 mg/ml n/a U.S. Pharmex [NLM]
Durandron Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Spain Organon [NLM]
Duratest-100-200 testosterone cypionate 100,200mg/ml 10 ml vial U.S. Roberts [NLM]
Duratest-100-200 testosterone cypionate 100,200 mg/ml 10 ml vial U.S. Hauck [NLM]
Steroid.com
371
Steroid Listings By Trade Name
Durateston Sustanon 250 (testosterone blend) 250 mg/ml 5 ml vial Australia Intervet VET
Durateston 250® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Bolivia Organon
Durateston 250® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Brazil Organon
Dura-Testosterone testosterone enanthate 200 mg/ml 10 ml vial U.S. Pharmex [NLM]
Durathate-200 Injection testosterone enanthate 200 mg/ml n/a U.S. Hauck [NLM]
Durathate-200 Injection testosterone enanthate 200 mg/ml n/a U.S. Roberts [NLM]
Dynabol nandrolone cypionate 50 mg/ml 10ml vial Australia Jurox [NLM] VET
Dynabolin 50 boldenone undecylenate 50 mg/ml 10, 50,100,250ml vial Columbia Kryovet VET
Dynabolon nandrolone undecanoate 80.5 mg/ml 1 ml ampule France Theramex [NLM]
Dynabolon nandrolone undecanoate 80.5 mg/ml 1 ml ampule Italy Farmasister [NLM]
Dynabolon nandrolone undecanoate 80.5 mg/ml 1 ml ampule Italy Foumier
Dynabolon Inj nandrolone decanoate 40 mg/.5 ml 1 ml ampule Korea n/a
Dynasten oxymetholone 50 mg tablet n/a Portugal Cilag [NLM]
Elpihormo nandrolone decanoate 50 mg/ml 1 ml Greece Chemica [NLM]
Enantat QV 250 testosterone enanthate 250 mg/ml 10,50 ml vial Mexico Quality Vet Vet
Enarmon-Depot testosterone enanthate 125 mg/ml n/a Japan Teskoku Hormone
Encephan methandrostenolone 5 mg tablet n/a Japan Sato [NLM]
Equibolin-50 nandrolone phenylpropionate 50 mg/ml n/a U.S. Vortech [NLM]
Equifort boldenone undecylenate 50 mg/ml 10, 50 ml vial Brazil Purina VET
Equi-gan boldenone undecylenate 50 mg/ml 10, 50,100,250 ml vial Mexico Tomel VET
Equilon 100 boldenone (blend) 100 mg/ml 6 ml vial Myanmar/Burma WDV VET
Equipoise® boldenone undecylenate 50 mg/ml 10, 50 ml vial Mexico Fort Dodge VET
Equipoise® boldenone undecylenate 50 mg/ml 50 ml vial U.S. Fort Dodge VET
Equipoise® boldenone undecylenate 25,50 mg/ml 50 ml vial Canada Ciba-Geigy [NLM] VET
Equipoise® boldenone undecylenate 25, 50 mg/ml 50 ml vial Canada Squibb [NLM] VET
Equipoise® boldenone undecylenate 50 mg/ml 50 ml vial Canada Wyeth VET
Equipoise® boldenone undecylenate 25, 50 mg/ml 50 ml vial Mexico Solvay [NLM] VET
Equipoise® boldenone undecylenate 25, 50 mg/ml 50 ml vial Mexico Squibb [NLM] VET
Equipoise® boldenone undecylenate 25. 50 mg/ml 50 ml vial U.S. Squibb [NLM] VET
Equitest 200 testosterone blend (misc) 200 mg/ml 6 ml vial Myanmar/Burma WDV VET
Esiclene formebolone 1 mg drops n/a Italy LPB [NLM]
Esiclene formebolone 2 mg/ml 2 ml ampule Italy LPB [NLM]
Esiclene formebolone 5 mg tablet n/a Italy LPB [NLM]
Esiclene formebolone 1 mg drops n/a Portugal Biofarma [NLM]
Esiclene formebolone 5 mg tablet n/a Portugal Biofarma [NLM]
Estano-Pets stanozolol (oral) 10, 25 mg tablet 100 tablet bottle Mexico Norvet VET
Estigor nandrolone phenylpropionate 10 mg/ml 250ml Argentina Bumet VET
Estrombol stanozolol (inj) 25mg/ml 10 ml vial Argentina Fundacion VET
Evabolin nandrolone phenylpropionate 25 mg/ml 1 ml ampule India Concept
Everone testosterone enanthate 100, 200 mg/ml 10 ml vial U.S. Hyrex [NLM]
Ex-Pois boldenone undecylenate 50 mg/ml 10 ml vial Argentina Agofarma VET
Extraboline nandrolone decanoate 50 mg/ml 2 ml vial Greece Genepharm
Facovit testosterone propionate 1 mg/ml 10 ml vial Italy Teofarma
Fenobolin nandrolone phenylpropionate 20 mg/ml n/a Russia Medexport Russia [NLM]
Ferona fluoxymesterone 1 mg tablet 30 tablet box Argentina Sidus
Fherbolico nandrolone phenylpropionate 50 mg/ml n/a Spain Fher [NLM]
Filybol methylandrostenediol (blend) 70 mg/ml 10, 20 ml vial Australia Ranvet VET
Finaject trenbolone acetate 30 mg/ml n/a France Roussel [NLM] VET
Finajet trenbolone acetate 30 mg/ml 50 ml vial U.S. Hoechst [NLM] VET
Steroid.com
372
Steroid Listings By Trade Name
Finajet trenbolone acetate 30 mg/ml 50 ml vial United Kingdom Hoechst [NLM] VET
Finaplix-H® trenbolone acetate 20 mg pellet 70,100 pellet cartridge Mexico Roussel [NLM] VET
Finaplix-H® trenbolone acetate 20 mg pellet 100 pellet cartridge U.S. Intervet VET
Finaplix-H® 20 trenbolone acetate 20 mg pellet 100 pellet cartridge U.S. Hoechst-Roussel [NLM] VET
Finaplix-S® trenbolone acetate 20 mg pellet 70 pellet cartridge U.S. Hoechst-Roussel [NLM] VET
Floxymesterone fluoxymesterone 5 mg capsule n/a Taiwan Chen Ho
Fluoxymesterone fluoxymesterone 10mg tablet 100 tablet bottle U.S. Rosemont
Fluoxymesterone cap fluoxymesterone 5 mg capsule n/a Taiwan Yuan Chou
Fortabol nandrolone laurate 20 mg/ml 10, 50 ml vial Mexico Parfam VET
Fortadex nandrolone laurate 25, 50 mg/ml n/a Germany Hydro VET
Fosteron fluoxymesterone 5 mg capsule n/a Taiwan Health Chemical
Fu Lao Shu fluoxymesterone 10 mg capsule n/a Taiwan Ming Ta
Fuloan fluoxymesterone 11 mg capsule n/a Taiwan New Chem & Pharm
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial Bolivia Laboratorios VM VET
Ganabol boldenone undecylenate 25, 50 mg/ml 10, 50,100, 250ml vial Bolivia Laboratories VM VET
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial Chile Laboratorios VM VET
Ganabol boldenone undecylenate 25, 50 mg/ml 10,50, 100, 250ml vial Chile Laboratorios VM VET
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial Columbia Laboratorios VM VET
Ganabol boldenone undecylenate 25, 50 mg/ml 10, 50, 100, 250ml vial Columbia Laboratorios VM VET
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial Dom. Republic Laboratorios VM VET
Ganabol boldenone undecylenate 25, 50 mg/ml 10, 50, 100. 250ml vial Dom. Republic Laboratorios VM VET
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial Ecuador Laboratorios VM VET
Ganabol boldenone undecylenate 25, 50 mg/ml 10, 50, 100, 250ml vial Ecuador Laboratorios VM VET
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial El Salvador Laboratorios VM VET
Ganabol boldenone undecylenate 25. 50 mg/ml 10,50, 100, 250ml vial El Salvador Laboratorios VM VET
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial Guatemala Laboratorios VM VET
Ganabol boldenone undecylenate 25, 50 mg/ml 10,50, 100, 250ml vial Guatemala Laboratories VM VET
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial Honduras Laboratories VM VET
Ganabol boldenone undecylenate 25, 50 mg/ml 10, 50,100, 250ml vial Honduras Laboratories VM VET
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial Panama Laboratories VM VET
Ganabol boldenone undecylenate 25, 50 mg/ml 10,50,100. 250ml vial Panama Laboratories VM VET
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial Paraguay Laboratories VM VET
Ganabol boldenone undecylenate 25, 50 mg/ml 10, 50,100, 250ml vial Paraguay Laboratories VM VET
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial Peru Laboratories VM VET
Ganabol boldenone undecylenate 25, 50 mg/ml 10, 50,100, 250ml vial Peru Laboratories VM VET
Ganabol boldenone undecylenate 50 mg/ml 500 ml vial Venezuela Laboratories VM VET
Ganabol boldenone undecylenate 25, 50 mg/ml 10, 50,100, 250ml vial Venezuela Laboratories VM VET
Ganabol methandrostenolone 25 mg/ml 50 ml vial Mexico Salud [NLM] VET
Ganekyl nandrolone phenylpropionate 50 mg/ml 10,100 ml vial Argentina Over Labs VET
Gen Tabs methyltestosterone 2 mg tablet 50, 200 tablet bottle Canada Vetcom VET
Gerabolin nandrolone decanoate 25 mg/ml 1 ml ampule Egypt Nile
Glando Stridox methyltestosterone 10mg tablet 20 tablet box Uruguay Ion
Halotestin® fluoxymesterone 5 mg tablet 50 tablet bottle Canada Pharmacia
Halotestin® fluoxymesterone 5 mg tablet n/a Denmark Upjohn [NLM]
Halotestin® fluoxymesterone 5 mg tablet n/a Finland Upjohn
Halotestin® fluoxymesterone 5 mg tablet n/a France Pharmacia-Upjohn [NLM]
Halotestin® fluoxymesterone 5 mg tablet 20 tablet box Greece Upjohn
Halotestin® fluoxymesterone 5 mg tablet 20 tablet box Italy Upjohn [NLM]
Halotestin® fluoxymesterone 2, 5 mg tablet n/a Japan n/a
Steroid.com
373
Steroid Listings By Trade Name
Halotestin® fluoxymesterone 5 mg tablet n/a Netherlands Upjohn [NLM]
Halotestin® fluoxymesterone 5 mg tablet n/a Norway Upjohn [NLM]
Halotestin® fluoxymesterone 5 mg tablet n/a Philippines Pharmacia & Upjohn
Halotestin® fluoxymesterone 5 mg tablet n/a Sweden Upjohn [NLM]
Halotestin® fluoxymesterone 5 mg tablet 100 tablet bottle Thailand Pharmacia
Halotestin® fluoxymesterone 2,5,10 mg tablet 100 tablet bottle U.S. Pharmacia & Upjohn
Halotestin® fluoxymesterone 10mg tablet 100 tablet bottle U.S. Wamer-Chilcott [NLM]
Halotestin® fluoxymesterone 5 mg tablet n/a YugoslaviaFRMRGalenika [NLM]
Hemogenin oxymetholone 50 mg tablet 10 tablet box Brazil Syntex [NLM]
Hemogenin oxymetholone 50 mg tablet n/a Brazil Aventis
Hemogenin oxymetholone 50 mg tablet 10 tablet box Brazil Sarsa [NLM]
Histerone Injection testosterone suspension 100 mg/ml n/a U.S. Roberts [NLM]
Histerone Injection testosterone suspension 25, 50, 100, mg/ml n/a U.S. Hauck [NLM]
Hormobin methyltestosterone 5 mg tablet 40 tablet box Turkey Munrin Sahin
Hubernol formebolone 5 mg dragee n/a Spain ICN Hubber [NLM]
Hubernol formebolone 1 mg drops n/a Spain ICN Hubber [NLM]
Hybolin methylandrostenediol dipropionate 50 mg/ml n/a U.S. Hyrex [NLM]
Hybolin nandrolone phenylpropionate 25,50 mg/ml n/a U.S. Hyrex [NLM]
Hybolin Decanoate nandrolone decanoate 50, 100 mg/ml 1, 2 ml vial U.S. Hyrex
Hybolin Imp. testosterone propionate 25, 50 mg/ml n/a U.S. Hyrex [NLM]
Hysterone fluoxymesterone 20 mg tablet 100 tablet bottle U.S. Major [NLM]
Implus-H testosterone propionate (implant) 20 mg/pellet n/a U.S. Upjohn
Jebolan nandrolone decanoate 50 mg/ml 1 ml ampule Turkey Etem [NLM]
Jenasteron Inj testosterone enanthate 250 mg/ml n/a Korea n/a
Jenasteron Inj testosterone enanthate 250 mg/ml 1 ml ampule Malaysia Jenahexal
Kanestron oxymetholone 50 mg tablet 100 tablet bottle Mexico Loeffler VET
KangJungBing methyltestosterone n/a n/a Korea n/a
Kicker Tab oxandrolone 2.5 mg tablet n/a Korea n/a
Laudrol LA nandrolone laurate 250 mg/ml 10 ml vial Mexico Loeffler VET
Laura bolin nandrolone laurate 25, 50 mg/ml 10ml vial Australia Intervet VET
Laura bolin nandrolone laurate 50 mg/ml n/a Austria Werffi-Chemie VET
Laura bolin nandrolone laurate 50 mg/ml 10, 50 ml Columbia Intervet VET
Laura bolin nandrolone laurate 20, 50 mg/ml 10, 50 ml vial Mexico Intervet VET
Laurabolin nandrolone laurate 25, 50 mg/ml 5, 10,50ml Germany Vemie VET
Laurabolin V nandrolone laurate 50 mg/ml 10, 50 ml Netherlands Intervet VET
libriol methylandrostenediol (blend) 75 mg/ml 10, 20 ml vial Australia RWR VET
Lipaw fluoxymesterone 10 mg capsule n/a Taiwan Long Der
Lipidex oxandrolone 2.5 mg tablet n/a Brazil Searle [NLM]
Lonavar oxandrolone 2.5 mg tablet 100 tablet bottle Israel BTG
Lonavar oxandrolone 2 mg tablet n/a Japan Dainippon [NLM]
Lonavar oxandrolone 2.5 mg tablet n/a Argentina Searle [NLM]
Long fluoxymesterone 10mg capsule n/a Taiwan Century
Longivol (plus estrogen) methyltestosterone 1 mg tablet n/a Spain Medical S.A.
Macrabone nandrolone phenylpropionate 25 mg/ml n/a Taiwan Ta Fong
Malogen testosterone suspension 100 mg/ml 10ml vial U.S. Forest [NLM]
Malogen Aqueous testosterone suspension 25, 50 mg/ml n/a Canada Germiphene [NLM]
Malogen Cyp testosterone cypionate 100,200 mg/ml 10 ml vial U.S. Forest [NLM]
Malogen In Oil testosterone propionate 100 mg/ml 10 ml vial Canada Germiphene [NLM]
Malogex LA200 testosterone enanthate 200 mg/ml 10 ml vial Canada Germiphene [NLM]
Steroid.com
374
Steroid Listings By Trade Name
Malotrone testosterone suspension 100 mg/ml 20 ml vial U.S. Bluco [NLM]
Masterid drostanolone propionate 100 mg/2ml 2 ml amp Germany Gruenthal [NLM]
Masteril drostanolone propionate 100 mg/2ml 2 ml ampule Bulgaria Syntex [NLM]
Masteril drostanolone propionate 100 mg/2ml 2 ml amp United Kingdom Syntex [NLM]
Masteron drostanolone propionate 100 mg/2ml 2 ml amp Belgium Sarva-Syntex [NLM]
Masteron drostanolone propionate 100 mg/2ml 2 ml amp Portugal Cilag [NLM]
Mastisol drostanolone propionate 5% injection sol. n/a Japan Shionogi [NLM]
Matogen 100/200 L.A. testosterone enanthate 100,200 mg/ml 10 ml vial U.S. Forest [NLM]
Maxibolin ethylestrenol 2 mg tablet n/a U.S. Organon [NLM]
Maxibolin Elixir ethylestrenol 2mg/5ml n/a U.S. Organon [NLM]
Maxigan boldenone undecylenate 50 mg/ml 10, 50 ml vial Mexico Inpei VET
Mediatric methyltestosterone 10mg tablet n/a U.S. Wyeth-Ayerst [NLM]
Megagrisevit-Mono clostebol acetate 15 mg dragee 30 dragee box Germany Pharmacia [NLM]
Megagrisevit-Mono clostebol acetate 10mg/1.5ml 1.5 ml vial Germany Pharmacia [NLM]
Melic methandrostenolone 5 mg tablet 1000 tablet box, bottle Thailand Phanmasant
Menabol stanozolol (oral) 5 mg tablet 100 tablet box India n/a
Menabolin nandrolone phenylpropionate 25 mg/ml 1 ml ampule Egypt Theramex / Memphis
Mesterolon mesterolone 25 mg tablet n/a Philippines Brown & Burk
Mesterolon mesterolone 25 mg tablet n/a Sweden Schering [NLM]
Mesteron methyltestosterone 10mg tablet n/a Poland Jelfa [NLM]
Mestoranum mesterolone 25 mg tablet n/a Denmark Schering
Mestoranum mesterolone 25 mg tablet n/a Norway Sobering [NLM]
Metabol nandrolone phenylpropionate 25 mg/ml 1 ml ampule India Jagsonpal
Metabolin nandrolone phenylpropionate 25 mg/ml n/a Taiwan Metro
Metaboline methandrostenolone 2 mg tablet 60, 500 tablet bottle Canada Desbergers [NLM]
Metabolon 25 methenolone acetate 25 mg tablet 100 tablet bottle Mexico Bratis Labs VET
Metadec nandrolone decanoate 25, 50 mg/ml 1 ml ampule India Jagsonpal
Metanabol methandrostenolone 5 mg tablet 20 tablet box Poland Jelfa
Metanabol methandrostenolone 5 mg tablet 20 tablet box Poland Polfa [NLM]
Metanabol methandrostenolone I mg tablet 20 tablet box Poland Polfa [NLM]
Metanabol methandrostenolone 0.5% cream n/a Poland Polfa [NLM]
Metandiabol methandrostenolone 25 mg/ml 50 ml vial Mexico Quimper VET
Metandienon methandrostenolone 5 mg tablet 100 tablet box Russia Bioreaktor
Metandren methyltestosterone 5 mg sub. dragee n/a U.S. Ciba [NLM]
Metandren methyltestosterone 10, 25 mg tablet n/a U.S. Ciba [NLM]
Metandren methyltestosterone 10, 25 mg tablet 100 tablet bottle U.S. Novartis [NLM]
Metandrol 10 methandrostenolone 10mg tablet 500 tablet bottle Mexico Bratis Labs VET
Metandrostenolon methandrostenolone 5 mg tablet 100 tablet box Russia Akrihin [NLM]
Metandrostenolon methandrostenolone 5 mg tablet 100 tablet box Russia Akrikhin
Metandrostenolon methandrostenolone 5 mg tablet 100 tablet box Russia Bioreaktor [NLM]
Metesto methyltestosterone 25 mg tablet 100 tablet bottle Thailand Acdhon
Methanabol methandrostenolone 5 mg tablet 500 tablet pouch Thailand British Dragon
Methanabol methandrostenolone 50 mg tablet 100 tablet pouch Thailand British Dragon
Methandienone methandrostenolone 5, 10mg tablet 100,1000 tablet bottle Mexico Ttokkyo VET
Methandon methandrostenolone 5 mg tablet 1000 tablet bottle Thailand Acdhon Co.
Methandriol methylandrostenediol dipropionate 75 mg/ml 10 ml vial Australia Ilium/Troy [NLM] VET
Methandriol Dipropionate Methandriol Dipropionate 75mg/ml 10ml vial Thailand British Dragon
Methasus 50 methylandrostenediol dipropionate 50 mg/ml 20 ml vial Australia Jurox [NLM] VET
Methyldiol methylandrostenediol 2 mg tablet n/a U.S. Vortech [NLM]
Steroid.com
375
Steroid Listings By Trade Name
Methyldiol Aqueous methylandrostenediol 50mg/ml n/a U.S. Vortech [NLM]
Methyltestosterone methyltestosterone 10 mg tablet n/a U.S. Goldline [NLM]
Methyltestosterone methyltestosterone 10mg tablet n/a U.S. Global
Metil Testosteron methyltestosterone 10mg tablet 50 tablet box Rumania Terapia
Metil Thomsina S methyltestosterone 10 mg tablet 20 tablet box Uruguay Celsius
Metil-Test methyltestosterone 50 mg tablet 100 tablet bottle Mexico Brovel VET
Metiltestosterona methyltestosterone n/a n/a Paraguay Botica
Metormon drostanolone propionate 100 mg/2ml 2 ml amp Spain Syntex [NLM]
Metyandrostendiol methylandrostenediol 10, 25 mg tablet n/a Poland Jelfa [NLM]
mibolerone drops mibolerone 100 meg/ml 55 mg bottle U.S. Wedgewood VET
Miotolan furazabol 1 mg tablet n/a Japan Daiichi Seiyaku [NLM]
Miro Depo testosterone cypionate 125 mg/ml 2 ml vial Korea Hanil Pharm
Mitgan 50 boldenone undecylenate 50 mg/ml 50 ml vial Columbia California VET
Myobolin nandrolone decanoate 25 mg/ml 1 ml ampule India Troikaa
Nabolic stanozolol (inj) 2mg/ml 50 ml vial Argentina Chinfield Ind. VET
Nabolic Strong stanozolol (inj) 25mg/ml 50 ml vial Argentina Chinfield Ind. VET
Nandoral ethylestrenol .5 mg tablet 100, 500 tablet bottle Australia Intervet VET
Nandrobolic nandrolone phenylpropionate 25 mg/ml n/a U.S. Forest [NLM]
Nandrobolic L.A. nandrolone decanoate 100 mg/ml 1 , 2 ml vial U.S. Forest [NLM]
Nandrolin nandrolone phenylpropionate 50 mg/ml 25 ml vial Australia Intervet VET
Nandrolin nandrolone phenylpropionate 25 mg/ml 10 ml vial Australia Intervet VET
Nandrolona 300 L.A. nandrolone decanoate 300mg/ml 10ml vial Mexico Ttokkyo VET
nandrolona decanoato nandrolone decanoate 50 mg/ml 1 ml ampule Chile Chile
nandrolone decanoate nandrolone decanoate 200 mg/2ml 2 ml vial Greece Norma Hellas
nandrolone decanoate nandrolone decanoate 100mg/ml 1,2 ml vial U.S. Lyphomed [NLM]
nandrolone decanoate nandrolone decanoate I00mg/ml 1, 2 ml vial U.S. Quad [NLM]
nandrolone decanoate nandrolone decanoate 50, 100, 200 mg/ml 1, 2 ml vial U.S. Steris [NLM]
Nandrolone Decanoate Inj nandrolone decanoate 100 mg/ml 2 ml vial U.S. Watson Pharma
Nandrolone Decanoate Inj nandrolone decanoate 200 mg/ml 1 ml vial U.S. Watson Pharma
nandrolone phenylpropionate nandrolone phenylpropionate 50,100mg/ml 2 ml vial India Hayrian Biotogicals [NLM]
nandrolone phenylpropionate nandrolone phenylpropionate 50 mg/ml n/a U.S. Quad [NLM]
Nandrosande nandrolone decanoate 25.50, 100 mg/ml 1 ml ampule Chile Sanderson
Nannismon Depot testosterone cypionate 50,100 mg/ml n/a Taiwan Chi Sheng
Nansmon Depot testosterone propionate 25 mg/ml n/a Taiwan Chi Sheng
Naposim methandrostenolone 5 mg tablet 20 tablet box Rumania Terapia
Neo Aphro methyltestosterone 5 mg tablet 30 tablet Egypt Misr
Neo-Anabolene methandrostenolone 5 mg tablet 10 tablet strip Indonesia Haurus
Neo-Durabolic nandrolone decanoate 100, 200 mg/ml 1, 2 ml vial U.S. Hauck [NLM]
Neo-Hombreol testosterone propionate 50 mg/ml n/a Netherlands Organon [NLM]
Neotest 250 testosterone decanoate 250 mg/ml 10 ml bottle Mexico Loeffler
Nerobol methandrostenolone 5 mg tablet 20 tablet box Bulgaria Gedeon Richter [NLM]
Nerobol methandrostenolone 5 mg tablet 20 tablet box Hungary Gedeon Richter [NLM]
Nerobol methandrostenolone 5 mg tablet 20 tablet box Yugoslavia/FRMRGalenika [NLM]
Nerobolil nandrolone phenylpropionate 25 mg/ml 1 ml ampule Bulgaria Godeon Richter [NLM]
Nerobolil nandrolone phenylpropionate 25 mg/ml n/a Hungary Godeon Richter [NLM]
Neurabol stanozolol (oral) 2 mg capsule 10 capsule box India Cadila
Neurabol Inj nandrolone phenylpropionate 25 mg/ml 1 ml ampule India Cadila
Neurophen nandrolone phenylpropionate 25 mg/ml 1 ml ampule India Ind-Swift
Nilevar norethandrolone 10mg tablet 30 tablet bottle France Searle
Steroid.com
376
Steroid Listings By Trade Name
Nilevar norethandrolone 10mg tablet 30 tablet bottle Switzerland Searie [NLM]
Nilevar norethandrolone 10 mg tablet 100 tablet bottle U.S. Searle
Nitrotain ethylestrenol 15mg/4gram 60, 250,1000 gram tube Australia Nature-Vet VET
Norabon nandrolone phenylpropionate 25 mg/ml 1 ml ampule Thailand Phihalab
Norandren nandrolone decanoate 50, 200 mg/ml 10, 50ml vial Mexico Brovel VET
Novandrol methylandrostenediol 10, 25 mg dragee n/a Yugoslavia/FRMRGalenika [NLM]
Nu-Bolic nandrolone phenylpropionate 25 mg/ml n/a U.S. Seatrace [NLM]
Nurezan nandrolone decanoate 50 mg/ml 1 ml ampule Greece Rafarm
Nuvir testosterone undecanoate 40 mg capsules 30 capsule bottle India Organon
ODK fluoxymesterone 5 mg capsule n/a Taiwan Winston
Omnadren Omnadren (testosterone blend) 250 mg/ml 1 ml ampule Poland Jelfa
Omnadren Omnadren (testosterone blend) 250 mg/ml 1ml ampule Poland Polfa [NLM]
Omnadren 250 Omnadren (testosterone blend) 250mg/ml 1 ml ampule Bulgaria Jelfa
Orabol-H ethylestrenol 100 mg/5g paste 30 ml plastic tube Australia Vetsearch [NLM] VET
Orabolin® ethylestrenol 2 mg tablet n/a Belgium Organon [NLM]
Orabolin® ethylestrenol 2 mg tablet 10 tablet box India Infar
Orabolin® ethylestrenol 2 mg tablet 100 tablet box Pakistan Organon
Orabolin® ethylestrenol 2 mg tablet n/a South Africa Donmed/Organon [NLM]
Orabolin® ethylestrenol 2 mg tablet n/a United Kingdom Organon [NLM]
Oralsterone fluoxymesterone 5 mg capsule n/a Taiwan Long Der
Ora-Testryl fluoxymesterone 5 mg tablet 100 tablet bottle U.S. Squibb Mark [NLM]
Oreton methyltestosterone n/a n/a Venezuela n/a
Oreton testosterone propionate 25 mg/ml n/a Mexico Goldline [NLM]
Oreton Methyl methyltestosterone 10 mg sub. tablet n/a U.S. Schering [NLM]
Oreton Methyl methyltestosterone 10mg tablet n/a U.S. Schering [NLM]
Orgabolin ethylestrenol 2 mg tablet n/a Indonesia Organon
Orgabolin ethytestrenol 2 mg tablet n/a Netherlands Organon [NLM]
Orgabolin ethytestrenol 2 mg tablet n/a Turkey Santa [NLM]
Orgabolin Drops ethytestrenol 2mg n/a Turkey Santa [NLM]
Oxafort oxandrolone 5 mg tablet 100 tablet bottle Mexico Loeffler VET
Oxanabol oxandrolone 5 mg tablet 100 tablet pouch Thailand British Dragon
Oxandrin® oxandrolone 2.5,10 mg tablet 100 tablet bottle U.S. BTG
Oxandrolone oxandrolone 5 mg tablet 30 tablet bottle Belize Planet Pharmacy
Oxandrolone oxandrolone 2.5 tablet 100 tablet bottle Mexico Ttokkyo [NLM] VET
Oxandrolone oxandrolone 5 mg tablet 100 tablet bottle Mexico Ttokkyo VET
Oxandrolone 10 oxandrolone 10 mg tablet 100 tablet bottle Mexico Bratis Labs VET
Oxandrolone SPA oxandrolone 2.5 mg tablet 30 tablet box Italy SPA [NLM]
Oxandrolone SPA (Export) oxandrolone 2.5 mg tablet 30 tablet box Italy SPA
Oxandrovet oxandrolone 5 mg tablet 100 tablet bottle Mexico Denkall VET
Oximetalon oxymetholone 75 mg tablet 100 tablet bottle Mexico Denkall VET
Oxitosona 5O oxymetholone 50 mg tablet 100 tablet box Spain Syntex [NLM]
Oxitron 5O oxymetholone 50 mg tablet 100 tablet bottte Mexico Bratis Labs VET
Oxybolone oxymetholone 50 mg tablet 20 tablet box Greece Genapharm
Oxydrol oxymetholone 100 mg tablet 50 tablet pouch Thailand British Dragon
Oxylone oxymetholone 50 mg tablet 100 tablet bottle Malaysia Duopharma
Oxymetholone oxymetholone 50 mg tablet 30 tablet bottle Belize Planet Pharmacy
Oxymetholone oxymetholone 50 mg tablet n/a Malaysia Sime Darby
Oxymetholone oxymetholone 50 mg tablet 100 tablet pouch Thailand British Dispensary
Oxymetholone Dongindang oxymetholone n/a n/a Korea Dongindang
Steroid.com
377
Steroid Listings By Trade Name
Oxymetholone HanBul oxymetholone 50 mg tablet n/a Korea HanBul
Oxymetholone HanSeo oxymetholone 50 mg tablet 100 tablet bottle Korea HanSeo
Oxymetholone Korea United oxymetholone 50 mg tablet n/a Korea Korea United
Oxymetholone Miverva oxymetholone 50 mg tablet 100 tablet Greece Minerva [NLM]
Oxymetolona 50 oxymetholone 50 mg tablet 100 tablet bottle Mexico Ttokkyo VET
Oxytone 50 oxymetholone 50 mg tablet 100 tablet bottle Thailand SB Laboratories
Panteston testosterone undecanoate 40 mg capsules 60 capsule bottle Finland Organon
Panteston testosterone undecanoate 40 mg capsules n/a Latvia Organon
Panteston testosterone undecanoate 40 mg capsules n/a Lithuania Organon
Panteston testosterone undecanoate 40 mg capsules 30,60 capsule bottle Peru Organon
Panteston capsules testosterone undecanoate 40 mg capsules n/a New Zealand Organon
Pantestone testosterone undecanoate 40 mg capsules 60 capsule bottle Estonia Organon
Pantestone testosterone undecanoate 40 mg capsules 60 capsule bottle France Organon
Parabolan trenbolone hexahydrobenzytearbonate 76 mg/1.5 ml 1.5 ml ampule France Negma [NLM]
Parabolan Tabs (Export) trenbolone acetate 25 mg tablet 20 tablet pouch Thailand British Dragon
Permastril drostanolone propionate 100 mg/2ml 2 ml ampule France Cassenne [NLM]
Plenastril oxymetholone 50 mg tablet n/a Switzerland Proto chemie [NLM]
Pluriviron mesterolone 25 mg dragee 30 dragee box Germany Asche [NLM]
PMS-Testosterone Enanthate testosterone enanthate 200 mg/ml 10 ml vial Canada Pharmascience
Polysteron 250 Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Venezuela Organon
Porkybol 1% boldenone undecylenate 10 mg/ml 10, 50,100 ml vial Columbia Compania California VET
Primobolan Depot methenolone enanthate 100 mg/ml 1 ml ampule Egypt Schering/CID [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a Austria Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a Belgium Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a Bolivia Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a Costa Rica Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a Dom. Rep. Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a Ecuador Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a El Salvador Schering [NLM]
Primobolan® methenolone acetate 50 mg tablet n/a France Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a Germany Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a Guatemala Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a Honduras Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet 100,1000 tablet box Japan Schering
Primobolan® methenolone acetate 5 mg tablet n/a Mexico Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a Nicaragua Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a Panama Schering [NLM]
Primobolan® methenolone acetate 5 mg tablet n/a South Africa Schering/Berlimed [NLM]
Primobolan® Acetate methenolone acetate 25 mg/ml 1 ml ampule Germany Schering [NLM]
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Austria Schering [NLM]
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Belgium Schering [NLM]
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Czech. Rep. Schering [NLM]
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Ecuador Schering
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule France Schering [NLM]
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Germany Schering [NLM]
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Greece Schering [NLM]
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Guatemala Schering
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Italy Schering [NLM]
Primobolan® Depot methenolone enanthate 50 mg/ml 1 ml ampule Japan Schering [NLM]
Steroid.com
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Steroid Listings By Trade Name
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Japan Schering
Primobolan® Depot methenolone enanthate 50 mg/ml 1 ml ampule Mexico Schering
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Paraguay Schering
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Portugal Schering [NLM]
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule South Africa Schering/Berlimed [NLM]
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Spain Schering
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Switzerland Schering [NLM]
Primobolan® Depot methenolone enanthate 100 mg/ml 1 ml ampule Turkey Schering
Primobolan® Depot mite methenolone enanthate 50 mg/ml 1 ml ampule Germany Schering [NLM]
Primobolan® S methenolone acetate 25 mg tablet n/a Finland Leiras [NLM]
Primobolan® S methenolone acetate 25 mg tablet n/a Germany Schering [NLM]
Primobolan® S methenolone acetate 25 mg tablet n/a Netherlands Schering [NLM]
Primobolan® S methenolone acetate 25 mg tablet 50 tablet bottle South Africa Schering/Berlimed
Primobolan® S methenolone acetate 25 mg tablet n/a Thailand Schering [NLM]
Primoniat®-Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Chile Schering-Chile [NLM]
Primoniat®-Depot 250 testosterone enanthate 250 mg/ml 1 ml ampule Chile Schering-Chile [NLM]
Primo-Plus 100 methenolone enanthate 100mg/ml 1 ml ampule Mexico Ttokkyo VET
Primo-Plus 50 methenolone acetate 50 mg tablet 100 tablet bottle Mexico Ttokkyo VET
Primoteston Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Australia Schering [NLM]
Primoteston Depot 50 Testoviron (testosterone blend) 75 mg/ml 1 ml ampule Australia Schering [NLM]
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Egypt Schering/CID
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Finland Leiras [NLM]
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Norway Schering
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule United Kingdom Sobering [NLM]
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Australia Schering Vet
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Ecuador Schering
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Guatemala Schering
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Jordan Schering
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Kuwait Schering [NLM]
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Mauritius Schering
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Mexico Schering
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml syringe New Zealand Schering
Primoteston®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Sudan Schering
Primoteston®-Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Egypt Schering/CID
Progro-H (plus estradiol) testosterone propionate (implant) 20 mg/pellet n/a Australia Pro Beef VET
Pronabol-5 methandrostenolone 5 mg tablet 100 tablet box India P&B Labs [NLM]
Propionat QV 1OO testosterone propionate 100 mg/ml 10 ml vial Mexico Quality Vet VET
Propionato de Testosterona testosterone propionate 25 mg/ml 20 ml vial Argentina Induvet VET
Protabol methylandrostenediol dipropionate 75 mg/ml 10 ml vial Australia Protabol VET
Protosin Inj nandrolone phenylpropionate 25 mg/ml n/a Taiwan Astar
Proviron mesterolone 25 mg tablet 20 tablet box Algeria Schering
Proviron mesterolone 25 mg tablet 50 tablet box Taiwan Schering
Proviron mesterolone 25 mg tablet 20 tablet box Turkey Schering
Proviron® mesterolone 25 mg tablet n/a Argentina Schering
Proviron® mesterolone 25, 50 mg tablet n/a Australia Schering
Proviron® mesterolone 25 mg tablet 50 tablet bottle Austria Schering
Proviron® mesterolone 25 mg tablet 50 tablet bottle Belgium Schering
Proviron® mesterolone 25 mg tablet 20 tablet box Brazil Schering
Proviron® mesterolone 25 mg tablet 20, 50 tablet box Bulgaria Schering
Steroid.com
379
Steroid Listings By Trade Name
Proviron® mesterolone 25 mg tablet 20 tablet box Colombia Schering
Proviron® mesterolone 25 mg tablet n/a Costa Rica Schering
Proviron® mesterolone 25 mg tablet 20 tablet box Croatia Schering
Proviron® mesterolone 25 mg tablet 20, 50 tablet box Czech. Rep. Schering
Proviron® mesterolone 25 mg tablet 20 tablet bottle Dom. Rep. Schering
Proviron® mesterolone 25 mg tablet 20 tablet box Egypt Schering/CID [NLM]
Proviron® mesterolone 25 mg tablet n/a El Salvador Schering
Proviron® mesterolone 25 mg tablet 20 tablet box Estonia Schering [NLM]
Proviron® mesterolone 25 mg tablet n/a Finland Leiras
Proviron® mesterolone 25 mg tablet n/a France Schering [NLM]
Proviron® mesterolone 25 mg tablet 50 tablet bottle Germany Schering [NLM]
Proviron® mesterolone 25 mg tablet 20 tablet bottle Greece Schering
Proviron® mesterolone 25 mg tablet n/a Guatemala Schering
Proviron® mesterolone 25 mg tablet n/a Honduras Schering
Proviron® mesterolone 25 mg tablet 10, 15, 20, 50, 100, 150 tab bottle Hungary Schering
Proviron® mesterolone 25 mg tablet 30 tablet box India Schering
Proviron® mesterolone 25 mg tablet n/a Indonesia Schering
Proviron® mesterolone 25 mg tablet 20, 50 tablet box Israel Schering
Proviron® mesterolone 25 mg tablet 20 tablet box Italy Schering
Proviron® mesterolone 25 mg tablet 20 tablet box Latvia Schering [NLM]
Proviron® mesterolone 25 mg tablet 20 tablet box Lithuania Schering [NLM]
Proviron® mesterolone 25 mg tablet 10 tablet box Mexico Schering
Proviron® mesterolone 25 mg tablet 50 tablet bottle Netherlands Schering
Proviron® mesterolone 25 mg tablet n/a Nicaragua Schering
Proviron® mesterolone 25 mg tablet n/a Panama Schering
Proviron® mesterolone 25 mg tablet 20 tablet box Paraguay Schering
Proviron® mesterolone 25 mg tablet 20 tablet box Poland Schering
Proviron® mesterolone 25 mg tablet 20 tablet box Portugal Schering
Proviron® mesterolone 25 mg tablet 20 tablet bottle Russia Schering
Proviron® mesterolone 25 mg tablet 20, 50 tablet bottle Slovakia Schering
Proviron® mesterolone 25 mg tablet 20, 100 tablet bottle South Africa Schering/Beriimed
Proviron® mesterolone 25 mg tablet 20 tablet box Spain Schering
Proviron® mesterolone 25 mg tablet n/a Switzerland Schering [NLM]
Proviron® mesterolone 25 mg tablet 20 tablet box Ukraine Schering
Proviron® mesterolone 25 mg tablet 30 tablet box United Kingdom Schering
Proviron® mesterolone 25 mg tablet n/a Uruguay Schering
Proviron® mesterolone 25 mg tablet 15 tablet box Venezuela Schering
Proviron® mesterolone 25 mg tablet n/a Yugoslavia FRMRAlkoid
Proviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Venezuela Schering
Provironum mesterolone 25 mg tablet 50 tablet box Singapore Organon
Provironum mesterolone 25 mg tablet 150 tablet box Thailand Schering
Psychobolan nandrolone undecanoate 80.5 mg/ml 1 ml ampule Greece Theramex [NLM]
Ptenastril oxymetholone 50 mg tablet n/a Austria Grunenthal [NLM]
Reforvit methandrostenolone 25 mg tab 100, 300 tablet bottle Mexico Loeffler VET
Reforvit-B methandrostenolone 25mg/ml 10, 50ml Mexico Loeffler VET
Restandol testosterone undecanoate 40 mg capsules 60 capsule bottle Denmark Organon
Restandol testosterone undecanoate 40 mg capsules 60 capsule bottle Greece Organon
Restandol testosterone undecanoate 40 mg capsules n/a Taiwan Organon
Restandol testosterone undecanoate 40 mg capsules 28, 56 capsule box United Kingdom Organon
Steroid.com
380
Steroid Listings By Trade Name
Restauvit methandrostenolone 2 mg tablet n/a Mexico Ciba, Rugby [NLM]
Restore mesterolone 25 mg tablet 20 tablet box India Brown & Burk
Retabolil nandrolone decanoate 25, 50 mg/ml 1 ml ampule Bulgaria Gedeon Richter [NLM]
Retabolil nandrolone decanoate 50 mg/ml 1 ml ampule Egypt Medimpex/Alxndria
Retabolil nandrolone decanoate 50 mg/ml 1 ml ampule Estonia Gedeon Richter
Retabolil nandrolone decanoate 25, 50 mg/ml 1 ml ampule Hungary Gedeon Richter
Retabolil nandrolone decanoate 25, 50 mg/ml 1 ml ampule Malaysia Gedeon Richter
Retabolin nandrolone decanoate 50 mg/ml 1 ml ampule Russia Medexport Russia [NLM]
Revator-200 (plus estradiol) trenbolone acetate 20 mg pellet 100 pellet cartridge U.S. Intervet VET
Revator-G (plus estradiol) trenbolone acetate 20 mg pellet 20 pellet cartridge U.S. Intervet VET
Revator-H (plus estradiol) trenbolone acetate 20 mg pellet 70 pellet cartridge U.S. Intervet VET
Revator-H (plus estradiol) trenbolone acetate 20 mg pellet 70 pellet cartridge Canada Intervet VET
Revator-H (plus estradiol) trenbolone acetate 20 mg pellet 70 pellet cartridge U.S. Hoechst-Roussel [NLM] VET
Revator-IH (plus estradiol) trenbolone acetate 20 mg pellet 40 pellet cartridge U.S. Intervet VET
Revator-IS (plus estradiol) trenbolone acetate 20 mg pellet 40 pellet cartridge U.S. Intervet VET
Revator-S (plus estradiol) trenbolone acetate 20 mg pellet 60 pellet cartridge U.S. Hoechst-Roussel [NLM] VET
Revator-S (plus estradiol) trenbolone acetate 20 mg pellet 60 pellet cartridge Canada Intervet VET
Revator-S (plus estradiol) trenbolone acetate 20 mg pellet 60 pellet cartridge U.S. Intervet VET
Ridrot Testosterone Inj. testosterone cypionate 75 mg/ml 250 ml vial Australia Troy VET
Roboral oxymetholone 50 mg tablet 100 tablets Israel Abic/Ramat-Gan [NLM]
Ropel Liquid Testosterone testosterone enanthate 75 mg/ml 200 ml vial Australia Jurox
Ropel Testosterone Pellets testosterone (implant) 23.5 mg pellet 450,600 pellet bottle Australia Jurox VET
Rubolin nandrolone phenylpropionate 25 mg/ml n/a Taiwan Ying Yuan
RWR Deca 50 nandrolone decanoate 50 mg/ml 10 ml vial Australia RWR VET
RWR Suspension testosterone suspension 25, 50, 100, mg/ml n/a Australia RWR VET
Sanabolicum nandrolone cyclohexylpropionate 25, 50 mg/ml 1 ml ampule Egypt Biochemie/Nile
Sanabolicum-Vet nandrolone cyclohexylpropionate 50mg/ml 10 ml vial Austria Werfft-Chemie VET
Scheinpharma Testone-Cyp testosterone cypionate 100 mg/ml 10 ml vial Canada Schein
Seidon stanozolol (oral) 2 mg tablet 100 tablet box Korea Seoul Pharm
Sidomon fluoxymesterone 5 mg capsule n/a Taiwan n/a
Silabolin ethytestrenol 25. 50 mg/ml 1 ml ampule Russia Farmadon [NLM]
Sinbolin nandrolone phenylpropionate 25 mg/ml n/a Taiwan Sinton
Sostenon 250® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Mexico Organon
Sostenon 250® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Spain Organon [NLM]
Spectriol methylandrostenediol (blend) 65 mg/ml 10 ml vial Australia RWR VET
Stabon stanozolol (oral) 2 mg tablet n/a Korea n/a
Stan QV 100 stanozolol (inj) 100mg/ml 20 ml vial Mexico Quality Vet VET
Stan QV 50 stanozolol (inj) 50mg/ml 20 ml vial Mexico Quality Vet VET
Stanabol stanozolol (oral) 5 mg tablet 250 tablet pouch Thailand British Dragon
Stanabol stanozolol (oral) 5 mg tablet 200,1000 tablet bottle Thailand British Dragon
Stanabol stanozolol (oral) 5 mg tablet 200 tablet pouch Thailand British Dragon
Stanabol stanozolol (oral) 50 mg tablet 100 tablet pouch Thailand British Dragon
Stanabolic stanozolol (inj) 50mg/ml 20 ml vial Australia Ilium/Troy VET
Stanazol stanozolol (inj) 50mg/ml 20, 50 ml vial Australia RWR [NLM] VET
Stanazolic stanozolol (inj) 50, 100mg/ml 20ml, 10ml vial Mexico Denkall VET
Stanazolic stanozolol (oral) 6mgcap 300 capsule bottle Mexico Denkall VET
Stanazolic stanozolol (oral) 10 mg tablet 100 tablet bottle Mexico Denkall VET
Stand-V stanozolol (inj) 50, 100 mg/ml 20 ml vial Mexico Ttokkyo VET
Stanol stanozolol (oral) 2 mg tablet n/a Taiwan Hua Shin
Steroid.com
381
Steroid Listings By Trade Name
Stanol stanozolol (oral) 5 mg tablet 200 tablet bottle Thailand Body Research
Stanol 10 stanozolol (oral) 10mg tablet 250 tablet bottle Mexico BratisLabs VET
Stanol 50 stanozolol (inj) 50mg/ml 20 ml vial Mexico BratisLabs VET
Stanol-V stanozolol (oral) 10 mg tablet 100,500 tablet bottte Mexico Ttokkyo VET
Stanosus stanozolol (inj) 50mg/ml 20 ml vial Australia Jurox [NLM] VET
Stanozodon stanozolol (oral) 2 mg tablet 1000 tablet bottte Thailand AcdhonCo.
stanozolol stanozolol (oral) 25 mg tablet 30 tablet bottle Belize Planet Pharmacy
stanozolol stanozolol (oral) 2 mg tablet n/a Taiwan Chen Ho
stanozolol Tab stanozolol (oral) 5 mg tablet 30 tablet box Greece Genepharm
Stanzol stanozolol (oral) 5 mg tablet 200 tablet bottle Thailand SB Laboratories
Sten Sten (testosterone blend) 50mg/ml 2 ml ampule Mexico Atlantis
Stenolon methandrostenolone 5 mg tablet 20 tablet box Czech. Rep. Leciva [NLM]
Stenolon methandrostenolone 1 mg tablet 20 tablet box Czech. Rep. Leciva [NLM]
Stenox fluoxymesterone 2.5 mg tablet 20 tablet box Mexico Atlantis
Steranabol clostebol acetate 20 mg/ml 2 ml ampule Italy Farmitalia [NLM]
Steranabol Ritardo oxabolone cypionate 12.5 mg/ml 2 ml ampule Italy Pharmacia & Upjohn [NLM]
Sterobolin nandrolone decanoate 50 mg/ml 1 ml ampule Finland Orion [NLM]
Stromba stanozolol (inj) 50 mg/ml n/a United Kingdom Sterling Research [NLM]
Stromba stanozolol (inj) 50 mg/ml n/a Sweden Sterling- Winthrop [NLM]
Stromba stanozolol (inj) 50 mg/ml n/a Sweden Winthrop [NLM]
Stromba stanozolol (oral) 5 mg tablet 10 tablet box Belgium Winthrop [NLM]
Stromba stanozolol (oral) 5 mg tablet 56 tablet box Greece n/a
Stromba stanozolol (oral) 5 mg tablet n/a Hungary Sterling-Health
Stromba stanozolol (oral) 5 mg tablet n/a Austria Berger [NLM]
Stromba stanozolol (oral) 5 mg tablet n/a Czech. Rep. Sterling-Health [NLM]
Stromba stanozolol (oral) 5 mg tablet n/a Denmark Winthrop [NLM]
Stromba stanozolol (oral) 5 mg tablet n/a Germany Winthrop [NLM]
Stromba stanozolol (oral) 5 mg tablet 100 tablet box Netherlands Sanofi
Stromba stanozolol (oral) 5 mg tablet n/a Netherlands Winthrop [NLM]
Stromba stanozolol (oral) 5 mg tablet n/a Sweden Winthrop [NLM]
Stromba stanozolol (oral) 5 mg tablet n/a Switzerland Winthrop [NLM]
Stromba stanozolol (oral) 5 mg tablet n/a United Kingdom Sanofi [NLM]
Stromba stanozolol (oral) 5 mg tablet n/a United Kingdom Sterling [NLM]
Strombaject stanozolol (inj) 50 mg/ml n/a Belgium Winthrop [NLM]
Strombaject stanozolol (inj) 50 mg/ml n/a Germany Winthrop [NLM]
Sunamon Depot Inj testosterone enanthate 130 mg/ml n/a Taiwan Astar
Sunamon Inj testosterone enanthate 250 mg/ml n/a Taiwan Astar
Super Test-250 Sustanon 250 (testosterone blend) 250 mg/ml 5,10 ml vial Mexico Tomel VET
Superanabolon nandrolone phenylpropionate 25 mg/ml 1 ml ampule Czech. Rep. Spofa
Superbolin methylandrostenediol dipropionate 75 mg/ml 10 ml vial Australia Vetsearch VET
Sustanon Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Ireland Organon
Sustanon Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Israel Organon
Sustanon Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Slovakia Organon
Sustanon "250" Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Argentina Organon
Sustanon "250" Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Indonesia Organon
Sustanon "250" Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Singapore Organon
Sustanon "250" Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Vietnam Organon
Sustanon (Cyctahoh 250) Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Russia Organon
Sustanon (Cyctahoh) Sustanon 100 (testosterone blend) 100mg/ml 1 ml ampule India Infer
Steroid.com
382
Steroid Listings By Trade Name
Sustanon 100 Sustanon 100 (testosterone blend) 100 mg/ml 1 ml ampule Germany Organon [NLM]
Sustanon '100'® Sustanon 100 (testosterone blend) 100mg/ml 1 ml ampule Egypt Organon/Nile
Sustanon '100'® Sustanon 100 (testosterone blend) 100 mg/ml 1 ml ampule Netherlands Organon
Sustanon '100'® Sustanon 100 (testosterone blend) 100 mg/ml 1 ml ampule United Kingdom Organon
Sustanon 250 Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Czech. Rep. Organon
Sustanon 250 Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Germany Organon [NLM]
Sustanon 250 Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule New Zealand Organon
Sustanon 250 Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Taiwan Organon
Sustanon 250 (Cyctahon) Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule India Infar
Sustanon 250® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Belgium Organon
Sustanon 250® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Estonia Organon
Sustanon 250® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Finland Organon
Sustanon 250® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Netherlands Organon
Sustanon 250® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Turkey Organon
Sustanon '250'® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Egypt Organon/Nile
Sustanon '250'® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Malaysia Organon
Sustanon '250'® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Pakistan Organon
Sustanon '250'® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule South Africa Donmed/Organon
Sustanon '250'® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Thailand Organon
Sustanon '250'® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule United Kingdom Organon
Sustanon® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Italy Organon
Sustaretard 250 Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule India BM Pharmaceuticals
Sustenan 250 Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Chile Organon
Sustenan Oral testosterone undecanoate 40 mg capsules n/a Chile Organon
Sustenon 250® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Portugal Organon
Sybolin boldenone undecylenate 25 mg/ml 10 ml vial Australia Ranvet VET
Synasteron oxymetholone 50 mg tablet 50 tablet bottle Belgium Sarva [NLM]
Synovex plus (plus estradiol) trenbolone acetate 25 mg pellet 80 pellet cartridge Canada Wyeth VET
Synovex plus (plus estradiol) trenbolone acetate 25 mg pellet 80 pellet cartridge Mexico Fort Dodge VET
Synovex plus (plus estradiol) trenbolone acetate 25 mg pellet 80 pellet cartridge U.S. Fort Dodge VET
Synovex plus (plus estradiol) trenbolone acetate 25 mg pellet 80 pellet cartridge U.S. Syntex [NLM] VET
Synovex®-H (plus estradiol) testosterone propionate (implant) 20 mg/pellet n/a Canada Ayerst
Synovex®-H (plus estrogen) testosterone propionate (implant) 25 mg/pellet 80 pellet cartridge Australia Fort Dodge VET
Synovex®-H (plus estrogen) testosterone propionate (implant) 20 mg/pellet n/a Mexico Fort Dodge
Synovex®-H (plus estrogen) testosterone propionate (implant) 20 mg/pellet n/a Mexico Syntex [NLM]
Synovex®-H (plus estrogen) testosterone propionate (implant) 20 mg/pellet n/a U.S. Fort Dodge VET
Synovex®-H (plus estrogen) testosterone propionate (implant) 23.5 mg pellet 450 pellets U.S. Syntex [NLM] VET
T. Lingvalete methyltestosterone 5 mg sub. dragee n/a YugoslaviaFRMRGatenika [NLM]
Tanoxol stanozolol (inj) 25 mg/ml 10 ml vial Argentina Bumet VET
Tealigen fluoxymesterone 5 mg capsule n/a Taiwan Ming ta
Tepro Hormone testosterone propionate 100 mg/ml 500 ml vial Australia Virbac VET
Terabon stanozolol (oral) 2 mg tablet 10 tablet strip Korea Jin Yang
Tesamone testosterone suspension 25, 50, 100, mg/ml n/a U.S. Dunhall [NLM]
Tesone L.A. testosterone enanthate 200 mg/ml 10 ml vial U.S. Sig [NLM]
Test 400 Test 400 (testosterone blend) 400 mg/ml 10 ml vial Mexico Denkall VET
Testabol Propionate testosterone propionate 100 mg/ml 10 ml vial Thailand British Dragon
Testabot Depot testosterone cypionate 200 mg/ml 10 ml vial Thailand British Dragon
Testa-C testosterone cypionate 200 mg/ml 10 ml vial U.S. Vortech [NLM]
Testacyp testosterone cypionate 100 mg/ml 2 ml vial India BM Pharmaceuticals
Steroid.com
383
Steroid Listings By Trade Name
Testadiate-Depo testosterone cypionate 200 mg/ml 10 ml vial U.S. Kay [NLM]
Testanate No. 1 testosterone enanthate 100 mg/ml n/a U.S. Kenyon [NLM]
Testaval testosterone enanthate 100,200 mg/ml 10 ml vial U.S. Legere [NLM]
Testen-250 testosterone enanthate 250 mg/ml 2 ml vial India BM Pharmaceuticals
Testenan Depot testosterone enanthate 250 mg/ml n/a Taiwan Sinton
Testenat Testoviron (testosterone blend) 100 mg/ml 1 ml ampule Russia Farmadon [NLM]
Testenon Testoviron (testosterone blend) 135 mg/ml 2 ml vial India BM Pharmaceuticals
Testenon Testoviron (testosterone blend) 135 mg/ml 1 ml ampule India BM Pharmaceuticals
Testenon 250 Sustanon 250 (testosterone blend) 250 mg/ml 5 ml vial Mexico Ttokkyo VET
Testermon testosterone enanthate 25 mg/ml n/a Taiwan CCPC
Testex testosterone propionate 50, 100 mg/ml n/a U.S. Pasadena [NLM]
Testex Leo testosterone propionate 25 mg/ml 1 ml ampule Spain Altana Pharma
Testex Leo testosterone propionate 25 mg/ml 1 ml ampule Spain Leo [NLM]
Testex Leo prolongatum testosterone cypionate 50,125 mg/ml 2 ml ampule Spain Altana Pharma
Testex Leo prolongatum testosterone cypionate 50,125 mg/ml 2 ml ampule Spain Leo [NLM]
Testinon-Depot testosterone enanthate n/a n/a Japan n/a
Testo testosterone propionate 50 mg/ml 10 ml vial Korea Samil
Testo LA testosterone cypionate 100 mg/ml 10 ml vial Australia Jurox [NLM] VET
Testo Tab methyltestosterone 25 mg tablet n/a Korea Samil
Testoderm testosterone (patch) 15mgpatch n/a Malaysia Alza
Testoderm testosterone (patch) 6 mg patch 10, 30 patch box Spain Esteve
Testoderm testosterone (patch) 4 mg patch 10 patch box Spain Esteve
Testoenan L/A testosterone enanthate 250 mg/ml 10 ml vial Mexico Loeffler Vet
Testo-Enant testosterone enanthate 125 mg/ml 2 ml ampule Italy Geymonat
Testo-Enant testosterone enanthate 250 mg/ml 1 ml ampule Italy Geymonat
Testogan testosterone propionate 25 mg/ml 50 ml vial Costa Rica Laguinsa VET
Testogan testosterone propionate 25 mg/ml 50 ml vial Dom. Rep. Laguinsa VET
Testogan testosterone propionate 25 mg/ml 50 ml vial Ecuador Laguinsa VET
Testogan testosterone propionate 25 mg/ml 50 ml vial El Salvador Laguinsa VET
Testogan testosterone propionate 25 mg/ml 50 ml vial Guatemala Laguinsa VET
Testogan testosterone propionate 25 mg/ml 50 ml vial Honduras Laguinsa VET
Testogan testosterone propionate 25 mg/ml 50 ml vial Nicaragua Laguinsa VET
Testogan testosterone propionate 25 mg/ml 50 ml vial Panama Laguinsa VET
Testogel testosterone (gel) 25, 50 mg single dose packet Australia Schering
Testogel testosterone (gel) 50 mg single dose packet Austria Schering
Testogel testosterone (gel) 25, 50 mg single dose packet Germany Jenapharm
Testogel testosterone (gel) 25, 50 mg single dose packet Netherlands Besins
Testogel testosterone (gel) 25, 50 mg single dose packet Sweden Besins
Testoject testosterone cypionate 100 mg/ml n/a U.S. Mayrand [NLM]
Testoject 50 testosterone cypionate 50 mg/ml n/a U.S. Mayrand [NLM]
Testoject-LA testosterone cypionate 200 mg/ml n/a U.S. Mayrand [NLM]
Testo-Jet L.A. Sustanon 250 (testosterone blend) 250 mg/ml 10 ml vial Mexico Norvet VET
Testolent testosterone phenylpropionate 100 mg/ml 1 ml ampule Rumania Sicomed [NLM]
Testolic testosterone propionate 50 mg/ml 2 ml ampule Thailand Body Research
Testolin testosterone suspension 100 mg/ml 10 ml vial U.S. Pasadena [NLM]
Teston methyltestosterone 25 mg tablet 30 tablet box Greece Remek
Teston QV 200 testosterone cypionate 200 mg/ml 10 ml vial Mexico Quality Vet VET
Testone-E testosterone propionate 25 mg/ml 1 ml ampule Egypt Misr
Testonon '250'® Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Egypt Nile
Steroid.com
384
Steroid Listings By Trade Name
Testonon'1001® Sustanon 100 (testosterone blend) 100 mg/ml 1 ml ampule Egypt Nile
Testopin-100 testosterone propionate 100 mg/ml 2 ml vial India BM Phanmaceuticals
Testopin-100 testosterone propionate 100 mg/ml 1 ml ampule India BM PharmaceutJcals
Testoprim-D Testoviron (testosterone blend) 250 mg/ml 1 ml ampule Mexico Labs. Tocogino
Testopro L/A testosterone propionate 250 mg/ml 10 ml vial Mexico Loeffler VET
Testopropon methyltestosterone 25 mg tablet n/a Malaysia Scanpharm
Testormon methyltestosterone 10mg tablet n/a Portugal Unitas
Testorone Depot testosterone cypionate 100 mg/ml n/a Taiwan Gentle
Testos 100 testosterone suspension 100 mg/ml n/a Canada Vetcom VET
Testosteron methyltestosterone 5 mg tablet n/a Germany Berco [NLM]
Testosteron testosterone propionate 25 mg/ml 1 ml ampule Rumania Sicomed [NLM]
Testosteron testosterone propionate 50 mg/ml 1 ml ampule Bulgaria Sopharma
Testosteron testosterone propionate 5, 10, 25, 50 mg/ml 1 ml ampule Hungary Hemofarm [NLM]
Testosteron testosterone propionate 50 mg/ml 1 ml ampule Switzerland Streuli & Co. AG [NLM]
Testosteron testosterone propionate 5, 10, 25, 50 mg/ml 1 ml ampule YugoslaviaFRMRGalenika [NLM]
Testosteron 250 Sustanon 250 (testosterone blend) 250 mg/ml 1 ml ampule Germany Rotex Medica [NLM]
Testosteron Depot testosterone enanthate 100 mg/ml 1 ml ampule Germany Rotex Medica [NLM]
Testosteron Depot testosterone enanthate 250 mg/ml 1 ml ampule Germany Rotex Medica
Testosteron Depot testosterone propionate 25 mg/ml n/a Taiwan Gentle
Testosterona testosterone propionate 50, 100 mg/ml 10, 20 ml vial Mexico Brovel VET
Testosterona 200 testosterone enanthate 200 mg/ml 10 ml vial Mexico Brovel Vet
testosterona enantato testosterone enanthate 100 mg/ml 1 ml ampule Chile Chile [NLM]
testosterona enantato testosterone enanthate 250 mg/ml 1 ml ampule Chile Chile
Testosterona IV L/A Sustanon 250 (testosterone blend) 250 mg/ml 10 ml vial Mexico Loeffler VET
Testosterona Propionato testosterone propionate n/a n/a Paraguay Botica
Testosterona Proptonat testosterone propionate 50, 100 mg/ml 1 ml ampule Russia Farmadon
Testosterona Ultra Lenta testosterone cypionate 100 mg/ml 20 ml vial Uruguay Dispert Labs. VET
Testosterona Ultra Lenta Fuerte testosterone cypionate 200 mg/ml 5 ml ampule Uruguay Dispert Labs. VET
Testosterona Ultra Lenta Fuerte testosterone cypionate 200 mg/ml 20 ml vial Uruguay Dispert Labs. VET
Testosteron-Depo testosterone enanthate 100 mg/ml 1 ml ampule YugoslaviaFRMRGalenika [NLM]
Testosteron-Depo testosterone enanthate 250 mg/ml 1 ml ampule YugoslaviaFRMRGalenika
Testosteron-Depo testosterone enanthate 100, 250 mg/ml 1 ml ampule YugoslaviaFRMRHemofarm [NLM]
Testosteron-Depot testosterone enanthate 250 mg/ml 1 ml ampule Germany Eifelfango
Testosteron-Depot testosterone enanthate 250 mg/ml 1 ml ampule Bulgaria Jenapharm
Testosteron-Depot testosterone enanthate 250mg/ml 1 ml ampule Germany Jenapharm
Testosterone 200 Depot testosterone enanthate 200mg/ml 10 ml vial Mexico Tomel vet
Testosterone 250 Sustanon 250 (testosterone blend) 250 mg/ml 10ml vial Costa Rica Qualityvet VET
Testosterone Berco Supp. testosterone propionate 40 mg/suppository 1 8 supp. box Germany Funke [NLM]
Testosterone CHP Theramex testosterone cyclohexylpropionate 296, 148, 37 mg/ml 1 ml ampule France Theramex [NLM]
testosterone cypionate testosterone cypionate 100 mg/ml 10 ml vial U.S. Geneva Geriatrics [NLM]
testosterone cypionate testosterone cypionate 100, 200 mg/ml 10 ml vial U.S. Goldline [NLM]
testosterone cypionate testosterone cypionate 50,100, 200 mg/ml 10 ml vial U.S. Huffman [NLM]
testosterone cypionate testosterone cypionate 200 mg/ml 10 ml vial U.S. Legere [NLM]
testosterone cypionate testosterone cypionate 100, 200 mg/ml 10 ml vial U.S. Schein [NLM]
testosterone cypionate testosterone cypionate 100,200 mg/ml 10ml vial U.S. Steris [NLM]
Testosterone Cypionate 200 testosterone cypionate 200 mg/ml 10ml vial Mexico Ttokkyo VET
Testosterone Cypionate Inj testosterone cypionate 200 mg/ml n/a Hong Kong Charmaine
Testosterone Cypionate Inj testosterone cypionate 200 mg/ml n/a Taiwan Gwo Chyang
Testosterone Cypionate Inj testosterone cypionate 200 mg/ml n/a Taiwan Tai Yu
Steroid.com
385
Steroid Listings By Trade Name
Testosterone Cypionate Inj. testosterone cypionate 100 mg/ml 2 ml vial Canada Cytex
Testosterone Cypionate Inj. testosterone cypionate 200 mg/ml 10 ml vial Canada Sabex
Testosterone Cypionate LA testosterone cypionate 100 mg/ml 10ml vial Mexico Ttokkyo [NLM] VET
Testosterone Depositum testosterone cypionate n/a n/a Italy SPA
testosterone enantato testosterone enanthate 250 mg/ml 1 ml ampule Chile Biosano
testosterone enanthate testosterone enanthate 100,200mg/ml 10 ml vial U.S. Geneva Geriatrics [NLM]
testosterone enanthate testosterone enanthate 100,200 mg/ml 10 ml vial U.S. Goldlline [NLM]
testosterone enanthate testosterone enanthate 100,200mg/ml 10 ml vial U.S. Quad [NLM]
testosterone enanthate testosterone enanthate 100,200 mg/ml 10 ml vial U.S. Schein [NLM]
testosterone enanthate testosterone enanthate 100,200 mg/ml 10 ml vial U.S. Steris [NLM]
Testosterone Enanthate 250 testosterone enanthate 250 mg/ml 1 ml ampule Iran Aburaihan
Testosterone Enanthate Dalim testosterone enanthate 250 mg/ml n/a Korea Dalim
Testosterone Enanthate Inj testosterone enanthate 200 mg/ml 10 ml vial Canada Taro [NLM]
Testosterone Heptytate testosterone enanthate 50,100,250 mg/ml 1 ml ampule France Theramex
Testosterone Jenaphamn testosterone propionate 25 mg/ml 1 ml ampule Germany Jenapharm [NLM]
testosterone propionate testosterone propionate 50 mg/ml n/a U.S. Quad & Lilly [NLM]
testosterone propionate testosterone propionate 100 mg/ml 10, 30 ml vial U.S. Rugby [NLM]
testosterone propionate testosterone propionate 100mg/ml 10ml vial U.S. Steris [NLM]
Testosterone Propionate Inj testosterone propionate 50 mg/ml 1 ml ampule China n/a
Testosterone Propionate Inj testosterone propionate 25 mg/ml n/a Hong Kong Charmaine
Testosterone Propionate Inj testosterone propionate 50 mg/ml n/a Hong Kong Hong Kong Med
Testosterone Propionate Inj testosterone propionate 25 mg/ml n/a Taiwan Tai Yu
Testosterone Propionate Inj. testosterone propionate 100 mg/ml 1 0 ml vial Canada Cytex
Testosterone Propionate Inj. testosterone propionate 100 mg/ml 10 ml vial Canada Dominion VET
Testosterone Propionate Inj. testosterone propionate 100 mg/ml 10 ml vial Canada Taro [NLM]
Testosterone Streuli testosterone propionate n/a 5, 10, 25, 50 mg/ml Austria Streuli & Co. AG [NLM]
testosterone suspension testosterone suspension 50, 100 mg/ml 10, 30ml vial U.S. Legere [NLM]
testosterone suspension testosterone suspension U.S. Schein [NLM]
testosterone suspension testosterone suspension 50, 100 mg/ml 10, 30ml vial U.S. Steris [NLM]
Testosterone Vitis testosterone propionate n/a 10, 25 mg/ml Germany Neopharma [NLM]
Testosterone-Prop. Disp. testosterone propionate 10, 25 mg/ml 1 ml ampule Austria Disperga [NLM]
testosteronpropionat testosterone propionate 50 mg/ml 1 ml ampule Germany Eifelfango [NLM]
testosteronpropionat testosterone propionate 25 mg/ml 1 ml ampule Germany Eifelfango
Testosteronum Prolongatum testosterone enanthate 100 mg/ml 1 ml ampule Belgium Polfa [NLM]
Testosteronum Prolongatum testosterone enanthate 100 mg/ml 1 ml ampule Bulgaria Jetfa [NLM]
Testosteronum Prolongatum testosterone enanthate 100 mg/ml 1 ml ampule Poland Jelfa
Testosteronum Prolongatum testosterone enanthate 100 mg/ml 1 ml ampule Poland Polfa [NLM]
Testosteronum Propionicum testosterone propionate 50 mg/ml 1 ml ampule Poland Jelfa
Testosure methyltestosterone n/a n/a Hong Kong Europharm
Testosus 100 testosterone suspension 100 mg/ml 20 ml vial Australia Jurox [NLM] VET
Testoviron Depot testosterone enanthate 250 mg/ml 1 ml ampule Taiwan Schering
Testoviron® testosterone propionate 10,25, 50 mg/ml 1 ml ampule Greece Sobering
Testoviron® testosterone propionate 10, 25 mg/ml 1 ml ampule Italy Schering [NLM]
Testoviron® testosterone propionate 50 mg/ml 2 ml ampule Spain Schering [NLM]
Testoviron® Depot testosterone enanthate 250 mg/ml 1 ml ampule Argentina Schering
Testoviron® Depot testosterone enanthate 250 mg/ml 1 ml ampule Hungary Schering [NLM]
Testoviron® Depot testosterone enanthate 250 mg/ml 1 ml ampule Ireland Schering [NLM]
Testoviron® Depot testosterone enanthate 250 mg/ml 1 ml ampule Peru Schering
Testoviron® Depot Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Argentina Schering [NLM]
Steroid.com
386
Steroid Listings By Trade Name
Testoviron® Depot Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Hungary Schering [NLM]
Testoviron® Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Austria Schering [NLM]
Testoviron® Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Dom. Rep. Schering
Testoviron® Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Germany Schering [NLM]
Testoviron® Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Greece Schering [NLM]
Testoviron® Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Italy Schering
Testoviron® Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Netherlands Schering [NLM]
Testoviron® Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Portugal Schering [NLM]
Testoviron® Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Spain Schering [NLM]
Testoviron® Depot 100 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Switzerland Schering [NLM]
Testoviron® Depot 135 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Denmark Schering
Testoviron® Depot 135 Testoviron (testosterone blend) 135 mg/ml 1 ml ampule Sweden Schering [NLM]
Testoviron® Depot 50 Testoviron (testosterone blend) 75 mg/ml 1 ml ampule Austria Schering [NLM]
Testoviron® Depot 50 Testoviron (testosterone blend) 75 mg/ml 1 ml ampule Germany Schering [NLM]
Testoviron® Depot 50 Testoviron (testosterone blend) 75 mg/ml 1 ml ampule Italy Sobering [NLM]
Testoviron® Depot 50 Testoviron (testosterone Wend) 75 mg/ml 1 ml ampule Spain Schering [NLM]
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Hong Kong Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Iceland Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Thailand Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Yemen Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 mi ampule Austria Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Bahrain Schering [NLM]
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Colombia Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Czech. Rep. Schering [NLM]
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Denmark Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Dom. Rep. Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Ethiopia Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Germany Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Greece Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule India Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Israel Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Italy Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Japan Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Lebanon Schering [NLM]
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Malaysia Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Malta Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Pakistan Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Paraguay Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Portugal Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Saudi Arabia Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Spain Schering
Testoviron®-Depot testosterone enanthate 250 mg/m! 1 ml ampule Sri Lanka Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Sweden Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Switzerland Schering
Testoviron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Uruguay Schering
Testovis methyltestosterone 10mg tablet n/a Italy SIT
Testovis testosterone propionate 20 mg/ml n/a Italy SIT
Testovjron®-Depot testosterone enanthate 250 mg/ml 1 ml ampule Qatar Schering [NLM]
Testoyohim methyltestosterone 25 mg dragee 30 dragee box Germany Paul Mehner [NLM]
Steroid.com
387
Steroid Listings By Trade Name
Testred methyltestosterone 10mg capsule 100 capsule bottle U.S. ICN
Testred Cypionate testosterone cypionate 200 mg/ml 10 ml vial U.S. INC [NLM]
Testrin-PA testosterone enanthate 200 mg/ml n/a U.S. Pasadena Res. [NLM]
Testron 4 250 Sustanon 250 (testosterone blend) 250 mg/ml 10 ml via! Mexico Bratis Labs VET
Testron Depot testosterone enanthate 125,250 mg/ml 1 ml vial Japan n/a
Ton Lin fluoxymesterone 10mg capsule n/a Taiwan Chin Teng
TP Men Hormone methyltestosterone 10mg capsule 24 tablets Thailand TP Drugs
Trembolone QV 75 trenbolone acetate 75 mg/ml 10 ml vial Mexico Quality Vet VET
Trenabol trenbolone acetate 75 mg/ml 10 ml vial Thailand British Dragon
Trenabol 200 Trenbolone acetate 200 mg/ml 10 ml vial Thailand British Dragon
Trenbol 75 trenbolone acetate 75 mg/ml 20 ml vial Mexico Ttokkyo VET
Trend 50 trenbolone acetate 50 mg/ml 6 ml vial Myanmar/Burma WDV VET
Tribolin methylandrostenediol (blend) 75 mg/ml 10, 20 ml vial Australia Ranvet VET
Trinergic methandrostenolone 5 mg capsule n/a India Unimed [NLM]
Triolandren testosterone blend (misc) 250 mg/ml 1 ml ampule Egypt Novartis
Triolandren testosterone blend (misc) 250 mg/ml 1 ml ampule Taiwan Novartis
Triolandren testosterone propionate 100 mg/ml 10 ml vial Switzerland Ciba Geigy CH [NLM]
Tri-Trenabol 150 Trenbolone Blend 150mg/ml 10 ml vial Thailand British Dragon
Trofbdermin Crema clostebol acetate cream 30 gram tube Italy Carlo Erba OTC
Trofbdermin Spray clostebol acetate n/a 30 ml spray Italy Carto Erba OTC
Turinabol nandrolone phenylpropionate 25 mg/ml n/a Bulgaria Jenapharm [NLM]
Turinabol nandrolone phenylpropionate 25 mg/ml n/a Czech. Rep. Germed [NLM]
Turinabol nandrolone phenylpropionate 25 mg/ml n/a Germany Jenapharm [NLM]
Turinabol Depot nandrolone decanoate 50 mg/ml 1 ml ampule Bulgaria Jenapharm [NLM]
Turinabol Depot nandrolone decanoate 50 mg/ml 1 ml ampule Czech. Rep. Jenapharm [NLM]
Turinabol Depot nandrolone decanoate 50 ma/ ml 1 ml ampule Germany Jenapharm [NLM]
Ultandren fluoxymesterone 1,5 mg tablet n/a United Kingdom Ciba [NLM]
Ultragan boldenone undecylenate 100 mg/ml 10 ml vial Mexico Denkall VET
Undestor testosterone undecanoate 40 mg capsules n/a Argentina Organon
Undestor testosterone undecanoate 40 mg capsules 60 capsule bottle Belgium Organon
Undestor testosterone undecanoate 40 mg capsules 60 capsule bottle Bulgaria Organon
Undestor testosterone undecanoate 40 mg capsules 60 capsule bottle Czech. Rep. Organon
Undestor testosterone undecanoate 40 mg capsules n/a Luxemburg Organon
Undestor testosterone undecanoate 40 mg capsules 60 capsule bottle Poland Organon
Undestor testosterone undecanoate 40 mg capsules 60 capsule bottle Rumania Organon
Undestor testosterone undecanoate 40 mg capsules n/a Slovakia Organon
Undestor testosterone undecanoate 40 mg capsules n/a Sweden Organon
Uni-Test Inj testosterone propionate 50, 100 mg/ml 1 ml ampule Canada Univet VET
Uni-Test Suspension testosterone suspension 100 mg/ml 30 ml vial Canada Univet VET
Uttragan boldenone undecylenate 50 mg/ml 50 ml vial Mexico Denkall VET
Vasorome oxandrolone 0.5 mg tablet n/a Japan Kowa [NLM]
Vasorome oxandrolone 2 mg tablet n/a Japan Kowa [NLM]
Vebonol boldenone undecylenate 25 mg/ml 10 ml vial Australia Ciba-Geigy [NLM] VET
Vebonol boldenone undecylenate 25 mg/ml 10 ml vial Germany Ciba-Geigy VET
Vebonol boldenone undecylenate 25 mg/ml 10 ml vial Switzerland Ciba-Geigy [NLM] VET
Veto-Test Sus testosterone suspension 100 mg/ml 30 ml vial Canada Austin VET
Vewon fluoxymesterone 5 mg tablet n/a Taiwan Yung Shin
Vi Jane fluoxymesterone 10mg capsule n/a Taiwan Shyh Sar
Virbac Tepro Pellets testosterone propionate (implant) 100 mg/ml 20 ml vial Australia Virbac VET
Steroid.com
388
Steroid Listings By Trade Name
Virigen testosterone undecanoate 40 mg capsules 30 capsule bottle Turkey Organon
Virilon (time released) methyltestosterone 10 mg capsule 100,1000 capsule bottle U.S. Star
Vironate testosterone cypionate 200 mg/ml 5 ml vial Philippines Xelox (export)
Virormone testosterone propionate 50 mg/ml 2 ml ampule Thailand Paines
Virormone testosterone propionate 50 mg/ml 2 ml ampule United Kingdom Ferring [NLM]
Virormone testosterone propionate 50 mg/ml 10 ml vial United Kingdom Nordic
Vistimon mesterolone 25 mg tablet 20 tablet box Germany Jenapharm [NLM]
Vistimon mesterolone 25 mg tablet n/a Korea n/a
Vistimon mesterolone 25 mg tablet 30 tablet box Taiwan Jenapharm
Vitabolic stanozolol (inj) 20 mg/ml 10. 100 ml vial Argentina Over Labs VET
VR Testprop testosterone propionate 22 mg/pellet n/a Australia Jurox VET
Waromom fluoxymesterone 5 mg tablet n/a Taiwan Washington
Weratestone 250 testosterone enanthate 250 mg/ml 1 ml ampule Algeria Weimer Pharma
Weratestone 250 testosterone enanthate 250 mg/ml 1 ml ampule Mozambique Weimer Pharma
Weratestone 250 testosterone enanthate 250 mg/ml 1 ml ampule Zimbabwe Weimer Pharma
Weratestone 250 testosterone enanthate 250 mg/ml 1 ml ampule Zimbabwe Weimer Pharma
Winstrol stanozolol (oral) 2 mg tablet n/a Japan n/a
Winstrol® stanozolol (oral) 2 mg tablet 20 tablet box Italy Zambon [NLM]
Winstrol® stanozolol (oral) 2 mg tablet 20 tablet box Spain Zambon
Winstrol® stanozolol (oral) 2 mg tablet 100 tablet bottle U.S. Sanofi
Winstrol® stanozolol (oral) 2 mg tablet 100 tablet bottle U.S. Upjohn [NLM]
Winstrol® stanozolol (oral) 2 mg tablet 100 tablet bottle U.S. Winthrop [NLM]
Winstrol® stanozolol (oral) 2 mg tablet n/a Greece Winthrop [NLM]
Winstrol® stanozolol (oral) 2 mg tablet n/a Portugal Winthrop [NLM]
Winstrol® stanozolol (inj) 50 mg/ml n/a Greece Winthrop [NLM]
Winstrol® Depot stanozolol (inj) 50 mg/ml 1 ml vial Italy Zambon [NLM]
Winstrol® Depot stanozolol (inj) 50 mg/ml 1 ml ampule Spain Zambon
Winstrol® V stanozolol (inj) 50 mg/ml 10, 30ml vial Canada Pharmacia VET
Winstrol® V stanozolol (inj) 50 mg/ml 10, 30ml vial U.S. Pharmacia & Upjohn VET
Winstrol® V stanozolol (inj) 50 mg/ml 10, 30ml vial U.S. Winthrop [NLM] VET
Winstrol-V® stanozolol (oral) 2 mg tablet 100 tablet bottle Canada Pharmacia VET
Winstrol-V® stanozolol (oral) 2 mg chewable tab 100 tablet bottle U.S. Pharmacia & Upjohn VET
Wmstrol-V® stanozolol (oral) 2 mg tablet 100 tablet bottle U.S. Pharmacia & Upjohn VET
Ziremilon nandrolone decanoate 50 mg/ml 1 ml ampule Greece Demo
Steroid.com
389
Steroid Listings By Trade Name
NOTES
NOTES
NOTES
NOTES
NOTES</beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></beta></p>TV REPAIR PARTShttp://www.blogger.com/profile/03272638773780329095noreply@blogger.com0