Anabolic Pharmacology SethRoberts 2009

p ~ o~
Seth Roberts
Seth Roberts' ANABOLIC PHARMACOLOGY, lie
Copyright 2009
All Rights Reserved.

This text may not be reproduced in part or in full in any form or by any means without written
permission of the author.
ANABOLIC PHARMACOLOGY II
Table of Contents
I. Introduction 7
II. Bro'iore 9
Ill. Steroids and the Law II
IV. Basic Chemistry 19
V. Units and Stoichiometry 24
VI. Anabolism/Catabolism 24
VII. Steroid Hormone Superfamily 31
VIII. Enzymes 57
IX. Binding Proteins 67
X. Crossover 73
XI. Synthetic AAS 76
XII. Counterfeits 76
XIII. Exogenous administration of AAS 77
XIV. Spot Injections 79
XV. Side Effects 83
XVI. Background Research 99
XVII. Selective Androgen Receptor Modulators 100
XVIII. Availability of AAS 102
XIX. Expectations 103
XX. AAS Profiles 107
XXI. Ancillary medication profiles 279
XXII. Pharmacokinetics 331
XXIII. Drug Metabolism 334
XXIV. Stacking 341
XXV. Dosing 343
XXVI. Stacks/Cycles 345
XXVII. Post-Cycle Therapy 385
XXVIII. Peptide Hormones 390
XXIX. Health Monitoring 399
XXX. Blood Tests 400
XXXI. The Addict Mentality 409
XXXII. Bibliography 410
III ANABOLIC PHARMACOLOGY

ANABOLIC PHARMACOLOGY 4
SECTION 1
5 ANABOLIC PHARMACOLOGY
DISCLAIMER
Absolutely no liability is assumed by the author, publisher or distributors of this text for the
information contained herein. This text is meant to be used for informational, educational and
entertainment purposes only. None of the information supplied is meant to diagnose or treat any
disease nor is meant to substitute in any way for the advice of a trained medical professional. None
of the opinions expressed in this text are to be construed as an endorsement of the use of any legal
or illegal substance.
INTRODUCTION
The consumption of various substances to enhance athletic performance has existed since ancient
times. Ancient Greeks knew bull and sheep testicles as a source of power and would ingest them in
various forms to enhance not only their performance in athletics but also in the bedroom I.
Throughout early history, advances in performance enhancement were slow and relied mostly on
anecdotal information as well as superstition. Strychnine, arsenic, cocaine, codeine and ether-laced
sugar cubes were all in widespread use by the time of the first modern Olympics in 1896.
Testosterone was isolated in 1935 and human trials were started as early as 1937 using testosterone
esters. Nazi Germany was apparently using testosterone and possibly other androgens on soldiers
during World War II to increase aggression and stamina on the battlefield. Scientific literature of
the early 1940's often speculated on the possible use of androgens to boost athletic performance.
Many in the bodybuilding community assume that steroid use began in the 1960's but anecdotal
evidence suggests that bodybuilders in California began experimenting with testosterone in the late
1940's and early 1950'SI.
The isolation and elucidation of the structure of testosterone ultimately led to the production of
many synthetic androgens, termed anabolic-androgenic steroids (AAS) that have been the
cornerstone of performance enhancement in the modern era2,3 In the 1980's and 90's, performance
enhancement moved beyond anabolic steroids to include growth hormone, insulin-like growth
factor-I, insulin, c1enbuterol, thyroid hormone, prostaglandin F-2, interleukin-15, erythropoietin and
a myriad of other exotic drugs. Even so, AAS continue to be TH E backbone of performance
enhancement in the new millennium. Even so, after almost a century since testosterone was first
isolated, the average steroid user still uses them haphazardly in an unscientific and often dangerous
manner. Anecdotal information has been the primary source of knowledge in the AAS community
but this information is often flawed and contrary to what the scientific world now knows regarding
AAS.
In 1990 , The teroid Control Act marked AAS as controlled substances and made their
use/possession a serious legal offense. Even so, the use of AAS only continues 10 grow. The
argument that using steroids is cheating is a na"ive one. Almost every sport and an overwhelming
majority of professional and Olympic athletes are using some form of "illegal" performance
enhancer. Although some commentators take the view that athletes using performance enhancers is
a minority position 4 , recent high profile admissions of athletes who had never tested positive
suggests otherwise. We will not eliminate this fact. Fans want to see superhuman performance with
records being broken at every competition. The exorbitant incomes of professional athletes
demonstrate the public's demand for these performances. At one time in the past, AAS use was
restricted in large part to only serious athletes (usually professional or Olympic caliber amateurs)
who had the benefit of team doctors and coaches with years of experience to guide their use. The
average user today is non-competitive in nature and does not have the guidance of doctor or coach
to direct their use of these powerful drugs with complex pharmacology.
In the last 15 years, several legal supplements were brought to market to satisfY the demand that is
ever present for AAS. These "prohormones" initially began as precursors to testosterone, which
could be enzymatically transformed in the body to active compounds. For anyone wishing to use
steroids but not wanting to break the law, these prohormones filled the void of AAS. Prohormones
evolved until eventually "prosteroids" were marketed. These prosteroids needed no conversion and
were active AAS that did not fall under the legislation of the Steroid Control Act and were therefore
not illegal. This loophole was largely closed with the passing of the Anabolic Steroid Control Act of
2004. This new law made existing prohormones and prosteroids illegal and scheduled them as
controlled substances. Most prohormones and prosteroids are now as illegal as those that fell under
the Steroid Control Act of 1990. More importantly, this new law makes it easier to schedule any
new steroidal supplements that come out in the future. The fact is, this new legislation will not
reduce the use of androgens, but instead, we will likely see a switch from the use of legal alternative
to the use of "traditional" illegal AAS.
As the government tries harder and harder to restrict access to androgenic steroids. the interest in
these compounds continues to grow. As awareness of anti-aging and maintaining optimum health in
wellness and disease increases, people are beginning to realize the positive role that androgens play
not only in men but also in women. Doctors and researchers are beginning to understand the
importance of maintaining healthy androgen levels as men age. Hormone replacement therapy
(HRT) for men is just now starting to be utilized more liberally and will only become more
widespread as men learn of the advantages of HRT. Furthermore, the use of AAS in people living
with HIV/AIDS has done a lot to revitalize the opinion of AAS in the eyes of healthcare
professionals.
Instead of trying to eliminate the use of AAS, we should instead look for ways to regulate their use
so that athletes are as safe and healthy as possible. We should also focus our attention on educating
the public and prevention among the youth who are especially vulnerable to the negative aspects of
AAS abuse 5 The argument is that steroid-using athletes set a bad example for young people.
However, athletes use alcohol and yet we can make a distinction between adults using alcohol and
kids using alcohol. We need to educate teenagers that they in fact have very high levels of
androgens naturally and that they can use this naturally high androgenic state to their advantage
without disrupting their pubescent physiology by using steroids prematurely.
The criminalization of AAS has not reduced their use, but rather has driven them underground.
Instead of doctors restricting access, we have underground dealers (who often also deal in hard
drugs) providing access to anyone who can pay. We also have numerous counterfeit drugs in
circulation, which are vastly more dangerous than the steroids they are supposed to contain. Even
worse, athletes (and even teenagers) have turned to other options such as insulin, IGF-I,
Interieukin-15, and others because they are undetectable, often easier to obtain and carry less legal
liability than steroids. However, the risk associated with the use of these compounds is much greater
than with AAS. The recent BALCO scandal illustrates the lengths that athletes will go to in order to
enhance their performance. These athletes were using an unproven, untested steroid whose side
effects and toxicity were unknown simply because it was undetectable.
BRO'LORE
Bro'iore is a term that originated on the internet to describe the folklore and mythology of steroid
use that is passed on from one "bro" to another. Bro'iore is usually not based in any scientific
reality but instead is a collection of anecdotes, superstitions and outright falsehoods. These beliefs
(often referred to as Bro'telligence) are taken as gospel in the steroid using community often
because they reinforce enabling types of behaviors. You are unlikely to come across bro'iore that
advocates lower doses, less frequent injections or the use of fewer drugs. Instead most bro'iore
recommends higher doses, more drugs used in combination, multiple accessory medications and
daily injections. Unfortunately, bro'iore is often very believable because it often contains a kernel
of truth or is a currently disproved scientific theory from yesteryear in addition to fulfilling the self-
reinforcing qualities of AAS.
Much of what you will read 111 this text is contrary to the principles and long-held beliefs of
bro'lore. This is likely to confuse many and even anger a few. Unfortunately, in the community of
steroid-users, it takes very little to be considered an "expert". Experiential/anecdotal knowledge is
often revered above scientific evidence and on the internet; the loudest voice (or the best name) is
considered to be the winner of atguments, especially when the loudest voice has misinterpreted
some valid scientific research. Those who propagate these misinformed opinions are often merely
trying to justifY their own addictive pursuits and promote these ideals in tho e who are less-
informed. My only suggestion is to take nothing at face value, educate yourself and consider the
source of every piece of information you come across.
Another thing to consider is that there is no absolute truth in SCIence. Scientific knowledge is
constantly evolving as new information comes to light. In addition, scientific data is often open to
interpretation so this allows for several lines of thinking to exist simultaneously that may be at odds
with one another. Many people take this to mean that science is somehow "wrong" and this leads to
a mistrust of science and a reliance on "everyday" experience to predict future events.
Unfortunately this approach is extremely lacking due to its subjective nature and lack of controls.
STEROIDS AND THE LAW
With the passage of the Steroid Control Acts of 1990 and 2004. AAS and most prohormones and
prosteroids were marked as controlled substances. They were assigned as schedule III drugs in the
same class as amphetamines and L D. This group is characterized by drugs that have a lower level
of abuse while still having some medicinal use with lower physical dependence but relatively high
psychological dependency. Simple possession is a felony under federal law as well as in many
states. This means that possession of personal use quantities could result in jail time. I am not a
lawyer but there is an excellent book, Legal Muscle, written by Rick Collins; who is a lawyer. This
book is an in-depth look at all of the legal aspects of steroid use and I highly recommend it for
anyone considering the use of AAS. The Steroid Control Act of 2004 is shown as a reference
below:
108th CONGRESS
2d Session
S.2195
To amend the Controlled Substances Act to clarii)' the definition of anabolic steroids and to provide
for research and education activities relating to steroids and steroid precursors.
IN THE SENATE OF THE UNITED STATES

March II, 2004
Mr. BIDEN (for himself, Mr. HATCH, Mr. GRASSLEY, Mr. HARKIN, Mr. TEVENS, Mr.
MCCAIN, Mr. NELSON of Florida, Mrs. FEINSTEIN, Mr. ALLEN, and Ms. MURKOWSKI)
introduced the following bill; which was read twice and referred to the Committee on the Judiciary
A BILL
To amend the Controlled Substances Act to c1arif'y the definition of anabolic steroids and to provide
for research and education activities relating to steroids and steroid precursors.
Be it enacted by the Senate and House of Representatives of the United States of America in
Congress assembled,
SECTION 1. SHORT TITLE.
This Act may be cited as the 'Anabolic Steroid Control Act of2004'.
II ANABOLIC PHARMACOLOGY
SEC. 2. AME DMENTS TO THE CO TROLLED SUBSTANCES ACT.
(a) DEFI ITIONS- Section 102 of the Controlled Substances Act (21 U.S.C. 802) is amended--
(I) in paragraph (41 )--
(A) by realigning the margin so as to align with paragraph (40); and
(B) by striking subparagraph (A) and inserting the following:
(A) The term 'anabolic steroid' means any drug or hormonal substance, chemically and
pharmacologically related to testosterone (other than estrogens, progestins, corticosteroids, and
dehydroepiand rosterone), and incl udes--
(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) I-androstenediol (3b, 17b-dihydroxy-5a-androst-l-ene);
(II) I-androstenediol (3a,17b-dihydroxy-5a-androst-l-ene);
(III) 4-androstenediol (3b, 17b-dihydroxy-androst-4-ene); and
(IV) 5-androstenediol (3b, 17b-dihydroxy-androst-5-ene);
(iv) androstenedione--
(I) I-androstenedione ([Sa]-androst-l-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) dehydrochloromethylteslosterone (4-chloro-17b-hydroxy-17a-methyl-androst-1 ,4-dien-3-one);
(x) *I-dihydrotestosterone (a.k.a. ' I-testosterone') (17b-hydroxy-5a-androst-l-en-3-one);
(xi) 4-dihydrotestosterone (17b-hydroxy-androstan-3-one);
(xii) drostanolone (17b-hydroxy-2a-methy 1-5a-androstan-3-one);
(xiii) ethylestrenol (17a-ethyl-17b-hydroxyestr-4-ene);
(xiv) n uoxymesterone (9-nuoro-17a-rnethyl-1 Ib, 17b-dihydroxyandrosl-4-en-3-one);
(xv) formebolone (2-formyl-17a-methyl-11 a, 17b-dihydroxyandrost-1 ,4-dien-3-one);
(xvi) furazabol (17a-methyl-17b-hydroxyandrostano[2,3-c]-furazan);
(xvi i) 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 (I a-methyl-17b-hydroxy-[5a]-androstan-3-one);
(xxii) methandienone (17a-methyl-17b-hydroxyandrost-l ,4-dien-3-one);
(xxiii) methandriol (17a-methyl-3b, 17b-dihydroxyandrost-5-ene);
(xxiv) methenolone (l-methyl-17b-hydroxy-5a-androst-I-en-3-one);
(xxv) methyltestosterone (I 7a-methyl-17b-hydroxyandrost-4-en-3-one);
(xxvi) mibolerone (7a,17a-dimethyl-17b-hydroxyestr-4-en-3-one);
(xxvii) 17a-methyl-* I-dihydrotestosterone (17b-hydroxy-17a-methyl-5a-androst-l-en-3-one) (a.k.a.
, 17-a-methyl-l-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
(I V) 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);
(xxxi i) 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-methy 1-2-hydroxymethylene-17b-hydroxy-[5a]-androstan-3-one);
(xxxvi i) stanozolol (17a-methyl-17b-hydroxy-[5a]-androst-2-eno[3,2-c]-pyrazole);
(xxxviii) stenbolone (17b-hydroxy-2-methyl-[5a]-androst-I-en-3-one);
(xxxix) testolactone (I 3-hydroxy-3-oxo-1 3, 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, I l-trien-3-one);
(xlii) trenbolone (17b-hydroxyestr-4,9, I l-trien-3-one); and
(xliii) any salt, ester, or ether ofa drug or substance described in this paragraph.'; and
(2) in paragraph (44), by inserting 'anabolic steroids,' after 'marihuana,'.
(b) AUTHORITY AND CRITERIA FOR CLASSIFICATION- Section 201(g) of the Controlled
Substances Act (21 U.S.C. 81 I(g is amended--
(I) in paragraph (I), by striking 'substance from a schedule if such substance' and inserting 'drug
which contains a comrolled substance from the application of titles 1\ and III of the Comprehensive
Drug Abuse Prevention and Control Act (21 U.S.c. 802 et seq.) ifsuch drug'; and
(2) in paragraph (3), by adding at the end the following:
(C) Upon the recommendation of the Secretary of Health and Human erVlces, a compound,
mixture, or preparation which contains any anabolic steroid, which is intended for administration to
a human being or an animal, and which, because of its concentration, preparation, formulation or
delivery system, does not present any significant potential for abuse.'.
(c) ANABOLIC STEROIDS CONTROL ACT Section 1903 of the Anabolic Steroids Control Act
of 1990 (Public Law 101-647) is amended--
(I) by striking subsection (a); and
(2) by redesignating subsections (b) and (c) as subsections (a) and (b), respectively.
SEC. 3. SENTENCI G COMMISSIO GUIDELI ES.
The United States Sentencing Commission shall--

(I) review the Federal sentencing guidelines with respect to offenses involving anabolic steroids;
(2) consider amending the Federal sentencing guidelines to provide for increased penalties with
respect to offenses involving anabolic steroids in a manner that reflects the seriousness of such
offenses and the need to deter anabolic steroid trafficking and use; and
(3) take such other action that the Commission considers necessary to carry out this section.
SEC. 4. PREVENTIO AND EDUCATlO PROGRAMS.
(a) IN GE ERAL- The Secretary of Health and Human Services (referred to in this Act as the
.Secretary') shall award grants to public and nonprofit private entities to enable such entities to carry
out science-based education programs in elementary and secondary schools to highlight the harmful
effects of anabolic steroids.
(b) ELiGIBILlTY-
(I) APPLICA T10N- To be eligible for grants under subsection (a), an entity shall prepare and
submit to the Secretary an application at such time, in such manner, and containing such
information as the Secretary may require.
(2) PREFERE CE- In awarding grants under subsection (a), the Secretary shall give preference to
applicants that intend to use grant funds to carry out programs based on--
(A) the Athletes Training and Learning to Avoid Steroids program;
(B) the Athletes Targeting Healthy Exercise and Nutrition Alternatives program; and
(C) other programs determined to be effective by the National Institute on Drug Abuse.
(c) USE OF FUNDS- Amounts received under a grant under subsection (a) shall be used primarily
for education programs that will directly communicate with teachers, principals, coaches, as well as
elementary and secondary school children concerning the harmful effects of anabolic steroids.
(d) AUTHORIZATION OF APPROPRIATIONS- There is authorized to be appropriated to carry
out this section, $15,000,000 for each of fiscal years 2005 through 2010.
SEC. 5. NATlONAL SURVEY ON DRUG USE AND HEALTH.
(a) IN GENERAL- The Secretary of Health and Human Services shall ensure that the National
Survey on Drug Use and Health includes questions concerning the use of anabolic steroids.
(b) AUTHORIZATION OF APPROPRIATIONS- There is authorized to be appropriated to carry
out this section, $1,000,000 for each of fiscal years 2005 through 20 I O.
END
Wording from the DEA website also states that:
This document is a general reference and not a comprehensive list. This list describes the basic or
parent chemical and does not describe the salts, isomers and salts of isomers, esters, ethers and
derivatives which may also be controlled substances.
This vague wording theoretically includes ANY steroidal derivative whether it is implicitly listed or
not even if it is unknown or a new chemical entity.
SECTION 2
BASIC CHEMISTRY
Steroids are molecules. Molecules are composed of different atoms bound to one another. Each
atom has different characteristics and when bound to other atoms in different arrangements, form
molecules with different chemical properties. Atoms have a nucleus of protons and neutrons.
Electrons circle the nucleus in orbitals:
Atoms differ from one another by their number of protons, neutrons and electrons. Atoms can form
bonds with one another by sharing electrons in what is called a covalent bond.
Carbon (C) is the basis for organic molecules such as steroids. Carbon has six protons, six electrons
and six neutrons (as in the simplified drawing above). Carbon has the ability to form four chemical
bonds. Hydrogen, on the other hand, is only able to form one bond. Therefore, carbon can bind four
hydrogens to form methane:
c
I
H./"' I'-......H
H
When attached to a molecule in the place of one of the hydrogens, this is known as a methyl group
(CH3).
Two carbons can bind to each other with each carbon binding to three hydrogens each to form
ethane (the carbons are inferred):
When attached to a molecule in the place of one of the hydrogens, this would be called an ethyl
group.
Oxygen is capable of forming two bonds. One oxygen molecule can bind to two hydrogens to form
H20, also known as waler:
o
H/"" H
Oxygen can also bind to another oxygen atom with a double bond to form 02, oxygen gas:
o 0
Carbon can form double bonds or even triple bonds as well. Double and triple bonds are not as
stable as single bonds and can be broken or reduced to a single bond more easily.
Some other functional groups that are common to steroid molecules are:
Keto group
A keto group is typified by a carbon double bonded to oxygen while also bound to two other
carbons.
OH
I
CH 3
Alcohol (OH) Group
An alcohol, or hydroxyl group, is typified by a carbon bound to oxygen, which is in turn bound to a
hydrogen.
Double bonds are generally weaker than single bonds (with triple bonds being the weakest).
However, when double bonds are alternated with single bonds, they are called conjugated double
bonds:
This conjugation often results in a characteristic referred to as aromaticity. Aromatic bond systems
are much stronger than normal double bonds and sometimes even stronger than single bonds
because they are very stable. When a 6-membered ring is conjugated it forms an extremely stable
structure known as a benzene ring:
o
Simple changes in a molecule can result in dramatic changes in its properties. For example, water as
shown above is one oxygen molecule bound to two hydrogen molecules:
o
H /'" H
On the other hand, two oxygen atoms bound to one another and each to a hydrogen forms hydrogen
peroxide, a molecule with properties quite different from water:
/H
0-0
/
H
The basic steroid structure is a four-ring system:
The carbons on this four-ring structure are numbered to allow for easy reference.
This introduction to basic organic chemistry should help you to understand the structural drawings
of the compounds in this book and how they differ from one another. However, for a greater
understanding of the chemical properties of the molecules discussed in this text one would need to
consult other texts dedicated to this subject.
One important thing to remember is that these molecules exist In three dimensions. On the
following page you can compare the side view of the three dimensional structure of testosterone,
dihydrotestosterone, estradiol and trenbolone. One can see how simple changes in structure, such as
alterations in the number and location of double bonds, can change the orientation and shape of
each molecule.
OH
Testosterone
OH
Dihydrotestosterone
OH
HO
Estradiol
OH
Trenbolone
UNITS AND STOICHIOMETRY
For the most part, AAS are taken in milligram (mg) quantities but a fe\ are taken in microgram
(ug) quantities. There are 1000 ug in a mg, there are 1000 mg in one gram and 1000 grams in one
kilogram. For those of you less familiar with metric measurements, one pound is equal 10 454 grams
and there are 2.2 pounds per kilogram. Injectable AAS are usually injected in milliliter (mL)
quantities. There are 1000 mLs in a liter and approximately 240 mL in a cup. A mL is also referred
to as a cubic centimeter or a cc. Therefore, one milliliter is equal to one cc. Injectable AAS also
have a milligram strength. For instance, you might have a 10 cc vial of 100 mg/ml testosterone
propionate. If you were to inject one cc (or one mL) of this preparation, then you would be injecting
100 mg. Three mL's would therefore be 300 mg.
ANABOLISM/CATABOLISM
For those who are new to cellular physiology: The body is composed of basic units known as cells.
A simplified prototypical cell is shown below:
Endoplasmic ~ticulum
00
GOiglBod"~
The cell is composed of a membrane that keeps the contents of the cell confined and controls what
may enter and leave the cell. The nucleus is the control center of the cell and contains D A. The
DNA codes for all of the proteins that the body is capable of producing. Transcription and
translation are the processes by which DNA is read and the message sent to the endoplasmic
reticulum (ER) where it is pieced together to form new proteins. These proteins are then released for
immediate use by the cell or can be stored for later use in what are known as Golgi bodies. The
mitochondria are the powerhouse of the cell whose purpose is to provide the cell and therefore the
body with energy.
Skeletal muscle is composed of specialized cells called myocytes. These myocytes are interspersed
throughout the muscle with connective tissue. Myocytes contain the usual cellular components but
are different from many other types of cells in that they are multinucleated and have a complex
system of contractile proteins6 These contractile proteins, when activated by calcium ions and ATP
cause a shortening of the cell (also known as a muscle fiber) length. This shortening pulls on the
fibrous connective tissue that connects myocytes to each other and extends to the bone as a tendon.
The shortening of the muscle fibers results in a muscle contraction, which moves the bone or other
muscle to which it is connected. As the fiber shortens, in length, it bulges in width. The contractile
proteins are pulled past one another in what is called the sliding filament model. The majority of
human musculature consists of muscles whose fibers span the entire length of a muscle from one
end to the other7 In order for a muscle to contract, all of the fibers in that muscle must contract.
This is known as the all or none principle of muscle contraction.
Skeletal muscle is the most abundant tissue in the body8 Muscle tissue, like most body tissues, is
constantly being broken down and repaired. The process of breaking down is known as catabolism
while building up/repair is known as anabolism. The net of these two processes is the equilibrium
state. This does not necessarily mean that anabolism equals catabolism at equilibrium. In fact,
beyond puberty, in the average, sedentary person, there is a net catabolism that increases as we age9
Anabolism/catabolism in skeletal muscle depends, in large part, on what is referred to as nitrogen
balance. Skeletal muscle is not built during the actual exercise but in the recovery period following
the exercise which can last up to 48 hoursIO,II.
(Xt"''''o'',...... CoJo-loo,,,""-
The contractile proteins in skeleta uscle are composed of amino aCi~re characterized by
the presence of nitrogen in their m cular structure. A e.ositive nitrogen balance is usually
correlated with anabolism while a ~gatiye nitrogen balance is usually found in catabolism. Adipose
(fat tissue) anabolism differs in that adipocytes (fat cells) contain little protein, instead containing
pools of triglycerides. Therefore, anabolism in adipocytes occurs with a positive triglyceride
balance and catabolism occurs with a negative triglyceride balance. Adipocytes and myocytes also
differ in that a positive triglyceride balance is itself, the stimulus for anabolism of adipocytes. This
is due to the storage nature of adipose tissue. Other timuli can augment anabolism of adipocytes,
but a positive triglyceride balance is all that is required.
There are multiple stimuli that can induce anabolism of skeletal muscle. Basically, these stimuli can
be broken down into mechanical and chemical. It has been shown that eccentric and concentric
. h' f I fib 10,11.12.13.14
overload is a stimulus for skeletal muscle ana b0 IIsm as IS stretc II1g 0 musc e I ers .
These mechanical stimuli are translated into biochemical stimuli 15, which are directed toward repair
of microtrauma of contractile proteins and if intense enough, towards adaptation of myocytes for
future bouts of mechanical stimuli - known as the "training effect".
Skeletal muscles can get larger by two processes: hypertrophy and hyperplasia. Hypertrophy is the
expansion of existing muscle cells through an increase in the quantity of contractile proteins or an
increase in intracellular fluid, glycogen - or both. Hyperplasia is the process in which new muscle
cells are produced. This is generally believed to occur through the differentiation of precursor cells
known as satell ite cells.
It has been demonstrated that certain chemical stimuli can result in anabolism in the absence of
mechanical stimulation. There are several, but the stimuli that are best documented are testosterone
-
and IGF-1.
Mechanical stimulus can result in catabolism, especially if it is too severe or if inadequate "repair
time" is allotted (known as "overtraining") or if the biochemical environment is not right for
anabolism. The primary chemical stimulus for catabolism is activation of the glucocorticoid
" d s
recep tor by g IUCOCOrtlCOI 91617
' . GI UCOCOrtlCOI
" d s, l'k . I'
1'e COrtlSO .. of an enzyme,
, II1crease the aCllvlly
glutamine synthetase, which result in the breakdown of skeletal muscle tissue and release of
glutamine from muscle cells l8 .19 This glutamine is shuttled to the liver where it is converted to
glucose through the process of gluconeogenesis. It has been shown that there is increased
expression of glucocorticoid receptors in hypertrophied skeletal muscle making them more prone to
the effects of cortisoI 20.21.
Androgens and glucocorticoids can therefore be considered to be opposing forces with regard to
anabolism and catabolism. The following is an incomplete list of anabolic and catabolic mediators
in skeletal muscle22.23.24.25.26.27,28.29,30.31 ,32.33,34,35:
Anabolic Catabolic
Androgens Inactivity
Insulin Glucocorticoids
IGF-I Thyroid Hormone Excess
GH Thyroid Hormone Deficiency
Glutamine PGE2
BCAAs Interleukin I
Contraction Interleukin 6
Stretch TNF-a
B-Adrenergics Interferon-y
PGF2-a Ciliary Neurotrophic Factor
Urocortin II Proteolysis-inducing protein
Interleukin-IS Myostatin
MGF NF-kappa-B
Calcineurin
HIMP
SECTION 3
STEROID HORMONE SUPERFAMILY
The steroid hormone superfamily (SHSF) consists of several classes of related compounds. Each of
these classes contains many derivatives resulting in thousands of chemically related steroid
molecules. This is one of the reasons why the term "steroid" is way too generic. For the purpose of
this discussion I will refer to the synthetic derivatives of testosterone as Anabolic Androgenic
Steroids (AAS). There have been plenty of anecdotal reports of misinformed people buying
"steroids" only to find out that they were not AAS but instead some form of synthetic
glucocorticoid (a derivative of cortisol). Therefore I find it necessary to discuss the major classes of
steroids to familiarize the reader with a basic level of knowledge with which to understand more
advanced topics.
To reiterate, the SHSF comprises a large group of chemical entities that have a certain functional
similarity. Specifically, the members of the SHSF exert their effect through Nuclear Hormone
Receptors (NHR)36.37 NHR are so named because they act within the cell nucleus to directly affect
transcription and translation of DNA and therefore the production of new proteins 38 . Some members
of the SHSF include:
PPAR (Peroxisome Proliferator-Activated Receptor)

PXR (Pregnane X Receptor)
CA R (Constitutive Androstane Receptor)
LXR (Liver X Receptor) Orphan
FXR (Farnesoid X-Activated Receptor) Group
RXR (Retinoid X Receptor)
RAR (Retinoic Acid Receptor)
VDR (Vitamin D Receptor)
LRH (Liver Receptor Homologue)
ERR (Estrogen Receptor Related)
ROR (Retinoid Orphan-Related)
Thyroid
Mineralocorticoids
Glucocorticoids Traditional/Core
Progestins Group
Estrogens
Androgens
I have split the above receptors into two subgroups based on differences in functionality. The
bottom group is the traditional/core group of the SHSF while the top group is known as the orphan
group. The thyroid hormone system has some similarities with both groups. The orphan group has a
wide variety of ligands, which are largely non-steroidal (a few, such as CAR or VDR have steroidal
or semisteroidalligands) and the receptors behave quite differently even though they act through the
39
nucleus like traditional steroid hormone receptors While all of the members of the SHSF are
integral to the function of the human body, we will only concern ourselves with the traditional/core
group, as they are most relevant to the topic of this book. With the exception of the thyroid
hormones, the classical SHSF members have ligands that are all steroidal and derived from
cholesterol as shown below:
o
CH,
CH,
HO
HO Pregnenolone
Cholesterol o
o
HO
17 alpha hydroxy
Pregnenolone
/ o Progesterone
o
CH,
OH
o
OH
HO o
# o #
Androstenedione 17 alpha hydroxy
o #
Progesterone Deoxycorticosterone
OH
HO OH
~ Androstanediol
0
0
OH
1 CH,
OH
0
HO
"<1"";'"
Corticosterone
Estrone 1
! L
Testosterone OH OH
OH OH
CH, 0 0
OH
HO
H Estradiol
Dihydrotestosterone Cortisol Aldosterone
The stereotypical action of a steroid hormone is illustrated below:
t
~.
_ _~~ HRC
~.
The steroid hormone (S) enters the cell where it binds to the steroid receptor forming what is known
as a hormone receptor complex (HRC). The steroid receptor resides in the cytoplasm of the cell in
an inactive state bound to other proteins, upon binding to the steroid hormone, these other proteins
disassociate from the receptor and the receptor becomes activated. The activated HRC moves into
the nucleus. Once inside the nucleus, two I-IRC bind together to form a homodimer (homo means
same, dimer means two). This homodimer recruits coactivators and binds to DNA at specific sites
called hormone response elements (HRE). Once bound to the I-IRE's the homodimer can enhance
(increase) or repress (decrease) production of proteins encoded by the section of DNA governed by
the I-IRE (see illustration below)38.39.40.41.
(oactl'o',ator
o 00
New Proteins
One might assume at each class of steroid hormone (androgen, estrogen, progesterone,
corticosteroids) would ave a specific HRE and this would lend specificity of action to each class of
steroid. Specific HRE's, however, have remained elusive40 but some evidence is
42
emerging ,43,44,45,46,47. Many different HRE's have been found but only estrogen receptors seem to
have specific HRE's that cannot be activated by the other members of the SHSF 39 The others
(androgen, progesterone, corticosteroids) all seem to share HRE's to varying degree48 . This is
strange since each class of steroid seems to have very specific actions. How can each class have a
specific action when they are acting through the same, non-specific HRE's? There are several
theories, but the one that makes the most sense is that each class, though acting through the same
HRE, has specific actions at the HRE that differ depending on interaction with cofactors. This
changes the end result of interaction with a given HRE. For example, an androgen receptor
homodimer may bind to the HRE for IGF-I and due to the cofactors it recruits and the way it
interacts with the HRE, may cause enhancement of IGF-I production (resulting in increased IGF-I
level). On the other hand, a glucocorticoid receptor homodimer may also bind to the same HRE for
IGF-I and due to the different cofactors it recruits and the different way it interacts with the HRE
may cause repression of IGF-I production (resulting in decreased IGF-I level).
This implies that in cells where both androgen receptors and glucocorticoid receptors are present,
that there is competition for /-IRE's with opposing action4o.49.5o In a state of higher GR occupation,
more GR would bind to the /-IRE's, which would exclude and out-compete AR resulting in lower
IGF-I production. As AR occupation increases (through the addition of more androgen) it begins to
out-compete GR for /-IRE occupation and IGF-I production increases. This is obviously simplified
for the purpose of discussion here. To add complexity, consider that each steroid class may act on
/-IRE's of hundreds of proteins, increasing the production of some while decreasing others. There
could potentially be some overlap, for instance AR and GR could both increase the production of 5
proteins and decrease the production of 5 proteins but have opposing actions on 10 additional
proteins. Again consider that each class may affect hundreds of proteins and that each class may
have a different combination of action and the result could be very different for each class.
Each class of hormone has its own specific receptor; however, each receptor has quite a bit of
51
similarity to the other members . Steroid receptors have three main parts: the DNA binding domain
(OBD) - responsible for binding DNA, the ligand binding domain (LBO) - responsible for binding
the specific hormone(s), and the n-terminal domain 52 ,53 The percent similarity of each receptor
compared to the glucocorticoid receptor is shown below in simplified form 51 :
DBD LBO
IUQQJO I 100 I GR
ICEJOI 57 IMR
I[]Q]O I 55 I PR
I~OI 55 I AR
I CillO I 30 ER
Because of the high amount of similarity in the LBO, the specific receptors are not necessarily so
specific. There is considerable ability of some steroids to crossover to receptors other than their
own 54 .55 .56575859
. . . , P rogesterone, an d rogens, g IucocorllCOI
. 'd S an d mll1era
' IOCOrtlCOI
" d s a II have some
ability to crossover. Estrogen (and its receptor) has the least amount of crossover because of the
relatively low amount of similarity in its LBO compared to the other members.
RECEPTOR BINDING
Steroid receptors are proteins. Like all proteins, steroid receptors are composed of many amino
acids. These amino acids are bound to each other in such a way to form a three dimensional
structure. This 3-D structure will differ based on the amino acids that make up the receptor
molecule. There are several important domains or regions of the receptor. One important region is
the DNA-binding domain (DBO). This region ofthe molecule determines how the receptor binds to
DNA. The ligand-binding domain (LBO) is the area of the receptor that binds the steroid molecule.
This area of the receptor forms a pocket, which the steroid molecule can slide into. Once the
molecule slides in, it comes into contact with amino acids on the interior of the pocket. The steroid
molecule, if it is the proper steroid for its receptor, will bind to these amino acids. This binding
changes the shape of the receptor molecule. If the binding is strong enough, the shape of the
receptor will change to cause a section of the receptor to fold over, closing the binding pocket
around the steroid molecule 6o This is a necessary step for the activation of steroid receptors. This
process can be visualized by thinking of the receptor as a box with a lid. The steroid goes into the
box and the lid folds over and closes the box:
Relative binding affinity (RBA) is a measure of how strongly a steroid binds to its receptor
compared to a standard molecule. Strength of binding is important because the stronger a steroid
binds; the more likely it is that the steroid will activate the receptor. Hypothetically speaking, a
steroid with an RBA of 100 may have a 70% chance of activating its receptor each time they come
into contact, while a steroid with an RBA of 40 may only have a 20% chance per each interaction.
RBA alone is not the only factor that determines a successful interaction. Concentration of a steroid
and concentration of the receptor also determine the likelihood of activation. Increasing
concentration of either the steroid or the receptor, or both, will increase the probability of activation.
For instance, 50 mg of steroid x with an RBA of 50 may have a 30% chance of activation, while
200 mg of steroid x may have a 40% chance (a doubling of concentration does not necessarily result
in a doubling of probability). If the number of receptors also doubles, then the likelihood may
increase to 70%. Therefore, the best-case scenario is a high affinity ligand in an environment of
high receptor density at an optimal concentration of ligand. Another important factor is the half-life
of the compound in plasma. A compound with a longer half-life in plasma will have a much beller
chance of binding the receptor. For example, oxymetholone has a relatively poor affinity for the
androgen receptor compared to testosterone. However, the half-life of oxymetholone is around eight
hours, while the half-life of testosterone is a matter of minutes.
K R
o R
K
N
DeC
R
N ""/P
Zn +
GA / '\ A
C C
KRAVEGOHNYL Ry
R
K
C
L
o
A
The problem is, the receptor concentration is unknown and is not steady. It can change in response
to several stimuli. It is a common beliefamong AAS users that the androgen receptor concentration
increases in response to stimulation by androgens. The fact is standard pharmacological theory
dictates that continued stimulation of receptors results in desensitization or downregulation of
receptors. The scientific literature is split, with some studies showing upregulation of androgen
. an d ot h ers si ' d ownregu I ' 0 f receptor quantity , , , , , . In my
7
receptor quanlity 10Wll1g atlon .616. -, 636465666768
experience, it seems much more logical that receptors desensitize or downregulate in response to
stimulation. Therefore, if you start out with a certain concentration ofa steroid, as time goes on, this
concentration will become less effective as the number of androgen receptors decreases, This is, in
fact, what we see in practical use of androgens. Users, at one time, used a pyramid scheme of
steadily increasing doses to help combat this effect. As the receptor density decreased, the
concentration of androgen increased, keeping receptor activation at roughly the same level. For
some reason, pyramiding fell out of favor with people opting for a scheme known as
"frontloading". With front loading, users start a cycle with the highest concentration of steroids that
they plan to use throughout the cycle. This results in a lot of receptor activation very quickly, but
also results in extreme receptor down regulation and a resulting faster loss in efficacy of the given
dose. It has also been shown that while androgen stimulation results in androgen receptor down
regulation, estrogen stimulation results in androgen receptor up regulation. This can be witnessed
with the fact that females have higher androgen receptor concentrations than do males.
Unfortunately, estrogen receptor activation results in several negative side effects, which has led
people to conclude that the lower the estrogen level the belter, mainly through the use of aromatase
inhibitors. Some have found it worthwhile to allow estrogen levels to rise while using an estrogen
receptor antagonist to combat the negative side effects. This also provides an argument for
including an aromatizable androgen in a cycle to help keep androgens receptor levels from
declining too severely.
ANDROGENS
Androgens are the class of steroid hormone of which testosterone and dihydrotestosterone (DHT)
are the primary members:
OH OH
~
o a
H
Testosterone DHT
Syntbesis
Testosterone is produced in the Leydig cells of the testes in response to luteinizing hormone (LH)
produced by the anterior pituitary. The Leydig cells also produce lesser amounts of DHT and
estrogen. Production of testosterone in normal men is about 5 mg per dai l . The stimulation of
testosterone secretion by LH is part of the hypothalamic-pituitary-gonadal axis (H PGA). The
hypothalamus and pituitary are two glands that reside in close proximity in the brain. The
hypothalamus produces a protein called gonadotropin-releasing hormone (GnRH) and secretes it in
pulses every 90-120 minutes into the pituitary giand sl . Once in the pituitary, GnRH stimulates the
release of LH and follicle stimulating hormone (FSH) into systemic (whole body) circulation. LH
and FSH bind to receptors in the testes. LH causes release of testosterone by the testes as described.
FSH, on the other hand, causes the release of androgen binding protein in the testes, which allows
for the maturation of sperm. Testosterone leaves the testes and circulates in the blood reaching the
hypothalamus and pituitary in the brain. Testosterone is aromatized to estrogen by the pituitary and
this is the signal for the pituitary to reduce the pulse amplitude of LH. DHT is also produced
through conversion by 5-alpha-reductase in the pituitary, which reduces LH pulse frequencl 9
Metabolism
In some androgen target tissues - hypothalamus, prostate gland, sebaceous glands, hair follicles -
testosterone is converted to DHT by the enzyme, 5-alpha-reductase. Approximately 6 to 8 % of the
daily production of testosterone (5 mg) is metabolized to DHT, amounting to about 0.3 mg per
dai'. DHT has approximately 25% greater affinity for the androgen receptor than testosterone.
This allows for a greater level of activity in these tissues without a change in the plasma levels of
testosterone. DHT also circulates in the blood, but binds more strongly to SHBG. Testosterone is
the primary androgen in skeletal muscle. Skeletal muscle has little 5-alpha-reductase activity but
possesses another enzyme, 3-alpha-hydroxysteroid dehydrogenase, which rapidly deactivates any
I
DHT that enters muscle cells from the circulation 70.7 .7 2
Testosterone is also metabolized to estrogens with about 0.3% of the daily production of
testosterone being converted to estradiol. This amounts to about 17 uglday with an additional 28
uglday (for a total of 45 uglday) arising from the peripheral conversion of androstenedione to
estrone to estradiol 5 '.
Receptor(s)
While androgen receptors are found in many diverse cell types, the tissues with the largest
concentrations are prostate and skeletal muscle. It has been assumed for quite some time that
activation of AR stimulates the production of more AR. However, castration causes AR levels rise
and when testosterone replacement is given; AR levels fall back to normal levels 73 This suggests
that androgens negatively regulate AR production. There has also been some conjecture that there is
an anticatabolic component of androgens. This would most likely occur through blockade of the
glucocorticoid receptor by testosterone (and derivatives) thereby disallowing catabolism of muscle
tissue through the action of cortisol at the glucocorticoid receptor. Another possibility is that
testosterone acts through the androgen receptor to decrease the activity of cortisol. A final
possibility is that androgens inhibit the production of cortisol resulting In a decrease In
glucocorticoid receptor activation and therefore decreased catabolism.
There is only one androgen receptor74 . All androgens act through this receptor. Research has found
a cell membrane receptor that is activated by some androgens. However, the role of this receptor is
75
currently being investigated and it is unlikely to playa major role in the anabolic effect of AAS
Even though there is only a single androgen receptor, there are many different AAS that seem to
produce varying effects. Several theories have been developed to try to explain these differences in
activity. The answer lies in the fact that there are multiple steroid receptors (other than the androgen
receptor), enzymes and binding proteins that androgens interact with to produce the variations in
effects. These factors and their influence on AAS activity will be discussed in future sections.
Protein Bindingrrransport
After being released into the blood stream, testosterone circulates primarily in the bound state.
Roughly fifty percent is bound to serum albumin while forty four percent is bound to sex hormone
binding globulin (SHBO) and four percent is bound to corticosteroid binging globulin (CBO). This
leaves about two percent of total testosterone in the free state in the plasmaS]. This free portion of
testosterone is available to act on cells that contain androgen receptors (termed androgen target
tissues).
Actions
Androgen is a generic term that refers to the fact that these are the hormones that arise during
puberty in the male to begin the process of developing secondary sexual characteristics (growth of
body hair, deepening of the voice, initiation of sperm/semen production etc.). This class of
hormones is the basis for almost all of the synthetic AAS used by athletes.
Testosterone levels are relatively low from birth to puberty. At puberty, levels rise and remain
elevated until puberty ends. This increase in testosterone initiates many changes including:
increased testicular size, axillary hair growth, sperm production, prostate enlargement, and increase
in linear growth, deepening of voice, growth of laryngeal cartilage (Adam's apple), increased
muscle mass and acne. As puberty ends, testosterone levels fall to normal adult levels and slowly
decline over the remainder of a man's life 76 . This decline in testosterone as a man ages is slowly
being recognized as an important physiological change that can and should be addressed n Termed
"male menopause" by some, "andropause" by others, this condition has been implicated in
everything from depression to lethargy to erectile dysfunction to heart disease and cancer.
Physicians are becoming more aware of HRT for men and more are willing to prescribe
replacement testosterone to men whose natural levels have fallen. HRT is still in its infancy but as
more men learn of the importance of maintaining healthy levels of testosterone, its popularity is
likely to increase.
Normal Levels
Total testosterone levels in normal adult males range from 300 to 1000 ng/dL with free testosterone
levels at 50 to 210 ngiL although ranges differ somewhat depending on the source 51 ,78 Total DHT
levels in normal adult males are in the range of 30 to 85 ngidL. In women, the rages are 15 to 70
ngidL for total testosterone and I to 8.5 ngiL for free testosterone and 4 to 22 ngidL for tolal
DHT 78
These may be higher than you would expect given the production of only 5 mg per day of
testosterone in normal males. This is due to the fact that sex hormone binding globulin (SHBG)
prolongs the half-life and helps to maintain plasma levels of androgens in the blood.
Excess/Deficiency
Excess androgens can be very detrimental in women but can also have negative effects in men as
well. Body and facial hair growth, voice deepening, acne, baldness, changes in skin thickness and
texture, loss of menstrual period, changes in cholesterol and enlargement of the clitoris are some of
the negative effects of excess androgens in women. In men, acne, prostate enlargement, changes in
blood lipids and male pattern baldness are the primary side effects of excess androgens.
Androgen deficiency in men can result in depression, lethargy, impotence, gynecomastia, reduced
sexual desire, decreased muscle mass, increased body fat and reduced bone mass. Androgen levels
tend to decline in men past the age of30 to 40 years 01d 79.8o
ANABOLfC PHARMACOLOGY 42
ESTROGENS
The body produces several different estrogens, the three most common are shown below:
HO o HO
CH 3 CH 3 CH 3
HO HO HO
Estradiol Estrone Estriol
As you can see there is an aromatic benzene ring as the first (A) ring member. All steroidal
estrogens share this benzene ring.
Synthesis
Estrogens are produced in men through the conversion of testosterone by the enzyme, aromatase, in
peripheral tissues, especially fat tissue. In women, the ovary directly produces estrogens.
Approximately 66 ug of estrone and 45 ug of estradiol are produced per day in the normal male
through peripheral conversion of androgens 51
Metabolism
Estradiol is converted into estrone and vice versa by 17-BHSD. Estrone is sulfated to form estrone
sulfate, which has a long half-life in the body and can be de-sulfated and converted back to estradiol
in times when estradiol production is low 81 .
Receptors
Unlike the other classical members of the SHSF, which only have one active receptor, there are two
functional estrogen receptors, ERalpha and ERbeta82 ,83,84,85 These two receptors are found in
different quantities in different tissues and have different functions, which greatly expands the
'b'l'
varia I lty 0 f actIOn
'f 0 estrogens82838485
' , . , S'
tlmu IatlOn
' 0 f estrogen receptors resu I
ts 'In upregu Iatlon
'
of estrogen and progesterone receptors 5l , Non-genomic effects of estrogens have been demonstrated
to occur through multiple mechanisms and unlike the other members of the classical steroid
86
hormone uperfamily members, are fairly well understood
Estrogens also circulate in the bound and free state. Seventy-eight percent of estradiol is bound by
albumin and twenty percent is bound by SHBG leaving two to three percent in the free slate. The
affinity of estradiol for SHBG is roughly one fifth that of DHT and about half of that of
testosterone. Estriol and estrone are about ninety percent bound to albumin with seven percent of
estrone and very little estriol bound to SI-18G. Roughly eight percent of estriol and four percent of
-I
estrone circulates unbound' .
Actions
Like androgens, estrogens comprise the set of hormones partially responsible for the development
of secondary sexual characteristics in females at the onset of puberty (growth of breast tissue, onset
of ovulation and menstruation, deposition of female pattern body fat distribution).
Although estrogens have traditionally been considered "female" hormones, they actually have very
important functions in both men and women besides female sexual development87 Estrogens
decrease bone breakdown, increase HDL, decrease LDL and have a role in libido in both men and
women 88
Normal Levels
Normal levels of estradiol in adult males are 10 to 50 pg/mL. In women, levels are more variable
due to the cyclical menstrual phase and can range from 20 to 750 pg/mL depending on the phase of
the menstrual cycle. Estriol increases in pregnancy but is usually less than 2 ng/mL in normal adult
men and women. Normal estrone levels in the adult male are 15 to 65 ng/L and in women are 15 to
250 ng/L 78
Excess/Deficiency
Although estrogens have many important functions in males, excess estrogens can have numerous
deleterious effects including gynecomastia. Estrogens are also known to facilitate the loss of
intravascular fluid into the extracellular space resulting in peripheral edema or bloating89 It is
important to note that although estrogens tend to worsen the appearance of water retention, they do
not necessarily cause water retention. There is a long held belief that estrogens cause water
retention during an AAS cycle. The fact is, androgens have a direct effect on the kidneys and result
91
in significant water retention and associated hypertension 90 . The presence of excess estrogens in a
steroid cycle will cause more water to accumulate subcutaneously resulting in the bloated
appearance. The use of anabolic steroids often increases estrogen levels either by displacing
resident estrogen from SHBG or through the conversion of the exogenous steroid to an estrogen or
estrogenic compound. Several strategies exist for the reduction of estrogen. Excess estrogen in
women can result in breast and uterine cancer.
Estrogen deficiency in males can result in decreased bone mass, altered cholesterol levels (higher
LDL or bad cholesterol and lower HDL or good cholesterol) and increased body fat levels92.9J.94
PROGESTINS
Progestins are the class of hormones that also arise in large quantities at puberty (in females) to
work in concert with estrogen to produce secondary sexual characteristics. Progestins are named for
their role in pregnancy (pro-gestational) in which they are essential. This is why the "Abortion pill"
Ru-486 (A.K.A. mifepristone), a progesterone antagonist, is so effective in terminating pregnancy.
Progesterone has a structure similar to testosterone:
o
CH:3
Synthesis
In women, progesterone secretion is mostly handled by the ovaries with the adrenals contributing
slightly. In men, the adrenals contribute the largest proportion of progesterone.
Metabolism
Progesterone is metabolized to 20-hydroxyprogesterone, 17-hydroxyprogesterone, allopregnenolone

and 5-alpha dihydroprogesterone. Progesterone is also an intermediary in the production of
aldosterone.
Receptors
There are two progesterone receptors termed PR A and PR B . PR A is a shorter from of the receptor and
only seems to have minimal transcriptional activity. Its larger role seems to be to inhibit the activity
of PRB. PR B is the major transcriptional isoform of the progesterone receptor and carries out most of
the actions of progesterone. The ratio of receptor isoforms differs from tissue to tissue and probably
plays a role in the differential effects of progesterone in different tissue types.
Protein Bindingffransport
Approximately 2.4% of progesterone circulates in the free state with about 17% bound to
sl
corticosteroid-binding globulin and about 80% bound to albumin .
Actions
Progestins were largely neglected in research until the past five or ten years. In the past decade a
new picture has been emerging that shows progestins to be more than just pro-pregnancy hormones.
There is a large amount of interplay between the progesterone and estrogen receptor systems.
Progesterone seems to reduce estrogen activity and estrogen, in turn, gives feedback to increase
progesterone action to a certain degree SI . While many side effects have been blamed on derivatives
of testosterone converting to estrogen, the role of progesterone in these processes is just now
coming to light. Most synthetic derivatives and even testosterone itself have some inherent
progestational activity due to the fact that the hormones and the receptors are so similar. Not all
AAS are agonists at the progesterone receptor. Some are antagonists and some are partial agonists
(or panial antagonists depending on how you look at it). This spectrum of activity can help to
explain some of the difference in activity among AAS. Since activation of the progesterone receptor
has been shown to decrease estrogen activity it can also be expected that antagonism of the
progesterone receptor will increase estrogen activi ty 9s. Therefore, the degree of progesterone
receptor activity can produce differing degree of effect on estrogen activity.
Normal Levels
What most people don't realize is that men have the same plasma levels of progesterone as a
woman who is in the follicular phase of her cycle; 0.2 to 1.4 ugIL. In the luteal phase, progesterone
levels can be as high as 27 ug/L and in the third trimester of pregnancy, levels can rise to 255 ugIL
in women. The level of progesterone in men is much higher than that of estradiol and is not too
78
much less than that oftestosterone .
ExcesslDeficiency
Excess progesterone in males is known to result in impotence and studies have shown that animals
lacking progesterone receptors have improved sexual function 96 . In fact, synthetic progestins have
97
been given to sex offenders to decrease sexual desire and frequency of erections Progesterone
receptor activation seems to severely disrupt the hypothalamic pituitary gonadal access resulting in
shutdown of testicular androgen synthesis. Deficiency of dihydroprogesterone, particularly with the
use of the S-alpha reductase inhibitor finasteride can result in altered levels of GABA production in
the brain, DHP, through the action of 3-alpha reduced metabolites increases GABA signaling
resulting in antidepressant and anti-anxiety effects. Deficiency in DHP can result in depression and
anxiety 51. Progesterone excess does appear to promote weight gain and appetite in both men and
women98
GLUCOCORTICOIDS
Glucocorticoids is the name given to the class of compounds of which cortisol is the representative
member. Its structure is similar to progesterone:
OH
o
CH3
" .. OH
Synthesis
Glucocorticoids and the next group mineralocorticoids are often lumped together under the term
corticosteroids because they are produced, in large part, in the adrenal cortex. The adrenal glands sit
on top of the kidneys. Within the adrenals, there are two different regions. The cortex primarily
produces corticosteroids while the other region, the medulla, produces epinephrine (also known as
adrenaline).
Glucocorticoid secretion is stimulated by adrenocorticotropic hormone (ACTH), which is released

in turn from the pituitary after stimulation by corticotrophin releasing hormone (CRH).
Glucocorticoids are secreted in a circadian rhythm with high levels secreted in the morning just
before rising. Glucocorticoids are also secreted in response to feeding and exercise. Glucocorticoids
are known as stress hormones because they are also released in response to stress.
Metabolism
Cortisol is interconverted to cortisone and back again by enzymes referred to as II-beta

hydroxysteroid dehydrogenases. This allows for a secondary pool of readily available
glucocorticoids. Glucocorticoids are primarily 5-beta reduced by the liver with little 5-alpha
reduction occurring. In addition, the 3-keto group is reduced by the 3-alpha hydroxysteroid
dehydrogenase enzyme to the 3-alpha tetrahydro derivatives (3-alpha hydroxyl, 5 beta_)52
Receptor
There are two primary glucocorticoid receptors, GR-alpha a nd GR-b .
transcriptional regulator of glucocorticoid action L'k h eta. GR-alpha IS the primary
. . . let e progesterone receptor the second
glucocorticoid receptor (OR-beta) acts as a negative modulator ofGR-alpha function. '
Under normal ~on~iti~ns, four percent of circulating cortisol is free, about ninety percent is bound
to corticosteroid binding globulin (CBG), also known as transcortin, and about seven percent is
bound to aibumin si .
Actions
The term glucocorticoid derives from the fact that one of the first effects discovered for these
hormones was their ability to affect glucose metabolism. Glucocorticoids increase gluconeogenesis
in the liver. Gluconeogenesis is the formation of glucose in the liver from other sources such as
amino acids. Glucocorticoids increase the pool of circulating amino acids through the breakdown of
skeletal muscle proteins (causing the release of glutamine) and increase lactate release from skeletal
muscles, which can also be used to release glucose.
Now, after 20 years of research, the role of glucocorticoids IS known to be much broader.
Glucocorticoids are responsible for many remarkably different functions. They are central to most
immune and inflammatory responses in addition to their glucose metabolism activities.
Glucocorticoids are well known in the AAS community for playing a role in the catabolism of
muscle and the anabolism of adipose tissue. They also playa role in bone metabolism. Often
demonized, this class of hormones is necessary for our survival. In fact, cortisol can be considered
the basic survival hormone. It plays a very big part in the response to stress and depression.
ormal Levels
Cortisol levels fluctuate throughout the day as part of the normal circadian rhythm with levels
highest upon rising in the morning and lowest levels during rest late at night.
Excess/Deficiency
Cortisol levels are tightly regulated because they are critical to human survival. Excess cortisol
results in muscle wasting, water retention, weight gain (especially central obesity) and depression.
Cortisol deficiency can result in anorexia, fatigue, weakness, weight loss, dehydration and joint pain
with calcification of cartilage in longstanding deficiency.
MINERALOCORTICOIDS
Mineralocorticoids, of which aldosterone is the representative member, are named because of their
ability to alter electrolyte (minerals like sodium and potassium) movements in the body (especially
in the kidney). They are very similar in structure to glucocorticoids:
OH
HO o
O-~"
'" OH
Synthesis
Though aldosterone is considered the major or stereotypical mineralocorticoid, the body produces
several other mineralocorticoids including deoxycorticosterone. These hormones, as mentioned,
control electrolyte balance, especially sodium. They act to retain sodium in the kidney resulting in
the retention of water and an associated increase in blood pressure.
Metabolism
Like cortisol, aldosterone is converted to tetrahydro derivatives through the action of 5-bela
reductase and 3-alpha hydroxysteroid dehydrogenase.
Receptor
99
Just as aldosterone and cortisol are very similar chemically, so are their receptors Just as with
estrogen and progestins, the interplay between glucocorticoids and mineralocorticoids is very
important. Glucocorticoids can stimulate the mineralocorticoid receptor and circulate at much
higher levels than mineralocorticoids99 . Without some kind of protection, glucocorticoids would
constantly stimulate mineralocorticoid receptors. The protective mechanism is an enzyme called 11-
beta-hydroxysteroid dehydrogenase 2 (II BHSD2). This enzyme inactivates glucocorticoids
allowing mineralocorticoids to act at the mineralocorticoid receptor.
Of all the steroid hormones mentioned here, aldosterone has the largest free circulating fraction.
Approximately 37 percent of aldosterone circulates in the unbound state. About 42 percent is bound
52
by albumin while the remaining 21 percent is bound to corticosteroid binding globulin .
Actions
Our understanding of mineralocorticoids has also benefited from the resurgence in "new" steroid
research. Instead of just controlling electrolyte movement in the kidney, mineralocorticoids and
their receptor are responsible for a range of activities on par with glucocorticoids.
Mineralocorticoids are very active in wound healing and are found throughout the body, often being
produced locally.
ExcesslDeficiency
Excess aldosterone results In sodium and water retention, which cause an increase in blood
pressure. High sodium intake decreases aldosterone secretion. Deficiency of aldosterone results in
dehydration, salt-wasting, hyperkalemia (high blood potassium) and metabolic acidosis.
5\ ANABOLIC PHARMACOLOGY
THYROID HORMONES
The thyroid hormone system is part of the steroid hormone superfamily even though the hormone
ligands are not steroids. The reason is that the thyroid receptors act in a steroidal fashion. Even so,
the thyroid hormone system is not part of the core family consisting of androgens, estrogens,
progestins, glucocorticoids and mineralocorticoids. I have chosen to include them here because they
are a topic of much interest and have considerable interaction with androgens. There are two
primary ligands in the thyroid system:
~~ ~.
'r---'JI-'OH
Thyroxine (T4) Tri iodothyroni ne(T3)
Synthesis
T4 is the major product of the thyroid gland and acts as a prohorrnone of T3 which is produced as
needed in peripheral tissues. Thyroid hormones are produced in the thyroid gland, which is located
just below the Adam's apple. Thyroid hormones are unusual in that they contain the trace element
iodine, which is scarce. The thyroid gland is responsible for concentrating iodine and storing it in
the form of thyroglobulin to compensate for periods when iodine intake is low. In the thyroid gland,
stored iodine is bound to tyrosine. Tyrosine is an amino acid derivative, which is found in the diet
or converted in the body from the amino acid, phenylalanine. Tyrosine is also utilized in the
production of dopamine, norepinephrine and epinephrine.
The release of thyroid hormone is controlled by the hypothalamus and pituitary in what is referred
to as the hypothalamic-pituitary-thyroid (HPT) axis. Thyroid releasing hormone (TRH) is released
from the hypothalamus into the pituitary gland where it stimulates the release of thyroid stimulating
hormone (TSH). TSH is released into circulation and stimulates the thyroid gland to release T4,
which is metabolized to n. T3 feeds back to inhibit secretion ofTRH and TSH.
Receptor
Since T3 is the active thyroid hormone, it binds to the thyroid receptor and causes activation in a
similar manner to the other steroid receptors. Thyroid hormone receptors form dimers and are
transported into the nucleus where they activate transcription of DNA
There are at least two thyroid hormone receptors TRalpha and TRbeta, which have different effects
when activated. Current efforts are underway to produce selective modulators of these receptor
subtypes to arrive at molecules that increase thermogenesis and basal metabolic rate or decrease
cholesterol levels without deleterious effects on the cardiovascular system.
Protein Bindingffransport
Thyroid hormones are transported in serum bound to carrier proteins. Only 0.04% of T4 and 0.4%
ofT3 circulate in the "free" state. It is this free portion that is able to bind the thyroid receptors and
result in hormonal action. There are three major binding proteins for thyroid hormones: thyroxine
78
binging globulin (TBG), thyroxine-binding prealbumin (TBPA) and albumin
TBG is synthesized in the Iiver and its levels are increased by estrogen while androgens decrease its
level. TBPA is a large peptide made up of several smaller peptides, known as a polypeptide, which
binds about 10% of circulating T4. Its affinity for T3 is about tenfold lower than for T4 so it carries
mostly T4. The dissociation of T4 and T3 from TBPA is rapid so TBPA is a source of rapidly
available T4. Albumin has a single strong binding site for T4 and T3 and several weaker ones.
Albumin is the most common protein in serum. Because of its high concentration, albumin
transports about 15% of circulating T4 and n. Thyroid hormones dissociate rapidly from albumin
making it a major source of free hormone in tissue 78
Actions
Thyroid hormones are essential for survival and have a multitude of effects. One of the main results
of thyroid hormone action is an increase in ATP utilization generating more body heat, greater
oxygen consumption and a higher basal metabolic rate due in large part to an increase in activity of
the enzyme, sodium-potassium ATPase. Thyroid hormone action also increases the production of
red blood cells and production of beta-adrenergic receptors, which also increase energy
5178
consumptIOn . .
Normal Levels
Thyroid hormone levels, though easily measured, are not easily interpreted. Simply measuring
absolute T4 and T3 levels will not necessarily give an accurate assessment of thyroid gland function
and thyroid hormone action.
Excess/Deficiency
Thyroid hormones are used illicitly to help burn fat. There are two types of medication available for
this purpose, synthetic T4 known as synthroid and synthetic T3 known as cytomel. Most people use
Cytomel<li> for fat burning since synthroid has to be converted to T3 to be active and the body will
adjust by reducing this conversion. Of course, Cytomel is very effective for helping to reduce body
fat but there are several serious side effects of its use. A hyperthyroid (too much thyroid) state can
result in catabolism of skeletal muscle as well as detrimental effects on the cardiovascular system.
Both excess levels of thyroid, known as hyperthyroidism, as well as a deficit of thyroid hormone,
known as hypothyroidism result in loss of skeletal muscle mass and an increase in cortisol
production.
SECTION 4
ENZYMES, CROSSOVER AND SIDE EFFECTS
One important thing to understand is the idea of equilibrium or balance. The human body is an
amazing biological machine, but it is not infallible. When you introduce a new situation, such as
administering AAS, the body will fight it, attempting to maintain the status quo. However, after a
time, ingesting these substances becomes the norm and a new equilibrium has been reached. As
mentioned in the section on androgens, the actions of AAS cannot be explained through androgen
receptor binding alone. In the preceding sections, the action of certain enzymes, such as 5-alpha
reductase and aromatase were mentioned. The action of enzymes on AA and the action of AAS on
these and other enzymes help to determine the specific activity of each individual steroid. In
addition, the ability to crossover to other steroid receptors (progesterone, glucocorticoid,
mineralocorticoid) is another determining factor in the differentiation of AAS and the generation of
side effects.
ENZYMES
5-ALPHA REDUCTASE
5-alpha Reductase (5AR) is an enzyme that is responsible for the irreversible conversion of C-4
double bond containing steroids to 5-alpha reduced analogues 100. A couple of examples of this
reaction are the conversion of androstenedione to androstanedione and testosterone to DHT:
H:31
CH:3 CH:3
5-alpha-reduetase

Androstenedione
Androstanedione
CH,OH
CH,
5-alpha-reduetase
o o
H
Testosterone
Clhydrotestosterone
The production of DHT in these tissues results in a local difference in androgen receptor activation.
DHT has a higher affinity for the androgen receptor and therefore, has a higher activity at an
equivalent dose. This allows for different levels of activation in different tissues without changing
the systemic (whole body) androgen level.
There are, in fact, two isoforms of 5AR - type I and type 2 100. \01 . 5A RIIS <,oun dIn many dIverse
tissues, but has .ItS I .
llghest expression Ieve Is In h < II I
air 10 IC e, se b i gd
aceous an , an d ,.Iver 100.101.102 .
5AR2 is most highly expressed in prostate, epididymis and seminal vesiciesloo.IOI Inhibition of the
type 2 enzyme is therefore specific to those tissues. Inhibition of type I, however, results in systemic
(whole body) reductions in DHT and can reduce androgenic side effects such as male pattern
baldness, acne and HDL reduction. Finasteride, a type II inhibitor is used for male pattern baldness
(MPS), but is only minimally effective because it is much more potent at the type II enzyme. 5AR
production is increased by androgens, therefore, the more androgen in the system, the more 5AR is
present.
Finasteride has been used to block 5AR activity, especially in cases of benign prostatic hypertrophy
(BPH) and prostate cancer. Finasteride is a selective 5AR2 inhibitor, which blocks DHT production
in those tissues with high levels of 5AR2 expression (prostate, seminal vesicle epididymis). It also
lowers circulating DHT by up to 70%. However, it does not reduce conversion to DHT in those
tissues in which 5ARI is present (sebaceous glands, hair follicles etc ... ) except at higher doses.
Also, the reduction in circulating DHT levels is transitory because levels of 5AR I are likely to
increase in a compensatory fashion, which will over time raise circulating DHT back to near normal
levels\Ol.
In most cases, 5-alpha reduction results in a more potent androgen. In the case of nandrolone and
nandrolone derivatives, 5-alpha reduction results in less potent derivatives lOJ :
H
OH
5-alpha Reductase
In this case, nandrolone is converted to dihydronandrolone CDHN). DHN has less affinity for the
AR than nandrolone. This is positive in the sense that for a given dose of nandrolone, there will be
greater activation in muscle than in the prostate. However, at higher doses, nandrolone will
overcome the capacity of 5AR resulting in higher levels of prostate AR activation. A-ring
substituents, such as a 2-methyl or a 4-chloro, result in some protection of the molecule from the
action of5AR.
5-alpha reductase also catalyzes the production of 5-alpha educed forms of progesterone such as
dihydroprogesterone (DHP)I02 DHP and its metabolites are known to produce anti-anxiety effects
in the brain 102 . Inhibition of5-alpha reductase could therefore interfere with this process.
An interesting side effect of 5-alpha reductase inhibition is an increase in testosterone production

due to a decrease in androgenic feedback at the hypothalamus. Also, less testosterone is "broken
down" to DHT; therefore, more remains in circulation 104
AROMATASE
Aromatase, an enzyme produced in many different tissues in the body, is responsible for converting
certain androgens into estrogens Androgens, like testosterone and androstenedione, which have a
double bond at position 4, are susceptible to aromatase action forming estradiol and estrone
respectivelylOO,IOS
OH
OH
CH,
CH3
Arornatase
o
HO
Testosterone Estradiol
Some androgens cannot be converted by aromatase. DHT is the prime example of a non-
aromatizable androgen. The lack of a double bond at carbon 4 changes the shape and electrical
properties of the molecule in such a way that ilS affinity for aromatase is very low. In fact, DHT and
other 5-alpha reduced androgens are known 10 be significant inhibitors ofaromatase activity.
5l
The testes produce only two percent of circulating estrone and 20% of circulating estradiol . The
vast majority of estrogens produced in the male are a result of the peripheral action of aromatase.
Fat tissue has a high level of aromatase activity and is, in fact, the largest source of estrogen
l05
production in males in the form of estrone
As stated, not all androgens are subject to aromatase activity. There is very little information in the
scientific literature as to which androgens are aromatized and which are nol. However, by taking
~..I what is in the literature and examining anecdotal reports, we can start to understand what
-:t. '\'
,.v Jscompounds are likely to be converted to estrogenic substances.
~~
""
s!
I r.!:r'" As previously stated, androgens with a C-4 double bond are subject to aromatization while 5-alpha-
redued steroids (like DHT) are not. Therefore, testosterone and androstenedione fit the profile
exactly. Nandrolone also seem to fit the profile; however, it is missing a methyl group at C-19.
This seems to reduce the affinity for aromatase considerably. Therefore, while nandrolone can be
aromatized, it is at a much lower potential than C-19 methylated androgens (like testosterone). One
must also realize that as the dosage of nandrolone is increased its potential for aromatization is also
increased.
Steroids like chlorotestosterone and oxymesterone are known to be non-aromatizable. This is due to
the fact that addition of a group to the A-ring (in this case -CL or -OH) results in a "protection" of
the molecule from aromatization (or 5-alpha reduction for that maller). These groups inhibit the
binding of the molecule to aromatase and the actions thereof.
One thing that must not be forgollen is that molecules undergo changes as a result of metabolism. If
a molecule with A-ring substiluents is metabolized in such a way that the group is removed then the
metabolized molecule is no longer "protected" and may undergo aromatization. The metabolism of
AAS is largely an unexplored area of study and therefore an unknown quantity. Animals lacking the
aromatase enzyme actually show increased adiposit/o 5
3-ALPHA/BETA-HYDROXYSTEROID DEHYDROGENASE
H H
3- alpha-hydroxys!eroid
dehydrogenase
o HO'"
H
Dhydrotestosterone
Androstanedjol
There are multiple isoforms of 3-alpha and 3-beta hydroxy steroid dehydrogenase enzymes, which
are expressed in various tissues throughout the body'06,I07,108 These enzymes are capable of
converting 5-alpha reduced androgens to 3-alpha or 3-beta diols:
This results in deactivation of the molecule since diols are much less potent. 3-alpha HSD is present
in skeletal muscle, so any DHT that reaches the muscle is rapidly deactivated. This means that using
DHT will not result in AR activation in skeletal muscle unless high enough doses are used to
overwhelm the enzyme action. Inhibition of 3aHSD in skeletal muscle is a potential method of
increasing anabolism that has not yet been explored. It is known that some drugs
(medroxyprogesterone) inhibit this enzyme and it is likely that some synthetic AAS do so as
well 109,1 10 3-beta HSD are bidirectional and can convert Diol prohormones to active 3-keto steroids.
II-BETA HYDROXYSTEROID DEHYDROGENASES
The II BHSD enzyme family consists of two isoforms: type I and type 2. II BHSD I is expressed in
almost every tissue in the body and is responsible for the conversion of inactive glucocorticoid
metabolites into active forms. This allows for local control of glucocorticoid levels in different
issues without altering systemic glucocorticoid levels.
OH OH
o
HO o
11-beta Hydroxvstergd
Dehydrogenase
o o
Cortlsol Cortisone
As stated earlier, the mineralocorticoid receptor and the glucocorticoid receptor are very similar to
one another and mineralocorticoids and glucocorticoids are capable of activating either receptor. In
fact, mineralocorticoids and glucocorticoids have a higher affinity for the mineralocorticoid
receptor than they do for the glucocorticoid receptor. Glucocorticoids, however, circulate at 100-
1000 fold higher concentration than mineralocorticoids ili . This necessitates a protective mechanism
if mineralocorticoids are to act at the mineralocorticoid receptor. Otherwise, glucocorticoids would
overwhelm them. This protective mechanism is II BHSD2. II BHSD2 is capable of deactivating
glucocorticoids by metabolizing them into II-Keto derivatives, which are inactive at
mineralocorticoid receptors and glucocorticoid receptors!! I. This allows mineralocorticoids to
activate mineralocorticoids without competition from glucocorticoids in mineralocorticoid target
tissues. This is important due to the fact that if II BHSD2 is blocked, then glucocorticoids can
"hyperactivate" the mineralocorticoid receptor. This leads to sodium retention, high blood pressure
and cardiovascular complications. Progesterone has been shown to be an inhibitor of I I BHSD2,
which partially compensates for in the antagonist effect of progesterone at the mineralocorticoid
receptor 11'-.
Since these enzymes control the local level of glucocorticoids, they are of vital importance to the
anabolic/catabolic process. It is very likely that some AAS antagonize one or both of these
enzymes. Unfortunately, since the discovery of these enzymes is a recent development. little work
has been done to determine the role that they play in skeletal muscle anabolism. Hopefully, more
work will be done in the future. II BHSDI antagonism in skeletal muscle and adipose tissue
lowering local glucocorticoid activity would be beneficial. Inhibition of I IBHSD2 can be very
detrimental to the kidneys and cardiovascular system.
17-BETA HYDROXYSTEROID DEHYDROGENASES
17-beta hydroxysteroid dehydrogenase is responsible for the interconversion of C-17

113
hydroxysteroids to Col? ketones and the reverse reaction as well ,114,11S A prime example of this
is the conversion of androstenedione into testosterone:
o H
H,
J {f J CH,
~~~$ ~---' Hobeta tNdroxysteroid
Dehydrogen ase
-1 tf~ o~ o
.,:j Androstenedione Testosterone
~~
-I
Since this reaction is reversible, testosterone can be deactivated by conversion to androstenedione
as well. C-17 alpha alkylation blocks the effect of this enzyme on a given steroid which is why
methylated androgens have increased oral bioavailability and longer half-lives than unmethylated
AAS. There are actually mUltiple isoforms of this enzyme that act preferentially on different
substrates and have some degree of preference for directionality as well 113,1 14.1 15.
This enzyme is also responsible for the interconversion of estradiol and estrone:
HO
CH 3 o
CH3
HO
HO
Estradiol
Estrone
Estrone is a longer-lived estrogen than estradiol and acts as a reserve for periods of low estradiol
production 107. 17BHSD inhibitors are currently in development for reducing estrogen levels in
conjunction with aromatase inhibitors for the treatment of breast cancer I16 ,117.118. The use of
aromatase inhibitors will reduce the levels of estradiol; however, estrone levels can remain elevated
and act as a source of estradiol through the actions of this enzyme Sl , This can also happen to men
using aromatase inhibitors, which is why some people choose to add an estrogen receptor antagonist
(like tamoxifen) in conjunction with aromatase inhibitors.
17-beta HSD is the enzyme responsible for converting Dione prohormones to active 17-beta
hydroxy steroids.
ll-BETA HYDROXYLASE
II-beta hydroxylase is an enzyme responsible for the addition of a hydroxyl group to the I 1-
position of steroid molecules. The two important reactions are the conversion of II-deoxycortisol to
cortisol and deoxycorticosterone to corticosterone:
OH OH
o o
OH OH
o o
11-Deoxycortisol
Cortisol
OH OH
o o
CH,
CH,

Deoxyccrticosterone Corticosterone
Testosterone is also converted in small quantities to I I-hydroxytestosterone, which in tllrn converts

to II-ketolestosterone. At higher doses, however, testosterone has been shown to inhibit II-beta
hydroxylase"9.'2o. This results in decreased production of cortisol and excessive amounts of
deoxycorticosterone in the body l21. Deoxycorticosterone is a potent mineralocorticoid. Elevated
levels of deoxycorticosterone result in salt and water retention and high blood pressure". It is likely
that other AAS also inhibit this enzyme although DHT does not. The other side effect is that as
cortisol levels are reduced, ACTH levels increase l21 . When testosterone inhibition is reduced, this
results in a rebound in cortisol production. A few elite bodybuilders supplement with synthetic
glucocorticoids as replacement therapy to try to prevent the body from overproducing ACTH.
.)... :z!>
#; rF" _4..0
21-HYDROXYLASE
~~",c.eP
~
21-hydroxylase is the enzyme that converts progesterone to deoxycorticosterone and 17-
hydroxy progesterone to Il-deoxycortisol:
OH
CH,
o
OH
17-alpha Hydroxy Progesterone 11-Deoxycortisol
Inhibition of this enzyme results in decreased production of cortisol and mineralocorticoids

(deoxycorticosterone and aldosterone)121. This results in the excretion of water and sodium and is
probably the mechanism by which certain AAS result in a "dry" physique. Unfortunately, very linle
work has been done to determine which, if any AAS inhibit the 2 I-hydroxylase enzyme
ENZYMES AS A WHOLE
All of the enzymes mentioned here do nOI operate in a vacuum. They are all acting in concert with
one another to maintain an equilibrium state. This also means that a given molecule can undergo
multiple conversions to arrive at a several different end points.
65 ANABOLfCPHARMACOLOGY
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BINDING PROTEINS
There are quite a few binding proteins that circulate in the blood and to which different hormones
and/or drugs bind. These binding proteins act as a reservoir where a certain portion of the total
hormone concentration is bound and can be released into or removed from free circulation as it is
needed without increasing or decreasing the production rate of a given hormones 1 It is considered
dogma that only the free portion of steroid hormones, that is, the portion not bound to carrier
proteins, is the active portion. In recent years, some evidence has come to light that challenges this
long held belief. The finding that some carrier proteins facilitate hormone entry into cells and may
122
in fact have receptors of their own is changing our view of bound and unbound steroid hormones .
These proteins also act to deliver hormones to specific tissues, such as the liver. Some of the
binding proteins have been theorized to have hormonal effects of their own. 1 will discuss some of
the binding proteins important to the topic of AAS in this section.
SEX HORMONE BINDING GLOBULIN
Sex hormone binding globulin (SHBG), also referred to as steroid hormone binding globulin, is a
protein that is largely produced in the liver and circulates in the blood. Recently some evidence has
123 124
demonstrated SHBG to be produced and regulated locally as well as in the liver ,125.
Historically, its function has been believed to be to bind sex hormones (testosterone, DHT,
estrogens) to transport them in the blood stream. Under nonmal circumstances, between 60 and 70%
of total testosterone, 70 and 80% of DHT, 35 and 40% of estradiol and 15 to 20% of estrone
circulate bound to SHBG S1 ,
Androgens, glucocorticoids, hypothyroidism and growth hormone decrease SHBG concentrations,

Hyperthyroidism, tamoxifen and estrogens increase SHBG concentrationssl , SHBG helps to keep
the equilibrium of sex hormone concentrations in the blood. Only free hormone can act, but steroid
can dissociate from SHBG to the free state as needed to keep free levels stable SI ,I22
Recently, a receptor for SHBG was found on the surface of some cells, When a given steroid is
bound to SHBG, the binding of SHBG to its receptor is inhibited, When not bound to steroid,
SHBG binds to its receptor and waits there until a steroid hormone binds to it l26,127 At this point,
SHBG plus the steroid molecule activate the SHBG receptor and dissociate together into
, I
Clrcu ' 128,129,130,131,132,133,134" Th e action
atlon ' 0 f SHBG at 'Its membrane receptor has been shown to
have an antiestrogenic effect and may be part of the mechanism whereby DHT exerts its
antiestrogenic effect 700 A reduction in the level of SHBG has been shown to augment the
proliferative effect of estrogen in breast tissue cells '25 ,135,136,137,138,139 Therefore, it appears that
SHBG acts as a hormone in its own right'40 It is unclear at this moment exactly what effects this
interaction has, however, as new information comes to light, it could change the way we look at
sex-hormone action. The herb, Urtica dioica, also known as stinging nettle, has been shown to
interfere with SHBG binding to the cell surface which is suspected to be the mechanism of stinging
nettle's effect on prostate hypertrophy 141.
SHBG binding by androgens plays an important role in AAS action notwithstanding this new
information regarding the SHBG receptor. Different AAS, when administered exogenously
(including testosterone) bind with different affinities to SHBG. This binding sequesters some of the
steroid rendering it inactive. Also, if the particular steroid binds with greater affinity than estrogen,
testosterone or DHT, then these molecules can be "bumped off' of the SH BG and into the free
state 51 ,142 Also, as stated, androgens reduce SHBG concentrations while estrogens increase levels,
While reducing SHBG levels will result in more circulating free androgen, it will also result in more
circulating free estrogen. If aromatizable androgens are used, SHBG concentrations can rise
significantly. The normal total capacity ofSHBG is 28nmol/L 5 '.
ALBUMIN
l43
Serum albumin is the most abundant protein in human plasma It is capable of binding many
different substances from fatty acids to hormones, drugs and body toxins 143 It binds steroid
hormones with Fairly low affinity (compared to SHBG) but because of its high circulating levels, it
has a very high capacity'43 This very high capacity makes albumin important in steroid hormone
equilibrium. Under normal circumstances, 60% of estradiol, 80% of estrone, 80% of progesterone,
30% of testosterone, 20% of DHT and 5% of cortisol are bound by albumin 51 . As the concentration
of testosterone in the body rises (as is the case when administered exogenously), SHBG becomes
saturated (at concentrations in the micromolar range) and albumin binding of testosterone increases.
Because of the action of albumin, the percent of unbound testosterone does not increase
proportionately with increasing doses. Within the physiological range, a two-fold increase in total
testosterone results in only a 17% increase in unbound testosterone14 4.
As with SHBG, increased binding of albumin by AAS results in the "bumping" of estrogen and
progesterone into the free state '44 This can result in estrogenic side effects from AAS that do not
convert to estrogen, In this case, an aromatase inhibitor will not help but rather an estrogen receptor
antagonist is required.
CORTICOSTEROID BINDING GLOBULIN
Corticosteroid binding globulin (CBG), also known as transcortin, is a protein that is similar to
SHBG in that it is produced by the liver, circulates in the blood and binds steroid hormones. In this
case, CBG is responsible for binding corticosteroids, like cortisol. Under normal circumstances,
51
18% of progesterone, 90% of cortisol but only 2% of testosterone is bound to CBG . Unlike the
case with SHBG, small changes in cortisol level results in large changes in free concentrations. The
corollary is also true, small changes in CBG results in large changes in free or bound cortisol
depending on the direction of the change in CBG. Several AAS are capable of altering the level of
144
CBG and therefore the circulating, non-protein bound level ofcortisol Finally, as is the case with
l45
SHBG, CBG is itself suspected of acting as a hormone, the effects of which are unknown . The
binding capacity of CBG in plasma is 690nmol/L. Plasma concentrations above this level result in
51
rapid increases in free cortisol. CBG levels are elevated in response to eSlrogens .
THYROID HORMONE TRANSPORT
Only 0.04% of T4 and 0.4% of T3 circulate in the free state. Thyroid hormone binding globulin
(TBG) binds 68% of T4 and 80% of T3. About II % of T4 and 9% of T3 are bound to thyroid
hormone binding pre-albumin (TBPA)51.
TBG is synthesized in the liver and its normal concentration is 15-30 uglml. Elevated estrogen
levels increase the production and serum levels ofTBG. Each molecule ofTBG has a single binding
site, which can accept either T3 or T4. Androgens and glucocorticoids lower TBG levels 51 . TBPA
is a circulating protein that can bind T4 or T3. Its normal level is 120-240 mglL. TBPA does not
bind thyroid hormones as strongly as TBG and acts as a source of rapidly available T4. Androgens
are known to increase levels ofTBPA 51 .
The importance of these binding proteins is apparent from their sensitivity to androgens, estrogens
and glucocorticoids. As stated, glucocorticoids and androgens decrease serum TBG and androgens
increase TBPA. These changes in binding proteins can acutely affect free thyroid hormone levels
and chronically affect the regulated level of thyroid hormones in the body.
Decreases in TBG have been shown to correlate well with skeletal muscle anabolism. This is most
likely due to an increase in free T3 levels. Many androgens, especially the C 17-alpha alkylated
AAS, cause a decrease in TBG with a corresponding increase in TBPA as the body tries to
l46
compensate .
SECTIONS
CROSSOVER
Earlier in this book I wrote about the SHSF and how members of this family are related. Because
they are related, they are therefore quite similar. This similarity allows for crossover to occur.
Crossover is when a steroid hormone acts at a receptor other than its "native" receptor or, in other
words, the receptor at which it normally binds. This interaction can result in agonism (or activation)
of the receptor, antagonism (or blocking) of the receptor or partial agonism which is a stimulation of
the receptor that results in less activation than the appropriate binding partner and therefore is also a
net antagonism to a certain degree. For instance, if testosterone activates the androgen receptor with
100 percent agonism but progesterone only activates the androgen receptor with 30 percent of the
agonism of testosterone, then you are actually reducing the net agonism of the system and you have
a net 70 percent antagonism of the level that testosterone provides.
ANDROGEN/PROGESTERONE
The ligand binding domain of the AR has greater than 50% homology to the same portion of the PR
that binds progestins 147 This means that this region of both receptors has greater than 50%
similarity. This similarity allows androgens to bind fairly well to the PR and the nature of the
similarity means that most androgen agonists that bind to the PR are also agonists to some degree at
the PRo Synthetic and natural progesterone receptor agonists also stimulate the AR to some degree.
Some androgens, such as trenbolone, mibolerone, methyltrienolone and THG bind very strongly to
t he PR an d may act as Iiu II agon .IStS 148149
. .ISO.lSI. Th'IS strong agonlsm
. 0 f t he PR resu I
ts 'In
downregulation of estrogen receptorsSI.IS2. Other androgens such as nandrolone and some
derivatives have lower levels of PR binding and act as antagonists of the progesterone receptor lS ]
Antagonism of the PR has been shown to result in upregulation of estrogen receptors SI . Those
androgens that also have strong binding to the progesterone receptor also seem to have improved
anabolic to androgenic ratios.
ANDROGEN /GLUCOCORTICOID
The ligand binding domain of the AR has greater than 50% homology with the same region ofGR
s1
that binds glucocorticoids . This means that this region is 50% the same in GR and AR. This
similarity allows some androgens to crossover and bind to GRI48.154. Because of the nature of the
similarity, most androgens that bind to GR act as antagonists of GR activityls4. This is actually a
somewhat desirable effect because antagonism of GR results in an anticatabolic effect, which
results in a greater net anabolism. The bad part is that while you antagonize the GR, more cortisol (a
glucocorticoid) builds up in your body, which will eventually overcome this effect necessitating the
need for higher doses of anabolics to maintain the same level of net anabolism. Also, cortisol can
crossover to AR as well so when the levels of cortisol get high enough they begin to antagonize AR
effects resulting in lower anabolic effect. In addition, antagonism of the glucocorticoid receptor
tends to make the user not feel very well since cortisol performs several vital functions such as
strengthening the immune system and providing anti-inflammatory actions.
As stated earlier, some androgens also inhibit the production of cortisol by interfering with the 11-
beta hydroxylase enzyme, which results in reduced production of cortisol. This can result in a
condition known as acute adrenal insufficiency that can result in fatigue, depression, weakness, and
insomnia 5!
G LUCOCORTICOIDIMINERALOCORTICOID
Glucocorticoid and mineralocorticoid probably have the greatest possibility for crossover since the
receptors and the molecules have the highest degree of similarity of all the steroid receptors/ligands.
Cortisol actual binds to the mineralocorticoid receptor with higher affinity than aldosterone and
with higher affinity than the glucocorticoid receptor. A Idosterone has about equal affinity for both
receptors 51 This is the reason for the existence of the II-beta hydroxysteroid dehydrogenase type II
enzyme. This enzyme acts as protection for the mineralocorticoid receptor by deactivating cortisol
in mineralocorticoid target tissues. Inhibition of this enzyme can result in excess stimulation of the
mineralocorticoid receptor by endogenous cortisol.
GLUCOCORTICOID/PROGESTERONE
There is some degree of crossover between cortisol and progesterone. Since progesterone acts as an
antagonist of the mineralocorticoid receptor and since there is so much similarity between
mineralocorticoid receptors and glucocorticoid receptors then it stands to reason that progesterone is
an antagonist of glucocorticoid receptors and this is probably one of the mechanisms behind some
of the anabolism/anticatabolism seen with the use of progestational compounds. Since androgens
themselves also have some potential for antagonism of glucocorticoid receptors, it is difficult to
differentiate these two activities. However, if a compound is a strong androgen and a strong
progestin (like tetrahydrogestrinone) then it is likely a strong antagonist of the glucocorticoid
l54
receptor .
PROGESTERONE/ESTROGEN
There is not really a crossover between progesterone and estrogen receptors in the sense of
progestins binding to the estrogen receptor. Even so, as stated previously, there is a large amount of
interaction between the two systems. Activation of the PR results in downregulation of PR and ER.
Antagonism of PR does just the opposite. Activation of the ER results in upregulation of the ER and
PR51.152
PROGESTERONE/MINERALOCORTICOID
There is quite a bit of crossover between progestins and the mineralocorticoid receptor.
Progesterone itself acts as an antagonist of the mineralocorticoid receptor with higher affinity than
aldosteronel55.156 Progesterone also acts as an inhibitor of II BHSD2, so in instances of high levels
of progesterone (like pregnancy) the antagonist activity of progesterone is offset by its inhibition of
II BHSD2 and mineralocorticoid activation by cortisol 157 . Also, progesterone can be enzymatically
altered to deoxycorticosterone, a potent mineralocorticoid 51 . Since many androgens also possess
progestational activity, it is likely that they also act as either antagonists or agonists of the
mineralocorticoid receptor and potentially as inhibitors of II-beta hydroxysteroid dehydrogenase
type II (and even possibly II BHSD I). Excessive activation of the mineralocorticoid receptor can
lead to serious consequences. Besides causing water retention and high blood pressure, it is also
responsible for the laying down of fibrous tissue in the heart and in arteries. This leads to
enlargement of the heart and stiffening of the heart walls and arteries. 17-hydroxyprogesterone acts
as a potent mineralocorticoid receptor antagonist l56 .
SYNTHETIC AAS
Almost all AAS are available in two basic forms: Tablets or capsules for oral administration and
oils or aqueous suspension for intramuscular (1M) injection. There are no AAS that are designed for
intravenous administration. Almost all of the oral AAS are C-17 alpha alkylated, which means that
they have a methyl group at position C-17 as shown below:
OH /'
,8
o
This methyl group is what makes it possible for the AAS to be taken orally by preventing
breakdown by the liver. The few orals that are not C-17 alpha alkylated have very poor
bioavailability and are readily broken down by the liver and therefore are not as effective. Of course
there are many other modifications that are made to the AAS core structure to try to alter the effects
of the molecule. These modifications and their effects are discussed later.
COUNTERFEITS
Counterfeit AAS come in two different cia ses. The first is an AAS that is manufactured under the
guise that it is produced by a legitimate pharmaceutical company. The second is an AAS that is
produced and marketed as an underground preparation. The first problem of counterfeit steroids is
that they often do not contain the drug they are supposed to contain. Often a cheaper AAS is
substituted for a more expensive one, for instance, methyltestosterone In place of
methandrostenolone. A second problem with counterfeits is that they may not contain the correct
amount of the AAS in question, for instance, the pills may contain only 7 milligrams of
methandrostenolone instead of 10 milligrams. A third problem with counterfeits is contamination.
This can be a very serious problem with orals and il~ectables. With injectables bacterial
contamination is one of the biggest concerns but so is contamination with heavy metals, viruses and
chemicals. Any of these contaminants, when injected can cause serious problems. One might think
that contamination of orals is not as serious because bacterial and viral contaminants are likely to be
nullified in the gastrointestinal system. While this is mostly true, there is a still a significant risk
with heavy metal and chemical contamination of oral medications.
EXOGENOUS ADMINISTRATION OF AAS
Injectable AAS are specially made and sterilized for deep muscular injection. Although an 1M
injection can be administered into any muscle if care is taken, larger muscles are best suited for this
purpose with the buttocks being preferred for its large muscle ma s and relatively few nerves and
blood vessels. As far as self-injection is concerned, let me say this: I am not a medical doctor and
most likely neither are you. Therefore, you should not be injecting yourself unless you are under
the supervision ofa medical doctor or have been trained to self-inject by a medical professional. 1M
injections are relatively simple to perform, even on one-self, but there are a number of things that
can go wrong if one is not properly trained. Hitting a nerve is not only painful but can lead to nerve
damage and dysfunction. Hitting a blood vessel will not only be messy but could also be life
threatening. Scar tissue is a concern with multiple injections over time, especially with large gauge
needles. The most common complaints are abscess and infection. These are caused either by
improperly sterilized black market products, by following less-than-sterile procedure when injecting
or by injecting too large of a volume. This can be potentially life-threatening if either an allergic
reaction (anaphylactic shock) or systemic infection (sepsis) occurs. "When in doubt, throw it out" is
a good rule to live by when the sterility of a product is in question. One's health is much more
valuable than the couple hundred dollars one just spent on some suspect black market products.
Syringes and needles come in many different sizes and in several different brands. A good rule to
live by is to use the smallest syringe needed (don't use a 3 cc for a Icc injection), with the smallest
gauge needle (the higher the number the lower the gauge) possible for the fewest possible
injections. Finding syringes and needles has become easier with the growth of the internet as there
are several onl ine sites which sell needles and syringes. I shouldn't have to say this but never, ever,
under any circumstances share a needle with ANYONE and never reuse a dirty needle. eedles and
syringes are too inexpensive to risk an infection or your life. Any gauge needle can be used for 1M
injections providing it is long enough to get into the muscle. Most gluteal injections require at least
1.5 inch and some larger glutes require 2 inch. Smaller muscle groups may require only 'Y., 5/8, or Y:z
inch needles. Many people use insulin needles for site injections. Gauge is only a concern insomuch
as the oil can be difficult to push through smaller gauges. Also, for longer needles, smaller gauges
tend to bend easily. Most people would use a 21-gauge 2-inch needle for a gluteal injection whereas
it might be wiser to use a 25 gauge 1.5 inch for this purpose. At some point it comes down to
per onal preference and comfort.
The injection procedure that a doctor will follow is as follows:
77 ANABOLlC PHARMACOLOGY
He removes the syringe from its packaging being sure only to touch the end that is meant to be held
in the hand - the other end (the place where the injection liquid comes out of) should not touch
anything. The needle is removed from its package being sure only to touch the protective shield
around the needle. Each piece is held in one hand and joined together. The needle guard is removed
and the needle is pushed through the stopper (or into the vial) and the liquid withdrawn. The needle
is removed from the stopper taking care not to touch any part of the needle to any unsterile surface.
Air bubbles are removed by inverting the needle/syringe (needle pointing up) and flicking the
syringe - air bubbles are then evacuated. The area for injection is rubbed with alcohol and the
needle is inserting quickly and somewhat forcefully into the injection site. Slight back pressure is
placed on the plunger to check for blood - if none is seen then the injection continues. If blood is
seen then the needle is removed and a new location is chosen (technically the entire
syringe/needle/drug should be discarded - but few follow this procedure). The plunger is depressed
steadily until all of the fluid is injected and the needle is withdrawn in one swift motion. A band-aid
is placed over the injection site to quell any bleeding and to protect the injection site until a scab
forms. The gluteus is divided into four quadrants with the injection placed in the upper/outer
quadrant. The area for a gluteal injection is displayed below:
Superior Gluteal Artery
Gluteus Maximus
Sciatic Nerve
There are several technical variations that can be used when injecting that depend on personal
preference. One method is to stretch the skin taught between the thumb and index finger and
injecting in the stretched area. Another (usually used with thigh injections) is to pinch the muscle
and skin into a bulge, which the needle is injected into. Another technique is useful when using a
larger gauge needle to prevent leakage. This is called the Z-Track technique. In this technique, the
skin is pulled taught from the side. The needle is inserted into the taught area and the injection
delivered. The needle is then removed and the skin is released. This seals the injection preventing
the injectable from leaking out.
SPOT INJECTIONS
Many people are now doing localized "spot" injections of injectable anabolic steroids. For a long
time, the only places people injected were the gluteals since they are a large muscle group with
fewer major blood vessels and nerves. However, as the use of a steroid called esiclene became
popular (and later Synthol), people figured why not inject the steroid into the muscles being worked
in the hopes that the steroid would exert a local effect. Esiclene caused a local, albeit temporary,
growth of the muscle it was injected into by causing an inflammatory response in the muscle tissue.
Other steroids can do this as well including testosterone propionate. Any local injection can enlarge
the muscle if the injection volume is large enough. Local injections, although popular, probably do
not exert any local growth through the androgen receptor, but rather by a stretching effect of the
volume on the muscle and the fascia. The steroid, once cleaved from its ester, is taken up into the
blood stream and doesn't really have a chance to act locally in the muscle.
Spot injections do carry somewhat greater risks than gluteal injections. The concentration of blood
vessels and nerves is often higher in smaller muscle groups, which, if injected into, can cause
injury, abscess, pulmonary embolism or possibly death. Also, the volume that a muscle can handle
is related to the size of the muscle. The gluteals can accept volumes up to and exceeding three ml
while the biceps might only take I or 1.5 (depending on the size of the biceps in question).
Virtually any muscle group can be injected: biceps, triceps, trapezius, delts, chest, lats, calves,
quads etc. The procedure is the same for spot injections as it is for regular gluteal injections (as
described above). Many people use insulin needles to perform sport injections because the needle is
a very small gauge and the needle does not need to be very long for most spot injections.
One other thing to consider is that the half-life of an injectable steroid can vary greatly from one
injection site to another due to the difference in the size of the muscle as well as the amount of
blood circulation. androlone decanoate may have a half-life of 7 days when injected into the
gluteals, but this may be reduced to 5 days when injected into the lateral deltoid l58 . Depending on
injection volume, working a muscle group that has just been injected may be difficult due to
localized muscle swelling.
One of the side effects of the criminalization of AAS is the quasi-legal marketing of sterile oils that
do not contain any active steroids. Users inject large volumes of these oils as site injections to
artificially enlarge individual muscles. Not only is this practice dangerous but just plain silly. In
many instances, the "muscles" that are created do not look anatomically correct. In my opinion,
these site-enhancing oils are much worse than AAS ever could be. The large volumes that are
injected carry a high risk of abscess. In addition, the sterility of these oils is not guaranteed which
could result in any number of serious adverse reactions. Scar tissue buildup is also common with the
use of these oils as well as nerve damage.
SECTION 6
SIDE EFFECTS
Side effects are any effect produced by a drug other than those that are intended. These side effects
can occur for various reasons such as impurities, crossover, spillover, and/or enzymatic conversion.
Considering the often-haphazard nature of their use, there are only a handful of cases where healthy
. I . k . h the use 0 f
athletes have suffered serious consequences 159160
. . Even so, there are potentia ns s Wit
any medication. Athletes have developed many strategies for diminishing side effects but in most
cases, preventing side effects from occurring would be the most desirable outcome. Listed below
are the most common side effects associated with AAS use and strategies that athletes use for
avoiding or reducing them where possible. The criminalization of AAS has reduced the availability
of many individual drugs so athletes often use whatever drugs are available rather than selecting the
most appropriate drug or drugs for their purpose.
Abscess
Abscesses due to injections given by medical doctors are quite rare however, with more and more
lay persons self-administering injectable AAS on a more frequent basis (often daily) the likelihood
for abscess increases. Other important factors in the alarming increase in abscesses are the increase
in contaminated underground preparations and the dangerous practice of "homebrewing".
Homebrewing is the production of home-made injectable AAS by purchasing raw powders and
dissolving them in various solvents. Often the raw materials are purchased from overseas and have
not been produced in a sterile environment. In addition, the solvents used are often not of
pharmaceutical grade and are not sterile. It is surprising that abscesses are not more common.
There are actually two types of abscess - sterile and septic. It seems that many of the abscesses that
AAS users experience are sterile abscesses that occur from improper injection location, technique,
too large an injection volume or frequent injections into the same location l61 . Sterile abscesses can
be painful but do not contain any bacterial infection. If the sterile abscess is severe, the resulting
inflammation can still cause muscle or nerve damage and scarring. The symptoms of an abscess
include heat, swelling, redness, and pain.
Septic abscesses occur when bacteria are injected into the muscle through contamination of the
drug, the needle or by carrying bacteria from the surface of the skin. The resulting heat, swelling,
redness and pain are hallmarks of an abscess. Septic abscesses can be dangerous if they are not
treated and can result in septicemia if the bacteria are picked up by the blood stream. Doctors will
treat bacterial abscesses by providing an exit route for the bacteria and pus (through an incision).
Antibiotics are sometimes necessary to clear up the infection. There are anecdotal reports of steroid
users draining their own abscesses. This practice is extremely dangerous and can make matters
worse by spreading the infection.
Acne
Acne is caused by bacteria attacking oil in sebaceous glands in the skin. Sebaceous glands have 5-
alpha reductase activity and androgens increase the amount of oil produced in these glandsl62.163
Bacteria attacking this oil results in eruptions on the skin (acne). These eruptions are generally only
mildly annoying but as they heal can result in pockmarks and scarring that most find aesthetically
displeasing. Athletes may attempt to reduce acne by using a 5-alpha reductase inhibitor; however,
any strong androgen may result in acne production even in the absence of 5-alpha reduction. It is
also important to keep the skin clean and free of bacteria. As a last result some people use salicylic
acid topical cream, ret in-A, or in extreme cases isotretinoin to combat acne. Accutane is generally
l64
reserved for use as a last result as it has been shown to be liver toxic and may also alter mood .165;
two side effects that AAS users often encounter as a result of using androgens that could be
compounded through the use of isotretinoin. Often, the final option is to the lower the dose of AAS.
This simple action can reduce every side effect yet, for obvious reasons, users are reluctant to do so.
Some dismiss acne as a minor nuisance and while acne usually subsides after cessation of AAS use,
the scars and blemishes will not. A pockmarked face is permanent, disfiguring hallmark of heavy
androgen use.
Addiction
There is considerable evidence that there is the potential for physical and psychological dependence
on AAS 166 The hormonal changes that occur in the AAS user can result in psychological effects
that result in a desire to continue using these drugs. In addition, the cessation of AAS use can result
in deleterious psychological effects, such as depression, as well as physiological effects including a
loss of body weight, tiredness, loss of libido, etc. that can further exacerbate the desire to continue
AAS use.
Baldness
Male pattern baldness is caused by the action of androgens in the hair follicle of those that are
genetically prone to this condition however; it seems that long term use of androgens results in
some degree of hair loss in the majority of users. 5-alpha reductase activity in the scalp causes
conversion of testosterone and other synthetic AAS to DHT or DHT derivatives, which results in
destruction of the hair follicle and hair IOSSI67. An androgen does need to be subjected to S-alpha
reduction to result in hair loss since any strong androgen can disrupt normal follicle function. There
are a few natural remedies that claim to reverse the balding process however none seem to work
very well. Prevention seems to be the best bet, that is, using, AAS that are not derivatives of DHT
and do not convert to DHT as well as staying away from very strong androgens. Also, many people
l68
have had success using topical creams containing either finasteride or spironolactone . Finasteride
blocks the conversion to DHT and DHT derivatives by inhibiting S-alpha reductase. Spironolactone,
on the other hand, acts as an antagonist at the androgen receptor. Of course finasteride would be
used only in combination with androgens that convert to more potent S-alpha reduced analogues
such as testosterone converting to DHT. Using finasteride with nandrolone or its derivatives would
be counterproductive since they convert to less potent S-alpha reduced derivatives. In all other
instances, spironolactone would be preferable since it blocks activation at the AR itself. Other, more
potent androgen receptor antagonists such as Flutamide have been successful in not only stopping
MPB but also in reversing the process. However, if flutamide spills over into systemic circulation, it
will severely limit gains on a cycle since it will block any androgens from binding at the AR. This
side effect should be considered permanent. Although some users have seen minimal hair regrowth
upon cessation of AAS use and some success ha been achieved by using minoxidil and/or
finasteride, the regrowth never seems to be adequate.
Benign Prostate Hypertrophy/Prostate Cancer
The prostate is a gland located along the urethra that contributes fluid to the ejaculate. It is small at
birth, but doubles in size during puberty due to stimulation from the high level of androgens
produced at this time. The prostate consists of a ductal gland surrounded by smooth mu c1e. The
smooth muscle contracts during orgasm squeezing the glandular portion which causes release of
prostatic fluid that contributes to semen volumesi .
Benign prostatic hypertrophy/hyperplasia is a condition where the prostate gland grows but no
cancer is present. As stated previously, the prostate is an androgen target tissue with high levels of
S-alpha reductase activity and AR expression. The prostate gland is very sensitive to androgen
stimulation and AAS will activate AR in the prostate gland. In most cases, this will lead to
hypertrophy and/or hyperplasia of the muscular portion of the prostate as well as expansion of the
secretory/fluid matrix. Although it has not been adequately proven that BPH leads to prostate
cancer, it is reasonable to assume that there is at least an increased risk of prostate cancer ifone has
BPH. It is therefore beneficial to try to reduce activation of AR in the prostate. Many athletes have
used a S-alpha reductase inhibitor such as finasteride (and to a lesser degree Saw Palmeno) to
8S ANABOLIC PHARMACOLOGY
reduce the conversIOn of some steroids to more potent reduced derivatives. Finasteride is not
prostate specific and will reduce conversion to DHT in other target tissues. Some have argued that
the use of finasteride will therefore reduce the effectiveness of a course of AAS treatment.
However, if you remember back to the enzymes section, DHT plays no part in skeletal muscle
hypertrophy do to the action of3-alpha HSD. Therefore, reducing conversion to DHT will have no
effect on muscular gains. The down side to using finasteride is that even if one could totally inhibit
S-alpha reductase activity, there would still be some level of AR activation in prostate and other
DHT target tissues because testosterone and other non-reduced synthetics are still capable of AR
activation in those tissues - just to a lesser degree than DHT. In any case, any help in reducing the
level of activation in the prostate is beneficial for long-term health. Symptoms of BPH include a
sense of fullness or pain in the lower abdomen, especially when urinating and difficulty initiating or
maintaining urine flow. There is some evidence that prolactin may play a role in prostate
enlargement independent of androgen levels l69 There is also some newer evidence showing that
estrogens may also playa role in prostate enlargement and prostate cancer through the actions of
SHBG and its receptor I70,171.
Blood Lipid Alterations
It is very common for AAS users to have altered cholesterol levels with higher LDL and lower HDL
as well as increased triglycerides l72 This is particularly true for those using C-17 alpha alkylated
l73
steroids As everyone reading this should know high total cholesterol and high LDL, high
triglycerides and low HDL lead to atherosclerosis (buildup of fatty particles in the arteries) and
heart disease. There is some evidence that the reduction in HDL levels is a DHT dependant
process 172,1 73 Additionally, using androgens that aromatize to estradiol has been shown in the
literature to diminish the effect of androgens on HDL 173 . Using weaker androgens and combining
finasteride with those androgens which convert to more potent 5-alpha reduced androgens seems to
help keep HDL levels from dropping as low. Even so, a western diet also plays a major role.
Everyone, AAS user or not, should do their best to eat a diet low in saturated fat and simple sugars
and high in dietary fiber which has been shown to reduce total cholesterol levels. Since AAS
innately affect cholesterol levels, it is even more important for the AAS user to eat a healthy diet.
Proper monitoring is a must and if cholesterol levels remain high even when on a proper diet, then
AAS use should be decreased until a more acceptable level is achieved. Cholesterol levels usually
return to normal after cessation of an AAS cycle, however, some of the damage caused by high
cholesterol has already been doile. Estrogen has a protective effect on blood lipid levels. The use of
aromatase inhibitors can have serious adverse effects on cholesterol, especially HDL, levels -
perhaps even more so than AAS. Tamoxifen and clomid provide some estrogenic stimulation and
l74
have beneficial effects on cholesterollevels .
Bone Closure/Short Stature
It is well documented that AAS can cause premature closure of the epiphyseal plates and a decrease
in terminal height in those who are still growing through aromatization to estrogens. What this
means is that taking AAS while you are still growing (mostly during the teen years) can stunt your
growth. The end of long bones (specifically the upper leg bone, the femur) is called the epiphysis.
This region of the bone is responsible for increases in length of the bones. The epiphysis closes in
51
response to stimulation by estrogens and once closed, no further increase in length occurs .
Therefore, only those AAS that convert to estrogen will result in closure of the epiphyseal plates. In
fact, androgens have been shown to stimulate the growth of long bones. Additionally, the use of
aromatase inhibitors has been shown in the literature to slow down the closure of the epiphyseal
plates and increase height 175 Once the epiphyseal plates have closed, no further increase in height
can be obtained.
Cancer
Although no link has been proven between the use of AAS and prostate cancer, it is uspected that
increased androgens can accelerate progression to cancer in those who are susceptible. Anabolic
steroids are listed as carcinogens and there is some evidence in the literature of liver tumors caused
by oral, C-17 alpha alkylated AAS 176.177,178,179. In addition, AAS directly increase levels of IGF-I
which is known to stimulate growth of tumors I80,18I,182,183,184. In fact, most pharmaceutical
companies are investigating inhibitors of the IGF-I pathway as a treatment for several types of
cancer. Steroid hormones in general are known to regulate oncogenes, which, if mutated can result
in cancer. The fact that steroid hormones interact with DNA and induce growth in a number of cell
types suggest that they could playa role in initiating or progressing cancerous processes. A study in
mice showed a shortened lifespan with androgen treatment with one of the causes being tumors of
the liver and kidneyl8S, Although no link has been proven as yet, it is reasonable to assume that
substances that cause cellular growth may at least increase the progression of disease in those who
are susceptible.
Cardiovascular Disease/Heat Attack, Stroke
There is an undeniable link between the abuse of AAS and negative cardiovascular health 186,187.188
The effects of AAS on blood lipids and blood pressure are well documented as are the ill effects of
high cholesterol and hypertension on cardiovascular health, There are several cases of stroke and
sudden cardiovascular death occurring in AAS using athletes documented in the scientific
literature I89 ,190,191,192 Using high doses of AAS for long periods of time combined with a poor diet
and lack of cardiovascular exercise is a recipe for disaster. On the other hand, there is some
evidence that maintaining normal androgen levels as men age is necessary for proper cardiovascular
functioning 193 Gening blood tests, eating a healthy diet with low levels of saturated fat and sodium
and incorporating aerobic exercise are important for everyone, but critical for AAS users.
Unfortunately, the effects of AAS on the cardiovascular system may not be realized for many years
and are likely to be ignored, especially in younger users,
Clitoral Enlargement
The use of androgens by women can lead to a lengthening and/or thickening of the clitoris. The
clitoris is composed of the same tissue as that found in the head of the penis and is responsive to
androgens, While some enlargement can lead to a greater sensitivity and ease in achieving orgasm
any gross enlargement is aesthetically unattractive as it takes on the appearance of a miniature
penis, While the clitoris will shrink to some degree when androgen use has ended, this side effect
should be considered permanent. Using AAS that do not convert to more potent androgens does not
seem to help as any degree of androgenic stimulation seems to cause some clitoral growth, Some
female athletes attempt to use only very small doses of weak androgens to help prevent this side
effect. Another strategy that is rumored to be in use is to create a topical nutamide cream to prevent
growth in this organ.
Clotting
AAS have verifiable effects on reducing blood clotting and prolonging bleeding time 194 ,195 There is
no way known to prevent this side effect but one should be cautious not to exaggerate the problem
by using other substances which are also known to affect cloning such as: aspirin, heparin,
coumadin etc ... Also, it is recommended that one should stop using AAS at least 6 weeks before
any surgery to prevent any unnecessary blood loss.
Edema
Edema, also know as water retention, is a potentially serious side effect of AAS use. There are two
types of water retention that AAS users frequently experience: I). Extracellular or subcutaneous is
when water collects just under the skin 2). Intracellular is when water loads within the cells causing
them to expand. Extracellular edema gives a person the bloated look with rounded facial features
and reduced muscle definition. Intracellular edema is considered aesthetically pleasing because it
pumps up the muscles making them look bigger. There are several causes of edema in the AAS
user. Firstly, the kidney is a target organ for testosterone itself and androgen receptors are present in
the kidney. Kidneys of males are significantly larger than those of females due to stimulation by
androgens l96 . While estrogens have been blamed for water retention, this is not necessarily so.
Estrogen is known to cause water to leak from the intravascular space into the extracellular space,
resulting in subcutaneous edema but not necessarily water retention. So, estrogens add to the
bloated look, but the actual retention of water is caused by several mechanisms. AAS with
progestational activity will also cause water retention by inhibiting II BHSD2 as previously
described which causes direct water retention by the kidney. Finally, steroids that inhibit II-beta
hydroxylase will result in water retention through the buildup of deoxycorticosterone in the
blood I97 ,198.199. While some consider water retention to be beneficial, for the most part it is not. A
very small amount of water retention is beneficial for joint function; however, any significant
amount of water retention will raise blood pressure leading to damage of the heart and the kidneys.
Some people enjoy the water retention because it makes them "feel big" and it looks good on the
scale, but as soon as AAS use is ceased, those gains go right down the toilet. Athletes wishing to
improve their health by limiting water retention do so by drinking plenty of water, keeping sodium
intake moderate (not too low, not too high) and by using AAS in doses that do not result in extreme
water retention.
FaciallBody Hair Growth
This side effect mostly applies to women but even some men (the less hairy ones) will notice
thicker, darker and generally more facial and body hair growth while using androgens. Axillary hair
is responsive to androgenic stimulation. The use of a 5-alpha reductase inhibitor can help to prevent
this side effect. For men this usually does not cause a problem since they are hairier anyway, but for
women it can be devastating. Needless to say that face and body hair on women is considered by
most to be extremely unattractive. While shaving, waxing and electrolysis can help and stopping
androgens will reduce the growth of hair this side effect should be considered permanent.
Hypertension
Hypertension refers to the elevation of blood pressure. As discussed under edema, increased water
retention will raise blood pressure. However, there is some evidence that AAS themselves have
some direct effect on the cardiovascular system that may cause elevations in blood pressure
independent of water retention 200 Elevated blood pressure can damage the cardiovascular system
and the kidneys. One of the primary mechanisms through which AAS increase blood pressure is the
inhibition of II-beta hydroxylase l2o This results in the increased production of deoxycorticosterone
which is a potent mineralocorticoid resulting in sodium and water retention 51 . In addition, chronic
excess ofmineralocorticoids has direct deleterious effects on the cardiovascular system, specifically
the heart. Some have attempted to mitigate these effects through the use of antimineralocorticoid
medications and antihypertensives.
Gynecomastia
Gynecomastia is the enlargement of breast tissue in the male. This enlargement is largely due to the
activation of estrogen receptors within the breast. AAS that convert to estrogen will result in some
growth, the amount of which will be determined by genetic susceptibility, the size of an individuals
breast tissue, the natural level of estrogen receptor in the breast, the degree of aromatization of AAS
used as well as the dose and ultimately the amount of estrogen produced in the breast. People have
noticed that the onset of gyno is detectable as an itching or tingling sensation in the nipple. Most
gyno can be avoided by not using those steroids that are known to convert to estrogen, or by using
them only in low doses. Also, people have used tamoxifen to block the estrogen and arimidex to
block the conversion of AAS to estrogen.
The breast is a complex tissue consisting ofa fat pad with ductal structures. In prepubescent females
and males, the fat pad is small with only a rudimentary ductal system that grows during gestation
under the influence of maternal growth hormone. In females, the breasts begin to grow in puberty as
estrogen levels increase. Estrogen causes both the expansion of the fat pad and propagation of the
ductal system. Further differentiation occurs during pregnancy as progesterone is secreted in large
quantities. Progesterone is responsible for further ductal branching as well as lobuloalveolar
structures (little sacs) at the end of ductal branches51.201. In males, the breast does not undergo
differentiation or proliferation unless stimulated. This occasionally occurs during puberty as
estrogen levels rise along with testosterone levels. In most cases, the growth is small and does not
progress following puberty.
There are several other possible causes of gyno that are only partially understood. When exogenous
AAS are used, they bind to SHBG and albumin to some degree. As discussed previously, estradiol
and estrone are also bound to SHBG and albumin under normal conditions and some may be
"bumped" off when more AAS are added. This estrogen then enters the free state and may
contribute to gyno even if no aromatizable AAS are used. Androgens, particularly those that do not
convert to estrogens, have been shown to decrease SHBG levels in the blood. As discussed in the
section about binding proteins, SHBG seems to have a protective role against estrogen induced
proliferation in the breastI25.135.136.137.138.139 With the reduction of SHBG levels, previously bound
estradiol and estrone circulate unbound and are much more likely to induce breast tissue growth in
the environment or reduced SHBG. Another potential cause of gynecomastia occurs as a result of
the inhibition of II-beta hydroxylase. The inhibition of II-beta hydroxylase results in excessive
production of DHEA which is known to exert direct estrogenic effects without conversion to
estrogen.
Progestational actions of AAS have been blamed for causing gynecomastia. Progesterone and
progestins are known to result in downregulation of estrogen receptors in the breast. In fact,
synthetic progestins have been used for this purpose in breast cancer. Some AAS that possess weak
agonist activity at the progesterone receptor may result in greater sensitivity to estrogen in the breast
but there is little evidence to support this possibility. Progestational effects have been the
explanation for the induction of gynecomastia by nandrolone esters. Nandrolone is converted to
estrogens but in smaller quantities than testosterone. Nandrolone does posses some affinity for the
progesterone receptor but the explanation for its ability to induce gynecomastia does not require the
reliance on progestational effects. Since nandrolone is 5-alpha reduced to a much weaker androgen
(dihydronandrolone), the androgen/estrogen ratio is reduced and the protective effect of DHT is
removed resulting in a much more estrogen sensitive environment.
The latest culprit blamed for causing gynecomastia is prolactin. Prolactin does playa role in breast
enlargement and initiation of lactation in women but only in an environment of high estrogen.
Unfortunately, the fear of prolactin has spread throughout internet message forums and people are
now using bromocriptine in an effort to stop prolactin-induced gyno which is claimed to be caused
most often by nandrolone or trenbolone. My personal opinion is that prolactin is seldom responsible
for gynecomastia in AAS users. Purthermore, treatment with bromocriptine is ill-advised since it
also lowers growth hormone levels and has quite a few other side effects of its own.
Another potential cause of gynecomastia is elevated IGP-1. IGP-I has shown the ability to activate
the estrogen receptor pathway in the absence of estrogen. Since androgens are known to increase
IGF-I levels, it is possible that androgens may initiate gynecomastia through this mechanism.
Aromatase inhibitors would not necessarily be effective in this instance but tamoxifen may be since
it has been shown to decrease IGF-I levels in the breast.
Headaches
Headaches frequently occur while using androgens. This is almost always a result of blood pressure
elevation. Often a user can feel his pulse beating in his head. This is a serious side effect and should
not be taken lightly (refer to Hypertension).
Impotence/ED
202
AAS have been shown to increase libido in some studies and to decrease libido in others There
are many potential causes of erectile dysfunction (ED) or impotence in men. The common causes in
AAS users are I. high blood pressure 2. disruption of HPA by estrogen and progesterone 3.
decreased androgenic stimulation. This side effect is often seen in those using nandrolones, hence
the nickname "Deca Dick". Deca has progestational activity and is often used with dianabol, which
readily converts to estrogen both of which can markedly reduce LH and FSH levels and in turn
natural testosterone production. Nandrolone also converts to a less potent androgen through 5-alpha
reduction which results in less androgenic stimulation in those tissues which are essential for male
sexual function. Some people have noticed a reversal of this effect if they add some testosterone to
the cycle. The argument is that some "androgen" is needed to balance out the estrogen and
progesterone effects. The fact is, adding any strong androgen, or an androgen that converts to a
strong androgen will help to alleviate this side effect of nandrolone. In addition, keeping blood
pressure and estrogen levels in check will also help but suppressing estrogen levels too far has also
been shown to have a negative effect on libido.
Joint Pain
Joint pain is more common with certain steroids (stanozolol) than with others. Some steroids are
known to relieve joint pain (nandrolone). All steroids can cause joint pain to some degree because
they increase the strength of the muscle but not necessarily the connective tissue. This can cause
strains and tears to occur much more easily. Also, many steroids can reduce the level or
effectiveness of cortisol in the body. Cortisol helps to keep the joints lubricated and reducing this
can cause the joints to ache.
Kidney Damage
While some androgens themselves can cause damage to the kidneys, more frequently it is the
associated hypertension that is the culprit. Unmitigated hypertension can lead to kidney damage
over time because the kidneys have to work harder to filter the blood. This is a serious side effect
that can, for the large part, be prevented. (see Hypertension)
Liver Abnormalities
The liver is a very important organ. It constantly removes toxins from the blood and deactivates
them - drugs are seen as toxins by the liver. The C17 alpha alkylated oral AAS are of most concern
with the liver. As the dose of these AAS increases, so does the "work" that the liver has to do to
deactivate them - this can lead to liver damage. A person should not assume that just because he
uses only injectables that he is safe. These drugs are still foreign bodies that, though gentler, are still
an increased load on the liver. There are a few cases of severe liver damage with steroid hormone
use in the literature but most of these occurred in individuals that had a preexisting
con d . .178.179. T ests s hou Id be d one peno
It Ion 176177 I"
. d'lca II y to be sure t hat t helver IS not un d u Iy
stressed. Milk thistle has often been used to help protect the liver, however, scientific research is
divided and some suggests that milk thistle may actually worsen the liver effects of oral AAS by
prolonging their half-life in the body.
Lower Back Pain/Pumps
Some AAS users have described experiencing back pain or a "pump" in the back muscles with the
use of certain steroids. The explanations for this side effect include altered electrolyte levels,
insufficient hydration, and too high a dose of offending AAS. Suggested cures range from taking in
large amounts of water, supplementing with taurine or supplementing with potassium. Though
supplementing with potassium is generally safe, some AAS are known to result in a borderline
hyperkalemic state which could make supplementing potassium risky. Another explanation for the
"back pumps" could be adrenal hyperplasia secondary to inhibition of II-beta hydroxylase or
excessive cortisol production through an antiglucocorticoid effect of certain AAS. (see
Hypertension, Kidney Damage)
Menstrual Irregularities
Women who use androgens will undoubtedly have disruptions in their normal cycle. With repeated
or ongoing cycling, women will eventually stop menstruating altogether. While this sounds like a
good thing for some it can lead to serious problems. Unfortunately, there is no real way to reduce
this side effect other than to minimize androgen use.
Mood
Many AAS are reported to have a euphoric effect when taken. The term "roid rage" has been used
by the media, often as an explanation for a murder that has been perpetrated by someone using
AAS 203 It has been proven scientifically that androgens have effects in the brain and can alter
mood 204 ,205,206,207 AAS use has also been linked to hypomanic symptoms including sleep loss,
increased energy and increased sexual feelings208.209. Another paper showed doses that would be
considered moderate by AAS users to have a low risk of psychosexual side effects in normal
males 2lO A placebo-controlled study demonstrated no increases in angry behavior with the
administration of testosterone in healthy males211 , Whi Ie these studies seem to contradict the media
notion of AAS-induced psychoses, it must be noted that none of these studies have looked at the
mega-dosing and long duration of use that some AAS users employ, It is likely that AAS use by
those susceptible to angry behavior or with underlying behavioral problems may experience
exacerbation with the use of AAS.
Nausea
While androgens can make the user big and strong, they can often make them feel sick at the same
time. Oral androgens seem to cause this side effect more often than injectables, especially
oxymetholone. Users often report stomach pain or nausea while using this steroid and it may be
related to the propensity for liver toxicity with oxymetholone.
Nosebleeds
Nosebleeds are a common side effect in those using androgens. While a nosebleed is not usually
serious, it can be an indication of an underlying problem, namely high blood pressure, High blood
pressure combined with the reduced blood clotting that AAS cause can result in frequent
nosebleeds. Checking one's blood pressure while on cycle should be mandatory anyway, but if you
ANABOLlCPHARMACOLOGY 94
are having nosebleeds while on-cycle, recheck your blood pressure and take the necessary steps to
get it in check. (refer to Hypertension)
Penile Shrinkage
This side effect is probably the biggest myth perpetrated by the popular media. It is no doubt that
anyone hearing this myth will think twice about using steroids, but it is silly in the extreme. While
testicular shrinkage is common with AAS use, there is no basis to the statement that they will result
in penile shrinkage. In fact, some men have reported an improvement in length and girth with the
use of androgens.
Steroid Flu
Many people report this side effect after starting a cycle, especially when using Sustanon 250.
Steroid Flu is typified by flu-like symptoms, which occur a week or two after the start of the cycle.
Some assume it to be due to impurities or the body's response to a foreign compound. Many people
will assume that they have gotten sick and will cut a cycle short. This side effect is more likely due
to alterations in glucocorticoid signaling brought on by the increase in androgen concentration at the
start of a cycle. The situation usually resolves itself over time.
Testicular Shrinkage
Testicular shrinkage is a very common side effect when using androgens. Using AAS will shut
down normal hormone production and when this occurs, the testes begin to shrink 212 ,213.214.
Generally, the longer a user is on AAS, the smaller they will get (of course there is a minimum size
that they will not shrink any further). Once a cycle ends the testes will begin to come back to
normal as testosterone production resumes. Some people will use HCG or c10mid during a cycle to
try to keep the testes from shrinking too much and proper PCT will help them come back quicker
after a cycle.
Urination PainlPressure
Androgens will cause the prostate to enlarge which can result in pain or pressure while urinating
(and sometimes even when not urinating). This can also lead to difficulty urinating or intermittent
urination where urine will stop flowing and then resume, sometimes even resulting in a wet spot on
the pants. The use of finasteride can help reduce prostate stimulation with androgens that undergo
5-alpha reduction but will not help when excessive doses of androgens are used. While this side
effect is usually only a nuisance, the cause is more serious (refer to BPH/Prostate cancer)
Voice Deepening
Women (and a few men) who use androgens will notice that the pitch of their voice will deepen as
time goes on. Many pro-bodybuilding women sound like men. This side effect has no serious health
problems but can cause the user psychological trauma. A deep voice for a woman is socially
unacceptable and will almost instantly identitY the owner as a steroid user (especially when the deep
voice is accompanied by large muscles). Though some have tried to correct this problem through
surgery, it is generally considered to be irreversible.
SECTION 7
BACKGROUND RESEARCH
A good portion of tile researcll into tile actions of AAS was carried out 30 to 40 years ago. Tile
.
works of VIda, , and otllers set tile groun dwor k fior wllat
Kocllaklan ~
we know to day215,216,217218,219
'.
Wllile tlleir work was revolutionary in tile time it was produced, today we realize tllat mucll of tile
work was lacking in its approacll. Tile determination of anabolic/androgenic ratios tllrough tile use
of laboratory animals (especially rats) was a major contribution to tile knowledge of AAS. To
determine tile anabolic/androgenic ratio, animals were given eitller a standard preparation
(testosterone propionate intramuscularly, metllyltestosterone orally) or tile test preparation (tile
steroid wllose ratio tlley wislled to determine). After dosing tile animals for a specific time period,
tile animals would be eutllanized and tile ventral prostate, seminal vesicle and/or tile levator ani
muscle would be taken from tile animals and weiglled. Tllis is known as tile Herscllberger assay.
Tile growtll of either tile ventral prostate or tile seminal vesicles would indicate androgenic activity
wllile tile growtll of tile levator ani muscle would indicate tile anabolic activity of tile compound in
question. Comparing tile androgenic activity to tile anabolic activity gives us tile anabolic to
androgenic ratio. In some studies, tile growtll of a cllickens comb was measured 220 Tile comb is an
androgen responsive tissue but tile results can be quite different tllan tllose obtained in rats.
Unfortunately, few of tllese studies were performed to tile standards tllat are expected of researcll
done today. Different lengtlls of treatment, different standards, different routes of administration,
different doses as well as misinterpretation of results call mucll of wllat was done in tile past to be
questionable at best. Little to no consideration was given to tile pllarmacokinetics and metabolism
of different drugs or to potential off-target effects, like tllose described in tllis text. As a guideline,
tile anabolic to androgenic ratios can be valuable but tlley sllould not be taken to be absolute.
SELECTIVE ANDROGEN RECEPTOR MODULATORS (SARMS)
Selective androgen receptor modulators, or SARMs, are androgen receptor agonists that selectively
activate androgen receptors in one tissue more so than in another. This is the pharmaceutical
221
industry's latest attempt to separate androgenic from anabolic actions in a single molecule .
Several pharmaceutical companies are actively researching nonsteroidal chemical entities that are
potential SARMs.
There are several approaches to producing a SARM 222 As noted elsewhere in this text, nandrolone
is actually a SARM. This is due to the fact that it is 5-alpha-reduced to a less potent androgen. This
means that at reasonable doses, nandrolone is more potent in skeletal muscle than it is in the
prostate. Therefore, it is selective for skeletal muscle. DHT is also a SARM. It is very active in the
prostate but is deactivated in skeletal muscle tissue by 3-alpha hydroxysteroid dehydrogenase.
Therefore, DHT is selective for the prostate. So, one mechanism for producing SARMs is through
enzymatic conversion 223 ,224 Another approach is to produce compounds that are more likely to
enter skeletal muscle cells than the cells of the prostate. Since the two tissues are different to some
extent, they have different properties regarding which substances can pass into the cells. This is a
difficult approach and will not necessarily offer selectivity over other tissue types such as sebaceous
glands, hair follicles etc. that are also responsible for androgenic side effects. Another approach is
to design molecules that change the shape of the androgen receptor in such a way to selectively
recruit coactivators to result in a different profile of gene expression than DHT225.226 Here are the
structures of several compounds that have been shown to be tissue selective androgens in the
literature22I.222. 224.227,228.229:
H3C CH 3
H,C
H CI
N OH
CH, -;?'
O,N
0 N
N(CH,), H
5-40503 LGD3303

BMS-564929
S-4
CF 3
o o N
H
LGD2941 LGD2226
o N N
H H
LDG120907
The structure labeled S-4 has found its way onto the underground market and people are reporting it
to have positive effects on energy and strength with only small increases in weight gain. There also
appears to be some effect on vision with this compound. S-4 is not known to be particularly potent
and was one of the first generation of selective androgen receptor modulators to be discovered.
This research is still in its early stages. Potential uses for SARMS that have been proposed include
treatment of hypogonadism, wasting conditions, osteoporosis, BPH, and male
contraception229.230,231. It will be interesting to see how this work progresses and how potential
abuse is addressed in the future.

AVAILABILITY OF AAS
The availability of AAS has seen its ups and downs. Before they were scheduled as controlled
substances in the Steroid Control Act of 1990, steroids were readily available in pharmaceutical
grade and were fairly inexpensive. There were a few counterfeit or underground products but for the
most part they contained the proper drug and dose. Once scheduled, prices increased rapidly as the
supply dried up and the risk to the seller increased. In this environment, counterfeits flourished.
There were some good counterfeits that contained the proper drug in the correct dose but there were
many more that contained no active ingredient and even some that contained harmful additives. Of
course the cleanliness of underground and counterfeit injectables was always questionable. Over
time, the supply increased as more legit pharmaceutical grade products became available and
underground labs became more sophisticated. The internet has also created an environment where
people can meet to discuss steroids, supplements and training as well as find sources for AAS.
Prices have stabi Iized at more reasonable levels since people can "shop around" for the best source.
While many people still desire only pharmaceutical grade preparations there are several
underground labs, which have become extremely popular and well known. While the identification
of all the available preparations and counterfeits of AAS is beyond the scope of this text, the
"Anabolics" publications by William Llewellyn are a good source of this information. Some of the
steroids I have outlined are not available from any source. I have chosen to include them because
they are interesting compounds and help us to understand how steroids differ from one another.
Also, different steroids are constantly becoming available from various underground sources so it is
difficult to predict what mayor may not be available in the future. A few good web sites to visit for
discussion of AAS, supplements and training are:
I: http://www.anabolex.com -- A hardcore site devoted to the discussion of anabolic steroids with

lesser emphasis placed on diet and supplements
2: http://forum.bodybuliding.com -- Less hardcore with more emphasis on supplements, dieting and
working out. Many notable experts including Patrick Arnold, William Llewellyn and Bruce Kneller
frequent this board and offer opinions.
3: http://forum.mesomorphosis.com -- A very good board with a lot of helpful discussion about
anabolic steroids
4: http://www.elitefitness.com -- This site has everything, the only problem is that to see everything
you must become a pay member.
5: http://www.fitnessgeared.com/forum/-- A lot of helpful people here with a lot of useful
information on everything from supplements to AAS.

6: http://www.cuttingedgemuscie.com/Forum/ -- A very informative board with some serious
discussion regarding the science behind AAS and supplements.
There are of course many other great forums to be found on the internet. A little searching will turn
up a wealth of information.
EXPECTAnONS
We live in a society that wants immediate gratification. No one is willing to wait in order to get
what they want. Unfortunately, it takes time to be the best, whether it is the fastest, strongest,
biggest or whatever. Mohammed Ali did not wake up one morning and say "I want to be the best
boxer in the world" and then the next day won the championship. It took years of training, eating
properly and mentally disciplining himself to become the champ. Many people look at AAS as
shortcuts and have the erroneous belief that more drugs will help them achieve their goals faster.
Along with the belief that AAS make things happen overnight is the concept of "feel". So many
times you will hear an athlete say that a drug must not be working because they don't "feel" it.
While it is true that people will feel different while using AAS, there is no indication that these
feelings have any relationship to the anabolic effect of the drugs. Of course, the aggression that
some of the harsher AAS produce is desirable in some sports (especially football and boxing) but
again, the aggression and anabolic effects do not appear to be linked in any meaningful way. The
fact is AAS are psychotropic drugs that do elicit changes in mood and do have addictive potential
from a psychological (as well as physiological) point of view166.204.20S.206.20J. Many people who use
AAS repeatedly begin to crave the psychological effects of the drugs.
Another source of unrealistic expectations is the scale. Of course bodybuilders are always watching
the scale but even runners, swimmers, baseball and football players will use the scale to determine
the progress of a cycle. Some athletes believe that if they aren't gaining 20 pounds in two or three
weeks that the drugs must not be working or that their cycle isn't strong enough. Many AAS cause a
good amount of water retention that is soon lost at the end of a cycle. The degree of water retention
on a cycle does playa role in strength gains due to leverage and joint lubrication. Of course, heavier
lifts do equate to greater mass gains, but just because one does not gain 20 pounds of water in the
first few weeks does not mean that the cycle is not working. True muscle gains come slowly while
side effects come immediately. It has been demonstrated in the literature that steroids can induce a
daily gain of about 60-75 grams of lean body mass per dal n This equates to a gain of about one
pound per week of lean body mass gains. Anything more than J 50-200% of this should probably be
attributed to gains in water or fat mass. While there is evidence that larger doses of AAS do equate

to larger lean mass gains (to a point), it is also a fact that larger doses do equate to more frequent
and more severe side effects.

SECTION 8

THE STEROIDS
This section will describe the properties of the individual steroids. I have included the structure of
each molecule for comparison and to show how I have arrived at the side effect profile. Each
steroid profile will have the following components:
Name: (the most common name for the drug)

(Other names): (other generic and trade names)
Chemical name: (the chemical name for the drug)
Structure: (the structure of the drug)
Chemical formula: (the chemical formula of the drug)
MW: (the molecular weight of the drug)
Description: (a description of the drug's properties)
AR affinity: (the affinity the molecule has for the androgen receptor)
PR affinity: (the affinity the molecule has for the progesterone receptor)
GR affinity: (the affinity the molecule has for the glucocorticoid receptor)
SHBG Affinity: (the affinity the molecule has for the sex hormone binding globulin)
Anabolic/Androgenic ratio: (a list of ratios from the literature)
Availability: (the general availability of the compound on the market)
Conversion to estrogen: (the degree to which the compound converts to estrogen)
The different receptor affinities are either taken from scientific literature or are estimated based on
the structure, properties and similarity to other molecules. Where estimated I have stated so with
the abbreviation "est."

STAND-BYS
The stand-bys are the AAS that have been used most commonly and are as such, the old "stand-
bys". They are usually the most available on the black market and many are still produced by
legitimate pharmaceutical companies. These are the AAS with which most users have the most
experience and will rely on for most cycles.

BOLDENONE
(Equipoise Qi" Ganabol, Boldebal, Vebonol, Sybolin, Pace, Equigain, Ultragan, Boldenon)
androsta-I,4-diene-17-beta-ol-3-one-undecyclenate
Formula: CI9H2602
MW: 286
Boldenone is a I-dehydro derivative of testosterone that has been sold as a veterinary preparation
under the name Equipoise and is largely known by this name. The formation ofa double bond in the
1,2 position changes the shape of the molecule slightly. This also changes the potency and
characteristics of the molecule. Boldenone has a lower affinity than testosterone for the androgen
receptor making it less potent on a mg for mg basis 233 This steroid can be converted to estrogen but
less so than testosterone, in addition, boldenone is metabolized to 1,4 dienedione which is a potent
aromatase inhibitor. Boldenone is converted by 5-alpha reductase to I-testosterone, a more potent
234
steroid as well as to the 5-beta isomer which is thought to be an inactive metabolite ,235. Binding
to SHBG is much lower with boldenone than with testosterone meaning a larger free plasma
concentration but a shorter half-life in plasma136 . There is linle to no binding to progesterone or
glucocorticoid receptors and no real data on the interaction of boldenone with the different enzyme
systems 233 The undecyclenate ester of boldenone was the ester marketed under the original trade
name but the free base as well as other esters are avai lable as underground preparations. On the
street equipoise is considered erroneously to have the same activity as deca and is often substituted
for deca in a stack. Dan Duchaine, ifnot the originator of this myth, at the very least promoted it in
his book "Underground Steroid Handbook II". If you look at the structure however, you can see that
it is structurally identical to dianabol without the C-17 alkylation, Most people experience much
less side effects with boldenone compared to methandrostenolone. This is due to the fact that
boldenone converts to estradiol while methandrostenolone converts to methylestradiol.
Methylestradiol is a much more potent and long lasting estrogen than plain estradiol. Since there is
no C-17 alkylation, there is no liver toxicity associated with boldenone. Boldenone is rumored to be
very good at increasing red blood cell production. While all androgens stimulate erythropoiesis,
there is no evidence in the scientific literature that boldenone is superior in producing this
f~ 237238.239.240 . B0 Id enone undecyclenate .
elect' . .
IS generally lI1Jected every four or five days but some
people will inject every day while others will inject once per week. The longer half-life of the
undecyclenate ester would dictate an injection frequency of every 10-14 days but there has been a
trend towards more frequent dosing by AAS users even with drugs known to have long half-lives.
Dosing is generally kept pretty low (300-500 mgs per week) however the low binding affinity

would argue for doses twice that which would be taken with testosterone. The anabolic to
androgenic ratios are favorable for boldenone however people do not consider boldenone to be a
particularly potent steroid, possibly due to the low doses that are utilized. Also, boldenone does not
cause much water retention so many people assume it is not working if they do not put on ten
pounds in one week. Boldenone is said to cause an increase in vascularity. There is no mechanism
to explain why boldenone would do this anymore than any other AAS.
I
AR AFFINITY:
II
75
I
I
PR AFFINITY:
II
0
I
GR AFFINITY: 0
I
SHBG AFFINITY:
II
Low
I
I
AlA RATIO:
II
100/54241
I
I II I
AVAILABILITY: I R"dily Availabl. a< V",,;....y P"pm"oo a<
Black Market Preparation and in Powder Form
I on Black Market
CONVERSION TO Low to Medium
I ESTROGEN: II I
III ANABOLIC PHARMACOLOGY

DROMOSTANOLONE
(Drostanolone, Drolban, Masteron, Permastril, Masteril)
2-a Ipha-methy I-d ihydrotestosterone
o
-
H
Form ula: C2o HJ2 02

MW: 304
Dromostanolone is a synthetic derivative of DHT. As I have discussed earlier, DHT binds more
strongly to the AR than testosterone but does not have an effect in muscle tissue because it is
deactivated by 3-alpha hydroxysteroid dehydrogenase. The methyl group at the 2 nd position allows
dromostanolone to stay active in muscle tissue by disallowing deactivation by this enzyme to some
degree, however, since Dromostanolone is converted primarily to the 2-methyl androsterone and 3-
alpha diol derivatives there is still considerable deactivation by 3-alpha hydroxysteroid
dehydrogenase 235 The presence of the 2-methyl group does reduce potency of dromoslanolone
compared to DHT but only to about the level of testosterone. Since dromostanolone is already 5-
alpha reduced, it is not converted any further. Therefore it is equipotent or slightly less potent in
skeletal muscle compared to prostate, hair follicles etc. This steroid is not prone to aromatization
due to the 5-alpha reduction. Additionally, 5-alpha reduced steroids have been shown to have anti-
aromatase activity. Dromostanolone, like DHT, binds strongly to SHBG and can displace bound
estrogen into circulation which can result in delayed gynecomastia when one goes "off' of this
steroid. No binding to progesterone or glucocorticoid receptors has been shown with this steroid.
Dromostanolone is traditionally injected as a propionate ester requiring it to be injected every two
or three days. It is a painful injection resulting in swelling and soreness. There are no legitimate
producers of dromostanolone propionate at this time, only underground suppliers. I would not be
surprised to see different esters of dromostanolone show up on the black market and there have
been some reports of oral dromostanolone being sold. Though many consider this steroid to be
similar to DHT and expect side effects to be similar, dromostanolone is actually somewhat less
harsh than DHT and more potent androgens. Its potency is similar to testosterone but without the
conversion to estrogen which is demonstrated in its anabolic to androgenic ratio (about 3: I).
Dromostanolone has build shown to build up red blood cells with a similar potency to
oxymetholone239 Among users, this drug is known as a "hardener" because it loads water into the
muscle without subcutaneous water retention (edema) resulting in a hard-looking physique.
Dromostanolone is also known for its positive effects on strength.

I
AR AFFINITY:
II
100
I
I
PR AFFINITY:
II
0
I
GR AFFINITY: 0
I II I
I
SHBG AFFINITY:
II
Medium to high
241
I
A/A RATIO: 62/24, 130/40
I II I
AVAl LABILITY: Low, Some availability on black market in
powder form however, testing has shown
everal batches to be trenbolone actetate instead
of dromostanolone DroDionate
CONVERSION TO None
I ESTROGEN: II I

ETHYLESTRENOL
(Maxibolin, Orabolin, Orgabolin)
I7-alpha-ethyl-4-estren-17-beta-ol
OH
... \'\\\
CH
Formula: C2o HJ2 0

MW:288
Ethylestrenol is an unusual derivative of nortestosterone. It lacks the double bonded oxygen at

position 3 and is 17-alpha ethylated as opposed to methylated (or alkylated). All classic steroid
hormones have some kind of functional group at the 3-position, in most cases a double bonded
oxygen (known as a ketone) or a single bonded oxygen bound to hydrogen (known as an alcohol).
While several researchers have shown a 3-functional group to be dispensable for androgen receptor
binding, the lack of such a group does decrease binding significantly. Ethylestrenol has very poor
binding affinity for the androgen receptor. In fact, it is virtually inactive at all receptors. There is
some evidence that this steroid acts as an aromatase inhibitor, which may increase natural
testosterone levels. It has been shown that ethylestrenolundergoes conversion to norethandrolone as
well as 3-hydroxy metabolites 235 There is little to no conversion to estrogenic metabolites and
while ethylestrenol is subject to 5-alpha reduction, like nandrolone, less potent metabolites are
formed. This results in a high anabolic to androgenic ratio 241 . Ethylestrenol has no binding to
SHBG 236 Unlike norethandrolone, eth,(ilestrenol has been shown to decrease total and free cortisol
levels without effecting CBG levels 2 2 When this steroid was originally marketed, it was used
primarily by women because it was considered to be weak and didn't seem to produce androgenic
side effects. Ethylestrenol is manufactured by some legitimate pharmaceutical manufacturers
around the world but it is not often found on the black market. Most consider it to be too weak.
However, at higher doses (100-150 mg per day), this steroid provides for a fairly potent anabolic
effect with very little androgenic or estrogenic side effects. The only real concern at this dose would
be liver toxicity but the 17-ethyl group seems to be less toxic than the traditional 17-methyl.

I AR AFFINITY:
II
Very low for parent
I
PR AFFINITY: Unknown
I II I
GR AFFINITY: Unknown
I II I
I
SHBG AFFINITY:
II Very Low
241
I
I AlA RATIO:
AVAILABILITY:
II 421/22,170121,200/40
Low availability as a pharmaceutical
I
preparation. Also available underground in
I I powder and tablet form
CONVERSION TO Low to none
I ESTROGEN: II I

FLUOXYMESTERONE
(Halotestin, Stenox, Android-F, Ultandren, Ora-Testryl)
9-alpha-tluoro-ll-beta, I7-beta-dihydroxy-17-alpha-methyl-4-androsten-3-one
OH
F
.'"
Formula: C20H29F03
MW: 336
Fluoxymesterone is actually derived from cortisol (a glucocorticoid) and as you can see from its
structure, shares the C-II hydroxyl (OH) group with cortisol-like steroids. The binding affinity of
fluoxymesterone for the androgen receptor is very low236 . It cannot be converted to estrogenic
metabolites but is converted to a more potent 5-alpha reduced form 243 The half-life of the parent
compound is 9.2 hours but the presence of active metabolites (such as the 5-alpha reduced form)
likely prolongs the active half_life 244 Fluoxymesterone is known to be very androgenic and to be
quite liver toxic. Halotestin is a steroid rumored to be good in a "cutting stack" because it seems to
not put on much weight but keeps a physique hard and increases aggression to get through workouts
on low calories. Some evidence suggests that fluoxymesterone is a potent glucocorticoid antagonist.
This suggests that tluoxymesterone has some level of inhibitory action on II-betahydroxysteroid
dehydrogenase. Since there is no literature demonstrating this effect, we can only speculate.
However, since fluoxymesterone is not known for producing a bloated effect, we can speculate that
if fluoxymesterone inhibits this enzyme system, that it is preferentially inhibiting the type I enzyme
which converts inactive glucocorticoids to active forms. Like oxandrolone, halotestin actually
242
increases total and free cortisol levels without while slightly reducing CBG levels Obviously the
effects on glucocorticoid signaling are quite complicated and difficult to dissect. In any case, the
likely scenario is that tluoxymesterone is anticatabolic with strong androgenic activity.
Fluoxymesterone binds somewhat weakly to SHBG but still is capable of displacing estradiol and
testosterone at higher doses236.245.246. Additionally, fluoxymesterone has a rather large suppressive
effect on TBG levels with only moderate compensatory increases in TBPA which is likely to cause
higher plasma levels of T4 and T3 with greater T3 uptake which may also explain the effectiveness
242
of this drug in a "cutting" stack Fluoxymesterone has been shown to be as effective as
oxymetholone in elevating red blood cell levels in the scientific literature2J8.24o Fluoxymesterone is
available as Halotestin in the US and as a pharmaceutical preparation in other countries, especially
Mexico as well as through black market suppliers. An interesting use of fluoxymesterone includes
the use of a 5-alpha reductase inhibitor, like finasteride. While this will not increase the anabolic
activity of tluoxymesterone, it will decrease the androgenic side effects. The purpose of such a
combination would be to harness the anticatabolic activity of fluoxymesterone.

I AR AFFINITY:
II 0.3
I
I PR AFFINITY:
II 0
I
40
I G R AFFINITY:
II I
SHBG AFFINITY: Low
I II I
AlA RATIO: 1745/120, 89/7524 \
I II I
AVAILABILITY: Available in US and several other countries as
pharmaceutical prep in tablet form. Availability
on the black market seems to be mixed, with
some availability of Mexican version and some
black market tablets and Dowder available
CONVERSION TO None
I ESTROGEN: II I

METHYLTESTOSTERONE
(Afro, Agovirin, Android, Androral, Arcosterone, Arcosterone, Hormobin, Longivol, Mediatric,
Mesteron, Metandren, Oreton Methyl, Teston, Testormon, Testosteron, T Lingvalete, Testovis,
Testred, Virilon)
I7-a Ipha-methy Itestosterone
OH
CH 3 .",IICH
Formula: C20HJoOZ
MW: 302
Methyltestosterone is a very crude synthetic derivative of testosterone. In fact, it was probably the
first orally available steroid ever marketed. Methyltestosterone is simply the C-17 alpha alkylated
version of testosterone. This added methyl group allows the molecule to survive long enough when
taken orally to have an effect. The effect however, is considered to be rather small.
Methyltestosterone has a short half-life, about 2.5 hours, and because of this, the drug needs to be
taken rrequently to have any real effect on muscle anabolism 248 Most people see little to no effect
even when using large doses but some athletes still use it to try and beat a drug tests and maybe
increase aggression a little just prior to competition. Methyltest is liver toxic due to the added
methyl group but no more so than other orals. The reputation for being more liver toxic is due to the
large amounts needed to make this drug worth taking. Most people do not knowingly use this drug,
but methyltest is found in a lot of the counterfeit dianabol that is available on the black market.
Methyltestosterone is converted by aromatase to the long-lived estrogen, methylestradiol. However,
methyltestosterone is a fairly potent inhibitor of the aromatase enzyme, so, with continued use,
estrogenicity peaks and then decreases. However, when methyltestosterone is stopped, there can be
a rebound estrogenic effect. This steroid is also converted by 5-alpha reductase to methylDHT
which is inactivated in skeletal muscle but very active in the prostate, hair follicles and other
androgen target tissues resulting in androgenic side effects Z47 The binding affinity of
methyltestosterone is about equal to that of testosterone, however, the longer plasma half-life and
the conversion to methylDI-IT result in a drug that has an anabolic to androgenic ratio of about I to
1233 241 . Methyltestosterone has been shown in the scienti fic literature to be a direct antagonist of the
glucocorticoid receptorZ49 This drug has no real effect on CBG levels or cortisol levels but it does
have a rather large suppressive effect on TBG with small compensatory increases in TBPA z42 The
binding affinity of methyltest is about equal to that of estradiol resulting in displacement of a good
amount of estradiol and testosterone from SHBG 245 . It is likely that methylandrostenediol is formed
through the metabolism of methyltest and methylandrostenediol has been shown to induce

2So
hypertension through potent inhibition of II-beta hydroxylase Methyltestosterone is cheap and
readily available in pharmaceutical preparations and the black market.
AR AFFINITY: 100
I II I
I
PR AFFINITY:
GR AFFINITY:
II
5
5
I
I II I
SHBG AFFINITY: Low to medium
I I 241
I
A/A RATIO: 1151103,159/168,280/356,150/130
I II I
AVAILABILITY: Available as several pharmaceutical
preparations in oral and sublingual form.
Readily available on the black market-
substituted for many other steroids especially
methandrostenoloen in black market
preparations
CONVERSION TO Medium
I ESTROGEN: II I

METHENOLONEACETATE
(Primobolan~
17-beta-hydroxy-l-methyl-5-alpha-androst-l-en-3-one
II
O-C-CH
CH 3
/-
H
Formula: C22H3203
MW: 344
Methenolone is a synthetic derivative of dihydrotestosterone. The acetate ester version is taken

orally though their used to be an injectable version of this ester in the past. A highly overlooked
steroid, many people do not consider primobolan to be very effective and coupled with its high
price, many do not consider it to be worthwhile. The oral form of methenolone acetate is relatively
weak due to the fact that methenolone is not 17-alpha alkylated. Instead, the I methyl group seems
to offer some protection from metabolism to I and 2 hydroxy metabolites. Even so, the acetate does
not have great oral bioavailability and a pretty high dose is needed to see significant effects. Since it
is a DHT derivative, methenolone does not aromatize nor does it have much progestational activity.
In fact, being a DHT derivative, primobolan likely acts as an aromatase inhibitor to some degree
which likely contributes to its reputation as a dry gainer with less suppressive effects. Since it is
already 5-alpha reduced, it does not gel metabolized by 5-alpha reductase. Methenolone still
underoes metabolism by 3-alpha hydroxysteroid dehydrogenase in skeletal muscle but less so than
DHT2 5 This results in a molecule that is somewhat less potent but still has a decent anabolic to
androgenic ratio. Furthermore it binds only moderately to SHBG and there is no evidence that
methenolone interacts to any degree with the glucocorticoid or progesterone receptors 236
Primobolan does not bring on massive weight gains, but this is due to the fact that there is very little
water and fat accumulated. Primobolan is used for adding quality mass with little to no side effects
but the injectable version is much preferred over the oral version. Low doses of primobolan have
been used by women with minimal side effects. Effective doses for men are considered to be 100-
150 mg per day with women taking 25 to 50 mg. Some have argued that primobolan can be used
without shutting down natural testosterone production. While suppression will be reduced with this
steroid because it does not convert to estrogen, there will still be some reduction in testosterone
production that will become worse as higher doses are used. A little known fact about methenolone
is that it has been shown to have similar levels of efficacy as oxymetholone for elevating red blood
cell count237 Methenolone, either the tablets or the injectable, has never been as available as most

of the other stand-bys and is often expensive when it is found. There are only a few pharmaceutical
preparations available and these items are often scarce even from black market sources.
AR AFFINITY: 50
I II I
I
PR AFFINITY:
II 0
I
I GR AFFINITY:
II 0
I
I
SHBG AFFINITY:
II
Low
24
I
AlA RATIO: 72/15, 36/6 \
I II I
AVAILABILlTY: Low as pharmaceutical prep and on black
I I market
CONVERSION TO None
I ESTROGEN: II I

METHENOLONEENANTHATE
(Primobolan Depot~
17-beta-hydroxy-l-methyl-5-alpha-androst-l-en-3-one
o
O-C
II CH
CH 3
-0
o -
H
Formula: C27 H42 03

MW:415
Methenolone enanthate is the injectable form of this steroid, referred to as Primobolan depot, its
original trade name. The enanthate ester provides for a relatively slow release from the injection site
and could be injected as infrequently as every 10 to 14 days though most users will inject it weekly
or even twice weekly. The injectable version of methenolone is much more effective than the oral
version since you do not have the effect of first pass metabolism to contend with. Once the ester is
stripped off you have just the parent methenolone molecule. As with the acetate version, this steroid
does not aromatize nor does it have much progestational activity. As higher doses are used, one
could expect to see greater incidence of androgenic side effects. The injectable version of
methenolone with the enanthate ester is a potent steroid. It is usually injected on a weekly or
sometimes shorter basis in doses of 400 to 600 for men and 50 to 100 mg for women. Women
actually do better with a longer injection period of 10 to 12 days to avoid a buildup in androgen
levels. Methenolone is considered to be one of the safest steroids but although this steroid is not C-
17 alpha alkylated, the I-methyl group can cause some elevations in liver enzymes (even with the
injectable) but less so than the C-17 alkyl derivatives such as methandrostenolone. This is definitely
not an instant gratification type of drug because it does not cause large amounts of water retention
and is less potent than other commonly used injectables like nandrolone or even testosterone. Some
people still prefer methenolone because even though it does not result in immediate gains, it
generally doesn't produce as much in the way of side effects as other drugs either. Methenolone, in
oral or injectable form is often stacked with other gentler drugs like oxandrolone. Though normally,
most users would avoid stacking two orals together, in this case, since methenolone has lower levels
of liver toxicity, it is not as much ofa concern.

AR AFFINITY: 50
I II
PR AFFINITY: 0
I II
GR AFFINITY: 0
I II
SHBG AFFINITY: Low
I II
AlA RATIO: 500/1 0, 30/2 241
I II
AVAILABILITY: Low as pharmaceutical prep and on black
I
CONVERSION TO
I market
None
I ESTROGEN: II I

MESTEROLONE
(Proviron, Mestoranum, Pluriviron, Vestimon)
I-alpha-methy 1-5-al pha-d ihydrotestosterone
o
H
Formula: C 2oH 32 02
MW: 304
Meslerolone is a simple derivative of dihydrotestosterone and is commonly known by its trade

name, Proviron. The addition of a methyl group to the I position, like methenolone, should help to
provide a small amount of protection from metabolism when taken orally. In fact the only
difference between methenolone and mesterolone is the presence of a double bond in the 1,2
position with methenolone. This double bond changes the shape of the A-ring as well as the location
of the I-methyl group. Though these drugs are so similar in appearance, they are quite different in
activity. While the I-methyl and I-double bond help to keep methenolone from being metabolized
to inactive metabolites, the presence of only a I methyl group seems to provide mesterolone with
little protection and it is likely deactivated quickly. Since mesterolone is already 5-alpha reduced, it
is not subject to further metabolism by 5-alpha reductase. Mesterolone, as a DHT-derivative, cannot
be converted by aromatase to estrogenic metabolites and has some degree of inhibition of aromatase
and likely some inhibition of 5-alpha reductase as well. In fact, many consider mesterolone to be an
anti-estrogen, and its use in the literature seems to support this to some degree. Mesterolone is one
of the stroniest binder of SHBG commercially available, in fact, only DHT binds to SHBG more
strongl/ 36.25 As discussed earlier, SHBG plays a very important role in testosterone metabolism.
Because mesterolone binds so strongly to SHBG it tends to bump other less strongly bound
molecules in the "free" state where they can bind the androgen receptor251 . Therefore, some athletes
have attempted to use mesterolone for this purpose. They add mesterolone to a cycle if the hopes
that more steroid will remain free and active. This would also be true for testosterone and estrogen.
Mesterolone would be capable of bumping both of these hormones into circulation as well which
may result in androgenic or estrogenic effects. There is no evidence that mesterolone binds to
glucocorticoid or progesterone receptors. Mesterolone is not known for being very anabolic even
though the anabolic to androgenic ratio when given subcutaneously is favorable. When 9iven orally,
mesterolone undergoes significant metabolism that greatly reduces any anabolic effecr 35 The fact
that mesterolone has been shown to have little effect on red blood cell production, unlike other
androgens, seems to confirm its rapid metabolism 252 Mesterolone has been studied quite
extensively in the literature as a fertility treatment to increase sperm quantity. There is quite a bit of
conflicting data showing mesterolone to have variable effects on LH and FSH, though it is generally

been shown to not reduce normal levels of LH and FSH 253 Though its use as an SHBG binder is
somewhat questionable, it may have use in blocking the metabolism of other DHT derivatives by 3-
alpha hydroxysteroid dehydrogenase since it seems to have significant affinity for this enzyme.
I
AR AFFINITY:
II 70
I
PR AFFINITY:
I
GR AFFINITY:
II
0
I
I II
0
I
SHBG AFFINITY: Very High
I II I
AlA RATIO: 130/15
I II
Readily available as pharmaceutical
I
AVAILABILITY:
preparation in oral form, less available as black
~arket preparation in tablet/capsule or powder
form
CONVERSION TO None
ESTROGEN: I I

METHANDROSTENOLONE
(Anabol, Anabolin, Andoredan, Bionabol, Dialone, Dianabol, Encephan, Metana?ol,
Methandrostenolonum, Nerobol, Pronabol-5, Stenolon, Trinergic, Naposlm, Anabolikum,
Methandrostenolone, Metandiabol)
I7-beta-hydroxy-17-alpha-methyl-1 ,4-androstadien-3-one
OH
CH 3
."" I CH
o
Formula: C2oH2802
MW:300
Methandrostenolone is a derivative of testosterone with double bonds at the I and 4 positions as

well as being C-17 alpha alkylated. Methandrostenolone, also known as methandienone or
methandienone, was originally produced under the trade name Dianabol, by which it is often still
referred to, making it one of the earliest synthetic androgens. Dbol, a shortened form of the trade
name that is common among steroid users, has been one of the most popular oral androgens ever
since its release. It has the reputation of being a very effective anabolic steroid (especially in
combination with deca durabolin) with fairly rapid weight gain, bloating and a marked increase in
appetite. There has been some disagreement over whether Dbol converts to estrogenic metabolites.
Though there is little evidence in the literature, it is pretty apparent from anecdotal experience that
Dbol is in fact converted to methylestradiol to some degree. Gynecomastia appears to be quite
common with the use of this steroid. There is evidence in the literature of the formation of 5-alpha
(and 5-beta) reduced metabolites from methandrostenolone and this is expressed in the fact that
Dbol is considered to be quite and rogen ic 235 ,254,255.256. The 5-alpha reduced form of
methandrostenolone, methyl-I-test, is known for inducing massive bloating and high blood pressure
at higher doses likely as a result of inhibition of the II-beta hydroxylase enzyme. SHBG binding of
this drufl is moderate so a good portion of the absorbed quantity of this drug circulates in the free
state 236,-. The binding affinity of methandrostenolone is low and as such, people have speculated
that this drug acts through a non-AR mediated effect. A more recent journal article has shown that
even th~~1h the binding affinities of some AAS are low, they are still. adequate to activate the
receptor- . Additionally, methandroslenolone has several active metabolites that likely have more
potent AR affinity. There is a small amount of interaction with the progesterone receptor but no
direct effect on the glucocorticoid receptor. This steroid has been shown to increase levels of CBG
while at the same time increasing serum cortisol and non-protein bound cortisol levels 242 This
could be the mechanism for the marked increase in appetite seen by those using Dbol. Increase in
the level of CBG is a common effect with estrogenic compounds while androgens tend to decrease
CBG levels demonstrating the propensity of methandrostenolone to convert to methylestradiol. The

increased cortisol levels could also contribute to the extreme amounts of water retention that users
experience with this drug. Dbol decreases TBG levels less than fluoxymesterone but with a slightly
greater increase in TBPA 242. Methandrostenolone is orally active due to the presence of the C-17
methyl group. As such, this compound is liver toxic but many do not consider it to be much of a
concern because users tend to consume doses in the 20 to 30 mg range and some report Dbol to be
effective in doses as low as 5 mg per day. A study in the literature reported a gain of ~ust over 5
pounds with just three weeks of methandrostenolone dosed at only 5 mg twice daily 59. Larger
doses are not uncommon (up to 100 mg per day) but with larger doses, liver toxicity could become a
concern. This drug has been shown to build up red blood cells in a similar manner to most other
androgens with similar efficacl 39 . Dbol is stacked with just about any other steroid due to the fact
that it is easily obtainable and very cheap. Some have suggested that methandrostenolone doses
should be split up through the day due to the short half-life while others report that once a day
dosing is sufficient. This steroid is probably the most avai lable as well as one of the cheapest on the
market. There are quite a few legitimate pharmaceutical preps available as well as a flood of black
market versions. The problem is that the popularity of this drug breeds many counterfeits. Even
though the raw material for methandrostenolone is extremely cheap, the raw material for
methyltestosterone is even cheaper (by about two thirds). Therefore, many unscrupulous
manu f;acturers WI'11 su b' h I
stltute metlYltest tior db o.I
I AR AFFINITY: II low I
PR AFFINITY: II 10 I
GR AFFINITY: II 0 I
SHBG AFFINITY: II Low I
A/A RATIO: II 125/55, 210/60, 30/6, 182/73, 89/450241 I
AVAILABILITY: Plentiful on the black market in tablet/capsule
I I form as well as iniectable and powder
CONVERSION TO Medium to high
I ESTROGEN: II I

NANDROLONE
17-Hydroxyestr-4-en-3-one
OH
o
Formula: CIsH2602
MW: 274
Nandrolone is the common name given to the C-19 demethylated derivative of testosterone, 19-
nortestosterone. While this seems like a minor alteration, its effects on the actions of the molecule
are profound. First of all nandrolone is a more potent binder of the androgen receptor with
approximately 50% great~r binding affinity than testosterone2J3,236,260. Secondly, since the 19-
methyl group plays a pivotal role in the aromatization process, the conversion to estrogenic
metabolites is reduced to about twenty percent with nortestosterone and its derivatives of the rate of
testosterone 261 . Thirdly the 5-alpha reduction of nortestosterone and its derivations results in
dihydronandrolone met~bolites which are considerably weaker than the parent compound235~6~.
A
Finally, binding to SHBG is significantly reduced with nortestosterone compared to testosterone ).
Nortestosterone is actually produced in small quantities in mammals, including man,
Nortestosterone is considered to be a derivative of progesterone and it does, in fact. have some level
of progestational activity, about twenty percent of the binding of progesterone233 .260. Much has been
made of this fact, especially with regard to nandrolone's ability to induce gynecomastia. Since
nandrolone does not convert to estrogen in nearly the same quantities as testosterone, all sorts of
explanations have been concocted to account for the apparent ease with which it causes
gynecomastia. The fact is that while nandrolone does convert to a smaller degree, significant
increases in estrone have been observed in the literature with nandrolone therap/61. Estrone is
sulfated to form estrone sulfate which has a very long half-life in the body and can act as a reservoir
of estradiol through back conversion. The main contributing factor is the fact that nandrolone is not
very androgenic. In fact, because of the formation of less potent, dihydronandrolone metabolites.
the total androgenic stimulation is much reduced with the use of nandrolone. This, combined with
the formation of estrone, results in a significant shift in the androgenic to estrogenic ratio. This is
also the largest reason for the major shutdown in natural testosterone production seen with
nandrolone and its derivatives 26J The fact that there is a small progestational activity does further
impact the shutdown of natural testosterone production but likely has minimal to no effect on the
propensity of nandrolone to cause gynecomastia. However, nortestosterone ha been shown to have
mixed agonist/antagonist activity at the progesterone receptor and antagonism of the progesterone
receptor may increase estrogen receptor concentration in the breast and hypothalamus which may
contribute to the estrogenic effects that some notice with nandrolone 264

Used in reasonable doses, nandrolone is almost the perfect steroid. The major drawbacks to
nandrolone are its reduced androgenic activity and its conversion to estrogen. Nandrolone is known
to dramatically affect libido in a negative fashion due to its reduced androgenic activity and results
in a condition known as "deca dick". This is due to the suppression of natural testosterone levels
and the lack of androgenic stimulation in DHT target tissues (such as the prostate). Many people
will add testosterone to nandrolone to help counteract the negative effect on libido. Others will add
a source of androgen such as mesterolone or dromostanolone to maintain androgenic tissues.
Another alternative is to use small doses ofa 5-alpha reductase inhibitor which will maintain some
of the more potent nandrolone in androgen target tissues - this would of course also increase the
risk of androgenic side effects. This is the opposite effect that 5-alpha reductase inhibitors have
when combined with other reducible steroids. Nandrolone, unlike most other androgens, actual
24
Ii
increases TBG and TBPA levels slightly resulting in reduced levels of free thyroid hormones .
One study showed nandrolone to be the most potent stimulator of red blood cell production
compared to testosterone and oxymetholone2JJ While many steroids (such as testosterone) inhibit
the production of cortisol through the inhibition of II-beta hydroxylase activity and the formation
of hypertensinogenic deoxycorticosterone, nandrolone has been shown to have little to no
hypertensinogenic effect due to a lack of inhibition of I I-beta hydroxylase 265 . On the other hand,
nortestosterone has been shown to inhibit cortisol production through the inhibition of 21
hydroxylase. This is demonstrated by the reduction in non-plasma bound cortisol shown in the
242
literature . This reduction in cortisol is likely due to chronic dosing because increases in cortisol
have been shown to occur early in therapy with nandrolone and may account for the relief in joint
266
soreness that some have attributed to nandrolone Different esters are attached to this molecule to
change the rate at which they are absorbed from the injection site. That is the only thing that the
different esters change. Once the ester is removed you have just plain nandrolone. Nandrolone is
well known for causing positive test results. In fact, most tested athletes will avoid nandrolone
because it can be detected for extended periods of time. Why this is so is somewhat of a mystery but
much of it has to do with the habits of the user. Most nandrolone esters tend to have a long half-life.
When injected on a period shorter than the half-life, nandrolone levels in the blood will rise to very
high levels which take a long time to be metabolized and cleared from the bod/ 67 ,268

Nandrolone Decanoate
(Deca Durabolin , Deca Durabol, Elpihormon, Anaboline, Androlone-D, Extraboline, Retabolin,
Turinabol Depot, Hybolin, Jebolan, androbolic, eo-Duraboltc, urezan, Retabold, Sterobohn,
Ziremilon, orandren)
o
Formula: C28H440J
MW:429
Since nandrolone decanoate is the most popular ester of nandrolone, most people will refer to all
nandrolones as "deca". The decanoate ester is a straight chain of 10 carbons. This results in a slow
release of nandrolone from the injection depot. Most people inject nandrolone decanoate every 7
days or so which is a little shorter than its half-life of 7 days. This results in a stepping up of total
plasma concentration of nandrolone over time. It can take 2 months or more to reach steady state at
the maximum plasma level. Physicians would administer nandrolone decanoate every 2 to 4 weeks
to help prevent this buildup in nandrolone levels. Injection volume and location can dramatically
alter the pharmacokinetics and pharmacodynamics of a depot. A study done with different esters,
injection volumes and locations of nandrolone showed a gluteal injection of 100 mg of the
decanoate ester in I ml of oil to have a much greater bioavailability (73%) compared to a 4 ml
gluteal or I ml deltoid injection(53-56%)269 In addition, a I ml gluteal injection of nandrolone
decanoate actual reached higher peak plasma levels (with a greater AUC) compared to a 4 ml
gluteal injection. A study utilizing nandrolone decanoate at a dose of 600 mg per week for 12 weeks
in HIV infected men showed a gain of about nine pounds with few adverse events including
gynecomastia 270 It is worth noting that the authors of the paper felt it advantageous althe end of the
study over the course of four weeks (400 mg, 200 mg, 100 mg, 50 mg). Most steroid users consider
the practice of tapering of dose (especially with long acting injectable esters) to be an ineffective
measure though this practice is common in the clinical setting.
Mg ofNandrolone per 100 mg: 64

Nandrolone Undecanoate
(Dynabolonilii, Psychobolan)
o
O'--U_,
CH,
-CH,
o
Formula: C29H4603
MW:443
The undecanoate ester consists of a straight chain of II carbons making it even more long lasting
than the decanoate ester. Its half-life is roughly 8-9 days and should probably be taken every two
weeks although athletes would probably use it on a weekly basis like decanoate. This more frequent
administration of a longer acting ester increases the plasma concentrations and the likelihood for
side effects. Metabolites have been detected for up to 8 months following injection of nandrolone
undecanoate; however, it is possible that metabolites could be detected for even longer.
Mg ofNandrolone per 100 mg : 62
Nandrolone Hexyloxyphenylpropionate
(Anadurilii, Anadurin)
o
CH
CH,
0-"-,
VVV '
Formula: C33H4604
MW: 507
The hexyloxyphenylpropionate ester is composed of 15 carbons containing a benzyl group. This

makes for a long and complicated ester which results in a very slow release of nandrolone form the
injection depot. With a 21-day half-life, an injection is only required every 3 to 4 weeks to maintain
steady plasma nandrolone levels271 Giving repeat injections shorter than the half-life would result
in a rapid build-up in plasma nandrolone levels. This can result in detection times of up to 19 weeks
as reported in the literature271 Also, because the ester is so large (it weighs almost as much as
nandrolone itself), you get only 54 mg of nandrolone per 100 mg of nandrolone
hexyloxyphenylpropionate however, the plasma level of nortestosterone has been shown to reach
double the levels given an equal dose of hexyloxyphenylpropionate ester compared to the decanoate
ester. Most athletes do not inject less frequently than once per week regardless ofa drug's half-life.

Some have suggested an "addiction" to the act of injecting itself. Self-injection can be quite
exhilarating with a rush of adrenaline and endorphins that some people actually start to crave.
Mg ofNandrolone per 100 mg : 54
Nandrolone Laurate
(Laurabolin"", Fortadex, Laudrol, Fortabol)
o
0---"-,
CH,
CH,
Formula: C30H 4S 03
MW: 457
LaUl'ate is also known as dodecanoate, which means that it is a straight chain of 12 carbons. This
results in a longer release than decanoate or undecanoate equating to a half-life of around 10 days.
Laureate should be taken every 12 to 14 days, but most athletes use it on a weekly basis. As Laurate
is often found in veterinary preparations, its cleanliness may not be up to human standards. Some
have reported getting flu-like symptoms from using nandrolone laurate.
Nandrolone Phenpropionate
(Activin, Androlone, Anabolin, Opopharma, Equibolin, Fenobolin, Fherbolico, Nandrobolic,
Nerobolil, Nu-Bolic, Superanabolon, Norandren, Kabolin, Durabolin, Hybolin, Stenabolin;
Docabolin (multi-ingredient preparation); Docabolina (multi-ingredient preparation)
o
Formula: C27H3403
MW: 407
The phenpropionate ester consists of a chain of 3 carbons with a benzyl group (a ring of 6 carbons)
on the end. This results in a rather short acting ester with a half-life of around 3 days although some

in the underground community have reported it to be I dal69 . A half-life of 3 days would require
this drug to be injected every 3-4 days to maintain plasma nandrolone levels. Athletes report fewer
side effects when using this ester than when using other longer acting forms of nandrolone. This is
likely due to the fact that with the shorter half-life there is less build up in plasma levels. This is
interesting considering that the phenpropionate ester actually reaches two to three fold hi~her peak
plasma levels after a single injection compared to the same dose of nandrolone decanoate 69. Even
so, many users will inject this drug daily which counteracts the increased safety aspect of the shorter
ester resulting in rapid and sustained high plasma levels of nortestosterone.
Nandrolone Propionate
(Norybol-19, Nortesto)
o
o~ .CH 3
CH 3 V
o
Formula: C21HJOOJ
MW: 330
The propionate ester is a straight chain of 3 carbons and is therefore an even shorter acting ester
than phenyl propionate, requiring injections every 2-3 days. The half-life of propionate and
phenylpropionate are only different by a matter of hours, however, you get 83 mgs of nandrolone
per 100 mg of nandrolone propionate compared to 68 mgs with nandrolone phenpropionate.
Mg ofNandrolone oer 100 mg: 83
I AR AFFINITY: II 154 I
1.=====11
PR AFFINITY: 20 I
CONVERSION TO II Low to medium I

I ESTROGEN:

OXANDROLONE
(Anavar, Oxandrin, Anatrophill, Lipidex, Lonavar, Yasorome)
5_alpha_androstan-2-oxa-17-alpha-methyl-17-beta-ol-3-one
OH
CH 3 . ,\\ "CH
o
H
Formula: Cl9H3003
MW: 306
Oxandrolone is an unusual derivative of DHT that was introduced by Searle in 1964, removed from
the market and reintroduced in the mid 1990's for the treatment of wasting in HIY patients.
Embedded in the A-ring is an oxygen atom at the 2-position forming what is referred to as a
heterocycle. This is referred to as a heterocycle. Oxandrolone has very low binding affinity but a
long half-life makes it reasonably potent258 Because it is a DHT derivative, and due to the presence
of the heterocycle, oxandrolone cannot be converted to estrogenic metabolites. Also, since it is
already 5-alpha reduced, it cannot be reduced further by 5-alpha reductase. Due to the presence of
the oxygen atom in the A-rin o , this steroid is not deactivated by 3-alpha hydroxysteroid
dehydrogenase in skeletal muscle1'J5 This steroid does not bind to SH BG so the entire circulating
drug is in the "free" state. Oxandrolone has been shown, like most androgens, to decrease SHBG
levels which may result in estrogenic side effects due to higher free levels of estradiol and
estrone 272 There is no evidence in the literature that oxandrolone interacts with the progesterone
receptor, but it is likely that oxandrolone has significant anti-glucocorticoid effects 273 Searle first
distributed Oxandrolone in the US under the trade name Anavar in 1964, the name by which it is
most frequently referred. For years, people were under the erroneous assumption that because
oxandrolone does not convert to estrogen it would not shut down natural testosterone production.
However, we now know that while estrogens reduce LH pulse amplitude, androgens decrease pulse
frequency which results in reduced natural testosterone production over time. In fact, a study by
Sheffield-Moore et al. demonstrated that a dose of only 15 mg/day in healthy young men for five
days reduced total and free testosterone levels 274 It has been postulated that oxandrolone has a
positive effect on creatine phosphate synthesis; however, there is no scientific data to support this
hypothesis. Oxandrolone increases nitrogen retention both through the anabolic effect of activating
androgen rece~tor but also through antagonism of the glucocorticoid receptor and the catabolic
effects thereor 73 ,274,275. Oxandrolone is often used by women because it is considered to be weak,
however, it can still produce androgenic side effects. High doses of oxandrolone (20 to 50 mg or
more) are needed to notice any appreciable mass gains while strength gains seem to corne more
easily though doses twice this amount are common. Oxandrolone is expensive and the high doses

needed often preclude its use. In addition, it tends to be less available on the black market than
methandrostenolone or oxymetholone. Oxandrolone increases free and bound cortisol levels, most
likely due to its actions as a glucocorticoid receptor antagonisr 42 Additionally, oxandrolone
decreases TBG concentrations pretty severely with large increases in TBPA resulting in increased
T3 uptake242 This correlates with the belief that oxandrolone is beneficial in a "cutting stack". This
is further evidence in studies showing a 4 pound decrease in fat mass while gaining 7 pounds of
lean mass with 20% increases in stren~th over the course of 12 weeks of treatment with only 20 mg
(10 mg, twice daily) of oxandrolone 6 There is also evidence in the literature that oxandrolone
enhances ketogenesis 277 Though oxandrolone is C-17 alpha alkylated, the literature and practical
experience shows this steroid to be fairly benign with regard to liver toxicity. Of course, higher
doses will increase the risk of liver toxicity. The half life of oxandrolone is about ten and a half
hours.
I AR AFFINITY:
II 0.38
I
I PR AFFINITY:
II 0
I
I GR AFFINITY:
II 30
I
I SHBG AFFINITY:
II Low to none
241
I
I A/A RATIO:
II 322/24
I
AVAILABILITY: Available as a pharmaceutical preparation in
oral form in several countries including the US.
Availability on the black market varies but is
generally good with both tablet/capsule as well
as powder forms available from various
sources.
CONVERSION TO None
ESTROGEN: I I

OXYMETHOLONE
(Anadrol, Anapolan, Anasteron, Hemogenin, Oxitosona, Dynasten, Plenastril, Roboral,
Synasteron, Androidin, Androyd, Nastenon, Pardroyd, Parvlsold, Others)
I7-beta- hydroxy-2-hydroxymethy lene-I 7-alpha-methy1-5-al pha-androstan-3-one
OH
HO
~
a
H
Formula: C21H3203
MW: 332
Oxymetholone is a synthetic derivative of DHT. It is considered to be a very potent and toxic oral
steroid. This is due to the fact that oxymetholone has a long half-life, about 8 hours, and several
active metabolites235.278 Oxymetholone, as a DHT derivative, is incapable of being converted to
estrogenic metabolites. Additionally, since oxymetholone is already 5-alpha reduced, it is not acted
upon by 5-alpha reductase but likely inhibits the action of this enzyme. Oxymetholone was
originally produced by Syntex in the US under the trade name Anadrol, by which it is commonly
known. Oxymetholone has the reputation of being very potent causing drastic size and strength
gains. It is also well known for its propensity for causing side effects including edema,
gynecomastia, balding, acne, increased aggressiveness and liver toxicitl 41 The average anabolic to
androgenic ratio reported in the medical literature is 5.8. Oxymetholone does not bind strongly to
the androgen receptor but it has been shown to activate the androgen receptor236.258 This steroid
does not bind to SHBG and has a long half-life in the body of about 8 hours 278 Oxymetholone is
metabolized in the body, in part, to 17-alpha-methyl DHT (17AMDHTi 3s 17 A~DHT does bind as
strongly to the AR and SHBG as DHT with slight affinity for the PR233 .2 3,. Oxymetholone is
considered to be exceptional at raising red blood cell levels. The fact is, all androgens cause this
effect to some degree and oxymetholone is actually not the most potent at producing this
effect237.279 The strong binding of 17AMDHT to SHBG displaces testosterone and estrogen into the
free circulation. This free estrogen can lead to gynecomastia. Although oxymetholone has a
reputation for dramatic size and strength gains, it is also well known that these gains tend to
disappear once treatment is ended. This is due to the fact that only a portion of the gains made while
using oxymetholone are attributable to actual muscle growth. This is likely due to a large degree of
water retention brought on through inhibition of I I-beta hydroxylase which would also explain the
bloating and elevated blood pressure that most people report while using this drug. Oxymetholone is
well known for its propensity for raising liver enzymes and with long-term treatment, causing liver

damage. This is due to the C-17 alkylation that makes oral administration possible and the relatively
large amount of drug that one must ingest to reach therapeutic levels. Much has been made of the
fact that anadrol seems to cause gynecomastia. Oxymetholone cannot be converted to estrogen so
many theories have been put forth to explain this effect. Some have theorized that oxymetholone
binds directly to the estrogen receptor but there is no scientific evidence to support this theory.
Others have blamed this effect on progestational activity of oxymetholone. Oxymetholone has been
shown in the literature to have anti-progestational effects 280 . As explained earlier, antagonism of the
progesterone receptor upregulates the estrogen receptor. This, coupled with the displacement of
estrogen from SHBG is the likely culprit in oxymetholone induced gyno. Mifepristone, a
progesterone receptor antagonist has also been shown to induce gynecomastia when taken
chronically. Like methandrostenolone, oxymetholone elicits an increase in CBG which is contrary
to most other AAS. Oxymetholone, unlike methandrostenolone, actually causes a slight decrease in
non-plasma bound cortisol 242 Oxymetholone decreases TBG pretty strongly resulting in increased
T3 uptake242
I AR AFFINITY:
II Unknown
I
I PR AFFINITY: II Unknown I
I GR AFFINITY: II Unknown I
I SHBG AFFINITY: II Medium for parent, High for metabolites I
I A/A RATIO: II 150/30, 320/45, 400/25 241
I
AVAILABILITY: Readily available as pharmaceutical
preparation in multiple countries. Black market
availability is high with tablet, injectable and
powder forms available.
CONVERSION TO None
I ESTROGEN: II I

STANOZOLOL
(Winstrol, Stanazol, Stromba, Strombaject, Stanol)
17_beta_hydroxy_17_alpha_methyl_5_alpha_androstano_[3,2-c]-pyrazol
OH
HN
~==-l
-
H
Formula: C21H32N20
MW: 329
Stanozolol is a highly modified synthetic version of DHT. As you can see, there is an additional
ring system attached to the traditional A-ring of the steroid structure. The binding data for winstrol
shows it to have very poor binding for the androgen re~eptor36 However the half-life of9 hours for
winstrol is quite long making up for the lower affinitl'8 Stanozolol is incapable of being converted
to estrogenic metabolites and is already 5-alpha reduced so it cannot be reduced further but does
seem to have some antiaromatase activity. Stanozolol has minimal binding to SHBG so it circulates
in the "free" state23.. It has been shown that although stanozolol does not interact directly with the
glucocorticoid receptor, it does interact with two glucocorticoid binding proteins known as STBP
and LAGS 281 ,282 This interaction "bumps ofF' bound cortisol into free circulation, At the same time,
stanozolol has been shown to interfere with cortisol release from the adrenal gland. This results in
reduced cortisol levels with chronic treatment. In fact, many people notice severe joint pain when
using stanozolol, especially when used alone. This can result in a rebound effect in cortisol
production when going off stanozolol. Even though stanozolol has a very large anabolic to
androgenic ratio, it is in fact quite androgenic. The anti-glucocorticoid effect of this drug likely
augments its anabolic/androgenic ratio beyond that of its androgen receptor binding effects alone,
Stanozolol decreases TBG levels but not as much as some of the other common AAS 242 In addition
to tablets for oral administration, stanozolol is also available as water based suspension for
injection. Because it is not esterified, this steroid needs to be injected every day. Also, water based
injections are a lot more prone to bacterial contamination so more care is needed to keep a multi-use
bottle sterile. The relatively large crystal size of some preparations limits the size of needle that can
be used because the crystals will jam smaller needles. There are some formulations available that
have smaller crystal size; however, these seem to have a shorter half-life - most likely due to the
crystals dispersing faster within the muscle. Because it is C-17 alpha alkylated, stanozolol has the
potential for liver toxicity though this is somewhat reduced with the injectable form because a lower
dose is often used. Stanozolol has a favorable anabolic to androgenic ratio but most do not consider
it to be very effective. This is largely due to the fact that stanozolol does not result in large water
weight gains.

AR AFFINITY: Unknown
I II I
I II I
I II
?
I
I
SHBG AFFINITY:
II 241
I
196/47.5,320/30,260/69,220/33
I
AlA RATIO:
II I
AVAILABILITY: Readily available as pharmaceutical
preparation in oral form, as veterinary
preparation in injectable and oral form and on
the black market in oral and powder form
CONVERSION TO None
I ESTROGEN: II I

TESTOSTERONE
1711-Hydroxyandrost-4-en-3-one
OH
,1
o
Formula: C I 9H 2S 02
MW: 288
Testosterone is the primary natural male androgen. Many people have argued that because it is
natural that it is the best. The body has several elaborate systems to prevent what it sees as an
overload of testosterone in the system. As you add more testosterone, enzymes such as aromatase
and 5-alpha reductase work harder to keep a state of equilibrium and therefore to lower testosterone
levels 262 This produces more estrogen and DHT. Testosterone binds very well to SHBG and only a
small fraction circulates in the free state 236 ,24S As with nandrolone, all esters of testosterone result in
the same drug being delivered to the muscle after the ester is stripped off. The ester controls how
slowly testosterone will be released into the body. Several things can influence the release of
testosterone from an ester depot including the size of the depot, the concentration of the steroid in
the oil vehicle, the type of oil used for vehicle, the injection site (gluteus, deltoid) and others269 .
Also, as the size of the ester increases, its percentage of the total molecular weight also increases.
This means that you get less testosterone per 100 mg of testosterone enanthate (72 mg) than you
would with 100 mg of testosterone acetate (87 mg). Testosterone is also available as a water-based
suspension. Suspension is very short acting requiring frequent (daily) injections. Many people will
use suspension in drug-tested competitions because it is cleared quickly. As this is a water-based
injection, it is more prone to bacterial contamination, so extra care must be taken to not contaminate
multi-use vials. As discussed previously, testosterone inhibits 1I-beta hydroxr,lase resulting in
decreased levels of free and total cortisol levels as well as decreased CBG levels- 42 This results in
increased levels of deoxycorticosterone which can cause sodium and water retention and increased
blood pressure 104. Testosterone does not affect TBG and TBPA in the manner described for some of
the synthetic AAS 242 .

Testosterone Cypionate
(Androcyp, Andronaq-LA, Andronate, Depo-Test, Depo-Testosterone, Durotest, Malogen Cyp,
Testa-C, Testadiate Depo, Testex, Testoject, Testred Cypionate, Cypiotest, Deposteron, Banrot,
Others)
o
o
Formula: C27H400J
MW: 413
The cypionate ester contains 8 carbons, which includes a 5 membered ring. This chain length and
level of complexity makes it more difficult for the body to cleave the ester from testosterone. This
makes for a slower release of testosterone from the injection depot. Because of this, testosterone
cypionate is injected every 5-7 days to maintain an even level of testosterone in the body.
Testosterone cypionate is one of the most popular esters of testosterone. As discussed in the section
on nandrolone, people are tending to inject steroids more and more frequently so it is not
uncommon for people to inject testosterone cypionate twice weekly as opposed to weekly.
Cypionate is readily and cheaply available on the black market. People consider cypionate to be
more likely to cause side effects than enanthate but as the half-lives are nearly identical and the
parent compound (testosterone) is the same, it is unlikely that these esters behave different in terms
of positive or negative effects. Water retention, high blood pressure, and acne are common with all
of the testosterone esters and gynecomastia can develop as well depending on dose and frequency of
injection. More frequent injections will increase the likelihood of side effects as the plasma levels of
testosterone will be higher.
Mg of Testosterone per 100 mg: 70

Testosterone Enanthate
(Andropository, Andryl, Androtardyl, Arderone, Delatest, Delatestryl, Dura-Testosterone,
Durathate, Enarmon Depot, Everone, Malogen, Primoteston, Tesone, Testanate, Testaval,
Testovion, Testrin)
o
o
Formula: C26H4003
MW: 401
The enanthate ester contains 7 carbons arranged in a simple straight chain. This results in a fairly
slow release from the injection site. In fact, even though the carbon chain is shorter than cypionate,
the release rate is in fact slower, albeit not by much. Enanthate should be taken every 7-9 days to
maintain constant testosterone levels but of course people tend to inject twice weekly with
enanthate just as they do with cypionate. Enanthate is a very popular drug and is used in doses from
200 mg every two weeks for replacement therapy all the up to gram ~uantities weekly. Doses as low
as 300 mg produce supraphysiologic plasma levels of testosterone28 . Doses as low as 125 mg per
week have been shown to produce gains in weight. A dose of 600 mg weekly for 20 weeks produce
a gain of 17 pounds of fat free mass with small decreases in fat mass284 Another study showed a
gain of 13 pound of fat free mass with a dose of 600 mg of testosterone enanthate weekly after 10
weeks oftreatment 285 .

Testosterone Propionate
(Testosteronea, Triolandren, Agovirin, Androfort-Richter, Testovis, Testoviron, Testogan, Testopro,
Anatest, Testex-Leo, Androlan, Virormone, Neo-Hombreol, In combination with other esters:
Sustanon 250, Omnadren)
o
o~ CH 3
CH 3 ~
o
Formula: C22H3203
MW: 344
Propionate is a simple ester with a straight chain of 3 carbons. This causes it to be a rather fast
acting ester, which needs to be dosed every 2 to 3 days to keep plasma levels steady. Propionate is a
painful injection with swelling and soreness lasting for several days. This is due to the acidic nature
of the ester as well as the relative insolubility of the testosterone propionate molecule. This
necessitates relatively high concentrations of solvents (such as benzyl alcohol and benzyl benzoate)
to be added to the oil to keep the steroid solubilized. Even so, when injected, the steroid can
crystallize in the muscle resulting in pain and damage to the tissue. This problem is present even
with legitimate pharmaceutical versions of this steroid, however, the underground versions are even
worse because they are often formulated with too high of a concentration of steroid and use very
high levels of solvent. Even so, some people will inject propionate every day rotating injection sites
around the body to avoid having to inject into a location that is still sore from the previous injection.
Users tend to see lower incidence of side effects with propionate compared to longer esters partly
because a lower total dosage is used. As users increase the dose and the frequency of injection, the
propensity for side effects increases.

Testosterone Undecanoate
(Restandol, Andriol, Androxon, Panteston, Undestor, Yirigen)
o
Formula: C30H4803
MW: 457
Testosterone Undecanoate has gotten a real bad name. It is available in an oral form known as
Andriol in several countries. The undecanoate ester allows for a greater oral bioavailability of
testosterone so a decent dose of testosterone can be obtained by taking TU orally. However, the
percent absorption is still pretty low requiring large, frequent doses to be taken. Also, the short half
life of Andriol requires that it be taken at least 3 times a day to achieve steady plasma levels. The
undecanoate ester consists of a straight chain of II carbon atoms. This makes it very fat-soluble and
resistant to cleavage. This is what allows andriol to be absorbed orally. It gets absorbed in the small
intestine as a fat and is transported via the lymphatic system. As an injection, this long chain ester
results in a very long lasting depot requiring injections only every 3 to 6 weeks to maintain steady
levels of testosterone.

Testosterone Blends
(Sustanon, Omnadren, Testoviron, Sten, Equitest)
There are multiple testosterone blends available on the black market, some by legitimate
pharmaceutical labs and some by underground labs. These products were created to give a long-
lasting steady supply of testosterone over several weeks time. They accomplish this by having a mix
of short and long acting esters that varies from product to product. Sustanon used to be a very
popular source of testosterone because it was cheap and rarely counterfeited. In recent years
however, people have begun to look down on Sustanon and other blend products. The derision
began with the belief that the shorting acting esters present in the product would "wear off' before
the longer esters so one would need to inject the product every two or three days to keep blood
levels stable. More recent criticism continues along the lines of blends producing "unstable" plasma
levels of testosterone. This criticism neglects the fact that the individual esters are not going to be
absorbed one by one as if they were individual injections. The esters instead will form a bolus that
will take on pharmacokinetic properties that are a mix of the esters contained therein. With the trend
toward increased injection frequency, I expect blends to stay out of favor because it does not lend
itself to frequent injections but rather once every two week or once a month injections.

TRENBOLONE
(Finajet, Finaject, Parabolan, Finaplix, Finabolan, Trenbol)
estra-4,9, I l-trien-17-beta-ol-3-one
OH
Formula: CISl-l2202
MW: 270
Trenbolone is a derivative of nandrolone in that it lacks the methyl group at position 19. As you can
see from the binding data, trenbolone binds strongly to both the AR and the PR 233 The strong
binding likely makes trenbolone an agonist of the progesterone receptor. Though people generally
believe progesterone agonists to cause gynecomastia, as described earlier in this book, progesterone
agonists actually result in the down regulation of estrogen receptors. This strong progesterone
receptor binding is also believed to be the source of the severe shutdown and loss of libido in a good
portion of users. Trenbolone binds strongly to the androgen receptor (stronger than any
commercially available androgen) and is not metabolized to 3-alpha metabolites in skeletal muscle
delivering rapid strength and size gains 23S It does not appear to be which makes it very potent It has
been shown to have strong anabolic effects while at the same time having an antiglucocorticoid
effect in animals but there is no reason to believe that this does not occur in humans as weI1 286,287,
Trenbolone cannot be converted to estrogens and although it is commonly believed that trenbolone
is not S-alpha reduced, there is a paper in the literature that shows trenbolone to be less potent in
tissues with high levels of S-alpha reductase287 This is exactly the same thing that is seem with
nandrolone and since trenbolone is also a 19-nor steroid it is reasonable to assume, based on this
evidence that trenbolone is in fact S-alpha reduced to less potent metabolites, This would also
explain the reports of gynecomastia as well as the shutdown that are seen with trenbolone even
though it does not convert to estrogen, The decreased androgenic stimulation as a result of the
production of less potent S-alpha reduced androgens upsets the androgen to estrogen balance that
results in greater net estrogenic signaling in the breast and hypothalamus. The main problem with
trenbolone is that it is very difficult (if not impossible) to find in a preparation that is made for
human consumption. Trenbolone used to be available as Parabolan but if it is made anymore (which
no one seems to be in agreement about) it is not readily available, Finaject was another product,
which contained trenbolone acetate but is no longer made. Most of the tren that is currently
available on the black market is made from canle implants called Finaplix. Several underground
labs have created injectable versions of this drug by dissolving the pellets in a solvent and bonling
the solution. Kits are also available through many sources that allow a person to make their own
injectable at home from the pellets. The problem with these underground versions and homemade

concoctions is that they are produced in a sterile fashion. This can lead to abscess, sepsis, and even
anaphylactic shock followed by death. Also, the solvents used to dissolve the pellets are not meant
to be injected and can cause the same problems with the additional possibility of poisoning.
Trenbolone has a reputation for being nephrotoxic (toxic to the kidneys). While all androgens have
some effect on kidney function, the exceptionally strong binding of trenbolone enhances this
negative effect. Another factor to consider is that many people's only experience with trenbolone is
through transdermal application (or injection) with DMSO. DMSO can be toxic to the kidneys as
well and probably augments that of trenbolone. Therefore, while trenbolone itself is toxic to the
kidneys, it may not be as toxic as some people have been led to believe through its use with DMSO.
Trenbolone is available with acetate, enanthate or occasionally the hexahydrobenzylcarbonate
esters. The acetate ester is injected daily or every other day and was previously available in a
veterinary product called Finaject that is no longer produced. The enanthate ester is produced by
underground labs and could be injected every 7-10 days but is probably injected more frequently by
AAS users. The hexahydrobenzylcarbonate ester was originally produced as a pharmaceutical grade
human-use product with the name Parabolan but hasn't been made in a long time. It seems to pop
up in underground preparations from lime to time and has a similar half-life as the enanthate ester
and therefore is injected weekly or biweekly.
I PR AFFINITY: II 74 I
I GR AFFINITY: II 5 I
I SHBG AFFINITY: II Low I
I A/A RATIO: II 500/500
241
I
I
~=~A~V~A~I~L~A~B~I~L~IT~Y=:=~I Readily available as veterinary cattle implants,
and on the black market as injectable and
powder forms
CONVERSION TO II None I.
I ESTROGEN:

EXOTICS
The exotics are AAS that have not been commonly used. They are much harder to find, ifat all on
the black market and are either no longer or have never been produced by legitimate pharmaceutical
companies. These are the AAS that most users have never tried but have intense curiosity about.

ANDROISOXAZOLE
(Neo Ponden)
I7-methyl-5-alpha-androstano-[3,2-cjisoxazol-17-beta-ol
OH
o
~=~
H
FORMULA: CZ1H31NOZ
MW: 329
Androisoxazole is a DHT derivative with an additional ring, much like stanozolol. There are two
isomers of this steroid with this isomer being the one that was marketed under the name eo
Ponden in Italy. This steroid is rare. In fact, very lillie is known about it because it is so rare. The
structure and anabolic/androgenic ratio suggests that it would be similar in effect to stanozolol but
the anabolic ratio suggests that androisoxazole would be less anabolic with similar androgenic
Z88
effects This steroid is incapable of converting to estrogen and is already 5-alpha reduced.
Additionally, this steroid most likely has poor androgen receptor binding affinity but a long plasma
half-life due to the additional ring and would require larger doses to see an anabolic effecl.
Androisoxazole was originally supplied as a tablet containing 5 mg. Dosing would be 25 to 100 mg
per day. This steroid is C-17 alpha alkylated which makes it orally active but also makes it toxic to
the liver. This steroid is nothing special but older steroids have been appearing on the black market
or as demethylated versions sold as dietary supplements.

II
II
II
SHBG AFFINITY: Low
II
AlA RATIO: 155/22 241
II
AVAILABILITY: Not Currently Available
II
CONVERSION TO None
ESTROGEN: II

ANDROISOXAZOLE 2
(none)
17_methyl_5_alpha_androstano_[2,3_d]isoxazol-17-beta-ol
HN
I
0-----<"..
-
H
Formula: CZI H3ZNOZ

MW: 330
Even less is known about this isomer of androisoxazole. It looks very favorable according to its
anabolic/androgenic ratio, but to my knowledge, this compound has never been marketed. This
isomer of androisoxazole would most likely perform much better than the marketed version. This
steroid would be unable to convert to estrogen. Although this steroid was never marketed, you never
know when something will turn up on the black market. A guess for dosing would be in the 25-50
mg per day range. Liver toxicity would be expected with this compound due to the C 17 alkylation
with it being more toxic than equal doses of methandrostenolone due to the resistance to
metabolism that the extra ring system provides. The androgenicity of this compound is roughly the
same as stanozolol; about 1/3 that of methyltestosterone. The anabolic activity of this isomer of
androisoxazole is better than the first isomer and even better than stanozolol. It is interesting that
this isomer was not marketed as it seems to be the better of the two and possibly even better than
stanozolol all around. Similar to danazol, this steroid likely undergoes ring-opening metabolism -
meaning that the extra ring is opened and hydroxylated to form 2-hydroxymethyl-17-alpha methyl
DHT,2 hydroxymethyl-l-en-17-alpha methylDHTand methylDHT:
OH OH
OH OH
CH,
H H
2-hydroxymethyl, 17-alpha methylDHT 2-hydroxymethyl-l-en-17-alpha methylDHT
Though this is speculation based on the known metabolism of danazol, this metabolic alteration
would account for the greater anabolic effect of this isomer compared to the other isomer since 2
hydroxymethylDHT is also a metabolite of oxymetholone. This steroid would likely perform like a

cross between stanozolol and oxymetholone. It would likely be quite potent and also significantly
more liver toxic due to the multiple active and methylated metabolites. There is also mention in the
literature of the 4-ene version of this isomer of androisoxazole known as
288
methylandrostenolisoxazole and it had an anabolic to androgenic ration of 8: 1
OH
CH,
o H
17-alpha methylDHT
I AR AFFINITY: II Unknown I
I PR AFFINITY: II Unknown I
I G R AFFINITY: II Unknown I
SHBG AFFINITY: Low for Parent, Medium to High for
I I Metabolites
I A/A RATIO: II 8.3-40:1 I
I AVAILABILITY:
II Not Currently Available
I
CONVERSION TO None
I ESTROGEN: II I

BOLASTERONE
(Myagen)
17-beta-hydroxy-7, 17-alpha-dimethylandrost-4-en-3-one
OH
CH 3 .",,,CH
Formula: C21 HJ2 0 2

MW: 316
The name "bolasterone" was used to not only describe the above steroid, but also by an
underground lab that for a counterfeit drug that consisted of anadroltabs ground up and dissolved in
testosterone cypionate. Underground labs and even supplement companies will occasionally use the
names or previously and currently marketed AAS in some form to give their products instant cache.
The true bolasterone, whose structure is shown above, was rumored to be the most effective steroid
on the market. It was also rumored to be very liver toxic, in fact, probably the most liver toxic of all
commonly available steroids. Also, while the addition of the methyl group at the C-7 position did
increase the binding to AR slightly, it also increased the binding to PR 3-4 fold resulting in a
substantially progestational molecule. This significant progestational activity combined with the
strong androgenic activity is probably what led people to believe that this was such an effective
molecule. This activity would cause rapid and large increases in skeletal muscle, body fat
accumulation as well as water retention, which would all result in large body weight increases. This
is evidenced in the anabolic/androgenic ratios of bolasterone that show it to be ten times more
anabolic than testosterone and twice as androgenic. The 7-alpha methyl group seems to interfere
with 5-alpha reduction but it is likely that this molecule was still vulnerable to aromatization 235 .
This steroid was removed from the market soon after its introduction because of problems with liver
toxicity. This created a new problem. The reputation of bolasterone's effectiveness inspired the
production of several counterfeit concoctions after it was removed from the market. None of these
counterfeits contained actual bolasterone but were instead a mixture of other steroids (usually a
testosterone, anadrol and deca) that was supposed to mimic bolasterone's effects. They slapped the
bolasterone name on the counterfeits and made a bundle off of the reputation of the real bolasterone.
Why did I bother to tell you about this when neither the real bolasterone nor the counterfeits are
currently available? There are several reasons. The first is that steroids have a way of popping up on
the black market. There are always several illicit manufacturers in operation around the world that
are capable of making just about any steroid. So, you never know if real bolasterone or a "new"
fake will pop up again in the future. Second, the structural motif of bolasterone is important in
understanding how different substitutions change a molecule's activity. Third, to make you aware of

the fact that, when it comes to counterfeits, you can never be quite too sure of what is really in the
bottle.
120
I
AR AFFINITY:
I 80
I PR AFFINITY:
I 0
I
GR AFFINITY:
SHBG AFFINITY:
I Low
I
AlA RATIO:
I 1140/224, 575/300
241
I
AVAILABILITY:
I Not Currently Available
I
CONVERSION TO
I Low to None
I ESTROGEN: I

CHLORDEHYDROMETHYLTESTOSTERONE
(Oral Turinabol)
4-Chloro-17~-hydroxy-17-methylandrosta-1
, 4-dien-3-one
OH
o
CI
Formula: C2oCIH2702
MW: 335
Oral-turinabol (OT) is very similar to in structure to methandrostenolone. The only difference, in

fact, is the addition of a chloride atom at the C-4 position. Oral-turinabol has a reputation of being a
very good steroid. The addition of the chloride atom removes the potential for aromatization by
blocking access by aromatase and also reduces conversion to DHT. The main differences are that
OT likely has a long half-life that makes up for its lower binding affinity and OT seems to have
higher affinity for SHBG than methandrostenolone which can result in testosterone and estrogen
being bumped into circulation 289 The half-life in the scientific literature after IV administration is
16 hours; however, the oral half-life is not necessarily the same289 Generally half-life for oral
administration is longer than that of IV administration, however, in this case it could actually be
shorter due to first pass metabolism and reduced peak plasma levels compared to the IV dose 289
Another paper suggests a fairly short half_life 290 A good estimate is at least eight hours for the half-
life of this steroid with the likely true value between 12 and 20 hours. The fact that metabolites of
this steroid can be detected for a long time after cessation argues for a longer half_life 235 Users have
reported pretty strong suppression of natural testosterone levels while using OT. This steroid is liver
toxic but likely only slightly more toxic than equal doses of methandrostenolone. This steroid is
well-known for its role in the state-sponsored doping program of the former East German Olympic
doping program. This drug was given to male and female athletes specifically to increase athletic
performance in the Olympics. Though men were also treated, women were the focus because they
responded much better to treatment. Doses of only 10 to 20 mg per day produced marked increases
in performance in women. This program also included other drugs like mestanolone, the II-beta
hydroxy form of Oral Turinabol, 4-chloro-methyltestosterone, 4-chloro-mestanolone,
methandrostenolone, testosterone and nandrolone esters as well as some stimulants and ~eptide
hormones. Even so, Oral Turinabol was the focus because it seemed to report the best results91 . OT
has shown up in recent years on the back market with people using in excess of 100 mg per day. At
this dose, one has to wonder if the product contains the correct steroid or is under dosed or if it is
just another case of "more is better".

~==AR=A=F=F=IN=I=T=Y=:=::::::II~======6=O======~
~==P=R=A=F=F=INI=T=Y=:=:::::;II~=======O======~
~==G=R=AF=F=INI=T=Y=:=:::::::II~=======O======~
;::==S=HB==G=A=F=F=INI==T=Y=:==II=======M=e=d=iu::::m;;:;::::======~
~==A/=A=RA==T=IO=:===I~I======>=1=O=O=/O=24=1======~
AVAILABILITY: I
Availability is low with only black market oral
;::========== and owder versions available
CONVERSION TO
ESTROGEN:
II. None

CHLOROMETHYLTESTOSTERONE
(none)
4_chloro_17_beta_hydroxy_17_alpha_methyl_androst_4_en_3_0ne
OH
.,,,,CH
o
CI
Formula: CzoCIH2902
MW: 337
Chloromethyltestosterone has good dissociation of anabolic to androgenic ratio. This is due to the
fact that the molecule interacts with 5-alpha reductase to from 4-chloro-dht derivatives, which are
inactive. Also, this affinity for 5-alpha reductase blocks the conversion of testosterone to DHT. This
results in lower stimulation in the prostate and other androgen target tissues. The 4-chloro group
also acts to block conversion to estrogenic metabolites and also blocks the conversion of
testosterone to estradiol. This makes cloromethyltest an effective anabolic with minimal side effects
associated with the C-17 alpha alkyl group. This steroid is C-17 alpha alkylated which makes it
orally bioavailable but also makes it toxic to the liver. Given effective doses this AAS should cause
quality lean mass gains with little to no bloating. This is one of the drugs used along with Oral
Turinabol in East Germany's state sponsored doping program 291 . Since OT was used preferentially
over this molecule, it would stand to reason that the athletes saw better results with OT than with
this compound. This steroid does not appear to be available on the legitimate or black market but
could be purposefully or inadvertently substituted in part or in full in black market versions ofOT.

AR AFFINITY: 100
PR AFFINITY:
11
0
I
II 0
I
GR AFFINITY:
SHBG AFFINITY:
II
Low
I
II 241
I
AlA RATIO:
AVAILABILlTY:
II
46/27, SOilS, 32/12
Not Currently Available

I
II I
CONVERSION TO None
ESTROGEN: II I

CHLORONANDROLONE
(norclostebol)
4-chloro-17-beta-hydroxy-estr-4-en-3-one
OH
o
CI
Formula: C l sCII-hs02
MW: 309
One would expect that some of what is said about 4-chlorotestosterone derivatives to apply to
chloronandrolone. The 4-chloro group does block conversion of nandrolone to estrogenic
metabolites and blocks conversion of testosterone to estradiol. The 4-chloro group blocks
conversion of test to DHT and results in the production of 4-chloro-dihydronandrolone, an inactive
metabolite. This results in less stimulation at the level of the prostate and in other androgen target
tissues as with other 4-chloro androgens. While the 4-chloro group does reduce the binding affinity
to the androgen receptor somewhat, it also reduces the affinity for the progesterone receptor. This
results in a nandrolone with less bloat and less fat retention. This is reflected in the
anabolic/androgenic ratio where one can see this compound has very little androgenic activity with
considerable anabolic activity. This steroid was marketed with an acetate ester, which required daily
injections_ Chloronandrolone is not available to my knowledge but has shown up recently as an
illegal growth promoter in cattle which suggests it is being manufactured somewhere. This steroid
would be a very effective anabolic if it were made with a longer ester. It would provide all of the
positive effects ofnandrolone with very little of the negative aspects.

AR AFFINITY:
II
90
I
PR AFFINITY:
II
10
0
I
GR AFFINlTY:
SHBG AFFINITY:
II
Low
I
II 241
I
A/A RATIO: 600/40, 112/26, 77/3
II I
CONVERSION TO
II
None
I
ESTROGEN: II I

CHLOROTESTOSTERONE
(Clostebol, Megagrivesit, Steranabol)
4-chloro-testosterone acetate
OH
~
o
CI
Formula: C 19C1 H27 0 2

MW: 323
Chlorotestosterone is a very simple derivative of testosterone made by attaching a chlorine atom at

the 4 position. This slight modification makes for a very different molecule than testosterone.
Clostebol has a slightly lower binding affinity for the AR than testosterone and no binding to the PR
or GR. The chlorine atom blocks the action of aromatase on this molecule. This means that
chlorotestosterone cannot be converted to estrogen and is converted to a less potent DHT
235
derivative Because testosterone is converted to DHT and estrogen to some degree and because
DHT and estrogen are inactive in muscle tissue, you lose a good portion of activity when using
testosterone. You also lose some of testosterone's activity due to binding to SHBG.
Chlorotestosterone binds much more weakly to SHBG than testosterone does. This makes ciostebol
a very good choice as an anabolic as can be seen from the anabolic to androgenic ratio. This steroid
was marketed with an acetate ester requiring daily injections. It is surprising that chlorotestosterone
is not used more often but this is probably due to the fact that this steroid does not offer instant
gratification in the form of "bloat". A longer ester would make this steroid much more attractive.

I ARAFFINITY: 11========12=0========1
I==:::::OP:::;R=AF~F:::;[NI=T;;;:Y:;=:===11 0 1
I GR AFFINITY: II 0 1

I AlA RATIO: II 126/55,68/14,10/3
241
I
AVAILABILITY: I Available as the acetate in pharmaceutical preparation
and on the black market as the enanthate and acetate
I
~=~~===:::::::::::::::::::~~~==: forms as iniectable and as powder
CONVERSION TO
ESTROGEN: .
I None

DANAZOL
(Danocrine, Danovol, Danotrol, Anargil, Winobanin)
I7-alpha-2,4-pregnadien-20-yno-(2,3-d)-isoxazol-1 7-01
OH
N~
I
0 - -......
Formula: C22 H27N0 2

MW: 337
Danazol has a structure that is very similar to that of stanozolol in that there is an additional ring
added to the steroid core. However, there are two main differences in danazol's structure that make
their activities quite different. First of all, whereas stanozolol is C-17 alpha alkylated, danazol is
not. It instead has two carbons joined to each other with a triple bond at the C-17 position. This is a
very progestational group that is found in several synthetic progestins. Danazol has been shown to
have glucocorticoid, androgenic, progestational and estrogenic properties292.293 This is due to the
products of metabolism of danazol in the body. This is the second area where danazol and
stanozolol differ. Unlike stanozolol, danazol undergoes ring-opening metabolism to form three
major metabol ites; 2-hydroxymethy lethisterone, 2-hydroxymethy I-I-en-eth isterone and
eth isterone294
OH OH
CH3 .... ,\\-CH
CH3 .",,\\_CH
OH
OH
CH,
o -
o H
2-hyd roxymethy lethisterone 2-hydroxymethyl-l-en-ethisterone
OH
CH,
Ethisterone

Ethisterone is a progestin that also has significant androgenic activity. The other two metabolites are
also androgenic progestins. This extended metabolism explains the broad range of effect that
danazol has in the body and illustrates how important the metabolism of a compound is in
determining its global effects. Danazol has been shown to reduce estrogen and progesterone
receptor levels, decrease 17-BHSD and reduce LH and FSH293.295. Danazol is a fairly potent
androgen but is not very anabolic292 Though danazol binds to CBG it does not increase circulating
245
cortisol levels because it binds more strongl~ to albumin .296. In fact, cortisol and SHBG were
shown to decrease with danazol treatmenr . Danazol is not used much by athletes, but the
combination of androgenic, progestational and estrogenic activity would be likely to cause
significant bloating and weight gain but curiously, danazol has been shown to be effective in
reducing gynecomastia in men 297 .
AR AFFINITY: 41
I II I
PR AFFINITY: 50
I II I
I GR AFFINITY:
II .
?
I
SHBG Medium for Parent, high for ethisterone metabolite
I AFFINITY:
A/A RATIO:
I ?
I II I
I AVAILABILITY: I Available as oral pharmaceutical prep
CONVERSION Low for parent, high for Ethisterone metabolite

TO ESTROGEN:

DIENOLONE
(none)
4,9-estradienolone
OH
Formula: Cl8H2402
MW:272
Dienolone is the unmethylated version of Methyldienolone, which was available as a prosteroid

before the ban. This steroid is a 9-dehydro derivative of nandrolone and is similar to trenbolone but
lacks its double bond at C-I I. The binding affinities for this compound show it to bind to the
androgen receptor with slightly less affinity than nandrolone but still stronger than testosterone with
similar affinity for the progesterone receptor as nandrolone233 ,26o. In fact, this compound has almost
identical binding to nandrolone. Unlike nandrolone, this compound would not be converted to
estrogen but may be converted to some degree by 5-alpha reductase to less potent metabolites,
similar to nandrolone. This is evident in its low androgenic activity. This molecule would have poor
oral activity and would need to be used transdermally or esterified and injected. The anabolic to
androgenic ratio for this compound is very favorable with low androgenicity and high anabolic
activity and is slightly misleading because the standard utilized was methyltestosterone. Like
nandrolone, this steroid has been shown to have mixed agonist/antagonist activity for the
progesterone receptor which will contribute to significant shutdown of natural testosterone and may
result in gynecomastia through upregulation of estrogen receptors in the breast and
hypothaiamus 2M Ultimately, this steroid would likely perform similarly to nandrolone with less
estrogenic and slightly more androgenic activity overall.

AR AFFINITY: 134
II
PR AFFINITY: 17
II
GR AFFINITY: 5
II
SHBG AFFINITY: Medium
II
AlA RATIO: 100110241
II
II
CONVERSION TO None
ESTROGEN: II

DIMETHAZINE
(none)
I7-beta-hydroxy-2-al pha, I7-d imethy 1-5-alpha-androstan-3-one-3.3'-azine
OH
N
H
Formula: C2 1HJ4NO
MW:316
Dimethazine is an unusual steroid. It is a methylDHT derivative with nitrogen in the place of

oxygen in the 3-keto position. There is no binding information available on this steroid and until
recently, hadn't been used in by athletes. Very recently however, this steroid has appeared on the
gray market as a prosteroid. It has favorable anabolic/androgenic ratios and would not convert to
estrogen being a 5-alpha reduced steroid. Some have compared superdrol to this molecule but the
presence of the nitrogen at the 3-position makes their activity somewhat different. This can be
witnessed in their markedly different anabolic to androgenic ratios. Like superdrol, this compound
is likely to be a potent inhibitor of II-beta hydroxylase inducing rapid gains in water weight
without subcutaneous edema. While this is desirable for some athletes, especially those looking for
quick gains, this would also bring on hypertension quite easily. Also, being dimethylated, this
steroid is expected to be harsher on the liver than those with a single methylation.

II
II
II
SHOG AFFINITY: Unknown
II
AlA RATIO: 210/95,27/6 241
II
II
CONVERSION TO None
ESTROGEN: I

DIMETHIAZOL
(none)
2',17-dimelhy l-androstan-2-eno-[3,2-dJ-thiazol-17-beta-ol
OH
-
H
Formula: C22 HJJ NOS

MW: 359
This steroid is similar in structure to furazabol and stanozolol but different because it includes a
sulfur heteroalom in the added ring. It is a DHT derivative and would not be able to convert to
estrogen. It is unclear whether this steroid was ever marketed, but it is unlikely that it was ever used
by athletes. It has an anabolic/androgenic ratio of 200/40 suggesting that it is more anabolic than
testosterone with about the same level of anabolic and androgenic activity as stanozolol at
equivalent doses. There is little information available for this steroid making it difficult to predict
how it would react. The presence of an additional methyl on the added ring suggests it may be more
liver toxic than equal doses ofstanozolol. Due to the presence of the sulfur atom, the additional ring
may be prone to ring opening reactions that could result in more potent metabolites and a longer
half-life. The 5-ring steroids (dimethiazol, stanozolol, danazol, furazabol, androisoxazole) all seem
to have very diverse physiological effects even though, at first glance, they look very similar.

II
II
II
SHBG AFFINITY: Low to None
II
A/A RATIO: 200/40 24 \
II
II
CONVERSION TO None
ESTROGEN: I

DIMETHANDROLONE
(none)
7-alpha, I l-beta-dimethyl-19-nortestosterone
Formula: CZOH300Z
MW: 302
Dimethandrolone, not to be confused with mibolerone which is also a dimethylated nandrolone, is a

new orally active androgen that is under development. It is not C-17 alpha alkylated but is usually
seen with an undecanoate ester attached. The absence of a methyl group at the 17 position should
result in little to no liver toxicity and studies with this steroid have shown good oral
bioavailabilitl 98 The androgen receptor binding of this steroid is better than DHT with
progesterone receptor binding more potent than nandrolone. Dimethandrolone has been shown to be
resistant to conversion by aromatase and 5-alpha reductase 298 ,299 The studies on this steroid show it
to be a potent andr~en with a good anabolic to androgenic ratio with prostate-sparing effects,
similar to a SARM 3 . Dimethandrolone was also shown to have potent suppressive effects on LH
release similar to nandrolone. Though this steroid may be pursued as a male contraceptive due to
the LI-I suppressive effects it would also be a potent anabolic, but like nandrolone would also reduce
endogenous androgen levels which could result in impotence and an imbalance in the
androgen/estrogen ratio which could induce gynecomastia. This steroid is not available on the
legitimate or black market but its presence in the literature makes it a possibility that it could wind
up on the black market at some point in the future.

AR AFFINITY: 150
I II I
PR AFFINITY: 40
I I I
I II I
SHBG AFFINITY: Low
I
AlA RATIO:
II
Unknown
I
I
AVAILABILITY:
II
I
I II I
I
CONVERSION TO
ESTROGEN: II
None
I

ll-BETA MNT
(none)
I l-beta-methyl-19-nortestosterone
Formula: Cl91-1zS0z
MW: 288
II-beta MNT, like dimethandrolone, may also be in development for male contraception or
hormone replacement. It is similar to dimethandrolone in that it binds strongly to the androgen
receptor. In fact, the one study where androgen receptor binding was determined showed II-beta
MNT to be a stronger binder of the androgen receptor than methyltrienolone z98 I I-beta MNT also
binds more stro~oly to the progesterone receptor than dimethandrolone but not as stro~B as
methyltnenolone-9B . ThiS steroid does not undergo aromallzallon but unlike dUllethandrolone -, IS
likely 5-alpha reduced to less potent metabolites. This steroid would likely not be very bioavailable
when given orally unless it was esterified like dimethandrolone. The very high progesterone
receptor affinity would likely produce the same LI-I suppressive effects of dimethandrolone and the
production of less potent 5-alpha metabolites would likely result in a disruption of the
androgen/estrogen ratio which could result in gynecomastia. As with dimethylnandrolone, this
steroid is not available on the black market, but steroid users and sellers are always looking for
something new so it is possible for this or any steroid to show up on the black market at any time.

AR AFFINITY: 170
II
PR AFFINITY: 50
II
II
SHBG AFFINITY: Unknown
II
AlA RATIO: Unknown
II
II
CO VERSION TO one
ESTROGEN: II

ETHYLDIENOLONE
(none)
I7-hydroxy-19-nor-17-alpha-pregna-4,9-dien-3-one
OH CH
CH 3 ." ,"I
Formula: C2oH2802
MW: 300
Little information is available on this compound. One would expect that it would be similar to
methyldienolone. I would guess that ethyldienolone would be even more progestational than
methyldienolone due the C l7-alpha ethyl group. The ethyl group seems to be less toxic than the
methyl group but also seems to be less effective in increasing oral bioavailability. This fact that this
steroid has fairly low androgenic activity suggests that it is 5-alpha reduced to less potent
androgens. The anabolic activity is good but this compound would likely require doses in the 50 to
100 mg range. This steroid would be similar in effect to norethandrolone but this steroid is not
capable of being converted by aromatase into estrogenic metabolites.

AR AFFINITY: 55
II
PR AFFINITY: 85
II
GR AFFINITY: 0
II
SHBG AFFINITY: Very Low
II
AlA RATIO: 100/10,150/30241
II
II
CONVERSION TO None
ESTROGEN: II
177
ANABOLIC PHARMACOLOGY
FORMEBOLONE
(Esiclene~
2-formyl-17-alpha-melhylandrosta-1 ,4-dien-1 I-alpha, 17-beta-diol-3-one
OH
o
I
Formula: C2l H2s0 4

MW: 344
Esiclene was never considered to be a very anabolic drug. In fact, the oral form of this steroid was
ignored completely. However, the injectable form was very sought after especially in the
competitive bodybuilding ranks. The reason it was so desired was because, when injected into
specific muscles this steroid caused a local inflammation and swelling of the muscle into which it
was injected. This effect was of course temporary, but allowed for lagging body parts to be brought
up by as much as an inch in some cases right before a competition. The cause of the swelling was
thought to be due to the large crystal size of the drug in suspension causing irritation and therefore
inflammation in the muscle or possibly due to the liquid that the steroid was suspended in. There is
evidence in scientific literature that there were several chemical impurities present in the
formulation that resulted from the manufacture of the formebolone molecule30I . All three of these
probably contributed to the inflammation. This steroid cannot convert to estrogen because of the
protection offered by the 2-formyl group. The molecule itself, although no direct binding data
exists, most likely has poor affinity for the AR. However, because of the hydroxyl group at the C-II
position as well as the formyl group at C-2, this molecule is most likely a fairly strong antagonist of
the OR, which would only add to the proinflammatory properties of this molecule. (Many people
know that cortisol is a terrific anti-inflammatory therefore if you oppose the actions of cortisol you
have pro-inflammation). This drug does not appear to be available on the black-market and even
though the oral was not used in the past it does have anticatabolic and androgenic activity.

I II I
I II I
I
SHBG AFFINITY:
II
Low
I
I II I
AlA RATIO: Unknown
I II I
AVAILABILITY: Questionable
I II I
I
CONVERSION TO
ESTROGEN: II
None
I

FURAZABOL
(Miotilan~
17a-Methyl-5a-androstano(2,3-c]-( I,2,5]oxadiazol-17p-ol
OH
Formula: C2oH 30N 2 0 2

MW: 330
Furazabol is a DHT derivative with an additional ring, similar in structure to stanozolol. This steroid
cannot convert to estrogen and is already 5-alpha reduced so it cannot be reduced further. Furazabol
is reported to have much effect on HPGA. Furazabol does not appear to undergo ring opening
metabolism like danazol. Unlike stanozolol, furazabol seems to have a fairly short half-life of only
about 2 hours J02 This steroid was actually used to lower cholesterol. Androgens reduce HDL
cholesterol without having much effect on LDL. This can result in a decrease in total cholesterol but
we now know that HDL cholesterol is "good" in the sense that it protects the heart while LDL
cholesterol is "bad". Therefore, even though total cholesterol may be reduced, there is actually an
increase in cardiovascular risk with these kinds of changes. Furazabol is C-17 alpha alkylated, so it
will have some potential for liver toxicity. Furazabol is available on the black market, but most
people report little muscular gain with this steroid. This is one of those steroids that seems to have
gained popularity in its absence. It was always difficult to find because it was only made in Japan
and rarely found its way to the black market. It hasn't been available for some time in Japan so it
took on a mythical quality because so few had actually used it. It is now available on the black
market and users are corning face to face with the fact that this steroid is not very effective. It has a
fairly good anabolic to androgenic ratio but it just doesn't seem to deliver significant results in real
world use. Perhaps it is due to the half-life or perhaps larger doses are needed to elicit an anabolic
response.

I AR AFFINITY: I Unknown I
I PR AFFINITY:
I
Unknown
I
I G R AFFINITY:
I
Unknown
I
I
SHBG AFFINITY:
I
Low to none
270173,330/94 241
I
I
AlA RATIO:
AVAILABILITY:
I
Low availability as a pharmaceutcal prep in
I
tablet form. Also available on black market in
I tablet and powder form
CONVERSION TO None
I ESTROGEN: I I

HYDROXYMETHYLTESTOSTERONE
(Oxymesterone,Oranabol)
4, 17-beta dihydroxy-17-methylandrost-4en-3-one
OH
CH 3 .",,,CH
o
OH
Formula: C2oH3003
MW:318
Hydroxymethyltestosterone was originally marketed under the trade names Oxymesterone and
Oranabol. No binding data is available for this compound but the anabolic/androgenic ratio suggests
that it would be even more potent than hydroxytestosterone. This compound cannot convert to
estrogen (or methylestradiol) or to DHT (or methyIDHT). It most likely acts as a fairly potent
aromatase inhibitor (as methyltestosterone and hydroxytest are both known to be aromatase
inhibitors) and may inhibit 5-alpha reductase to some degree as this has been seen with
hydroxyandrostenedione. Furthermore, as is evidenced from the androgenic value, the hydroxyl
group decreases the potency of this compound for the androgen receptor. This should be a relatively
mild compound with low androgenic side effects and lower propensity for suppression of the HPGA
due to the likely inhibition of natural production of estrogens and DHT and the fact that this steroid
is not aromatized or 5-alpha reduced. The C-17 alpha alkylation will cause some liver enzyme
elevation, which should be similar on a mg per mg basis to methandrostenolone. Oxymesterone
would not cause subcutaneous edema and would likely not result in much shedding of the hail'
excefst at higher doses. Oxymesterone is excreted largely unmetabolized suggesting a longer half-
life 2 '. This steroid was released briefly as a gray market supplement but was quickly removed.
Most likely the manufacturer realized a little late that it was a controlled substance since there did
not seem to be any FDA or DEA involvement. For those who are worried about prostate
enlargement, high blood pressure and hair loss, this compound seems to be a good alternative to
methy Itestosterone or even to methandrostenolone.

I
AR AFFINITY:
I
80 est
I
I
PR AFFINITY:
GR AFFINITY:
I
0
I
I
SHBG AFFINITY:
I
0
Low
I
I
AlA RATIO:
I
134/61, 330/50 241
I
I
AVAILABILITY:
I
Currently available in Spain as a
I
I
CONVERSION TO
I Pharmaceutical prep. Does not appear to
currently be available on black market
None
I ESTROGEN: II I

MESTANOLONE
(MethyIAndrostanolone)
17~-Hydroxy-17-methyl-5a-androstan-3-one
OH
CH 3
.. ""CH
o
H
Formula: C2oH3202
MW: 304
Mestanolone is the C-17 alpha alkylated version of DHT. This, of course, makes it orally
bioavailable. It also adds some progestational activity to the molecule 233 Methyl DHT cannot
convert to estrogen, but it does bind strongly to SHBG which can displace estrogen into circulation
possibly resulting in estrogenic side effects. As stated, DHT is deactivated in skeletal muscle by 3-
alpha hydroxysteroid dehydrogenase as will Mestanolone23s However, if large enough doses are
taken, it is possible that this enzyme may be overwhelmed and mestanolone would therefore bind to
the AR resulting in quite strong anabolism but it has not been determined scientifically if this is
possible and what dose would achieve this effect. Some people have an abnormal attraction to DHT
and methyl DI-IT. They reason that since DHT is a stronger androgen that it must be a better
anabolic and they refuse to acknowledge that these steroids are deactivated in skeletal muscle. The
reason is probably due to the strong effect that DI-IT has on the psyche of the user. DHT will
increase aggression and can cause significant strength gains though nervous stimulation.
Additionally, increased strength often does equate to mass gains even in the absence of an anabolic
effect of this compound. Methandrostanolone and its derivatives seem to have a potent effect on the
inhibition of II-beta hydroxylase which results in water retention but since methylDHT does not
convert to estrogen and likely inhibits aromatase and the endogenous production of estrogen there is
no subcutaneous edema. This results in greater scale weight as well as contributes to strength gains.
The down side is that I I-beta hydroxylase inhibition also results in sodium retention and high blood
pressure which are not very good for the heart. The anabolic to androgenic ratio is further
confirmation of the lack of anabolic effect of Mestanolone since the ratio is in favor of androgenic
effects by two to one compared to anabolic effects. This steroid is capable of producing all of the
negative side effects of androgens such as acne, mood swings, male pattern baldness, and
hypertension.

AR AFFINITY: 125
I II I
PR AFFINITY: 10
I II I
GR AFFINITY: 0
I II I
SHBG AFFINITY: High
I II I
A/A RATIO: 107/254,24/20,26/64241
I II I
AVAILABILITY: Low, available on the black market in
I
CONVERSION TO
I capsule/tablet form and as powder
None
I ESTROGEN: II I

- = =
METHANDRIOL DIPROPIONATE
(Andris, Arbolic, Crestabolic, Durandrol, Hybolin, Methyldiol, Metylandrostendiol,
Metylandrostendiol, Novandrol, Novandrol, Protabol)
I7a-Methyl-5-androstene-3p, I7P-diol
Formula: C26H4004
MW: 416
Methandriol is a steroid that is very similar to the prohormone 5-androdiol except that it is C-17
alpha alkylated and also esterified at both ends. It is present in combination with several other
steroids especially those manufactured in Australia. In Dan Duchaine's Underground Steroid
handbook II, Duchaine postulated that methandriol enhanced the activity of any steroid used in
combination with it. He stated that methandriol did this by binding very strongly to SHBG thereby
knocking other steroids into the free and active state (similar to what has been described for
mesterolone). Although methandriol does bind to SHBG, it does so fairly weakly and is not capable
of knocking most steroids off. Methandriol is very prone to aromatization (like androdiol) and it has
been suggested that it can bind directly to the estrogen receptor without the need for aromatization.
When used with other aromatizing steroids, methandriol most likely occupies aromatase to the point
that the other steroid is unable to be aromatized allowing it to stay free and active. While this
sounds like a good idea at first, the excess estrogen that is produced by adding methandriol could
lead to gynecomastia Quickly. Methandriol has been found to be a potent inhibitor of II-beta
hyd roxy IaseJOJJ04J05J06J07
' , , ' . Th'IS resu I ts 'In a b UI'Id up 0 f d eoxycortlcosterone,
. a ~otent
J08
mineralocorticoid that elicits retention of sodium and water resulting in hypertension ,J09. 10. A
potentially disturbing aspect of the hypertension induced with methandriol was its apparent
irreversibilityJII. The inhibition of II-beta hydroxylase reduces the production of cortisol and
results in a reduction in the size of the adrenals, also known as adrenal atrophy, which can result in
a stale of acute adrenal insufficiency upon withdrawal of the use of steroids that inhibit I I-beta
hydroxylase. Methandriol is metabolized to methyltestosterone, estrogenic metabolites and 5-alpha
2JS
reduced androgens that contribute to the side-effect profile of this steroid The "increase in
efficacy" that this steroid induces when used in combination with other androgens as proposed by
Duchaine and others may be related to the inhibition of II-beta hydroxylase which will result in
water weight gain and an anticatabolic effect through the reduction in serum cortisol. As mentioned

elsewhere, the inhibition of II-beta hydroxylase can cause hypertension and other negative
cardiovascular effects.
AR AFFINITY: 5
I I I
PR AFFINITY: 0
I I I
GR AFFINITY: 0
I I I
SHBG AFFINITY: Low
I
A/A RATIO:
I
0.7-1.8
I
I I I
AVAILABILITY: Available in several pharmaceutical
I preparations
CONVERSION TO Medium to high
I ESTROGEN: I I

7-ALPHA-METHYL-19-NORTESTOSTERONE
(MENT, Trestolone)
4-estren-7a-methyl-3, 17-dione
~
o
Formula: Cl9H2S02
MW:288
7-alpha-methyl-nortestosterone (MENT) is currently under investigation for use in men as hormone

replacement and a contraceptive. As can be seen from the binding data, MENT has a higher affinity
for the androgen receptor than testosterone and a fairly high affinity for the progesterone
receptor233 This bears out in the anabolic to androgenic ratio as well which shows MENT to have
high anabolic as well as androgenic activity. MENT is very similar in structure to mibolerone
except that it is lacking the C-17 alpha alkylation. This reduces its progestational activity
considerably but it still quite strong, being more potent than nandrolone and about as potent as
dimethandrolone 298 MENT is not converted by 5-alpha reductase to less potent metabolites so it
would be expected to be more androgenic than nandrolone312.313.314. Originally, MENT was believed
to not convert to estrogenic metabolites through the action of aromatase; however, studies have
shown that MENT is, in fact, aromatized313.315 This compound has been shown to be effective at
reducing sperm count in healthy men while not causing excessive stimulation at the prostate and
allowing for sufficient AR stimulation in other tissues312.316.317 However, the fact that this
compound has significant progesterone receptor binding and is converted to a potent estroSen
causes severe HPGA shutdown, which is good for contraception, but bad for athletes316.3IS.319. 20
One would have to assume that these affinities would also cause significant water and fat retention
as well as a high propensity for gynecomastia. MENT, unlike mibolerone, is not C-17 alJlha
alkylated so it has very low bioavailability and is generally administered intramuscularl y320.321.3 22
The C-7 alpha methyl can still cause some elevations in liver enzymes. This steroid is touted as
being the optimal steroid for hormone replacement and is apparently under development for that
purpose. This steroid should produce effects similar to nandrolone but with greater progestational,
androgenic and estrogenic effects. MENT produces quick weight and strength gains that would be
useful in a bulking cycle. This steroid has shown up on the black market in recent years in both the
raw base and an injectable acetate form. The acetate form would need to be injected daily since
322
MENT acetate was shown to have relatively high clearance in pharmacokinetic studies in man
The free base of MENT would be metabolized very quickly and would likely not offer much
benefit. Some have apparently been attempting to use the raw base and the acetate orally but since

the oral bioavailability is so low, this would require large, frequent doses to see any effect. While
this steroid would produce significant gains in mass it should also be expected to cause significant
shut down in natural testosterone production.
AR AFFINITY: 125
I
PR AFFINITY:
I 75
I
GR AFFINITY:
I 0
I
SHBG AFFINITY:
I None
I
AlA RATIO:
I 590/250, 1340/300
241
I
AVAILABILITY:
I
CONVERSION TO
I Low to medium
I ESTROGEN: I

17-ALPHA-METHYL-3-METHYLENE-I-ANDROSTEN-17-BETA-
OL
(none)
17-alpha-methy i-3-methy lene-I-androsten-i 7-beta-ol
OH
." 111 CH
Formula: C21~b20
MW: 300
This steroid is very similar to methyl-i-test. Instead of a 3-keto group, it has a 3-methylene. This
would presumably reduce enzymatic deactivation by 3-alpha hydroxysteroid dehydrogenase.
Although there are no binding values available, this compound has a very favorable
anabol ic/androgenic ratio. One could expect this molecuie to behave in a simi lar way to meth-I-test
but would most likely have a longer half-life. This 3-methylene steroid cannot be converted to
estrogen and is already S-alpha reduced. The literature suggests that like other 3-methylene
323
androgens, this steroid would also be a very good inhibitor of the aromatase enzyme Methyl-I-
test is known for bringing on rapid gains and severe side effects. This is likely due to significant
suppression of II-beta hydroxylase. It is unknown if this steroid would cause similar side effects
but even though its anabolic to anabolic ratio is high, it is well below that if methyl-I-test. This
steroid was never marketed nor is it currently available nor is it on any banned lists or lists of
controlled substances that I am aware which could make it a primary target for black market or gray
market suppl iers.

I
PR AFFINITY:
II
Unknown
I
I II I
I II I
I
A/A RATIO:
II
266/12 241
I
I
AVAILABILITY:
II
I
I II I
CONVERSION TO None
I ESTROGEN: II I

METHYLDIAZINOL
(none)
3-azi-17-alpha-methyl-5-alpha-androstan-17-beta-ol
OH
N
II
-
H
Formula: CZOH3ZNz 0
MW:316
Methyldiazinol is a methyl DHT derivative with a strange group at the 3 position consisting of two
nitrogens with a double bond to each other. There is no binding information available for this
compound and it has never been marketed to my knowledge. However, it has a very advantageous
anabolic to androgenic ratio of 300/20. One would expect this compound to not be affected by 3-
alpha hydroxysteroid dehydrogenase. This steroid would not be capable of being converted to
estrogen and would likely inhibit II-beta hydroxylase like other methylDHT derivatives which may
help to explain its favorable ratio due to loading of water into the skeletal muscle. Since it is C-17
alpha alkylated it would increase liver enzymes but not necessarily more so than other alkylated
androgens. As with the previous compound, this compound is very interesting but because it is
currently unavai labIe, its effects are somewhat of a mystery.

I I
I
PR AFFINITY:
"II Unknown
I
I II I
I
A/A RATIO:
II
300/20
241
I
I II I
I II I
CONVERSION TO None
I ESTROGEN: II I

METHYLTRIENOLONE
(R 1881, methyltrenbolone)
I7-beta-hydroxy-17-alpha-methyl-estra-4,9, I l-triene-3-one
OH
CH 3
." ", CH
o
Formula: Cl9H2J02
MW: 284
Methyltrienolone is an experimental steroid that has found its way onto the black market to a
limited degree. As you can see from its structure it is very similar to trenbolone except that it is C-
17 alpha alkylated which makes it orally active. It is sometimes referred to as methyltrenbolone.
While this is technically true, as you can see from the binding data, methyltrienolone is very
different from trenbolone. It was designed to have a very large anabolic index and as such it binds
very strongly to the androgen receptor. It also binds very strongly to the progesterone receptor and
the glucocorticoid receptor2JJ ,324 This molecule is often used as the standard in scientific literature
because it is the strongest binder of the AR of any common anabolic steroid. It binds to the AR with
2 to 3 times the affinity of testosterone. However, its affinity for the PR is more than 40 times that
of testosterone and 2 to 3 times that of even progesterone. Because of its strong affinity to the AR,
much stronger than DHT, this steroid does not need to be converted to a DHT derivative to exert
androgenic effects in the scalp, skin and prostate. This strong androgenic effect would likely cause
HDL levels to plummet to very low levels. The anabolic to androgenic ratio of this steroid is
basically off the chart with anabolic effects being 120 times that of testosterone and androgenic
effects being 60 times that of testosterone - and this was compared to methyltestosterone orally.
Methyltrienolone does not bind to SHBG and cannot convert to estrogen 24 ,.J25 In the scientific
literature, methyltrienolone has been shown to be very liver toxic. Doses as low as 100 mcg (0.1
mg) per day resulted in elevations of liver enzymes by as much as eight-fold in the span of just one
week l54 Because of the high propensity for liver toxicity, it would be unwise for anyone to use this
steroid for any length of time. In recent years, methyltrienolone has shown up on the black market.
Most users seem to justifiably be fearful of the liver toxicity of this drug and thus, there are few
reports on its effectiveness.

AR AFFINITY: 200-300
I II I
PR AFFINITY: 200-300
I II I
GR AFFINITY: 60
I II I
SHBG AFFINITY: none
I II 241
I
AlA RATIO: 12000/6000
I II I
AVAILABILITY: I~ow availability in tablet or powder form on the
I black market
CONVERSION TO None
I ESTROGEN: II I

MIBOLERONE
(Cheque drops)
7-alpha,17-alpha-dimethyl-19-nortestosterone
OH
.. ,\ItCH
Formula: C20H3002
MW: 302
Cheque drops, containing the steroid mibolerone, were originally produced as an aid in keeping
female dogs from going into heat. Technically it is considered and androgen, however, mibolerone
260
is also very progestational which is the mechanism for its effects in female dogs In fact,
mibolerone has about twice the affinity for the progesterone receptor as progesterone itself. This
drug had a reputation as being a very potent steroid useful in attaining mass and for drastically
increasing aggression. This drug is the nor-19 derivative of bolasterone and as nandrolone is more
potent and more progestational than testosterone, so is the case with mibolerone compared to
bolasterone. The addition of the methyl group at C-7 not only increases AR and PR activity but also
increases the toxicity of the molecule. Mibolerone is a derivative of nortestosterone (nandrolone);
however, it is not metabolized to a less potent dihydronandrolone metabolite due to the shielding
effect of the 7-alpha methyl group235 Like MENT, it is likely that mibolerone is aromatized to form
estrogenic metabolites. This steroid is dosed in micrograms (I milligram is equal to 1000
micrograms) and even so, people still experience significant side effects due to its potent nature.
This steroid does not bind to SHBG and even though it is not 5-alpah reduced, it is a very potent
androgen on its own and can still exert strong androgenic effects. Mibolerone is well known for
causing shedding of hair. It comes as a liquid and a few drugs are taken sublingually under the
tongue. Mibolerone is known for causing severe elevations in blood pressure and aggression. It is
rumored that a certain professional boxer was using this steroid when the well-known ear-biting
episode took place. This steroid is relatively rare, but still pops up from time to time. Most people
use it for the strength gains it imparts or for a burst of aggressive energy in strength sports;
however, used at a low dose, due to its high AR and PR affinities, this drug can result in pretty
substantial mass gains over time. Unfortunately, the liver toxicity of this compound make prolonged
dosing an extreme liability.

AR AFFINITY: 108
I II I
PR AFFINITY: 214
I
GR AFFINITY:
II
10
I
I
SHBG AFFINITY:
II
Low
I
I II 241
I
A/A RATIO: 4100/1800,320/220,365/320
I II I
AVAILABILITY: Low to none
I II I
CONVERSION TO Low
I ESTROGEN: II I

NORBOLETHONE
(Genobol)
13-ethyl-17-beta-ol-18,19-norpregn-4-en-3-one
,,'1\1'\
CH
Formula: C2 1HJ202
MW:316
Norbolethone is a steroid that is very similar to nilevar but instead of the standard methyl at position
C-18 it instead has an ethyl group in this location. As a derivative of nandrolone this steroid is
progestational but the addition of the ethyl group at C-18 adds to the already high progestational
activity of nilevar making norbolethone a strong binder of the progesterone receptor. Norbolethone
327
is also a bit more toxic to the liver than nilevar Norbolethone probably undergoes 5-alpha
reduction to a less active metabolite in DHT target tissues and aromatizes in small quantities to
estrogen derivatives. The anabolic to androgenic ratio for this steroid is very favorable and suggests
that norbolethone is significantly stronger than nilevar in both its anabolic and androgenic effects.
In fact, using norethandrolone as the standard, norbolethone is shown to be eight times as anabolic
and three times as androgenic as norethandrolone. Norbolethone was originally developed and
marketed by Wyeth under the trade name Genabol and was investigated for use in children with
stunted growth at doses up to 2.5 mg per dal 28,329 It was not used widely by athletes until recently
when it was used to evade drug tests due to its lack of detectability, When its use was discovered,
norbolethone was used as a starting point in developing THG, orbolethone delivers results similar
to nandrolone with bloating and mass gains with less strength gains, Suppression of natural
testosterone levels would be severe with norbolethone,

AR AFFINITY: 80
I I
PR AFFINITY: 120
I I
GR AFFINITY: 0
I I
SHBG AFFINITY: Low to none
I I
AlA RATIO: 350/17, 860/280241
I I
AVAILABILITY: Low to none
I I
CONVERSION TO Low
I ESTROGEN: I

NORETHANDROLONE
(Nilevar)
I7-alpha-ethyl-19-nortestosterone
OH
,,1'\\'\
CH
Formula: C2oH3002
MW: 302
Nilevar is the C-17 alpha ethylated derivative of nortestosterone (nandrolone). This modification
renders norethandrolone even more progestational than nandrolone. This steroid is also very similar
to norbolethone, having only a methyl group at C-18 instead of an ethyl. This makes
norethandrolone less progestational than norbolethone. People often refer to nilevar as "oral deca"
and it is often substituted for anavar. Nilevar does have stronger binding to the AR than testosterone
but less than that of nandrolone. On the other hand, its binding affinity for the PR is twice that of
nandrolone that likely makes it less of a partial agonist and more of a full agonist, similar to
trenbolone. Nilevar may not be an "oral deca" but it has advantages over nandrolone. Nilevar can be
taken orally and is less liver toxic than equal does of methandrostenolone due to the fact that the
ethyl group seems to have less effect on the liver than the methyl group. Like nandrolone,
norethandrolone is 5-alpha reduced to less potent dihydro metabolites 23S Unlike nandrolone,
norethandrolone converts to ethylestradiol that has almost no activity at the estrogen receptors and
may actually act as an antagonise 3o . Nilevar is a potent steroid that delivers quality gains. Those
who receive nilevar as a counterfeit version of anavar will likely notice the difference as they are
very different compounds. Nilevar should be effective in doses as little as ten milligrams but most
would use it at doses of 30 mg or more. A study in the literature showed that 25 mg per week of
norethandrolone produced gains of about half a pound per week or six Rounds in twelve weeks with
few side effects. 50 mg did not show improved efficacy over 25 mg3 '. Like methandrostenolone,
Nilevar cause increases in free and total cortisol levels and increases appetite242 . Norethandrolone
decreases TBG to the same degree as oxandrolone with a compensatory increase in TBPA. This will
result in higher free T3 and T3 uptake. The anabolic to androgenic ratio for norethandrolone shows
it to be anabolic with lower levels of androgenic activity with both being similar to nandrolone with
slightly higher androgenic activity.

I~=~P==R=A::::F:::::F::::INI:::::::::T==Y=:==11 130 I
I GR AFFINITY: II 0 I
I AlA RATIO: II 103/33,200/57
241
I
A V AILABILITY: I Medium to low availability as pharmaceutical
preparation as well as black market prep in oral
I form or powder
CONVERSION TO II. Low I
I ESTROGEN:

NORMETHANDROLONE
(N ormethandrone)
17~-hydroxy-17-methy lestr-4-en-3-one
OH
Formula: CI9H2802
MW: 288
Normethandrone is the C-17 alpha alkylated version of nandrolone. Like nilevar, it is sometimes
referred to as oral deca. Normethandrolone has slightly higher binding affinity for the androgen
receptor and sli~htly lower binding affinity for the progesterone receptor than
norelhandrolone23J.2o This steroid also shows am small amount of binding to the glucocorticoid
23J As opposed to nilevar, normethandrolone
receptor, likely giving it some anticatabolic effect
converts to the more potent and long-lasting estrogen, methylestradiol. This steroid is converted by
5-alpha reductase to the less potent 5-alpha reduced version, methyldihydronandrolone which has
less than half of the binding affinity for the androgen and progesterone receptor compared to
23J
normethandrolone Since this steroid is C-17 alpha alkylated, it has the potential for liver toxicity,
more so than norethandrolone and similar to equal doses of methandrostenolone. The anabolic to
androgenic ratios that can be found for this compound show a lot of variability, even when utilizing
the same standard demonstrating some of the difficulty in interpreting these types of studies.
Normethandrolone is a more estrogenic and androgenic version of norelhandrolone.

AR AFFINITY: 130
I II
PR AFFINITY: 110
I II
GR AFFINITY: 5
I
SHBG AFFINITY:
I Low
I
A/A RATIO:
I 325/125, 580/1 I 0 241
I
AVAILABILITY:
I I
CONVERSION TO Low to medium
I ESTROGEN: I

QUINBOLONE
~Anabolicum Vistar)
17-cyclopent-1 --enyloxy-androsta-I,4-dien-3-one
Formula: C24H3202
MW: 352
Quinbolone was never produced in the US and has only been marketed in Italy under the trade name
Anabolicum Vistar by Parke Davis. Quinbolone's structure is very similar to methandrostenolone
and boldenone. It is taken orally, but is not C-17 alpha alkylated; instead it contains a cyclopentenyl
ether, making it more similar to equipoise than to dianabol. This eliminates the worry of liver
toxicity; however, quinbolone is not very active orally because of the lack of C-17 alkylation.
Quinbolone has a very short half-life and a probability of aromatization to estrogen and moderate
affinity for the androgen receptor. This steroid can also be converted to potent 5-alpha reduced
metabolites. There is some disagreement over whether the ether is removed through metabolism or
not. If the ether is not removed, then the binding affinity for this steroid is likely to be reduced.
Most of what can be said for boldenone applies to quinbolone except that quinbolone's half-life is
very short and the gut destroys much of it before getting into circulation. The anabolic to
androgenic ratio shows this steroid to be fairly weak compared to methyltestosterone orally.

AR AFFINITY: 75
I I
I"
PR AFFINITY: 0
I
GR AFFINITY:
I
0
I
SHBG AFFINITY:
I Low
I
I
AlA RATIO:
I 60/20 241
I
I
AVAILABILITY:
I
I I I
CONVERSION TO Low to Medium
I ESTROGEN: I I

STENBOLONE
(Anatrofin)
I(5a)-androsten-2-methyl-17p-ol-3-one
OH
o
H
Formula: C2oH3002
MW: 302
Stenbolone is very similar to both dromostanolone and oxymetholone. It is a derivative of DHT

with a double bond between carbon I and 2 and a methyl group at position 2. The methyl group at
position 2 protects the molecule from both aromatization to estrogen and to some degree,
inactivation in muscle tissue by 3-alpha hydroxysteroid dehydrogenase. This 2-methyl group does
decrease binding to the androgen receptor somewhat. This makes for a molecule that has lightly
less binding affinity for the androgen receptor than primobolan but like primobolan, this steroid
cannot be converted to estrogenic metabolites through aromatization. Stenbolone is considered by
some to be a gentler version of oxymetholone. This steroid has a similar structure to oxymetholone
but is not C-17 alpha alkylated so it has minimal effects on liver function. Stenbolone builds up red
blood cells like oxymetholone and is metabolized to some degree to dromostanolone which has also
been shown to increase red blood cells235.239. Stenbolone does not seem to result in as much size
gain as anadrol or as much bloat so it likely does not have as much inhibitory activity on II-beta
hydroxylase. Stenbolone tended to be injected daily because of the short half-life of the acetate
ester. Additionally, the acetate ester seems to produce pain and swelling at the injection site.
Stenbolone has similar androgenic activity compared to I-testosterone, the unmethylated version of
this drug, but with higher anabolic activity. This is likely due to the reduced conversion to 3-alpha
hydroxy metabolites. Stenbolone offers many of the advantages of oxymetholone with less bloating
and elevated blood pressure.

I II I
I II I
I II I
SHBG AFFINITY: Medium to High
I II 241
I
AlA RATIO: 300/130
I II I
I II I
CONVERSION TO None
I ESTROGEN: II I

TETRAHYDROGESTRlNONE
(THG, "The Clear")
o
Formula: C21H2802
MW:312
Tetrahydrogestrinone (THG) has been inlhe news lately. It was developed underground for the sole
purpose of evading drug tests while improving athletic performance. This "designer drug" was
made and distributed to top-level Olympic and professional athletes and was undetectable on a drug
test. That is, until a coach turned in a sample to testers at USADA, the anti-doping agency.
USADA was then able to develop a method to test for THG and several athletes tested positive.
This scandal has elevated public scrutiny of doping in sports and has brought a lot of negative
publicity to AAS, prohormones and the supplement industry. THG is a derivative of the progestin,
gestrinone:
o
TI-IG has ver:?; strong binding to the androgen, progesterone, glucocorticoid and mineralocorticoid
receptors JJ2 .3 J. THG has been shown to have strong androgenic and anabolic actins as well as
antiglucocorticoid and progestational effects. People reported feeling ill while using this drug which
is not surprising considering the C-17 and C-18 ethyl groups which would tend to make this
compound quite liver toxic. This steroid cannot convert to estrogenic metabolites through
aromatization but may be converted to less potent 5-alpha metabolites since it is a 19-nor steroid.
There is no doubt that this steroid is an effective anabolic, however, now that it is detectable, its use
will most likely wane or completely disappear. THG stands as a reminder of the lengths that athletes
will go to evade drug tests. They were using an unknown steroid that had not been tested for safety

simply because it was not detectable. I would not be surprised though, to see it turn up on the black
market at some point.
AR AFFINITY: 200
PR AFFINITY:
I I
300
GR AFFINITY:
I 10
I
I I
SHBG AFFINITY: ?
I ?
I
A/ARATIO:
AVAILABILITY:
I
I None
I
CONVERSION TO
ESTROGEN: I I

THIOMESTERONE
(Emdabol, Emdabolin, Protabol, Tiomesterone)
I,7-Bis (acetylthio)-17-hydroxy-17-methylandrost-4-en-3-one
OH
Formula: C24H3404S2
MW:451
Thiomesterone is a very unusual and interesting drug. The basic structure is like that of methyl
testosterone, however, two groups containing sulfur, called acetylthio groups, are found at positions
I and 7. The group at position I protects thiomesterone from aromatization to estrogen. The group
at position 7 increases binding affinity for both the androgen receptor and the progesterone receptor
and prevents 5-alpha reduction. These groups also act to increase the half-life of this drug
significantly. The bulkiness of these acetylthio groups suggests that they might be metabolized
since it is unlikely that they would be accommodated within the binding pocket of the androgen
receptor. Thiomesterone has gotten very good write-ups in scientific literature and by Dan Duchaine
in USH2 as being very anabolic. Thiomesterone has, therefore, taken on a sort of mythological
status because so few people have used it to determine if the myth lives up to reality. It is very
difficult to find this drug on the black market. However, there are many underground labs that are
capable of producing this drug and one never knows when it will make a comeback to the black
market. Liver toxicity may be a problem with this molecule, but unfortunately, not enough data is
available to make that determination at this time. The anabolic to androgenic ratio is very favorable,
likely due to the lack of conversion to more potent 5-alpha metabolites.

I II
I II
I II
SHBG AFFINITY: Low to none
I II
AlA RATIO: 456/61
I II
I II
CONVERSION TO None
I ESTROGEN: II

PROSTEROIDS
Prosteroids are or were "quasi legal" compounds that are or were sold as dietary supplements. They
are active steroids that do not require enzymatic conversions. Some of these compounds were made
illegal under the Anabolic Steroid Control act of2004. Even though some of these compounds were
not listed in the new legislation, their legality still remains in question and their presence in the legal
market is tenuous at best.

5-ALPHA MEDROXYPROGESTERONE
(none)
o
.. ,,'OH

o -
H
Formula: C22HJ40J
MW: 346
5-alpha Medroxyprogesterone (5aMP) is a progesterone derivative that is very similar to

medroxyprogesterone. Medroxyprogesterone has been prescribed to prevent skeletal muscle
catabolism associated with cancer and HIV/AIDS. It works through several mechanisms including
the reduction of catabolic cytokines, the inhibition of aromatase and the inhibition of 3-alpha
hydroxysteroid dehydrogenaseJJ4.JJ5.JJ6 Catabolic cytokines, such as Interleukin-6, Tumor Necrosis
Factor AIpha, and Interleukin-I cause the breakdown of skeletal muscle proteins. Inhibition of these
cytokines results in reduced catabolism and a shift to anabolism. As discussed previously, DHT is
not anabolic in skeletal muscle because it is deactivated by 3-alpha hydroxysteroid dehydrogenase.
The inhibition of 3-alpha hydroxysteroid dehydrogenase by medroxyprogesterone prevents the
deactivation of DHT in skeletal muscle resulting in increased anabolism. Although
medroxyprogesterone is a progestin, it is also quite androgenicJJJ. The 5-alpha reduced form of
medroxyprogesterone is even more potent in producing these effects. In addition, 5-alpha
medroxyprogesterone also acts to stimulate GABA receptors in the brain producing a sense of well-
being and stimulation of GH release. 5aMP and several similar derivatives are available as gray
market supplements. The 3-reduced versions on the market are likely to be estrogenic since 3-
reduced progestins are known to have this activity. This product is likely to cause significant
shutdown of natural testosterone production due to the progestational effects.

I II I
I II I
I II I
I II I
AlA RATIO: Unknown
I
AVAILABILITY:
II
Unknown
I
I II I
I
CONVERSION TO
ESTROGEN: II
none
I

17_ALPHA-METHYL-I-DEHYDROANDROSTANOLONE
(methy I-I-testosterone)
17-alpha-methyl-5-alpha-androst-l-en-17-beta-hydroxy-3-one
OH
CH 3 .. ""CH
o -
H
Formula: Czol-i)oOz
MW: 302
17-alpha-methyl-l-dehydroandrostanolone, or MIT for short, was the first methylated prosteroid

introduced and initiated the "methyl craze" in the supplement market. No receptor binding studies
have been performed on this molecule and the anabolic/androgenic ratios vary widely as well. Users
have reported gaining 10 pounds or more in short periods of time (1-2 weeks). This compound
cannot be converted to estrogen, is probably not appreciably progestational and is a DHT derivative.
Side effects are those typical to androgens: acne, high blood pressure, altered lipids, prostate
hypertrophy and male panern baldness. It seems to be pretty potent and also seems to cause
significant HPGA suppression. This compound is C-17 alpha alkylated so it does carry the risk of
elevated liver enzymes, which should be similar or slightly more than equal doses of
methandrostenolone. Methyl I-test seems to cause lethargy in the same way as I-test and reduces
HDL levels quite severely. MIT was the most popular prosteroid until it was removed from the
market with the passage of the 2004 Anabolic Steroid Control Act. The likely mechanism for the
rapid weight gain as well as the hypertension witnessed with MIT is an increase in water retention
secondary to inhibition of II-beta hydroxylase. Because MIT does not convert to estrogen, this
water retention does not leak into the subcutaneous space resulting in the "bloated" look. The
anabolic to androgenic ratios for this steroid range from weak to extremely potent. It is important 10
remember that water makes up 60-80 percent of the mass of muscle tissue. The water loading effect
of some steroids will increase body weight quickly but transiently. This steroid has a reputation for
being quite toxic but people still love it because it gives an instant gratification. Some have reported
gynecomastia either while using M IT or post-cycle, often referred to as "delayed gyno". As with
oxymetholone, theories have been put forth to explain this effect including progestational effects
and increases in prolactin. A more likely scenario, particularly for strong androgens with no
conversion to estrogen, is that androgens reduce SHBG levels which can upset the androgen to
estrogen ratio, particularly post-cycle when the androgenic stimulation of the cycle has subsided
and back conversion of estrone to estradiol can upset the androgen/estrogen ratio. Another
possibility is that inhibition of II-beta hydroxylase will decrease cortisol levels but increase DJ-IEA

production by the adrenals. DHEA has been shown to be capable of directly stimulating the
estrogen receptor.
I I I
I I I
I
SHBG AFFINITY:
I
Medium to high
I
I I I
AlA RATIO: 50/25,910/180241
I I I
AVAILABILITY: Previously available as a prosteroid,
I questionable now
CONVERSION TO None
I ESTROGEN: I I

I-DEHYDROANDROSTANOLONE
( I-testosterone)
17_beta_hydroxy_5_alpha_androst_l_en_3_one
OH
~
o
H
Formula: C19H2802
MW: 288
I-test was, at one point, a legal supplement. This being so, many considered it to be a
'prohormone"; however, it is clearly an anabolic androgen as it does not require enzymatic
conversion to be biologically active. It is also considered by many to be "less potent" than other
"real" steroids because it was legally available. I-test was the first "prosteroid" to be introduced to
market. It is a DHT derivative and its anabolic/androgenic ratio agrees with this fact. I-test cannot
be converted to estrogen and does not appear to be significantly progestational. However, no
binding data is available for this compound. I-test has been used in transdermal preparations and
seems to work well; however, its short half-life requires almost constant application to keep plasma
levels up. Some have tried to inject I-test, but have found it to be extremely irritating at the
injection site. Some have hypothesized that the molecule itself is an irritant but the likelihood is that
the irritation is caused by contaminants or by too high of a concentration of benzyl alcohol or
benzyl benzoate, or the steroid itself. The cypionate ester of I-test has been produced and seems to
be relatively painless as an injectable with an anecdotal half-life of about 4-5 days. As an androgen,
I-test can cause elevated blood pressure, prostate hypertrophy and male pattern baldness. I-test also
seems to cause a marked lethargy, which has yet to be explained. I-test cannot be converted to
estrogen in any appreciable amount and is therefore free of estrogenic side effects. On a mg per mg
basis, I-test seems to have only about 75% of the potency of testosterone most likely due to the lack
of water retention. The anabolic to androgenic ratio shows this steroid to be twice as anabolic as
testosterone with similar levels of androgenic activity. I-test was made illegal by the 2004
legislation but may still be available on the black market.

AR AFFINITY: 85 est
I
PR AFFINITY:
I 0
I
I I I
GR AFFINITY: 0
I
SHBG AFFINITY:
I medium
I
I
AlA RATIO:
I 210/135,200/100 24 (
I
I
AVAILABILITY:
I
I
CONVERSION TO
I None
I
I ESTROGEN: I I

3-DESOXYMETHYLTESTOSTERONE
(DMT, Madol, Pheraplex)
3-desoxymethyltestosterone
-
H
Formula: CZO H32 0

MW: 288
Desoxymethyltestosterone, also known as DMT or Madol, is a designer steroid that was recently
discovered to be in use by athletes to avoid drug tests. The absence of a 3-keto group makes this
steroid similar in appearance to ethylestrenol. However, as DMT was undetectable in urine tests, it
is unlikely that DMT converts to a 3-keto derivative although it has been shown in the literature that
ethylestrenol does in fact convert, to some degree to norethandrolone. DMT is 5-alpha reduced;
however, the absence of a 3-keto group makes it impossible for the enzyme 3-alpha hydroxysteroid
dehydrogenase to deactivate it in skeletal muscle. This compound cannot convert to estrogen but it
is likely a strong binder of SHBG and can displace estrogens which may result in increased chance
of developing gynecomastia. It is also likely that this steroid is a potent inhibitor of II-beta
hydroxylase which could also playa role in the induction of gynecomastia as described elsewhere in
this tex!. While some have claimed that this steroid will not result in reduction of natural
testosterone production, this is, in fact, untrue. DMT has achieved somewhat of a cult following
since it was discovered. II is fairly potent in spite of the lack ofa 3-keto group and the presence of
the C 17 methyl group makes it toxic to the liver, but no more so than equal doses of
methandrostenolone. The anabolic to androgenic ratio shows this steroid to be 12 times more
anabolic compared to methyltestosterone with almost twice as much androgenic activity. This also
supports the likelihood of inhibition of II-beta hydroxylase as does a study in the literature showing
338
increased heart weights in animals treated with DMT DMT is found in several nutritional
supplements, however, as DMT is on the radar as a designer steroid, it is unlikely that these
products will remain legal for very long. In fact the DEA has signaled its intentions to schedule this
steroid though it has not yet been scheduled.

I
AR AFFINITY:
PR AFFINITY:
II
Unknown
Unknown
I
I
GR AFFINITY:
II
Unknown
I
I II I
I II I
AlA RATIO: 1200/187241
I II I
AVAILABILITY: Available as a prosteroid
I II I
CONVERSION TO none
I ESTROGEN: II I

2,17-DIMETHYLDHT
(numerous)
2,17-alpha-dimelhyl-androslanolone
OH
CH
3 .. ",,, CH
o -
H
Formula: C21H3402
MW: 318
Superdrol was released as a dietary supplement just before the 2004 Prohormone Ban wenl into
effect. As this compound was new, it was nol listed in the legislalion as a banned steroid. Somehow
this steroid has flown under the radar for the past five years. This prosteroid is the C-17 alpha
alkylated version of dromostanolone and is likely to cause similar effects. Superdrol is a DHT
derivative but is due to the protection of the 2 alpha methyl group there is Ie s deactivation by 3-
alpha hydroxysteroid dehydrogenase. This steroid cannol be converted to estrogenic metabolites
through aromatization. When superdrol was first introduced, it was touted as being free of side
effects but it became apparent quite quickly that this was not the case. The dimelhylation is likely to
improve the bioavailability, but will also increase liver toxicity. Androgenic side effects are also
likely and will depend on dose. Because of its strong androgenic activity, superdrol causes rapid
reductions in HDL levels and produces side effects such as acne, hair loss, oily skin, high blood
pressure and the other common androgenic side effects. Users report rapid strength increases with
similar weight gain compared to M IT. As with M IT, this steroid is likely a potent inhibitor of 11-
beta hydroxylase resulting in water retention and elevated blood pressure with linle subcutaneous
edema. There have been reports of gynecomastia occurring either during or after a cycle of
superdrol. The same explanation used for M IT would probably apply to superdrol as well.

I II I
PR AFFINITY: 0
I II I
GR AFFINITY: 0
I II I
SHBG AFFINITY: Medium to high
I II
400120 241
I
AlA RATIO:
I II I
I II I
CONVERSION TO None
I ESTROGEN: II I

HYDROXYMETHYLNANDROLONE
(none)
4,17-beta-dihydroxy-17-methylestr-4-en-3-one
OH
CH 3
.,,"ICH
OH
Formula: CI9H2803
MW: 304
Hydroxymethylnandrolone (MeOHN) was available as a legal gray market supplement until the
2004 legislation. No binding data is available on this compound and the anabolic/androgenic ratios
are variable. If one looks at methylnandrolone, one can see that the addition of a methyl group to
nandrolone actually decreases AR binding affinity by about 10% but it increases progesterone
receptor binding 5 fold. The AR and PR binding of methyl nandrolone are nearly equal. If we were
to extrapolate these values to MeOHN, we would expect it to be more androgenic. In fact, the
hydroxyl group will prevent conversion to DHN, which is one of the benefits of using nandrolone.
The conversion to DHN in the prostate and other target tissues results in less activation at those
siles. The positive is that the hydroxyl group will also prevent conversion to estrogen. The hydroxyl
group will also reduce some of the binding affinity {or the androgen and the progesterone receptor.
What you are left with is a compound that has roughly equal affinity for the progesterone and
androgen receptors, does not convert to estrogen, but should not be used with aromatizable
compounds. Also, the C-17 alpha alkylation will raise liver enzymes and as this is a nandrolone
derivative, one could expect the affect on the liver to be greater than equal amounts of
methandrostenolone. Dosing has generally been conservative with 10 to 20 mg per day common;
however, some have pushed the dose up to 40 to 60 mg per day without adverse reactions.
Anecdotally, people have reported this compound to produce lean gains with little to no water
retention. The anabol ic to androgen ic ratios seem somewhat at odds with the real world appl ication
of this steroid. There is also some degree of variability with androgenic activity of3 to 10 times and
anabolic activity 10 times that of methyltestosterone.

II
II
II
SHBG AFFINITY: Low
II
A/A RATIO: 1304/1024, 1304/281 24 \
II
AVAILABILITY: Formerly available as prosteroid. Questionable.
I
CONVERSION TO Low
ESTROGEN: II

HYDROXYNANDROLONE
(Oxabolone, Steranabol, Steron)
4, I7-beta-dihydroxyestr-4-en-3-one
OH
o
OH
Formula: ClsH2603
MW: 290
Hydroxynandrolone was available as a legal gray market supplement until the passing of the 2004
legislation. It is considered a "prosteroid" because it does not need to be converted to be
biologically active. There is no binding data available on this compound, but its
anabolic/androgenic ratios show it to be relatively mild. Depending on which values you believe,
hydroxynandrolone is either as anabolic or halfas anabolic as testosterone. The hydroxyl group will
prevent this molecule from conversion to estrogen, but will also prevent conversion to DHN - this
will result in less protection for the prostate than nandrolone. The hydroxyl group will decrease
binding affinity for both the androgen receptor and the progesterone receptor. Taken orally, this
steroid would have little or no activity since it is not orally bioavailable. If this steroid was available
with a long lasting ester, this compound might be a good alternative to nandrolone.

AR AFFINITY: 120
I II I
PR AFFINITY: 10
I I I
GR AFFINITY: 0
I I I
SHBG AFFINITY: Low
I I I
AlA RATIO: 92/46, 50120241
I
AVAILABILITY:
I
LOW availabity as a pharmaceutical preparation in
I
the cypionate form. Previously available as a
I prosteroid in the cypionate form - Questionable
CONVERSION TO None
I ESTROGEN: I I

HYDROXYTESTOSTERONE
(none)
4, 17-beta dihydroxy-androst-4en-3-one
OH
o
OH
Formula: C I9H2803
MW:304
Hydroxytestosterone was available as a legal supplement, but was made illegal by the 2004
Anabolic Steroid Control Act. It is considered a prosteroid because it does not need to be converted
to be biologically active. It has been used orally, but has poor bioavailability even with some of the
long chain esters that have been attached. Some used it transdermally several times a day to combat
its quick half-life. There is no binding data available on this compound; however, its
anabolic/androgenic ratio suggests that it is not a very potent androgen receptor binder.
Hydroxy testosterone has about half the anabolic activity of testosterone with one quarter of the
androgenic activity. The hydroxyl group prevents this molecule from being converted to estrogen or
DHT. This molecule also acts as an aromatase and 5-alpha reductase inhibitor as does its metabolite
4-hydroxyandrostenedione, also known as fonnestane. The hydroxyl group would be expected to
reduce androgen receptor binding. This molecule is advantageous for those who are concerned
about their prostate or their hairline. It is only mildly suppressive (depending on dose of course) and
offers modest gains with little side effects. This compound has been seen with either the cypionate
or the undecanoate ester attached providing for a longer half-life. Unfortunately, the esterified
compounds are difficult to solubilize and a concentration of 100 mg/ml with a high concentration of
benzyl alcohol and benzyl benzoate is needed. Taken in reasonable doses, hydroxytest results in
quality mass gains with little water retention and few side effects and could be compared to
primobolan only less androgenic. It has been largely overlooked due to the fact that it was
previously available as a legal prosteroid. Unfortunately, there are people who believe that anything
legal must not be effective. Additionally, since hydroxytest does not load water, users do not see
quick mass gains with this steroid. I wouldn't be too surprised to see hydroxytest show up on the
black market where it might gain some respect as a pretty good anabolic with few side effects.

AR AFFINITY: 70
I
PR AFFINITY:
II I
0
I II I
GR AFFINITY: 0
I II I
SHBG AFFINITY: Low
I II 241
I
A/A RATIO: 52/28
I II I
AVAILABILITY: Previously available as a prohormone,
I I Questionable now.
CONVERSION TO None
I ESTROGEN: 11 I

METHYLDIENOLONE
(none)
17-alpha-methyl-4,9-estradienolone
OH
o
Formula: CI9H2602
MW: 286
Methyldienolone is a "prosteroid" that was brought to market before the 2004 ban and is now
illegal. Methyldienolone looks similar to methyltrienolone except that there are two double bonds
instead of three. The C-17 alpha alkylation means that this compound can be taken orally and like
all C-17 alpha alkylated androgens, there is the possibility of liver enzyme elevation. Also, the 4,9
double bonds and the fact that this is a nortestosterone derivative make the potential for liver
toxicity even greater. Although being fairly close in structure to methyltrienolone, it is quite
different in action. As one can see from the binding affinities, Methyldienolone has more affinity
for the progesterone receptor than it does for the androgen receptof33260 In fact, MD has less
affinity for the androgen receptor than testosterone. Like methyltrienolone and THG,
Methyldienolone has some antagonist activity toward the glucocorticoid activity which would result
in some anticatabolism. This steroid has a high anabolic to androgenic ratio likely due to a long
half-life because of the resistance to metabolism that the double bonds contribute. MD cannot
aromatize to estrogenic metabolites but may be 5-alpha reduced to less potent metabolites in the
same manner as nandrolone. Some have reported gaining ten pounds in as little as three weeks with
MD at doses of only one or two mg. It has also been stated that this steroid is better suited to a
"CUlling" stack to maintain muscle mass while losing weight. Since MD has anticatabolic effects
through its antiglucocorticoid activity this seems reasonable. In any case, since MD is now an
illegal steroid, it remains to be seen if it will gain much popularity on the black market.

AR AFFINITY: 64
I II I
PR AFFINITY: 71
I II I
GR AFFINITY: 10
I II I
I
SHBG AFFINITY:
A/A RATIO:
II
Low
130/30, 1000/200 241

I
I II I
I
AVAILABILITY:
CONVERSION TO
I Previously available as a prosteroid,
questionable now
None
I ESTROGEN: II I

METHYLEPITIOSTANOL
(none)
2a,3a-epithio-17a-methyl-5a-androstan-17b-ol
Formula: C20H300S
MW:318
Methylepithiostanol is currently being sold as a gray market prosteroid. As a DHT derivative, this
prosteroid is androgenic but has also been investigated as an antiestrogen. It is rumored to be very
effective at reducing breast tissue growth. Methylepithiostanol cannot convert to estrogen but there
are some reports of gynecomastia with this prosteroid however, these reports are largely
unsubstantiated. This prosteroid is C-17 alpha alkylated and is thought to be more liver toxic than
other methylated steroids though there is no hard evidence for this to be true. The anabolic to
androgenic ratio for this prosteroid is very high but this does not seem to translate to real world
effects. Methylepithiostanol is said to have pretty severe effects on HDL, likely due to its
antagonistic actions on estrogen. Doses range from 10 to SO mg per day. Users generally do not
report large mass gains with this prosteroid and describe it as a dry, lean product.

I II
I II
I II
I II
A/A RATIO: 1100/91 24 \
I II
I II
CONVERSION TO None
I ESTROGEN: II

METHOXYTRENBOLONE
(none)
trenbolone methyl ether
o
Formula: CJ9H2402
MW: 284
Methoxytrenbolone is suspected to be the ingredient in an over the counter gray market prosteroid
that is marketed as an oral version of trenbolone. There is still some debate as to what is actually in
the product with some suggesting that it may contain actual trenbolone. Trenbolone has some oral
bioavailability but is illegal for sale - especially as a dietary supplement. If the product contains
methoxytrenbolone then its legality would still be in question since it would simply be the methyl
ether of trenbolone. This product is dosed in the low milligram range and its feedback has been
varied. As with many prosteroids that are sold primarily online, it is difficult to get accurate
feedback from users. Companies will often hype up their products by posing as users who are
"logging" their experiences in a favorable light. Orals ethers tend to not be as effective as C-17
alpha alkylated androgens but since trenbolone has some bioavailability of its own, it is possible
that this product may produce an anabolic response but likely at much higher doses. The flip side is
that the methyl ether should not have much negative effect on the liver. If this is in fact the
compound that is contained in the product, and if a sufficient dose is taken, then one would expect
to see similar effects to those of trenbolone.

I II I
I II I
I II I
I II I
AlA RATIO: Unknown
I II I
I II I
CONVERSION TO None
I ESTROGEN: II I

PROSTANAZOL
(none)
I7-beta-tetrahydropyrany I-methy 1-5-alpha-androstano-[3,2-c]-pyrazol
HN
~==-l.
H
Formula: C25H3SN202
MW: 398
Prostanazol is one of the newer prosteroids released after the 2004 legislation. This prosteroid is the
C-17 demethylated derivative of stanozolol. Obviously, the lack of this methyl group reduces the
oral bioavailability of this compound dramatically. The manufacturers have added an ether group at
the C 17 position but this improves oral bioavailability only slightly. Anecdotal reports indicate that
doses of at least 200 mg are necessary to see any results from this compound. The lack of C 17
alkylation also decreases the half-life of this molecule considerably. Since stanozolol has relatively
low binding affinity that is only made up for by its long half-life, this prosteroid is not likely to
produce simi lar results even if taken in divided doses throughout the day. If esteri lied, instead of the
added ether, and injected, this molecule might produce similar gains to injectable winstroJ. One
possible use for this compound would be to take a good dose immediately before workouts only.
This would provide some AR activation but because of the short half-life, will likely not cause
much, if any, suppression. This steroid is not capable of being converted to estrogenic metabolites
through aromatization. To my knowledge, there have not been any reports of joint pain with this
product as is commonly reported with stanozolol which is likely a result of its rather low activity.
This prosteroid is still available on the gray market but the high doses needed and the low level of
activity do not make it very attractive.

AR AFFINITY: Very Low
I II I
PR AFFINITY: ?
I II I
GR AFFINITY: ?
I II I
SHBG AFFINITY: Very Low
I II I
AlA RATIO: ?
I II I
AVAILABILITY: Readily available as a prosteroid
I II
None
I
CONVERSION TO
I ESTROGEN: II I

PROHORMONES
Prohormones are steroidal supplements that, like Prosteroids, are or were sold in a quasi-legal
fashion in the supplement market. Some of these products were made illegal in the 2004 legislation
while some are currently still sold under the radar.

5-ALPHA ANDROSTANEDIOL
(none)
5a-androstan-3a, 17~-diol
OH
HO'\'
Formula: CI9H320Z
MW: 292
5-alpha-androstanediol is a prohormone that is purported to convert to DHT. This ~rohonnone does

have some androgen receptor binding affinity of its own although it is very low)] The problem
with this prohormone is that while it is converted to DHT in the liver, it is deactivated in the skeletal
muscle. In fact, when DHT is deactivated in skeletal muscle, 5-alpha androstanediol is the
metabolite that is produced. Only with very high and frequent doses would a person see any
significant skeletal muscle anabolism, but even at low doses would experience negative androgenic
side effects. You can see from the anabolic/androgenic ratio that this prohormone is actually a
selective modulator with the selectivity towards the androgenic activity. The beta isomer has a
slightly higher androgen receptor affinity than the alpha isomer but it is still quite low 2)]
Androstanediol cannot be converted to estrogen and has some antiestrogenic activity as well.
Anecdotal evidence suggests that 5AA (and methyl5AA) is more potent in building muscle than
DHT (or methyIDHT). Although 3-alpha hydroxysteroid dehydrogenase is considered to be
unidirectional meaning that in skeletal muscle, it is much more likely to deactivate DHT under
normal conditions. However, when 5AA (or methyl5AA) is taken, it may push the enzyme in the
reverse direction resulting in higher skeletal muscle DHT levels. Taking 5AA or methyl5AA in
conjunction with DHT or methylDHT would likely increase the effectiveness of those compounds
in skeletal muscle due to interference with the 3-alpha HSD enzyme. This prohormone was made
illegal in the Steroid Control Act of 2004 and since it is a prohonnone, it is unlikely to show up on
the black market unless it is put into a product as a cheaper alternative to the active ingredient.

AR AFFINITY: 10
I II
PR AFFINITY: 0
I II
GR AFFINITY: 0
I II
SHBG AFFINITY: High
I II 241
AlA RATIO: 30/34,65/276,110/187
I II
I II
CONVERSION TO None
I ESTROGEN: II

17-ALPHA-METHYL-I-ANDROSTENEDJOL
(none)
17-alpha-methy I-I-androstenediol
HO'"
Formula: C2o H32 0 2

MW: 304
17-alpha-methyl-l-androstenediol is a prohormone that is not listed in the 2004 legislation. This

prohormone is the diol version of methyl-I-testosterone and requires conversion to be fully active
although it does have some activity in its own right. Only a portion of the dose taken will convert to
methyl-I-test but because methyl-I-test is so potent a dose of only 20 mg of the prohormone seems
to be sufficient to produce gains. This prohormone is toxic to the liver but at doses of 20 mg the
toxicity should be no more than effective doses of methandrosteno lone. This prohonnone will likely
convert at a rate of 10 to 20%, therefore, a dose of20 mg of the prohormone will deliver a dose of2
to 4 mg of MIT. This dose of MIT, along with the activity of the prohormone itself, produces
significant gains without the side effects that many were experiencing with larger doses of MIT.
The anabolic to androgenic ratio of this prohormone show it to be four times as anabolic as
methyltestosterone with about the same level of androgenic activity. Neither the prohormone or
M IT can convert to estrogenic metabolites through the actions of aromatase. Both however, are
likely to inhibit II-betahydroxylase resulting in water retention and elevated blood pressure not to
mention all of the potential androgenic side effects.

I II I
I II I
I II I
I II I
A/A RATIO: Unknown
I II I
AVAILABILITY: IFormerly availableunknown
as a prohormone, currently
I
CONVERSION TO
I ESTROGEN: II I

t -ANDROSTENEDIOL
(numerous)
l-androsten-3~, 17~-diol
OH
HO
-
H
Formula: C I9H3002
MW: 290
IAD was considered to be one of the more potent pro hormones and was one of the first
prohormones that delivered noticeable results. It converts to I-testosterone and has some intrinsic
activity of its own. Neither lAD nor I-test can convert to estrogen and both are fairly strong
androgens. High doses of IAD were required to see significant gains since the conversion rate was
roughly 10-15 'Yo. It was not uncommon for doses of 800 mg per day in divided doses to be used.
IAD was made illegal by the Anabolic Steroid Control Act of 2004 and is no longer legally
available and prohormones do not seem to show up on the black market. There are some newer
prohormones available that require a two step conversion to produce I-testosterone. The original
IAD seemed to produce lethargy in a similar manner to I-testosterone and like any steroid could
result in shutdown of natural testosterone production. Side effects with prohormones tend to be mild
because they seem to be less active. In this case, since there is no conversion to estrogen, only slight
androgenic side effects would be encountered unless high doses were taken.

I II I
I
PR AFFINITY:
II Unknown
I
I II I
I
AlA RATIO:
II
40/50 241
I
I
AVAILABILITY:
II
Previously available as a prohormone. Now
I
I
CONVERSION TO
I iIIel!:al.
I ESTROGEN: II I

4-ANDROSTENEDIOL
(numerous)
4-androsten-3p, 17p-diol
HO
Formula: Cl9H300Z
MW: 290
4-adiol was the first prohormones to be released and is a direct precursor to testosterone. 3-beta
hydroxysteroid dehydrogenase converts 4AD into testosterone. This prohormone although an
improvement over androstenedione still has very poor bioavailability. Very little is actually
absorbed by the gut and still even less survives the liver. Even after all this, the amount of
conversion is quite low and the half-life of activity is very short. This necessitates taking relatively
high doses of androdiol throughout the day (3 x 300mg+). Many companies offered esterified or
etherified versions of 4AD that promised better absorption and a longer duration of action. Other
companies offered transdermal versions that bypassed the liver, resulting in beller absorption;
however, the duration of action was still rather short. This prohormone converts into testosterone,
which can then convert into DHT or estrogen. In fact, many people report a high level of
estrogenicity when taking androdiol. Androdiol itself does have minimal AR binding affinity and
can be converted to androstanediol, which is androgenic. The anabolic to androgenic ratio shows
androdiol to be more androgenic than anabolic suggesting that the conversion to androstanediol is
preferential to the conversion to testosterone. There are two isomers of this prohormone, the 3-alpha
and the 3-beta. The 3-alpha appears to be less androgenic. This prohormone was made illegal by the
2004 legislation and is no longer available.

AR AFFINITY: --5
I II I
PR AFFINITY:
I
GR AFFINITY:
II 0
0
I
I II I
SHBG AFFINITY: Low
I
AlA RATIO:
II
Unknown
I
I II I
AVAILABILITY: Questionable
I II I
I ESTROGEN: II I

5-ANDROSTENEDIOL
(none)
5-androsten-3~, 17~-diol
OH
Formula: C 191-13002
MW: 290
5-adiol hit the market soon after androstenedione as many manufacturers scrambled to get new and
interesting prohormones into the hands of anxious consumers. 5-adiol is very similar to a marketed
steroid called methandriol. Methandriol is the C-17 alpha alkylated version of 5-adiol. 5-AD
converts very easily to estradiol and many users experienced negative estrogenic side effects,
especially gynecomastia. It has been reported in the literature that 5-AD has a direct eflect on
estrogen receptors although the evidence is somewhat questionable. Even worse, this prohormone
had little to no anabolic activity as can be seen with the anabolic to androgenic ratio being 10/20.
This prohonnone has long since fallen by the wayside and scheduled or not, it is unlikely that
anyone would ever want to use it but it shows the desperation that existed on the part of consumers
to get their hands on a legal alternative to steroids and the willingness of manufacturers to produce
said alternative.

AR AFFINITY: 14
I I
PR AFFINITY: 0
I I
GR AFFINITY: 0
I I
SHBG AFFINITY: Medium
I I
A/A RATIO: 10/20241
II I
II I
ESTROGEN: II I

ANDROSTENEDIONE
(none)
4-androsten-3, 17-dione
Formula: C l9 Hz60z
MW: 286
Androstenedione, known popularly as Andro, was the first "prohormone" to be put on the market. It
has little androgen receptor binding affinity and undergoes conversion to testosterone via 17BHSD.
Androstenedione is normally produced by the testes and adrenals at a rate of about 3.2 mg/day and
circulates at a concentration of about 5.4 nmol/L 51 Of this, only about 7.5% circulates in a free,
unbound state with 6.6% bound to SH BG and 85% bound to albumin. Only about 7% of the
androstenedione produced in the body is converted to testosterone while 1.7% is converted to
estrone51 Estrone is a weaker estrogen than estradiol, but can be directly converted to estradiol as
well. Soon after it was put onto the market, people began to realize that androstenedione was not
very anabolic and tended to produce unwanted side effects (such as gynecomastia) quite easily most
likely due to its high affinity for albumin and the fact that high doses were necessary to see any
anabolic effect. Androstenedione is known to be a fairly potent aromatase inhibitor but either
because it was metabolized quickly or some other reason; it still produced significant estrogenic
side effects. Andro could be metabolized to more potent androgenic 5-alpha reduced metabolites
and as such, could produce side effects such as acne, hair loss, prostate enlargement and others.
Andro was targeted by the media after Mark Macguire admitted to using it during the time when he
broke the home-run record. Andro was removed from the market as a consequence of this attention
but other products were quickly produced to fill the vacuum. It has been theorized that one could
use androstenedione with testosterone to interfere with 17-beta hydroxysteroid dehydrogenase to
decrease the metabolism of testosterone.

AR AFFINITY: <1
I
PR AFFINITY:
II I
0
I II I
I
GR AFFINITY:
II 0
I
I
SHBG AFFINITY:
II Low
241
I
AJARATIO: 55/131,53/110,22/39,32/32
I
AVAILABILITY:
II
I
I II I
I
CONVERSION TO
ESTROGEN: II
Medium
I

BOLADIOL
(none)
7, 17-alpha-dimethyl-androsten-3, 17-diol
HO
HO
Formula: C21H3402
MW:318
This prohormone has been rumored to be in development for release as a dietary supplement. It is
the diol version of the infamous steroid bolasterone. Bolasterone is the 7,17 dimethylated version of
testosterone and has a reputation as being one of the most potent steroids ever sold as a legitimate
pharmaceutical product. It was also removed from the market due to potential liver toxicity.
Bolasterone has an anabolic to androgenic ratio that shows it to be six times more anabolic than
methyltestosterone and three times as androgenic. This diol prohormone would likely be very potent
requiring only a few milligrams to see strong anabolic and androgenic effects. The 7-methyl group
likely protects this steroid from 5-alpha reduction but it would likely still possess strong androgenic
activity on its own. Also, the diol and bolasterone both have the capacity to be converted to
estrogenic metabolites. The fact that this diol is dimethylated and that bolasterone was removed
from the market due to concerns over liver toxicity strongly suggest that this prohormone would
also be quite liver toxic. Additionally, one would expect to see strong estrogenic and androgenic
side effects from this prohonnone.

II
II
GRAFFINITY: Unknown
II
II
AlA RATIO: Unknown
II
CONVERSION TO
ESTROGEN: "I Unknown
253
ANABOLIC PHARMACOLOGY
I-DEHYDROEPIANDROSTERONE
(I-DHEA)
I-ANDROSTEN-3P-OL-17-0NE
Formula: Cl9Hz80Z
MW: 288
I-DHEA is a newer pro hormone that is a naturally occurring metabolite of DHEA. It is converted
through a two step process, first to I-androdiol and then to I-testosterone. There is no data on the
efficiency of these conversions but like most pro hormones, they are likely to be in the 10% range
for each conversion resulting in 1 mg of I-testosterone for every 100 mg of I-DH EA consumed.
While this may not sound like a lot, I-AD is active in its own right and some of the manufacturers
have included accessory ingredients in with the prohormone to enhance bioavailability and
conversion so that the rate could actually be double or triple what it would be for the prohormone
alone. Neither I-DHEA nor its metabolites can be converted to estrogenic metabolites. The lack of
estrogenic metabolites and the improved androgenic and anabolic effects of I-DI-IEA offer a real
improvement in efficacy and side effect profile compared to standard DHEA.

I II I
I
GR AFFINITY:
II
Unknown
I
I
SHBG
II
Unknown
I
I AFFINITY:
A/A RATIO:
II
Unknown
I
I II I
AVAILABILITY: II Unknown
I I
CONVERSION I none
TO ESTROGEN: I

4-DEHYDROEPIANDROSTERONE
(4-DHEA)
4-ANDROSTEN-3!3-0L-17-0NE
HO
Formula: Cl9H1SOl
MW: 288
4-DHEA is another newer prohonnone derivative of DHEA. The only difference is the switching of
the double bond from position 5 to position 4. Though this seems like a relatively minor change it
alters the molecule in several aspects. First of all, DHEA is suspected to act directly at the estrogen
receptor due to the presence of the double bond in the fifth position. For 4-DHEA this is not likely
and would require actual aromatization to estrogenic metabolites. So, while 4-DHEA does lessen
the estrogenic side effects of DHEA, it does not eliminate them unless an aromatase inhibitor is also
applied. As with I-DHEA some manufacturers are including accessory ingredients with 4-DHEA to
increase metabolism to the desired metabolites while reducing metabolism to estrogen and DHEA.
This prohormone converts to testosterone through androstenedione and androstenediol in a two step
process.

I
AR AFFINITY:
PR AFFINITY:
II
Unknown
Unknown
I
I II I
I II I
I
SHBG
AFFINITY:
AlA RATIO:
II
Unknown
Unknown
I
I II I
AVAILABILITY: II Legally available
I I
CONVERSION I Unknown
TO ESTROGEN: I

DEHYDROEPIANDROSTERONE
(DHEA)
5-ANDROSTEN-3~-OL-17-0NE
Formula: CI9H2S02
MW: 288
DHEA is a crude prohormone that occurs naturally in the human body. DHEA is considered an
adrenal androgen because it is made in the adrenal glands instead of the testes (like testosterone and
DHT). DHEA is readily converted in the adrenal glands, liver and kidneys into DHEA Sulfate, an
inactive form of this prohorrnone. DHEA is produced in large quantities and circulates in the blood
at concentrations higher than cortisol and second only to cholesterol 339 DHEA is converted in
peripheral tissues into androstenedione and testosterone, however, DHEA only accounts for about
5% of total androgen production in the normal maiesi . I n females, DHEA is the major source of
androgen production. DHEA has also been suspected to act directly at the estrogen receptor
producing estrogenic side effects. Conversion of DHEA is not very efficient in that it must undergo
two enzymatic conversions to arrive at testosterone. For this reason, DHEA has not been considered
to be very effective or very popular for building lean mass. Some companies have begun to include
ingredients along with DHEA to channel the conversion to testosterone while reducing conversion
to estrogenic and androgenic metabolites while increasing bioavailability and prolonging half-life.
DHEA is reputed to have other effects beyond and conversion to estrogen or androgen and is very
popular among anti-aging proponents. This is likely to occur through its conversion to 7-keto and 7-
hydroy metabolites which appear to play a role in modulating the effects of cortisol in the
bodi 3 ,340 While DHEA may not be as strong as other prohormones or prosteroids currently on the
market, it is legal and taken with the proper accessory ingredients, can produce anabolism with few
side effects.

AR AFFINITY: 0.02
I II I
PR AFFINITY: 0
I II I
I
GR AFFINITY:
SHBG
II
0
Low to medium
I
I AFFINITY: II
A/A RATIO: 12/34 241
I
I II I
I I
CONVERSION I medium
TO ESTROGEN: I

a
NORDEHYDROEPIANDROSTERONE
(norDHEA)
5-ESTREN-3~-OL-17-0NE
Formula: ClsH2602
MW: 274
NorDHEA is yet another newer prohormone derivative of DHEA. The only differences with this
pro hormone is that it is demethylated at the 19 position just like nortestosterone and instead of a
double bond at the 5 position, it has a double bond at position 4. NorDhea converts to
nortestosterone through a two step conversion with norandrostenediol and norandrostenediol as
intermediate metabolites. Since nortestosterone has less conversion to estrogenic metabolites and is
5-alpha reduced to less potent metabolites, this prohormone should have less estrogenic and
androgenic side effects than DHEA. Furthermore, 19-nor steroids are more potent at the androgen
receptor and are more anabolic. As with DHEA, the inclusion of accessory ingredients can further
reduce the conversion to estrogenic and androgenic metabolites reducing side effects considerably
while also increasing the metabolism to the target hormone, nortestosterone. The only drawback is
that 19-nor steroids seem to result in pretty severe shutdown of natural testosterone production.

I II
I II
I II
SHBG Unknown
I AFFINITY: II
AlA RATIO: Unknown
I II
I
CONVERSION
TO ESTROGEN:
I Low

DIENEDIONE
(numerous)
4,9-estradiene-3,17-dione
Formula: C 1s H22 02
MW:270
Dienedione was purported by its makers to be a precursor to trenbolone. However, as you can see,
dienedione lacks a double bond in the II position. There is no process in the body that would
produce this double bond. This prohormone is actually a precursor to dienolone. It is unknown how
well this PH will convert. As a dione, it would require conversion at the C-17 position by 17 beta
hydroxysteroid dehydrogenase, which does not see to be an efficient conversion for PH's. This
being said, dienolone has a favorable anabolic to androgenic ratio with about equal anabolic activity
to testosterone but only one tenth the androgenic activity. This prohormone cannot convert to
estrogenic metabolites through aromatization but likely converts to less potent 5-alpah reduced
metabolites like other nortestosterone derivatives. Like other prohormones, dienedione has a very
short half-life and requires fairly large and frequent doses to maintain plasma levels necessary for
an anabolic effect. Also, since this prohormone is a nortestosterone derivative it likely results in
significant shutdown of natural testosterone production and since it has minimal androgenic activity
will likely result in decreased libido and may induce gynecomastia through disruption of the
estrogenic/androgenic ratio.

AR AFFINITY: 5
I II I
GR AFFINITY:
II
Unknown
I
SHBG AFFINITY:
II
Low
I
AlA RATIO:
II
?
I
AVAILABILITY:
II
Available, Legal
I
II I
CONVERSION TO None
ESTROGEN: II I

HALODROL
(none)
4-chloro-1 ,4-androstadiene-17-alpha-methyl-3, 17-diol
OH
HO
CI
Formula: C2oH29C102
MW: 337
Halodrol is a new prohonnone released after the 2004 ban. This compound is supposed to convert to
the steroid Oral Turinabol (OT) through the actions of 3-beta hydroxysteroid dehydrogenase. The
presence of the 4-chloro group partially inhibits this conversion so little OT is actually produced.
The 4-chloro group also inhibits the conversion to estrogen and results in less potent 5-alpha
reduced metabolites being produced. The rule of thumb is that diols convert at about 10-20%. I
estimate that Halodrol converts at 1 to 5%. The prohormone alone may have some small intrinsic
activity and if large enough doses are taken then one may see results similar to OT, however, since
the prohormone is methylated, such large doses would be quite toxic to the liver. This product was
originally contaminated with significant quantities of DMT but has since been cleaned up. Though
reports on this prohormone vary, most are indicating that higher doses are needed to see any
anabolic effect. Doses up to 100 mg per day are not uncommon but since this product is methylated,
higher doses increase the risk of liver toxicity. Even a dose of 100 mg per day with a ten percent
conversion would only result in a dose of 10 mg of OT being produced. For comparison, women in
the East German program of doping were taking 20 mg per day.

I
PR AFFINITY:
I Unknown
I
I
GR AFFINITY:
I Unknown
I
I
SHBG AFFINITY:
I Unknown
I
I
AlA RATIO:
I Unknown
I
I
AVAILABILITY:
I Available as a prohormone
I
I
CONVERSION TO
I none
I
I ESTROGEN: I I

MENTDIONE
(none)
7-al pha methy lestrene-3,17-d ione
Formula: Cl9H2602
MW: 286
MENT dione is another potential prohorrnone that has been discussed on the internet and may be
introduced at some point in the future. This prohormone is the dione derivative of 7-
methylnortestosterone and would convert to some degree to MENT. Much of what applies to
MENT would also apply to the prohormone. MENT does not convert to less potent 5-alpha reduced
metabolites but can convert to 7-methylestradiol. Additionally, MENT has pretty strong binding to
the progesterone receptor and causes significant shutdown of natural testosterone production. It is
known that MENT has fairly poor bioavailability but the prohormone may actually improve this
since it would be metabolized to MENT. The anabolic to androgenic ratio of MENT dione shows it
to have very high anabolic activity; almost ten times that of methyltestosterone with about fifty
percent more androgenic activity. Liver toxicity would be minimal since this prohorrnone is not C-
17 alpha alkylated. Estrogenic and androgenic side effects would still occur with MENT dione but
one would suspect that doses as low as ten milligrams may provide sufficient anabolic response.

I II
I II
I II
I II 241
AlA RATIO: 1241120,960/165
I II
AVAILABILITY: Unknown
I II
CONVERSION TO low
I ESTROGEN: II

METHYL ANDROSTANEDlOL
(none)
5a-androstan-17a-methyl-3~,17~-diol
OH
."",CH
HO
H
Formula: C 2oH 34 0 2
MW: 306
Masterdrol was a legal prohormone until the passage of the 2004 legislation. It is methylated which
makes it much more bioavailable than non-methylated prohormones. The methylation also protects
the C-17 hydroxyl from 17 BHSD converting it to a C-17-one. This prohorrnone is converted to
meslanolone and would therefore share some of the properties of that compound. Also, the
unconverted prohormone has some binding affinity of its own. This is a fairly potent prohormone.
This compound cannot convert to estrogen. Methyl-DHT does have more progesterone receptor
binding than does DHT; however, it is still relatively small. The anabolic to androgenic ratios
renect the fact that this prohormone is very androgenic with little anabolic activity. Larger doses
would be required to keep the prohormone and any methylDHT that is produced by conversion
from being deactivated in skeletal muscle. Like most DHT derivatives, this compound is used for
strength gains and to maintain sexual function when stacked with other less androgenic steroids.
Since this prohormone is C-17 alpha alkylated, there is a possibility of elevated liver enzymes that
will increase as dose increases.

AR AFFINITY: 15
I II I
PR AFFINITY: 10
I II I
GR AFFINITY: 0
I II I
SHBG AFFINITY: High
I II I
AlA RATIO: 22/72 241
I II I
AVAILABILITY: Previously available as a legal prohormone,
I I questionable now
CONVERSION TO None
I ESTROGEN: II I

MIBOLERONE DIOL
(none)
7, 17-alpha-dimethyl-estren-3~, 17~-diol
OH
", ,II CH
HO
Formula: C2oHn02
MW: 304
Mibolerone diol is another unmarketed prohormone that may come to market in the future. This
pro hormone is the diol version of the potent steroid mibolerone. Mibolerone has a reputation for
being very potent and very toxic. Since mibolerone is dosed in microgram quantities, this
prohonnone could likely be dosed as low as two or three milligrams since a conversion of 10%
would result in 200 to 300 micrograms of mibolerone. Mibolerone has very strong binding to the
androgen and progesterone receptors and this prohonnone is likely to have significant binding
affinity even without conversion. Mibolerone diol is likely to cause significant shutdown of natural
testosterone production with strong androgenic side effects. The presence of two methyl groups
makes mibolerone more likely to cause liver toxicity and this is also true for the diol prohormone.
This is mitigated somewhat by the low doses necessary to induce an effecl. Since so few people
have used legitimate mibolerone, or bolasterone for that matter, there is intense curiosity about its
effects which is probably the driving force behind the discussion of this prohormone and other
unmarketed prohormones.

I II I
I II I
I II I
I II I
AlA RATIO: Unknown
I II I
AVAILABILITY: Unknown
I II I
CONVERSION TO Unknown
I ESTROGEN: II I

NORANDROSTENEDIOL
(none)
19-nor-4-androsten-3,17-diol
HO
Formula: CIsH2s02
MW: 276
Norandrostenediol is a prohormone that is converted to nandrolone in the body. This prohormone

has a favorable anabolic to androgenic ratio, which attests to its potency. Both the prohormone and
the active metabolite (nandrolone) are converted by 5-alpha reductase to less potent dihydro
metabolites which allow for reduced androgenic side effects when taken at reasonable doses. The
negative side effects of nordiol are similar to those for nandrolone, bloating, fat accumulation, blood
pressure elevation and gynecomastia due to disruption of the estrogenic/androgenic ratio. Without
some kind of ester or ether to enhance half-life it needed to be applied frequently in either oral or
transdennal fashion. This made achieving a consistent plasma level difficult. This PH, like the dione
version was made illegal by the 2004 legislation. Nordiol seemed to be pretty potent for a
prohormone but most seemed to prefer androdiol due to the notion that the nor prohonnones would
cause gynecomastia.

AR AFFINITY: 10
I II I
PR AFFINITY: 0
I II I
GR AFFINITY: 0
I II I
SHBG AFFINITY: Low
I II I
AlA RATIO: 50/5241
I I I
AVAILABILITY: Previously available as a legal prohormone,
I I Questionable now
I ESTROGEN: II I

NORANDROSTENEDIONE
(none)
19-nor-4-androsten-3,17-dione
Formula: C1sH2402
MW: 272
Nordione is a prohormone that undergoes conversion to nandrolone through the action of the
enzyme 17 BHSD. As with most PH's, nordione has poor oral bioavailability and a very short half-
life necessitating high doses to be taken frequently. The use of this prohormone could result in a
positive test or nandrolone. Norandrostenedione is now illegal, but most people didn't think it to be
worthwhile. Many considered it to be very estrogenic, but the evidence would suggest that it is less
so than androstenedione or androstenediol. Used in high doses, this PH seemed to deliver more
than either androstenedione or androstenediol. It is interesting to note that nordione has more
androgenic activity than the diol version. The first generation prohonnones like nordiol, nord ion
androstenediol and androstenedione were often used in very high amounts (approaching one gram
per day in divided doses) in order to see an effect. These high doses often produced unwanted side
effects such as gynecomastia, hair loss, acne and prostate enlargement.

AR AFFINITY: 5
I II I
PR AFFINITY: 0
I II I
GR AFFINITY: 0
I
SHBG AFFINITY:
II
Low
I
I II I
AlA RATIO: 58/45,37/55
I II I
AVAILABILITY: IPreviously available as a legal prohormone, now
I iIIee:al
I ESTROGEN: II I

11-0XOANDROSTENEDIONE
(adrenosterone)
3, II, 17-androstenetrione
o
o
Formula: Cl9H240j
MW: 300
Adrenosterone is a relatively new pro hormone that does not fall under the 2004 legislation. This
prohorrnone is the I I-keto substituted version of androstenedione. There is not much data on this
prohormone but it is produced naturally in humans. Presumably, some portion is converted to 11-
ketotestosterone which has some degree of androgen receptor binding. Another proposed
mechanism of action for this prohormone is the inhibition of II-bela hydroxysteroid dehydrogenase
type I. Adrenosterone inhibits this enzyme selectively over the type 2 enzyme and prevents the
conversion of inactive cortisol metabolites to active cortisol. This results in an anticatabolic activity
and supposedly makes this prohormone effective in a cuning stack. Anecdotal reports show this
pro hormone to be very mild with higher doses needed to elicit a response. The anabolic to
androgenic ratio for this prohormone bears this out. One test shows it to have 70% of the anabolic
activity of testosterone with half of the androgenic activity while another study shows it to have
only 10% of the anabolic activity.

241
AlA RATIO: 70/48, 10/7
AVAILABILITY: Available as a prohormone

ESTROGEN:

ANABOLlCPHARMACOLOGY 278
ANCILLARY MEDICAnONS
The following are medications, which are used before, during or after a steroid cycle to increase the
potency ofa cycle while alleviating side effects.

AROMATASE INHIBITORS

AMINOGLUTETHIMIDE
(Cytadren@, Elipten, Orimeten)
3-(4-am inopheny1)-3-ethy1-2,6-piperid ined ione
H
o N o
NH
Formula: C I 3H J 6N 202
MW:232
Aminoglutethimide inhibits several enzymes that are responsible for steroid synthesis including
aromatase. It has been used to not only inhibit estrogen production but also to lower cortisol levels.
Clinically it has been used to treat breast cancer in doses of 500-1000 mg/day along with
hydrocortisone 20 mg twice per day to replace glucocorticoid levels 5J . This is to prevent cortisol
levels from dropping too low (acute adrenal insufficiency), or to prevent a rise in ACTH that might
overcome the inhibition. This drug has also been used to treat Cushing's syndrome which is a state
341
of cortisol excess . Along with inhibiting cortisol synthesis and aromatase, aminoglutethimide has
342
also been shown to disrupt thyroid function Aminoglutethimide is a very potent inhibitor of
aromatase, offering up to 90% inhibition. However, it is also very effective at suppressing cortisol
levels and therefore its use can be dangerous. Some steroid users will use Cytadren without
knowing about its suppressive effects on cortisol. Since some steroids also suppress cortisol
production, this effect may go unnoticed but once aminoglutethimide is stopped, the user may
experience significant side effects due to acute adrenal insufficiency.
Classification: Aromatase Inhibitor, Steroidogenesis Inhibitor

LETROZOLE
(Femara)
4,4'-( I H-I ,2,4-triazol-l-ylmethylene)dibenzonitrile
o N
N==
Formula: C l7 H lI N s
MW:285
Letrozole is a non-steroidal competitive inhibitor of aromatase. Unlike the steroidal suicide

inhibitors letrozole does not reduce levels ofaromatase in the body. It is the most potent inhibitor of
aromatase and results in 90-100% inhibition of estrogen formation 343 ,344. It takes about 2 to 3 days
to reach maximal inhibition, but may take as much as 2 months to reach steady state levels in the
45 344
bodl Letrozole has also been shown to suppress cortisol and aldosterone levels Suppression
of cortisol can be a positive thing both on and off-cycle; however, one must realize that there is a
significant rebound effect which can result in higher cortisol levels following letrozole therapy. It is
well known that the use of an aromatase inhibitor can reduce HDL cholesterol levels and it is
suspected that reduction of estrogen through the use of aromatase inhibitors can result in a
compensatory mechanism that may increase sensitivity to eSlrogen 346. Though this mechanism has
not yet been determined it may be increased aromatase or estrogen receptor expression or
something else entirely347 Aromatase inhibitors have gained in popularity in recent years among
steroid users because of the mistaken belief that the lower the estrogen the better. As stated earlier
in this text, estrogen plays important roles in male physiology and too much suppression can result
in side effects.
Classification: Aromatase Inhibitor

6-KETO ANDROSTENEDIONE
(numerous)
4-androsten-3,6,17-trione
Formula: C19H2403
MW: 300
6-Keto Androstenedione (6KAD) is a suicidal aromatase inhibitor. Like formestane and

348
exemestane, it binds irreversibly to aromatase, which terminally inactivates the enzyme . 6KAD
was brought to market as a legal testosterone booster and is used quite extensively as post-cycle
therapy by those who want a legal anti-aromatase product. 6KAD has about a 15 fold lower Ki than
349
formestane which means that a much higher dose is needed to get the same level of inhibition ,35o,
In a study funded by the manufacturer, significant increases in free and total testosterone as well as
DHT were seen with 3 weeks of an unspecified dose of 6KAD. However, while there was a trend
towards reduced estradiol levels, one would expect that an effective aromatase inhibitor would
significantly reduce estradiol levels. There was also a rather large increase in estrone levels. 6KAD
is converted to 6-oxoestradiol and 6-oxoestrone, and although the estrogenicity of these compounds
is unknown, it would seem that this increase in estrogen levels might interfere in the hypogonadal
state following prohormone or steroid use.

1,4,6 ANDROSTATRlENE-DIONE
(numerous)
androsta-I ,4,6-triene-3, 17-dione
Formula: C19H2202
MW: 282
Androstatrienedione is a legal supplement marketed as an aromatase inhibitor. Although weaker

than nonsteroidal, pharmaceutical inhibitors, this AI is a suicidal inhibitor, which means that it
inactivates the aromatase enzyme349,351 This AI was rumored to produce very large increases in
natural testosterone production however; the metabolites of 1,4,6 interfere with the testosterone
assay producing falsely high readings 352 In actuality, this AI is probably about as potent as 6-oxo,
which is not that potent at all. In addition since 1,4,6 is a suicidal aromatase inhibitor, it is likely
that the body will either increase its production of aromatase, the estrogen receptor, or both.
Furthermore, while it is claimed that 1,4,6 does not convert to an androgenic metabolite, it does in
fact convert to 1,4,6 testosterone which has about one third the activity of testosterone.

FORMESTANE
(Lentaron@)
4-Hydroxyandrost-4-ene-3,17-dione
HO
Formula: CI9H2603
MW:302
Formestane is a suicidal aromatase inhibitor. Formestane competes with testosterone and other
substrates at the bindin site of aromatase. It then forms metabolites, which bind to the aromatase
molecule irreversibl/ 5 . This inactivates the aromatase molecule completely. Aromatase activity
levels will stay low even when formestane use has been stopped as it takes time for the levels of
aromatase to be built back up. Formestane has been shown to inhibit estrogen formation by about
50%354. Formestane can convert to 4-hydroxytestosterone in the bod/ 55 Although this conversion
can occur, it most likely occurs only in very small amounts. Furthermore, hydroxytestosterone is a
weaker androgen than testosterone and therefore will have less of a suppressive effect on the
HPGA. Also, formestane and 4-0HT have inhibitory effects on 5-alpha reductase, which will
reduce the levels of DHT in the body356. Formestane has been shown to decrease sex-hormone
binding globulin levels when given ora II/ 53 This can cause a temporary increase in free estrogen
levels when use of formestane has just begun. For this reason, it is advisable to use an estrogen
receptor antagonist in conjunction with formestane (and probably with other aromatase inhibitors as
well). Since formestane does not inhibit aromatase that strongly, there is less chance of side effects
since estrogen levels are not reduced too severely.

EXEMESTANE
(Aromasin~
6-Methyleneandrosta-l ,4-dien-3, 17-dione
Formula: C2oH2402
MW: 296
Exemestane is suicidal aromatase inhibitor. Exemestane takes up to 7 days to reach maximal

357
inhibition of aromatase . Maximal suppression with exemestane only reaches about 60-70% for
J57
estradiol and estrone though another paper shows near 100% inhibition of estrone production J58
Exemestane has been associated with androgenic and progestational side effects, which bring its
usefulness for post-cycle therapy into question. Not many athletes use exemestane as an aromatase
inhibitor. A dose of 25 mg resulted in an increase in testosterone levels of 60% in healthy young
males 359 . As stated, it is probably not the best choice for post-cycle therapy but is used as on-cycle
therapy to keep estrogen levels low. As with other aromatase inhibitors, exemestane will alter lipid
profiles and may result in compensatory upregulation of sensitivity to estrogen especially when
using higher doses.

ANASTROZOLE
(Arimidex)
I,3-Benzenediacetonitrile, (alpha), (alpha), (alpha)', (alpha)'-tetramethyl-5-( I H-I ,2,4-triazol-l-
ylmethyl)
Formula: C17HI9N5
MW: 293
Arimidex is an aromatase inhibitor that prevents steroids that are prone to aromatization from
converting to estrogen. Unlike suicidal inhibitors, arimidex does not reduce the level of aromatase
enzyme in the body. It can take up to four days to reach maximal suppression of estrogen levels
with this drug 357 . Suppression of estrogen production up to 90% has been reported with arimidex357
The potency of this aromatase inhibitor is apparent in the fact that it is taken in such a low dose.
AAS users take aromatase inhibitors to try to prevent the rise in estrogen when using aromatizable
steroids, primarily to prevent gynecomastia. Arimidex has been shown to reduce breast tenderness
associated with gynecomastia without reducing the size of the tissue 360 Unlike other aromatase
inhibitors, arimidex has been shown to not alter lipid profiles or to affect adrenal steroid
synthesis J57 Many of the name brand aromatase inhibitors are sold on the gray market over the
internet through "research" companies and are sold in either pill, powder or liquid form but the
quality of these items is not assured.

G G52
ADRENERGIC AGONISTS

CLENBUTEROL
(Spiropent, Ventopulmin, Broncodil, Broncoterol, Cesbron, Contrasmina, Contraspasmina,
Monores, Novegam, Prontovent,)
4-amino-3,S-dichloro-alpha-[[( I, l-dimethylethy I)amino]methyl]benzenemethanol
CI
OH
CI
Formula: Cl2H1SCI2N20
MW: 314
Clenbuterol is sometimes referred to as a steroid by the media. By looking at the structure, you can
clearly see that it is not a steroid. It is, in fact, a beta-adrenergic agonist very similar to epinephrine.
Clenbuterol is used by athletes for several purposes. The primary purpose is as a stimulant and
weight loss agent but secondarily it is also believed to be anabolic. Clenbuterol has been shown to
be anabolic in animals and to cause muscle fiber type switching from slow to fasr3 61 ,362,363. There is
some evidence from animal studies that this anabolic response is at least partly mediated through
increased muscle content oflGF_I J64 For this reason, it has been used as a feed additive to increase
bulk of farm animals used for meat. Most people do not report anabolic effects from clenbuterol but
this is likely due either to the much lower doses used in humans compared to animals or to
comparison of results to those obtained from steroids. Clenbuterol does not cause bloating and will
increase metabolic rate causing fat to be burned 36s This results in a lower scale weight and since
most people equate scale weight to gains, they do not consider c1enbuterol to be anabolic. One
problem with the use of c1enbuterol is that beta-adrenergic receptors adjust quickly. For this reason,
most cycle the use of c1enbuterol in a two-week on, two-week off cycle. Some have advocated
using c1en on a 2 week on 2 week off cycle, but as the half-life of c1en is rather long (about 36
hours) this cycle is probably not going to prevent receptor downgrade. Side effects are similar to
other stimulants including rapid heartbeat, increased body temperature, nervousness, tremor,
headache, perspiration, nausea and insomnia366,367 A particularly disturbing side effect is that
clenbuterol has been shown in the scientific literature to cause enlargement of the heart368 . Some
have suggested that using clenbuterol between AAS cycles could help retain muscle mass by
increasing androgen and thyroid receptor levels in skeletal muscles.
Classification: Beta Adrenergic Agonist

FENOTEROL
(none)
4-( l-hydroxy-2-{[2-(4-hydroxyphenyl)-I-methylethyl]amino}ethyl)benzene-I ,2-diol
HO
NH
HO
Formula: CI7H21 NO 4
MW: 303
Fenoterol is a beta-adrenergic agonist similar to c1enbuterol. In the literature, fenoterol has been
shown to have greater anabolic effect than c1enbuterol J69 Since most people do not notice much of
an anabolic effect with clenbuterol, it is unclear is any anabolic effect would be noticed with
fenoterol. Even though fenoterol has been shown to have anabolic effects, like clenbuterol, these
effects will not be comBarable 10 those of AAS. Fenolerol would have similar effects to clenbuterol
with regard to fat 10ssJ 2 Fenoterol was removed from the market in the US due to the potential for
overdose. The use of beta agonists for weight loss is quite common. This is due to the fact that they
increase thermogenesis, increase fat burning and stimulate the C S. The down side is the cardiac
risk that is common to this class of medications. Increased heart rate blood pre sure, and direct
effects on cardiac contractility as well as potential heart enlargement are potentially dangerous side
effects; particularly when combined with androgens.

ALBUTEROL
(numerous)
Alpha 1-[[( 1, I-Dimethylethyl)amino]methyl]-4-hydroxy-1 ,3-benzenedimethanol
OH
HQ--{
OH
Formula: C13 H21 NO 3

MW: 239
Albuterol is yet another selective beta-2 agonist that athletes use as a stimulant and to burn fat 370 .
Albuterol has been shown to have androgenic activity but is quite 10w371 . A study in Parkinson's
patients with 4 mg of albuterol sulfate given orally four times a day for 14 weeks showed a 10%
372
increase in fat free mass suggesting that albuterol has anabolic effects in humans Athletes only
use the oral forms of beta-2 agonists since the inhaled forms do not seem to offer the same benefits.
As with all bet agonists, there is concern with side effects such as tremor, nervousness, increased
heart rate, sweating nausea and others. Chronic use of beta-2 agonists results in desensitization and
loss of effect. Some have attempted to use the histamine antagonist, ketotifen to prevent the
desensitization since there is some evidence in the literature of this effect373 Some have suggested
that Benadryl may also have this effect since it is also a histamine antagonist and while this may be
so, there is no evidence in the literature. In addition to Clenbuterol, Fenoterol and Albuterol, there
are other long acting beta agonists such as Formoterol and Salmeterol among others that may be
substituted based on price and availability.

EPHEDRINE
(numerous)
Alpha-[ I-(Methylamino]ethyl]- benzene-methanol
CH
/
NH
Formula: CloHISNO
MW: 165
Ephedrine is a naturally occurring alkaloid from plants of the genus Ephedra. It can also be made
synthetically. Ephedrine is used as a stimulant and fat loss aid. Unlike the beta-2 agonists, ephedrine
is not specific for any subtype of adrenergic receptor and stimulates several subtypes. Ephedrine has
been the subject of much attention because it can be used to manufacture methamphetamine and
there were a few deaths surrounding its use as a party drug. While there are side effects similar to
those discussed for the beta-2 agonists, the risk is greatly enhanced when used with other stimulants
and/or alcohol. The legality of ephedrine is now a complicated issue and while it is available over
the counter, the ephedrine content is controlled and the sale is monitored to prevent diversion to
methamphetamine manufacture.
Classification: Adrenergic Agonist

SELECTIVE ESTROGEN RECEPTOR MODULATORS
(SERMS)

CLOMIPHENE
(Clomid, Milophene, Serophene)
2-[4-(2-Ch loro-I ,2-di phenyletheny I) phenoxy]-N,N-diethylethanamine
~CH
o----.lNH
CI
Formula: C26H28CINO
MW: 406
Clomid is selective estrogen receptor modulator. This means that it binds to the estrogen receptors
but selectively activates certain responses while not activating others. Clomid is used to maintain
and/or restart testicular function during and after a steroid cycle 374 ,375 Clomid seems to be much
more effective than HCG; however, most people use c10mid in too high a dose which can result in
estrogenic stimulation. Clomid, if used at too high a dose and for too long, will actually shut down
testicular production of testosterone because it will activate the estrogen receptor to a greater
degree. A common dose of clomid is 100 mg per day in a single dose while 50 mg twice per day or
even once per day usually works just as well with less chance of side effects. Some have even seen
positive results with only 25 mg once or twice per day. Some have had success with a five day
course of 100 mg while others prefer a longer course of treatment with 50 mg per d ay 376 There is
even some evidence that 50 mg every other day for three days per week for 8 weeks will raise
377
testosterone and LH levels Clomiphene has been known to cause blurred vision, dizziness and
headaches and is also toxic to the liver to a small degree.
Classification: Selective Estrogen Receptor Modulator

TAMOXIFEN
(Nolvadex, Tamofen, Apo-Tamox, Tamone)
2-[4-( I,2-Diphenyl-l-butenyl)phenoxy]-N,N-dimethylethanamine
~CH
O~NH
Formula: C26 H29NO

MW: 372
Tamoxifen is a selective estrogen receptor modulator similar to clomiphene. Many steroid users will
use tamoxifen to block the effect of estrogen at the estrogen receptors. Tamoxifen has also been
shown to increase the levels ofSHBG in the blood 378 This is generally considered to be a bad thing
by steroid users because it is believed that high SHBG will reduce the effectiveness of a stack by
reducing circulating AAS levels. In reality, strong androgens cause a decrease in SHBG levels that
can result in higher circulating free estradiol and estrone levels in addition to free androgens which
can contribute to the formation of gynecomastia. Additionally, many AAS have little binding to
SHBG and circulate largely in the free-state or bound to albumin. It may therefore be advantageous
to increase SHBG levels to help sequester circulating estrogens. As stated in the side effects section
under gynecomastia, SHBG has been shown to have a protective role against estrogen induced
proliferation in the breast 125,135.136,137,138,139, Though there is little evidence showing tamoxifen to be
effective in preventing gynecomastia, there is considerable evidence that tamoxifen can be used to
shrink breast tissue, particularly when it is of the lump variety as opposed to the fatty
type 379,380,381,J82, More so than with clomiphene, the problem with tamoxifen is that most people
think that more is better and use too high of a dose, Doses as low as 10 mg per day have been
shown to be effective for the treatment of gynecomastia while some will use five or ten times this
amount382 Higher doses of tamoxifen may result in stimulation of estrogen receptors producing the
opposite effect to what is desired especial ~ when endogenous estrogen levels have been driven to
very low levels with aromatase inhbiitors 3 Tamoxifen has been shown in the literature to have
similar effects to clomiphene for increasing LH and testosterone levels37 S, While most aromatase
inhibitors have been shown to decrease HDL levels, tamoxifen has been shown in some cases to
increase it.

RALOXIFENE
(Evista)
[6-hydroxy-2-(4-hydroxypheny I)benzo[b]thien-3-yl][4-[2-( I-piperidiny I)ethoxy]phenyl]-,
hydrochloride
OH
HO
O~O
Formula: C2sH27N04S
MW: 474
Raloxifene is the next-generation of selective estrogen receptor modulators. Raloxifene, like other
SERMs, acts as an estrogen receptor agonist in some tissues but as an antagonist (or partial agonist)
in others384 . Raloxifene is used in post-menopausal women to help prevent osteoporosis since it is
an active estrogen in bone. It is also an agonist with regard to its ability to lower LDL and total
cholesterol levels. Raloxifene acts as an antagonist in breast and uterine tissues. Raloxifene is newer
so it has not been used much for this purpose in men. Unlike tamoxifen, raloxifene is not available
in generic form which makes it more expensive. Studies have shown raloxifene to be better than
tamoxifen in treatment of gynecomastia with a greater response rate and degree of response380
Raloxifene has also been shown to increase LH, FSH, SHBG and total and free testosterone in
males 385 Even though raloxifene appears to be a better choice than tamoxifen, it is unlikely that its
use will increase until it is available as a generic. Tamoxifen and clomid may not be as good, but
they are cheap and readily available. There has been some talk of estrogen antagonists reducing
IGF-I and the effect that this could have on skeletal muscle hypertrophy. Aromatase inhibitors have
been shown to increase IGF-I levels 386 ,38J SERMS on the other hand have been shown to decrease
IGF-I levels. The fact is, serum IGF-I levels do not have any correlation with muscle growth but
rather, it is the release of IGF-I within the muscle that has an anabolic effect. Increasing circulating
IGF-I levels may actually be detrimental and promote tumor growth 388 As discussed later, the IGF-
I system is very complex with multiple binding proteins that modulate its actions so simply
elevating circulating levels doesn't mean much in and of itself.

TOREMIFENE
(Fareston~
2-[4-(4-chloro-1 ,2-diphenyl-but-l-enyl)phenoxy]-N,N-dimethyl-ethanamine
CI
Formula: C26H28CINO
MW: 406
Toremifene is one of the newer SERMs to come to market in the past ten years. Toremifene has
been shown to increase LH, SHBG and testosterone in men in a similar manner to tamoxifen 389,390
This SERM is also in clinical trials to prevent the progression of prostate cancer391 . Many of the
things that were said about tamoxifen would apply to toremifene as they seem to perform in very
similar manners. Toremifene seems to perform better than tamoxifen with regard to elevation of
HDL and reduction oftriglycerides 392 . There have not been any studies done with toremifene with
regard to gynecomastia as yet. Because this is a newer drug that is still under patent, it tends to be
much more expensive than generic tamoxifen.

ORMELOXIFENE
(Centchroman)
trans-I-[2-{ 4-(7-methoxy-2,2-dimethy1-3-pheny1-3,4-dihydro-2H-
l-benzopyran-4-y I)-phenoxy }-ethyl]-pyrrolidine hydrochloride
o
o
Formula: C30H3SN03
MW:457
Ormeloxifene is a very interesting SERM that not available by prescription in the US. It is sold
under the trade names Centron and Sehali in India. It is rumored to be a very effective birth control
agent and many women are buying it through online pharmacies for use in this purpose.
Ormeloxifene is a very potent anta~onist in breast tissue with a very long half-life which
necessitates dosing only twice a week 3,394 Ormeloxifene is also active in bone and is effective in
lowering cholesterol levels. Unlike tamoxifen, centchroman has no partial agonist activity in breast
or hypothalamus. Furthermore, this SERM has been shown to increase LH in normal males 395
Ormeloxifene has been around for quite some time but has not undergone extensive testing. On
paper it seems to have clear advantages over tamoxifen but since it is not readily available, it is
unknown for now ifit will live up to its reputation.

FULVESTRANT
(Faslodex~
7-alpha-[9-(4,4,5,5,5-penta tl uoropentylsul ph iny I)
nonyl]estra-I ,3,5-( I 0)- triene-3, 17-beta-diol
HO
Formula: C32 H47F s03S

MW: 607
Fulvestrant is a new estrogen antagonist, which has no agonist activi~ and actually down-regulates
the level of estrogen receptor alpha and progesterone receptors 39 .397. It has been shown that
ERalpha is the primary receptor in the pituitary responsible for negative feedback inhibition of LH
secretion. Fulvestrant has been shown to increase LH and testosterone secretion in rodents but this
effect has not yet been tested in human males. Fulvestrant is in injectable that is administered
intramuscularly at a dose of 250 mg once per month. It is used clinically for the treatment of breast
cancer. It is reasonable to assume that fulvestrant would be very effective in preventing or treating
gynecomastia, however, it has not been clinically tested for this purpose. There are serious potential
down-sides to downregulating estrogen receptor levels since estrogens are important for bone health
as well as for keeping cholesterol levels low. Another potential negative for the use of fulvestrant in
males is a paper showing that fulvestrant also downregulates androgen receptor in the prostate 398 .
While this could be good for those with prostate cancer, it may result in reduced libido and leaves
open the question of what effect fulvestrant has on androgen receptor in skeletal muscle.
Classification: Antiestrogen/Estrogen Receptor Downregulator

=
5-ALPHA REDUCTASE INHIBITORS

FINASTERIDE
(propecia, Proscar'"')
N-( I, I-Dimethylethyl)-3-oxo-4-aza-5a-androstane-l-ene-1713_amide
o N
H
H
Formula: C23H36N202
MW: 373
Finasteride is a 5-alpha reductase inhibitor. This prevents steroids that can be converted to DHT
from doing so. As discussed earlier, DHT causes baldness, prostate enlargement and under normal
circumstances does not contribute to skeletal muscle growth. If a steroid is converted to DHT at a
rate of 20%, that means there is 20% less steroid working to increase muscle growth. Therefore,
finasteride is very useful not only in decreasing hair loss and prostate growth, but may also increase
the effectiveness of a stack that contains steroids that convert to DHT. Most AAS users believe that
adding finasteride will decrease the effectiveness of the stack. In fact, several papers have shown
that finasteride does not reduce the anabolic effect of testosterone when co-administered to
animals 3994OO Since DHT is deactivated in skeletal muscle before it can act, it makes sense that
inhibiting conversion to DHT would not reduce anabolism. Reducing conversion to DHT will
reduce the increase in aggressiveness and some of the strength gains of a cycle but the effect on
anabolism should be minimal. As discussed previously, DHT is partly responsible for feedback
inhibition of natural testosterone production. The use of finasteride can help to reduce shutdown and
to increase testosterone levels40I . Reducing DHT levels too low can result in a loss of libido and
may result in gynecomastia from offsetting the estrogen/androgen ratio.
Classification: 5-alpha Reductase Inhibitor

OUTASTERlOE
(Duagen, Avodart'") .
(5a, 17~)- -{2,5 bis(triOuoromethyl) phenyl}-3-oxo-4-azaandrost-l-ene-17-carboxamlde
F
F
F
NH
~ F
CH 3
F F
~
o N
H -
H
Formula: C27H30F6N202
MW: 528
DUlasteride is a next-generation 5-alpha reductase inhibitor. While finasteride is a selective inhibitor

402
of 5-alpha reductase type 2, dutasteride inhibits both type I and type 2 . This results in a much
greater effectiveness in reducing DHT and therefore a greater therapeutic benefit in BPH, prostate
cancer and male pattern baldness. While finasteride reduces DHT by about 70%, a dose of only 0.5
mg of dUlasteride suppresses DHT by about 95%403 While finasteride is capable of increasing
testosterone levels slightly due to reduction in androgenic feedback inhibition of LH secretion.
dutasteride is more effective in this regard 40J . Dutasteride has been shown to be 30% more effective
than finasleride for regrowing hair404 The down side is that reducing DHT levels too far can result
in sexual dysfunction and gynecomastia. Dutasteride has been used by athletes, but even though it is
more effective, it is also much more expensive so most opt for generic finasteride instead.
Classification: 5-alpha Reductase Inhibitor

SAW PALMETTO
Saw Palmetto is a natural product that has been used for the treatment of benign prostate
hypertrophy. The berries of the saw palmetto plant contain high concentrations of beta sitosterol as
well as other sterols and a good amount of fatty acids. Beta sitosterol has been shown to act as a 5-
alpha reductase inhibitor and this is one of the mechanisms through which saw palmetto works. The
fatty acid component also appears to ~Ia~ a role in S-alpha reductase inhibition with gamma linoleic
acid having the most potent effect4 5.4 . The use of saw palmetto in clinical trials has shown
convincing evidence of a moderate effect in reducing DHT and prostate size with a better side effect
profile than finasteride405.4o7. Saw palmetto has also been shown to have a positive effect on hair
loss406.
Classification: S-alpha Reductase Inhibitor

STINGING NETTLE
Stinging nettle has been used as a natural treatment for benign prostate hypertrophy. Some people
erroneously believe that stinging nettle inhibits 5-alpha reductase. It was recently found that
components of stinging nettle not only bind to SHBG but also interfere with the binding of SHBG
to its membrane receptor408,409 There is some evidence that the binding of SHBG to its membrane
receptor plays a role in prostate hypertrophy and prostate cancer. Stinging nettle has been shown to
shrink the prostate 41 0.41 . This herb has also been shown to inhibit the aromatase enzyme412 It is
unclear what effect nettle would have in the breast with this combined effect of aromatase inhibition
and blockade ofSHBG at its cell surface receptor since SHBG has been shown to have an inhibitory
effect on estrogen proliferation in the breast.
Classification: SHBG Binder

GONADOTROPINS

HCG
(human chorionic gonadotropin, Pregnyl, Chorex, ovarel, Profasi)
237 amino acid structure consisting of two subunits (A and B)
HCG is a dru" that is almost identical to luteinizing hormone and is used to stimulate the testes to
produce testo~erone. HCG is prescribed for low testosterone in doses of 1000 to 4000 i.u. injected
intramuscularly once or twice per week. HCG is sometimes given in combination with
Urofollitropin a synthetic version of follicle stimulating hormone, to help induce sperm
production 13,414. Steroid users will sometimes use HCG as replacement for LH as levels of this
hormone drop during a cycle. This is proposed to help to keep normal testosterone production as
well as normal testicular size. There is evidence in the literature that HCG will help to maintain
spermatogenesis during the use of AAS but little evidence that normal testosterone secretion will be
maintained415.416 Users mistakenly associate testicular size with testosterone production when it is
more likely an indicator of functional spermatogenesis. HCG is also used as post-cycle therapy to
try to restart testosterone production following a cycle. There are many different dosing regimens
used for this purpose. Aside from the above regimen, which is the usual way in which HCG is
prescribed by physicians, athletes will sometimes use 1000-2000 i.u. once per week for three
weeks,. Another option is to use 3000 i.u. initially, 3000 i.u. 5 days later, and then 1500 i.u. for two
injections 5 days apart. The problem is, since HCG is nearly identical to LH, it can also be
suppressive. Therefore, some have seen beller results trom using smaller doses (500 i.u.) every five
days and still others choose to either decrease dose over time or increase the time between doses to
try to trick the body into producing more normal levels of LH. A recent study demonstrated that low
doses of HCG (250 to 500 IU) given every other day could maintain intratesticular testosterone at
normal levels which is required for normal testicular function 417 .
Classification: LI-I Mimetic

LIVER PROTECTANTS

=
L1V52
Liv52 is a proprietary blend of seven herbs: capers, chicory, black nightshade, arjuna, Negro coffee,
yarrow and tamarisk. This product has been used since 1955 when it was first introduced as a liver
tonic. It acts as a potent antioxidant and has been shown to reduce ALT levels induced by toxins.
Liv52 has been approved as a drug in at least one country and has been popular in the past with
steroid users although milk thistle seems to be more popular now. There are conflicting studies
418
showing Liv52 to be effective or ineffective at protecting the liver against various insults .419
Most of these studies deal with damage induced by ethanol and there are no studies on the effects of
Liv52 when taken in combination with alkylated anabolic steroids. While the evidence may be
inconclusive it is generally accepted that Liv52 may offer some protective effect to the liver and
likely will not cause any detrimental effect.

MILK THISTLE
(Silybum Marianum)
Milk thistle is an herb that is used to help combat liver toxicity associated with the use of oral PH's
and steroids. Milk thistle contains a component called silymarin which has been shown in the
scientific literature to have therapeutic effects on treating several types of liver damage including
cirrhosis, hepatitis and fatty infiltration of the liver. Silymarin has also been shown to protect
against toxic chemicals including alcohol, acetaminophen and carbon tetrachloride42o Milk thistle
helps to stimulate production of new liver cells to replace damaged ones. The standard dosage of
milk thistle extract based on 70 - 80 percent silymarin content is from 70-210 milligrams three
times daily, most steroid users will take doses between 500mg-lOOOmg divided into equal doses
twice daily. While both Liv52 and Milk thistle are both considered to be safe, there seems to be
stronger clinical evidence for the hepatoprotective effective of Milk thistle although there is no
direct evidence of any protective effect when combined with alkylated AAS.
Classification: Liver Protectant
L 309 ANABOLIC PHARMACOLOGY

ANTI-ACNE

ACCUTANE
(Isotretinoin)
13-cis-retinoic acid
Formula: C2oH 2S 0 2
MW: 300
Accutane is an isomer of retinoic acid, which inhibits sebaceous gland function. It is prescribed in
cases of severe acne, which do not respond to other first-line treatments (antibiotics, retin-a cream).
Steroid using athletes use Accutane to combat oily skin and acne that androgens produce. Accutane
is a very harsh drug with the potential for serious side effects including: liver toxicity, inflammatory
bowel disease, increased triglyceride levels, decreased HDL levels, dry skin, dry mouth, depression
. .
' ,.t21.424
thoughts421422 , ,425 ,4 -6 . For acne, treatment With
.
1
and sUIcidal Accutane sounds worse than the
disease. There are several better options such as retin-A cream and antibiotics and of course
decreasing the dose of the offending steroids. Women who are pregnant or may become pregnant
should never use Accutane since it can cause severe birth defects. The psychological and hepatic
effects of Accutane are particularly dangerous in the context of AAS use since they are also often
associated with behavioral changes and hepatotoxicity.
Classification: Antiacne

RETIN-A
(Avila, Renova, Relisol-A, Stieva-A, Stieva-A Forte, Yitinoin, Relirides)
Retin-A is a vitamin A derivative, which is applied topically as a cream or gel to reduce acne. Thus
drug is available in several strengths to address varying degrees of acne. Retin-A is much safer than
accutane but does have some side effects including greater sensitivity to sunlight and redness,
blistered or crusting skin. Some have noticed that Retin-A causes a temporary worsening of acne,
however, if treatment is continued, the acne usually subsides. Unfortunately, some find applying a
cream to be bothersome so instead lhey resort to the easier oral remedy, Accutane. Accutane has
serious side-effects which should not be taken lightly and for milder cases of acne, retin-A is
preferred.

DIURETICS

EPLERENONE
(Inspra)
Pregn-4-ene-7,21-dicarboxy Iic acid, 9, I l-epoxy-17 -hydroxy-3-oxo-;y-lactone, methy I ester
(7,11,17-alpha)
,,
'0
.' \\
Formula: C24HJ006
MW:414
Eplerenone is a next-generation mineralocorticoid antagonist427 ,428 Like spironolactone it acts as a

diuretic and hel~s to ftrevent mineralocorticoid-induced cardiovascular damage and reduces high
blood pressure U ,430,4 I, Like spironolactone, eplerenone can cause a dangerous build-up of
potassium in the blood (called hyperkalemia) so extreme care must be taken when using these
drugs, Unlike spironolactone, eplerenone has no antagonist activity at the androgen receptor so it is
unlikely to cause gynecomastia, Eplerenone is virtually unknown in the steroid using public because
it is very new and is not available in generic (orm, Epleronone has distinct advantages over
spironolactone but like other brand name only medications, is much more expensive than the readily
available generic versions of spironolactone, The inhibition of II-beta hydroxylase by certain AAS
results in elevated levels of deoxycorticosterone in the blood, Deoxycorticosterone is a
mineralocorticoid and will result in sodium and water retention, high blood pressure and adverse
cardiovascular effects, Employing a mineralocorticoid antagonist could, theoretically, reduce these
side effects of those AAS that inhibit II-beta hydroxylase, The largest concern in doing so would
be the potential for hyperkalemia with the use of antimineralocorticoids since some AAS have been
reported to cause potassium retention as well.
Classi fication: Diuretic/Antimineralocorticoid

SPIRONOLACTONE
(Aldactone)
7-(Acetylthio)-17-hydroxy-3-oxo-pregn-4-ene-21-carboxylic acid y-lactone
Formula: C24H3204S
MW:417
Spironolactone is a mineralocorticoid receptor antagonist. This causes spironolactone to act as a

mild diuretic. It is also used in topical form to help combat male pattern baldness because it also has
some degree of antagonism at the androgen receptor. Many bodybuilders use diuretics such as lasix
to help shed water for competitions. Lasix, however, is very harsh and can lead to serious health
problems as witnessed in recent years as some bodybuilders have collapsed on stage and a few have
even died from diuretic use. Spironolactone is a gentler diuretic that gets to the root cause of much
of the water retention brought on by steroid use. Unfortunately, the anti-androgenic activity makes
its use somewhat of a liability to the steroid-using athlete. Spironolactone will help to excrete some
of the excess water from a cycle, which will result in lowered blood pressure. While potassium may
need to be replaced while using lasix, it should never be given with spironolactone. Spironolactone
will also help to prevent the negative cardiovascular effects of AAS by antagonizing excessive
mineralocorticoid stimulation. As explained under eplerenone, some AAS have been reported to
cause potassium retention so combination with an antimineralocorticoid may be ill advised since
elevated blood potassium can cause a fatal heart attack432
Classification: Diretic/Antimineralocorticoid

HYDROCHLOROTHIAZIDE
(Dyazide~ . ' .
6-Chloro-3,4-dihydro-2H-1 ,2,4-benzolhiadiazine-7-sulfonalnlde I, I-dioxide
HO OH
,,/
H2 NS02 s
~ ........ NH
I ~ N)
CI
H
Formula: C7HgCINJ04S2
MW: 298
Hydrochlorothiazide is a diuretic and antihypertensive. It has a different mechanism than

spironolactone and furosemide and is considered to be much safer and gentler than furosemide.
HCT can potentially cause low potassium levels so supplementation may become necessary. Steroid
using athletes will use HCT to reduce bloat and high blood pressure brought on by a cycle. The use
of diuretics by bodybuilders to shed water for competitions and by other athletes who compete in
weight classes, particularly when limiting water intake is a potentially dangerous practice.
Dehydration, cramping and electrolyte disturbances that can cause abnormal cardiac rhythms are
potentially serious side effects. Hydrochlorothiazide is generally considered to be safer in with
regard to these side effects than furosemide but the danger still exists. Used in low doses to help
keep blood pressure low and to reduce sodium retention, hydrochlorothiazide will improve the
cardiovascular risk of AAS.
Classification: Diuretic
ANABOLfC PHARMACOLOGY 316

FUROSEMIDE
(Lasix)
5-(A minosu Ifony 1)-4-chloro-2-[(2- furany Imethy I)amino]-
benzoic acid
o OH
NH
I
o
CI
Formula: C12 H"CINzOsSz

MW:331
Furosemide is an extremely potent and dangerous diuretic with the potential for serious side effects.
It is available in both an oral form and as an injectable. Furosemide can cause dehydration and a
reduction in blood volume which can lead to circulatory collapse and possibly stroke and can result
in kidney damage. Furosemide can deplete potassium and sodium levels resulting in dangerous
heart arrhythmias. Calcium can also become depleted resulting in severe muscle cramping and
tetanus (freezing). Furosemide is used by competitive athletes to drop weight to stay in a weight
class and by bodybuilders to reduce subcutaneous water before a competition. The use of
furosemide is extremely dangerous and should not be used without medical supervision.
Classification: Diuretic

ANTI-PROLACTIN

CABERGOLINE
(Dostinex~
6-A Ily I-N-[3-(dimethy lamino)propyl]-N-(ethylcarbamoy I)ergol ine-8-carboxam ide
Formula: CZ6H37NsOz
MW: 452
Cabergoline is a dopamine agonist that is used to reduce prolactin433.434 Over the past few years
there has been a growing belief that prolactin is causing gynecomastia among steroid users. This is
fueled by the apparent ability of certain AAS to induce gynecomastia even though these steroids are
unable to be converted to estrogen. Cabergoline will reduce prolactin levels but it will also reduce
433
GH levels .434 Though prolactin levels may occasionally become elevated during or after a steroid
cycle, prolactin only exerts a tropic effect in the presence of estrogen 51 . This trend toward
controlling prolactin is typical of the polypharmacy that occurs with the use of AAS. Many of the
so-called cases of prolactin-induced gynecomastia can be explained through increased estrogen,
altered estrogen/androgen ratio or even possibly through progesterone receptor antagonism. Cardiac
valvular disease, a potentially serious side effect has been noted in the literature with the use of
cabergoline435 .
Classification: Antiprolactin

BROMOCRIPTINE
(Bromocryptine mesylate, Parlodel, Alti-bromocriptine, Apo-bromocriptine)
2-Bromo-12' -hydroxy-2' -( l-methylethyl)-5' -(2-methylpropy l)ergotaman-3' ,6', 18-trione
H3C CH 3
0
OH
H" NH 0
", '" N
H
N O~
~CH3 ~
N
H2
'. " 0
H3C CH 3
N
!J
H Br
Formula: CnH40BrNjOj
MW: 655
Bromocriptine, like cabergoline, is one of the newer ancillary medications being used by those on a
. . .IS a d
cyc Ie. B romocnptll1e ' receptor agonist,
opamll1e . w IllC
. h decreases t he re Iease 0 fprolactin
' 433434
. .
Prolactin levels can rise during a cycle resulting in reduced libido and contributing to gynecomastia,
sometimes even inducing lactation. As explained under cabergoline, the use of bromocriptine to
reduce prolactin levels is a misguided practice. In most cases, prolactin levels can be reduced by
lowering estrogen levels. The reduction of prolactin through dopaminergic stimulation is likely to
decrease growth hormone levels as well as prolactin. Furthermore, playing around with the
dopaminergic system is not advisable since changes in the activity of this system can result in
serious side effects. Bromocriptine has been shown to decrease LH and plasma testosterone and it is
believed to be through the dopaminergic activit/ 36 Bromocriptine can worsen high blood pressure
and can cause dizziness and dry mouth.
Classification: Antiprolactin

CHASTE TREE BERRY
(vitex)
Chaste tree berry has been used since ancient times for various purposes. The plant and berries
contain several flavonoids as well as progesterone, hydroxy progesterone, testosterone and
androstenedione. Chaste tree berries are known to be antiandrogenic and progestational. Steroid
users have used vitex to suppress prolactin levels and it has been proven to do this in the scientific
literature by binding to dopamine receptors437 438.4 39 Furthermore, chaste tree berry has been shown
to act as an antagonist at estrogen receptors and to upregulate progesterone receptors440 . As with
bromocriptine, it is my opinion that directly lowering prolactin levels, especially through dopamine
receptor stimulation is not a good practice. That being said, the antiestrogenic actions of chaste tree
berry would explain its effectiveness as a treatment for gynecomastia, however, a study showed
436
both bromocriptine and vitex to decrease LH and plasma testosterone levels .
Classification: Anti-prolactin

ANTI-HYPERTENSIVES

CLONIDINE
(Catapres)
CI
H
Cj=N--<//_)
H
CI
Clonidine is a medication used to treat high blood pressure. The use of AAS often results in an
increase in blood pressure. For some, blood pressure increases so much that they choose to use
some form of antihypertensive medication. Some would argue that it might be better to lower the
dose of AAS, reduce sodium intake, eat healthier and maybe even go off of AAS altogether, but
some people do not see those options as desirable. Clonidine is an alpha-2 adrenergic receptor
agonist which causes vasodilatation and inhibits the release of norepinephrine. Clonidine can result
in sleepiness and is sometimes used off-label as a treatment for insomnia. Clonidine is also used
because scientific evidence indicates that the higher dose (O.3mg) increases growth hormone levels.
Classification: Antihypertensive

HAWTHORNE BERRY
Hawthorne berry is a natural ~roducl lhat has been used to treat high or low blood pressure,
arrhythmia and atherosclerosis 1,442, The flavonoid components of Hawthorne have proven effects
on increasing coronary flow and cardiac contractility. Hawthorn also has vasodilatory activity and
has been shown to reduce cholesterol, triglycerides and blood viscosity as well as enhancing
cholesterol degradation. Hawthorne can have a sedative effect and in high doses can cause
dangerously low blood pressure. teroid-using athletes use Hawthorne to combat hypertension
caused by androgens. As can be seen, there are other added benefits of using Hawthorne while on a
cycle including cholesterol lowering and cardioprotection. As the cardiovascular risks of AAS are
well-documented, this herb could have a positive role in mitigating these risks to the user.
C lassi fication: Hypotensi ve/Card ioprotectant

MISCELLANEOUS

RU-486
(mifepristone, Mifeprix
4, 9-estradien-17a-propynyl, I I ~-[ 4-dimethynylamino ]phenyl-17~-01-3-one
OH
CH 3 .. ,,\,===--CH
Formula: C29H35 N02

MW:430
RU-486 is a progesterone antagonist that has been used for a decade in Europe to induce abortions
in pregnant women. Termed "the Abortion Pill", it was recently approved for this purpose in the
US. It is very effective as a progesterone antagonist but as described previously, progesterone
antagonists actually increase estrogen receptor levels443 It also acts as a potent glucocorticoid
antagonist and some have anempled to block cortisol using this drug to provide some degree of
anticatabolic effect. This practice is ill-advised since the body compensates by increasing the
O'f COrtlSO
en d ogenous pro d uctlon . . . . Th'IS d rug was once t houg h t to be a pronllslng
. 1444445446447 .. new
find among AAS users. In reality it has no beneficial effect for the steroid-using athlete.
Class ificalion: AnI iprogesl in/AnI iglucocorl icoid

CYPROHEPTADINE
(Periactin~
Formula: C21H21N
MW:287
Cyproheptidine is an antihistamine and antiserotonergic that also has the side effect of increasing
appetite. Some level of success has been seen using cyproheptadine in illnesses like anorexia, cystic
fibrosis and cancer to increase appetite. In the past, AAS users have used periactin while bulking in
order to increase the number of calories they can consume and therefore the amount of weight they
could gain. This drug also tends to cause drowsiness and irritability as well as other potential side-
effects. Although it is still used in some circles it seems that as bulking as fallen out of favor, so has
the use of this appetite stimulant. The number of potential accessory medications is almost limitless.
As stated earlier, the culture of polypharmacy among AAS users is all too willing to seek out some
sort of pharmacological intervention to produce any desired or to combat any undesired effect.
Combining different drugs and supplements in this haphazard fashion can produce many kinds of
unintended consequences as the interactions become difficult to predict.
Classification: Antihistamine/Appetite Stimulant

SECTION 9

PHARMACOKINETICS
Pharmacokinetics is the study of the time course of a drug in the body and investigates the processes
of absorption, distribution, metabolism and excretion (ADM E). Pharmacokinetic parameters are
determined through the measurement of drug concentrations in blood, plasma or tissues over time.
A drug can be administered in several ways: oral, intravenous, intramuscular, subcutaneous,
intraperitoneal, transdermal, topical, intraocular, intranasal etc. Androgens are usually given
intramuscularly, orally or transdermally.
INTRAMUSCULAR
Androgens that are administered intramuscularly are usually esterified (two notable exceptions are
testosterone suspension and stanozolol suspension). An ester is attached to the steroid at the C-17 -
OH group, which makes the steroid molecule even more lipophilic. The ester prolongs the
absorption of the molecule from the injection depot with different esters having a different effect on
the absorption rate. More lipophilic esters have longer absorption times448 The esterified androgens
are dissolved in oil and injected into the muscle in a depot. The steroid is absorbed from the depot
(which is lipophilic) into the muscle (which is hydrophilic) as it is de-esterified. This de-
esterification reaction is the first step in metabolism. The drug enters the circulation (bypassing first
pass metabolism in the liver) and is distributed to the organs, tissues and cells of the body. During
this process, the drug will eventually be distributed to organs of extraction. Organs of extraction are
generally the liver and kidney. These organs metabolize the drug into metabolites that can result in
449
effects of their own :
Toxicity
Toxic Metabolite
Active Metabolite
Inactive Metabolite
Reversible Metabolite
Prolonged
Activity

The metabolism of the drug eventually leads to excretion of metabolites from the body (usually in
the urine or feces, or both). The time that it takes for the drug concentration present in the
circulation to decline to 50% of the current value is called the half-life (this is a simplification but
will serve for the purposes of discussion).
A single injection results in an increase in plasma concentrations of a drug which reaches a peak
and then declines over time. The shape of this curve is dependent on the pharmacokinetics of the
drug in question.
35
30
25
20
15
10 -<
5 -
0
0 5 10 15
When a drug is taken at a given interval, a steady state will eventually be reached where drug
elimination is equal to drug availability. The rise and fall in drug concentrations will eventually be
equal between each dose. The half-life ofa drug is generally considered to be a good estimate of an
appropriate dosing interval~50:
70
60
50
40
ij
30 -j
20
10
o-
0 1 2 3 4 5 6

There is a common belief among AAS users that dosing on a more frequent interval will decrease
variability in plasma concentration. Dosing more frequently than the half-life of a drug will result in
less variability in plasma levels; however, it will still take about 4 half-lives for the drug to reach
steady state in the plasma. Also, more frequent dosing will result in higher plasma levels and
increase the likelihood for side effects. The degree of variability of plasma levels when a drug is
given at an interval equal to the half-life is acceptable and will not result in a plasma level below the
therapeutic range if a sufficient dose is administered 451 .
One strategy to combat the time it takes to reach steady state is called "frontloading" which his
equivalent to the concept of a "loading dose". Frontloading involves administering a larger dose
45o
initially and then reducing the dose for all of the following doses . For instance, 800 mg is given
the first week and 400 mg each week after. This produces a theoretical graph as follows:
250
200
150
100
50
0 ..... _
o 1 2 3 45 6 78 91011121314151617181920212223242526272829
In this instance you can see that the peaks remain fairly consistent with only a slight drop-off. The
advantage to this dosing scheme is that you get drug concentrations high quickly and sustain this
high level.
As mentioned under the description for nandrolone, there are many variables that can alter the
pharmacokinetics of a drug. The ester, volume of injection, concentration of the drug, and injection
site can all influence the rate at which the drug is absorbed into the blood stream 448 If two different
steroids are mixed in the same injection site, this will also influence the rate of absorption.

ORAL
The same basic principles hold true for oral administration but in a much tighter time frame. Oral
drugs are absorbed from the gut and travel directly to the liver where they undergo "first-pass
metabolism". First-pass metabolism occurs in the liver after oral absorption of drugs. Whatever
drug survives this process passes into the blood stream and is distributed to tissues throughout the
body. Eventually, the drug returns to the liver (or goes to the kidneys) where it is metabolized and
eventually excreted. Orals have a much shorter half-life than injectables and can range from hours
to days depending on the drug in question. As with intramuscular dosing, oral dosing should be
administered in a time frame equal to or shorter than the half-life of the drug. Even though the half-
life is shorter, oral drugs actually have a much longer 'active-life". For example, when testosterone
is cleaved from its ester and released into circulation, it has an active life of only a matter of
minutes. Oral drugs, once they reach the blood have a much longer active life because they are
much more resistant to metabolism than unmethylated injectables.
DRUG METABOLISM
Clearance of drugs from the body normally occurs through the actions of the liver and the kidneys.
Drug metabolism is typically divided into Phase I and Phase II. This is based on the fact that drugs
first undergo oxidative attack (addition of an -0H group), termed Phase I, and then the hydroxyl
group undergoes conjugation (glucuronidation or sulfation) in Phase II. A large group of enzymes,
called Cytochrome P450 enzymes, are mainly responsible for Phase I metabolism. There are about
30 CYP450 enzymes with six (CYPIA2, CYP2C9, CYP2CI9, CYP2D6, CYP2EI and CYP3A4)
being the major metabolizing enzymes452 CYP3A4 is the most abundant and clinically important
enzyme in humans, metabolizing about one half of all available drugs. Testosterone and many
synthetic androgens are metabolized by CYP3A4. One thing to keep in mind is that there is a wide
variation in enzyme concentrations and activities from person to person 452 This variability can
result in marked differences in how an individual metabolizes any given drug.
The primary site of metabolism for testosterone by CYP3A4 is through 6-hydroxylation forming 6-
hydroxytestosterone. CYP3A4 is also capable of forming 2-beta hydroxy, I-beta hydroxy and 15-
alpha and beta hydroxy metabolites453

OH OH
CH, CH,
OH OH
CH, CH,
OH OH
CH, CH,
OH OH
CH,
OH
These hydroxy metabolites then undergo a process of conjugation with glucuronic acid or sulfate
and are excreted. As with other enzymes that have been discussed, certain functional groups can
block the action of the CYP3A4 enzyme. A functional group (such as a methyl) in position 6 or 7
can block the formation of 6-hydroxymetabolites454 . This is why 7-methylation increases oral
bioavailability and toxicity of androgens. Androgens with functional groups at position 6 or 7
undergo other routes of metabolism, possibly greater I or 2-beta hydroxylation. The same is true for
positions I and 2. A functional group in either of these positions will block the formation of I-beta
or 2-beta hydroxy metabolites. This will help to increase oral bioavailability and increase toxicity
but to a much lesser degree than groups at position 6 or 7 since I-beta and 2-beta hydroxylation are
secondary pathways compared to 6-hydroxylation.

Following the Phase I addition of hydroxyl groups, the Phase II reactions occur to increase water
solubility of metabolites to allow for excretion in urine or feces. Steroid hormones undergo two
primary Phase II reactions: glucuronidalion and sulfation. Sulfation attaches a sulfate group to a
hydroxyl and is performed by sulfotransferase enzymes found primarily in the liver and
gastrointestinal tract. There are several types of sulfotransferase enzyme each with different
substrate preference. Glucuronidation attaches a glucuronic acid group to a hydroxyl and is
performed by UDP-glucuronosyltransferase enzymes found in the liver, kidney and gastrointestinal
452
tract There are many types of UDP-glucuronosyltransferases each with a different specificity for
substrate. Most steroid hormones undergo both glucuronidation and sulfation.
OH
CH,
CH,

Sulfotransferase
01? .//' rF .//'
Testosterone Testosterone Sulfate
OH O----~I
CH,
OH
CH, H
..-J-------' H0
H-'"---OH

GI ueu ron osyl tran sferase
~
o1?
Testosterone Testosterone -B-Glucuronide
One of the more common questions asked with regard to AAS is "How long will it take for Drug X
to clear from my body? This is a very difficult question to answer since there is a good bit of
variability in how and how well an individual metabolizes different steroids. Aside from this
variability, there are also other factors, which complicate the answering of this question. The route
of administration, the dose of the drug in question as well as the duration of use will have a role in
clearance from the body. Another factor is the combination of drugs that are used. Since most AAS
and even some accessory medications are metabolized by the same enzymes in the body they will
often inhibit each other's metabolism. For example, a person taking 200 mg of testosterone
propionate every two days for 8 weeks could expectlhe drug to clear after 20 days or so. If the same

cycle were used, but with the addition of 50 mg of oxymetholone per day the clearance rate of
testosterone could be doubled or tripled.

SECTION 10

STACKING
From the early 1900's when testosterone was first isolated to the production of the first synthetic
androgen, athletes only had one option as far as AAS were concerned: Testosterone. Even when
dianabol was first starting to gain popularity people tended to use it by itself. In the early days,
athletes were very conservative with AAS use and the idea of "stacking" was considered to be a
major advance. This is hard for some to believe with the "more is better" philosophy of today, but
these compounds were new and people of the time had no idea what negative effect they would
have in the long term. Of course as time went on, doses moved up and as people used them for
longer periods of time they began to realize that AAS, though potent, were generally forgiving as
far as serious side effects were concerned.
By most accounts, stacking began in earnest in the seventies with the most popular stack being Deca
Durabolin and Dianabol. This is the prototypical stack in most peoples' minds and is still quite
popular today. Unfortunately, the ideas behind stacking were based more on superstition and
guesswork than they were in science. It was believed in the scientific community at this time that
one could separate anabolic and androgenic activities and wind up with a molecule that was purely
anabolic with no androgenic side effects. This led people to classify synthetic AAS as either more
anabolic or more androgenic (and even as a ratio of the two: the androgenic to anabolic ratio) based
on experiments that were primarily done in lower animals. The idea is not necessarily wrong, and
pharmaceutical companies have resumed the search for selective anabolics in the form of SARMs.
Very little was known at the time about aromatization, conversion to DHT, androgen crossover to
progesterone receptors etc. Even with the advances in knowledge that have been gained over the
past twenty years, users are still haphazardly throwing stacks together based on anecdotal
information and "feel".
The basic reasoning behind "stacking" is to combine two or more AAS that together have more
beneficial and less negative effects than either drug would have by itself. As I stated earlier, there is
only one true androgen receptor and it is the activation of this receptor in the muscle that results in
skeletal muscle hypertrophy. Therefore, in the absence of any effect other than AR activation, only
magnitude of AR activation would be in question. As has been explained in this text, all AAS have
some side effect other than AR activation, such as: interaction with various enzymes, conversion to
estrogen, progestational effects, conversion to DHT, antiglucocorticoid effects and binding to
SHBG and albumin that all contribute to the anabolic, anticatabolic and other effects.

The current popular belief is that every person has his own genetic limit to how much muscle can be
gained naturally. It is also believed that AAS should not come into play unlilthe genetic maximum
is reached and should be used to break through this genetic limit. AAS make it possible to exceed
one's genetic limits and therefore one would assume that once steroids are stopped, a user will
revert back to their genetic maximum. This is not necessarily so. While it will be impossible to
maintain all of the gains made while using steroids, it does seem that users do retain a greater than
natural level of muscularity after going off. This is likely due to the increase in fibrous tissue and
contractile proteins that are built up and are more difficult for the body to break down as well as the
production of new muscle fibers through the process of satellite cell differentiation.
Another observation is that there seems to be a second genetic maximum that AAS use alone cannot
bring a person through. Some believe that this second limit can only be breached through the use of
growth hormone, insulin and IGF-1. These three peptide hormones have extremely potent growth
effects and are credited with the increasing muscularity witnessed in recent years in the top ranks of
pro bodybuilding. Their use has increased in "amateur" circles mainly because they are "legal" and
undetectable. This is an unfortunate side effect of the criminalization of AAS. Some athletes have
turned from effective and relatively safe use of AAS to the more dangerous use of GH, insulin and
IGF-I for legal and competitive advantages at the expense of their health. These hormones carry a
much greater risk/reward profi Ie than that of AAS.
Perhap the biggest misconception with regard to the use of anabolic steroids is that, upon coming
off, all gains made will eventually be lost. The amount of muscle retained after stopping AAS is not
only a function of what one does after cessation of use, but also of what one does while on a cycle.
A person can make great gains by haphazardly taking anything they can get their hands and staying
"on" indefinitely. While this approach will produce increases in muscular gains, it will also
jeopardize the health of the user. In my correspondence through message boards on the internet, I
have learned that there are many sensible users who realize that they can't stay on forever, some for
health reasons, some for economic reasons.
There is a current belief among users that testosterone should be included in every stack as a "base"
upon which other drugs are added. There are various lines of reasoning behind this with one of the
most popular being to support libido. There are many idiosyncratic "rules" and myths that users
seem to apply to stacking. In most cases, there is little reason to include testosterone as a "base" ofa
cycle and in some cases, is actually at odds with the goal of the cycle. If a stack only includes
weakly androgenic steroids then it may be necessary to supply a source of androgen, but any
moderate or strong androgen would serve this purpose.

Another popular notion is that there are two classes of steroids. Class I steroids that bind strongly to
the androgen receptor and exert their effects through the androgen receptor and class II steroids that
bind weakly to the androgen receptor and mediate their effects through mechanisms other than the
androgen receptor. Going one step further, one is supposed to stack class I steroids with class II
steroids to take advantage of the different mechanisms. This classification has little base in reality.
Yes, some AAS have low affinity for the androgen receptor, but a recent paper showed that even
with the low androgen receptor binding, these steroids were still able to activate the receptor to
produce an effect258 Though this theory has been debunked, the concept of combining different
steroids with different effects is key. For example, methandrostenolone has been shown to increase
free cortisol levels while nandrolone has been shown to decrease cortisol levels 242 Also,
methandrostenolone has been shown to decrease TBG levels while nandrolone has only a minimal
stimulatory effect on TBG 242 Nandrolone converts to less potent 5-alpha reduced metabolites which
can upset the estrogen/androgen ratio while methandrostenolone converts to potent 5-alpaha
reduced metabolites, restoring the estrogen to androgen ratio. These effects help to explain why
nandrolone and methandrostenolone have been viewed as complementary in a stack.
Often the driving force behind the choice of drugs to stack together in a cycle is one of availability
or cost or both. Certain steroids are harder to come by on the black market and cost can vary greatly
from one product to another. Although, for the most part, any two or more steroids could be stacked
together, one might be better served by using a higher dose of a single agent if the combination of
two drugs does not offer a benefit beyond an increase in overall dose. Some people feel that they are
not being "hardcore" enough if they are not stacking when, in reality, there seems to be a maximum
rate at which muscle tissue can be laid down so, beyond that point, any additional drug serves only
to increase the degree of side-effects.
DOSING
Dosing of AAS is always a controversial subject. We live in a "more is better" world where people
want results yesterday. The psychology of the average person is that of more is better. If I use
higher doses of more types of drugs then I will grow faster. The fact is these are drugs with potent
neurological side effects and a strong potential for psychological dependence. This sometimes
results in a disconnect between what is the best way to use steroids for promoting growth and what
the user wants to use to "feel" a certain way.
Doses of just 100 mg per week or 200 mg every other week of testosterone enanthate have been
shown in scientific studies to produce significant gains in lean mass and strength in as little as ten

weeks in normal men. It has also been shown that as dose increases, so do muscular gains in a dose-
dependant fashion up to 600 mg/week. No scientific studies, to my knowledge, have been
performed with higher doses. One thing to keep in mind is that, as dose increases, so does the
likelihood for side effects and there is a maximum rate at which muscle tissue can be laid down.
One logical approach would be to start low and increase the dose as needed to attain the desired
effect and keep the dose as low as possible while still achieving growth. This will keep side effects
to a minimum while benefiting from the positive effects of AAS and will make recovery easier once
the user stops using.
This being said, the choice of dose is a very personal decision. People often have very different
goals and are willing to accept different levels of risk for different levels of reward. People do
respond differently and will require lower or higher doses depending on their own genetic makeup.

STACKING AND CYCLES
The following stacks and cycles are examples of the approaches that have been or are currently
being utilized in combining different drugs. There is a good deal of mythology around AAS
selection and "rules" to stacking laid down by anecdotal information and the aforementioned
Bro'iore. Any list of stacks is likely to draw criticisms and derision from self-appointed experts who
attempt to elevate themselves through perpetuating the mythology of the community. In any case,
this list of stacks is not meant to serve as an example of what should be done, but rather a record of
what has been done and what is being done. As there is very little legitimate research in how to
combine different AAS to maximize the results obtained from different combinations, any method
to stacking and cycling is likely to be a matter of personal choice and therefor highly individualized.

TESTOSTERONE ONLY
Testosterone alone is a very popular stack, especially for beginners. Testosterone eSlers are usually
plentiful on the black market. There are therefore many options to choose from. Most people choose
longer acting esters to avoid having to inject too often. People will sometimes mix esters to take
advantage of different duration of action. Many feel lhat testosterone is the best because it is the
body's natural androgen. No matter which ester is used, once it is cleaved you are left with plain
testosterone. Many people report different effects with diflerent esters. For example, some feel that
they gel less water retention and propensily for gynecomastia with propionate compared to
cypionate. This likely is a result of the liming of injeclions and the level of "bu ild-up" of androgens
in the body. If one injects at a frequency greater than the half-life then plasma levels will rise to
higher levels. The first example stack is a combination of testosterone enanthate and testosterone
propionate. Testosterone cypionate could be substituted for enanthate since their half-lives are
roughly the same. In this stack, enanthate is injected every other week while propionate is injected
every olher day. The propionate will get the testosterone levels up more quickly while the enanthate
takes some time. Most inject enanthate and cypionate once per week and some even more
frequently. Physicians, on the other hand, will inject every two weeks for enanlhate. This slack will
not produce the instant gratification that many desire; however, it is a safe stack lhat can be lIsed
long term with steady gains and low likelihood for side-effects.
Examples:
Week Testosterone Enanthate Testosterone Propionate

I 300 mg/EOW 50 mg/EOD
2 300 mg/EOW 50 mg/EOD
7 300 mglEOW 50 mg/EOD
1I 300 mg/EOW 50 mg/EOD

This version of the test only stack is more typical of current users. In this stack, cypionate is
injected weekly and propionate daily. This will result in escalating plasma levels that will peak in
the third or fourth week. Though this is a fairly potent stack, many would opt for even higher doses
in search of quick gains. Accessory meds are likely to be needed with this stack, particularly an
antiestrogen or anti-aromatase. The likelihood for side-effects will limit the duration of this stack.
Of course, it is very common for only a single ester to be used but with the longer lasting esters, it
takes time for the effects to become noticeable.
Week Testosterone Cypionate Testosterone Propionate

1 400 mg/wk 50 mg/day
I1 400 mg/wk 50 mg/day

DECA AND DBOL
Deca and dbol (nandrolone decanoate and methandrostenolone) is the granddaddy of all stacks, in
that it was probably one of the first combinations of steroids to be used in a "stacking" fashion. It is
often said that if you can't grow on deca and dbol, then you can't grow. This is a potent stack that
causes fairly rapid size and strength gains. The first example utilizes pretty low doses similar to
what may have been used in the 1970's or early 80's. These doses would probably be laughed at
today but this stack would provide decent gains and though I have shown an eight week cycle, the
low dose of dianabol could allow for a longer duration. Some would argue that a testosterone "base"
would be needed for this stack, but the methandrostenolone should provide a sufficient level of
androgenicity to maintain libido.
Examples:
Week Deca Dianabol

This second example is more typical. The dose of deca is doubled while the dose of Dianabol is
quadrupled. This results in quick bloat, which satisfies the impatient user. This dose of Dianabol
should not be used for too long so a taper is started at week six. Most would continue the deca
through week ten without reducing the dianabol dose since tapering has fallen out of favor. This
results in side effects including bloating, gynecomastia, high blood pressure and acne.
Week Deca Dianabol

I 400 mg/wk 40 mg/day
5 400 mglwk 40 mg/day
6 20 mg/day
7 10 mg/day
8 10 mg/day
9 5 mg/day
10 5 mg/day

This last example incorporates frontloading of the deca with a pyramid of the dianabol. Peak levels
of nandrolone will be reached in week four with the highest dose of dianabol. Long esters like deca
are self-tapering because blood levels slowly decrease over time. Most have all but abandoned ideas
like pyramiding and tapering because they want immediate "feelable" effects. What they get are
massive spikes in blood levels which results in immediate and prolonged shutdown as well as rapid
desensitization.
Week Deca Dianabol

1 500 mg/wk 5 mg/wk
2 400 mg/wk 10 mg/wk
6 20 mg/wk
7 10 mg/wk
8 5 mg/wk
9 5 mg/wk

DECA AND ANADROL
Deca and anadrol is a stack that not too many people would consider. Similar to the Deca/Dianabol
stacks but more potent, the anadrol provides enough androgenic stimulation that one probably
wouldn't have to worry about loss of libido. There may be a concern with gynecomastia, but with
the doses kept reasonable, this shouldn't be a problem but most would probably include an anti-
estrogen just to be on the safe side. This first cycle is a low dose cycle that would not get the
attention of most users. Many would state thaI the doses are simply too low. As with the above
example, this is still a pretty potent stack that should deliver sizable gains. The lower doses will
help to keep side effects manageable and the duration can therefore be spread out.
Examples:
Week Deca Anadrol

6 200 mg, wk 25 mg/day
7 200 ml;iwk 25 mg/day
1I 200 mg/wk 25 mg/day
This second example would satisfy those that prefer higher doses. Deca is dosed at 400 mg a week
with anadrol added at 100 mg in the middle of the cycle when the nandrolone starts to kick in.
Week Deca Anadrol

I 400 mg/wk
2 400 mg/wk
3 400 mg/wk
8 400 mg/wk
9 400 mg/wk
10 400 mg/wk

TEST AND DBOL
Test and dianabol has probably replaced the deca and dbol stack as one of the favorites since test
esters and dianabol are easily and affordably obtained on the black market. The first example stack
has testosterone cypionate dosed at 400 mg per week with 40 mg of dianabol per day. This is a
pretty potent stack although some may argue that a higher dose of both drugs are needed. No matter
how high of a dose, there will always be someone arguing that it needs to be higher still. In any
case, this stack will produce appreciable gains but will also be likely to produce side effects like
bloating, high blood pressure and gynecomastia. Most will include an anti-estrogen or anti-
aromatase or both to help combat these side effects and maybe some finasteride to help prevent hair
loss and prostate swelling. I would argue that if you need a slew of accessory medications to combat
side effects that it might be wiser to lower the doses. One could reduce the frequency of injections
of the cypionate to 400 mg every other week and reduce the dianabol dose to 20 mg per day and
still see significant growth with much lower occurrence of side effects.
Examples:
Week Testosterone Cypionate Dianabol

351 ANABOLlCPHARMACOLOGY
This second example utilizes testosterone propionate, which, when injected every other day does
not seem to result in as much of an increase in blood pressure, bloating or estrogenic side effects. A
reduction in the dianabol dose to 20 mg also aids in reducing side effects.
Week Testosterone Propionate Dianabol

I 100 mg/EOD 20 mg/day
2 100 mg/EOD 20 mg/day
~
.) 100 mg/EOD 20 mg/day
6 100mg/EOD 20 mg/day
7 100 mg/EOD 20 mg, day
8 100 mg/EOD 20 mg,day
10 100 mg/EOD 20 mg, day
1I 100 mg/EOD 20 mg, day

NANDROLONE AND TEST
Nandrolone alone is not a popular stack because many seem to suffer from "deca dick"; a pretty
severe loss of libido. The solution was to add replacement levels of test to keep the libido up while
still getting the benefits of nandrolone. Of course instead of replacement levels of test, some opt for
much higher levels of test. This, of course, increases the likelihood of side effects, especially water
retention and gynecomastia requiring the use of accessory drugs to help prevent them. The first
stack is a fairly potent dose of nandrolone with a pretty standard replacement dose of testosterone
enanthate added. This level of nandrololle is still a little too high as far as side effects are concerned
and it is likely that an anti-estrogen would be needed.
Examples:
Week Deca Testosterone Enanthate

1 400 mg/wk 200 mg/EOW
2 400 mg/wk 200mg/EOW
10 400 mg/wk 200 mg/EOW
11 400 mg/wk 200 mg/EOW
12 400 mg/wk 200 mg/EOW

This second example utilizes shorter duration esters to help reduce side effects. The shorter acting
esters, especially when dosed less frequently, seem to produce fewer side effects due to lower peak
plasma levels. These doses are pretty low but produce decent steady gains with less bloat and less
side effects. This stack could be used for very long durations without many side effects.
Week Durabolin Testosterone Propionate

I 100 mg 2X/wk 50 mg2X/wk
2 100 mg 2X/wk 50 mg 2X/wk
3 100 mg 2X/wk 50 mg 2X/wk
4 100 mg 2X/wk 50 mg 2X/wk
5 100 mg 2X/wk 50 mg2X/wk
8 100 mg 2X/wk 50 mg 2X/wk
10 100 mg 2X/wk 50 mg2X/wk
II 100 mg 2X/wk 50 mg 2X/wk
12 100 mg 2X/wk 50 mg 2X/wk
13 100 mg 2X/wk 50 mg 2X/wk
14 100 mg 2X/wk 50 mg2X/wk
15 100 mg 2X/wk 50 mg 2X/wk
16 100 mg 2X/wk 50 mg2X/wk

TREN AND TEST
Tren and prop is considered to be a "cutting stack". I am not a believer in cutting versus bulking
stacks. In my opinion, almost any stack could be used to bulk or cut with diet being the determining
factor. Tren and prop is a good combination for many of the same reasons as deca and test. Tren is a
strong AR binder with considerable progestational activity which results in pretty severe HPGA
suppression which results in a lack of libido. The addition of testosterone helps to counteract this
effect. Tren is also a modulator of glucocorticoid activity. Prop is chosen as the ester in this case
because the frequency of injections can be synced with tren acetate. Users will inject these steroids
either every other day or every day.
Examples:
Week Trenbolone Acetate Testosterone Propionate

1 50 mg/day 50 mg/day
I
l 355 ANABOLIC PHARMACOLOGY
In this example, longer lasting esters of each drug are used allowing for once a week injections.
Both of these stacks will produce dramatic results. This particular stack could be dosed in an every
other week fashion either alternating drugs or injecting them both at the same time. Although some
would consider 300 mg of tren and 200 mg of test every other week to be too low, it is still well
above replacement levels and will still produce good results with less propensity for high blood
pressure.
Week Trenbolone Enanthate Testosterone Enanthate

I 300 mg/wk 200 mg/wk
2 300 mg/wk 200 mg/wk
~
.> 300 mg/wk 200 mg/wk
4 300 mg/wk 200 mg/wk
5 300 mg/wk 200 mg/wk
6 300 mg/wk 200 mg/wk
7 300 mg/wk 200 mg/wk
8 300 mg/wk 200 mg/wk
9 300 mg/wk 200 mg/wk
10 300 mg/wk 200 mg/wk
1I 300 mg/wk 200 mg/wk
12 300 mg/wk 200 mg/wk

TREN AND PRIMO
Tren and primo seems to be a popular stack currently. I am not really sure why that is. Trenbolone
is a very strong androgen and binds tightly to the androgen receptor. Methenolone on the other hand
is substantially weaker.
Examples:
Week Trenbolone Enanthate Methenolone Enanthate

1 300 mg/wk 300 mg/wk
2 300 mg/wk 300 mg/wk
3 300 mg/wk 300 mg/wk
4 300 mg/wk 300 mg/wk
5 300 mg/wk 300 mg/wk
6 300 mg/wk 300 mg/wk
7 300 mg/wk 300 mg/wk
8 300 mg/wk 300 mg/wk
9 300 mg/wk 300 mg/wk
10 300 mg/wk 300 mg/wk
11 300 mg/wk 300 mg/wk
12 300 mg/wk 300 mg/wk

DURA BOLIN AND EQUIPOISE
Durabolin and equipoise is a safer alternative to deca and dbol. Many people consider equipoise to
be similar to deca most likely because Dan Duchaine stated this to be so in the USHII. Equipoise is
actually much more similar to methandrostenolone than to deca. Boldenone is a relatively weak
binder with GC modulating activity and a propensity to convert to estrogen. It is different from
methandrostenolone in that it is neither orally active nor liver toxic and converts to a less potent
estrogen (estradiol) than dbol (methylestradiol). Durabolin is a shorter acting ester of nandrolone,
which has less propensity for side effects due to less build up of plasma levels. Durabolin and eq
can be taken every 4-7 days with many of the positive aspects of a deca-dbol stack with less
bloating and estrogenic side effects.
Examples:
Week Durabolin Equipoise

I 200 mg 2XJwk 300 mg 2XJwk
2 200 mg2XJwk 300 mg 2XJwk
3 200 mg 2XJwk 300 mg 2XJwk

TEST AND ANADROL
Test and anadrol is not as popular as it once was. Anadrol is a very potent compound with many
side effects associated with its use. I think that many users have become more conscious of their
health and, with this; the use of anadrol in general has diminished. This being said, test (usually
cypionate) and anadrol was a very popular stack at one time. Anadrol causes rapid weight gains due
to water retention and causes rapid increases in strength. This stack was known for its ability to
cause severe bloating and hypertension as well as hair loss. The first example is a relatively high
dose of testosterone cypionate (although some would opt for a gram or more) with 100 mg of
anadrol. This stack will cause rapid increases in weight as well as a large propensity for side effects.
Examples:
Week Testosterone Cypionate Anadrol

This second example is a gentler version utilizing a lower dose of testosterone in the form of the
propionate ester with a much lower dose of anadrol. While this stack will not satisi)' those wanting
instant gratification, it will produce decent gains with less side effects and could be used for a
longer duration, perhaps even 16 weeks provided liver values to not climb to high.
Week Testosterone Propionate Anadrol


TEST AND ANAVAR
Anavar is considered to be relatively weak, expensive and more difficult to obtain on the black
market so many people do not have the opportunity or desire to use it in a stack. However, when
stacked with testosterone, anavar really shines. Anavar really seems to build up strength and has
potent anti-glucocorticoid effects. The first example combines a moderately high dose of
testosterone cypionate with a higher dose of anavar. This level of anavar will keep cycle duration
shorter because even though it is considered to be less liver toxic, the higher dose will result in
elevated liver enzymes. This stack will produce good strength gains but care must be taken as the
anti-glucocorticoid effect of the anavar combined with the II-beta hydroxylase inhibiting effect of
higher doses of test can result in high levels of deoxycorticosterone being produced resulting in
water and sodium retention and high blood pressure. An anti-mineralocorticoid diuretic could be
added to combat this effect.
Examples:
Week Testosterone Enanthate Anavar

This second example utilizes lower doses of both drugs which will help to prevent the bloating with
the first stack.
Week Testosterone Enanthate Anavar

9 300 mg, wk 25 mg/day
10 300 mg, wk 25 mg/day
II 300 mg/wk 25 mg/day

TREN ANDEQ
Tren and eq is not as popular as it should be. This stack would be a more potent version of a
durabolin/EQ stack. Tren would be taken either every other day or every day unless you have the
enanthate version, which can be taken weekly. Eq could be taken weekly or spread out in several
injections with the tren. Tren is similar to nandrolone but with greater AR and PR binding but with
no conversion to estrogen. Eq, like methandrostenolone, increases free and total cortisol levels. Tren
has strong glucocorticoid receptor antagonist effects which would counteract the effect of increased
cortisol.
Examples:
Week Trenbolone Enanthate Equipoise

1 300 mg/wk 300 mg/wk
2 300 mg/wk 300 mg/wk
3 300 mg/wk 300 mg/wk
4 300 mg/wk 300 mg/wk
5 300 mg/wk 300 mg/wk
6 300 mg/wk 300 mg/wk
7 300 mg/wk 300 mg/wk
8 300 mg/wk 300 mg/wk
9 300 mg/wk 300 mg/wk
10 300 mg/wk 300 mg/wk
1I 300 mg/wk 300 illg/wk
12 300 mg/wk 300 mg/wk

TEST+ NOLVA + FINASTERIDE
This stack is probably the safest stack that a man could take. It utilizes the natural androgen,
testosterone but blocks negative estrogenic and androgenic side effects. Since tamoxifen is a
selective estrogen receptor modulator, it blocks estrogenic stimulation of the breast but allows some
positive estrogenic activity, such as stimulation of bone and positive effects on blood lipids. Some
may argue that aromatase inhibitors may be more effective, but aromatase inhibitors tend to be too
effective, driving estrogen levels too low resulting in upregulation of estrogen sensitivity. In many
cases, aromatase inhibitors would be preferred, but in this stack, to keep it as safe as possible,
tamoxifen is favored. Finasteride will reduce androgenic stimulation of the prostate and other
androgen target tissues such as the hair follicle and skin. Dosing is critical in this stack since too
high of a dose of tamoxifen can cause increased estrogenicity and too high of a dose of finasteride
can cause a reduction in libido. Of course, both of these doses will be dependant on the dose of
testosterone, which esters are chosen and each person's unique physiology. If doses of test are kept
reasonable, then bloat can be minimized as well. Very high doses of test would require a
mineralocorticoid antagonist (such as spironolactone or eplerenone) to combat deoxycorticosterone
induced water and sodium retention and the high blood pressure they bring. However, care should
be taken with spironolactone since is does have some antagonistic action at the androgen receptor.
If the doses of testosterone, finasteride and tamoxifen are kept in balance and testosterone doses are
kept reasonable, natural testosterone production may continue since the feedback of estradiol and
DHT will be kept in check.
Examples:
Week Testosterone Cypionate Nolvadex Finasteride

1 400 mg/wk 30 mg/day 2.5 mg/day
3 400 mglwk 30 mglday 2.5 mg/day
8 400 mglwk 30 mglday 2.5 mglday

A low, intermittent dose of the aromatase inhibitor anastrozole could be added to help reduce
estrogen levels without driving them too low. Dosing twice a week with anastrozole has been
shown to partially reduce estrogen levels
Week Testosterone Nolvadex Anastrozole Finasteride

Cypionate
I 400 mg/wk 30 mg/day Img 2X/wk 2.5 mg/day
2 400 mg/wk 30 mg/day Img2X/wk 2.5 mg/day
3 400 mg/wk 30 mg/day Img 2X/wk 2.5 mg/day
1I 400 mg/wk 30 mg/day Img 2X/wk 2.5 mg/day
13 400 mg/wk 30 mg/day Im!l2X/wk 2.5 mg/dav
14 400 mg/wk 30 mg/day 1mg 2X/wk 2.5 mg/day

DECA + NOLVA + FINASTERlDE
This stack will probably ruffle a few feathers. Everyone knows that nandrolone is 5-alpha reduced
to a less potent dihydronandrolone derivative. While this is good for the prostate and the hairline, it
is bad for the libido and is one of the main reasons for the high likelihood of gynecomastia with
nandrolone. People have invoked the progestational activity of nandrolone as the culprit for years.
The fact is the reduction of nandrolone to DHN results in reduced androgenic stimulation in the
breast which has been shown to be a negative regulator of breast tissue growth. If you reduce
androgenic stimulation in the breast and add in an aromatizable AAS like nandrolone, you upset the
androgen to estrogen ratio and gynecomastia is likely. Adding finasteride to nandrolone will not
only increase the potency of the cycle but will also greatly reduce the likelihood of gynecomastia.
The addition of nolvadex makes it even less likely. Shutdown will still be a problem (this is likely
due to the progestational activity) with this cycle.
Examples:
Week Nandrolone Decanoate Nolvadex Finasteride

1 400 mg/wk 30 mg/day 1 mg/day
2 400 mg/wk 30 mg/day 1 mg/day
3 400 mgJwk 30 mgJday I mg/day
4 400 mg/wk 30 mg/day I mg/day
5 400 mJwk 30 mQ/dav I mgJdav
7 400 mg/wk 30 mgJday I mg/day
8 400 mQ/wk 30 mQ/dav I mg/day
9 400 mgJwk 30 mQ/dav I mgJday
10 400 mgJwk 30 mg/day I mg/day
1I 400 mQ/wk 30 mgJdav I mg/day
13 400 mQA.vk 30 mQ/dav I mgJdav
14 400 mg/wk 30 mg/day I mgJdav
15 400 mgJwk 30 mg/day 1 mg/day
16 400 mgJwk 30 mgJday I mg/day

In this variation, a moderate dose of letrozole is added to help prevent any increase in estrogen
levels.
Week Nandrolone Nolvadex Letrozole Finasteride

Decanoate
1 400 mg/wk 30 mg/day 2.5 mg/day 1 mg/day
9 400mg/wk 30 mg/day 2.5 mg/day 1 mg/day
12 400 mg, wk 30 mg, day 2.5 mg/day 1 mg/day
13 400 mg, wk 30 mg, day 2.5 mg/day 1 mg/day

OXANDROLONE AND PRIMOBOLAN
This stack is considered to be a very safe stack, so much so that it is often used by women. Some
will use the oral form of methenolone with oxandrolone as an oral only stack. This is not advisable
since methenolone has very poor bioavailability. Both methenolone and oxandrolone are relatively
weak with low androgenic side effects and neither converts to estrogen. Some users have the
erroneous belief that these two compounds will not shut down natural testosterone production.
While they certainly do suppress HPGA function, it is through androgenic feedback rather than
estrogenic feedback. While Oxandrolone is C 17-alpha alkylated, it is considered to be less toxic
than other oral androgens and primobolan has only a small ability to raise liver enzymes due to its
C-I Alkylation. The major down side of this stack is that both oxandrolone and methenolone are
difficult to come by and can be quite expensive.
Examples:
Week Oxandrolone Primo Tabs

I 50 mg/day 100 mg/day
4 50 mg/day 100 mg/dav
5 50 mg/dav 100 mg/dav

This second example utilizes a lower dose of anavar with a good dose of the injectable enanthate
ester of primobolan. This stack could be used for a longer duration due to the lower dose of anavar.
While probably not potent enough for those wanting quick gains, this stack will produce quality
gains without bloat or many side-effects at all.
Week Oxandrolone Primo Depot

I 25 mg/day 400 mg/wk
2 25 mg/day 400 mg/wk
3 25 mg/dav 400 mg/wk
9 25 mg/day 400mg/wk

ORABOLIN AND PRIMO
Orabolin is pretty difficult to find on the black market nowadays, but at one time this was
considered to be a very safe and effective stack for men and women. The first example combines
the oral version of primobolan with orabolin. Oral primobolan is pretty weak but is only very
slightly liver toxic. Orabolin has an ethyl group at the C-17 position and is considered to be very
mild on the liver as well. Again, this stack will not produce huge gains in weight over night but will
add solid mass over time.
Examples:
Week Orabolin Primo Tabs

8 50 mglday 100 mg/day
This second example utilizes the injectable version ofprimobolan which is much more effective.
Week Orabolin Primo Depot

1 50 mg/day 400 mglwk
4 50 mglday 400 mg/wk
10 50 mg/day 400 mglwk
I1 50 mg/day 400 mg/wk

ORABOLIN AND ANAVAR
An orals-only stack that includes two difficult to obtain AAS. This stack would likely be too weak
for most men but would provide good anabolism for women.
Examples:
Week Orabolin Anavar

3 50 mg, day 50 mg/day
4 50 mg, day 50 mg/dav

TEST+ANADROL+TREN
This is probably one of the most potent and dangerous stacks that are commonly used. In this stack,
Testosterone is often used at over a gram per week with high doses of oxymetholone (100 - 150 mg
per day) and trenbolone (75-100 mg/day). This slack will cause rapid increases in strength and
weight gain but will also cause severe side effects. Blood pressure is likely to be dangerously
elevated with HDL levels near zero. Hair loss can be rapid for those who are prone to male pattern
baldness. Prostate enlargement is also very likely due to the large amount of androgenic stimulation
with this stack. Unfortunately, the type of user who prefers this stack is not too concerned about his
health and will likely not use accessory medications to combat side effects for fear of decreasing the
stack's potency. The first example utilizes moderately high levels of each component although these
doses have been doubled.
Examples:
Week Testosterone Cypionate Tren Enanthate Anadrol

I 400 mg/wk 300 mg/wk 100 mg/day
2 400 mg/wk 300 mg/wk 100 mg/day
This second example reduces both the cypionate and the anadrol doses. This level of cypionate wi II
help to prevent loss of libido that some report with tren while the anadrol will increase red blood
cells at this level with reduced toxicity.
Week Testosterone Cypionate Tren Enanthate Anadrol

I 100 mg/wk 300 mg/wk 50 mg/day
6 100 mg/wk 300 mg/wk 50 mg, day
7 100 mg/wk 300 mg/wk 50 mg, day

This final example uses short acting esters of test and tren to help reduce side effects and a minimal
dose of anadrol to build up red blood cells. This would still be a very potent stack and though the
doses are not high it still amounts to over 500 mg of AAS per week.
Week Testosterone Tren Acetate Anadrol

Propionate
1 50 mg/EOD 75 mg/EOD 25 mg/day
3 50mg/EOD 75 mg/EOD 25 mg/day
4 50 mg,fEOD 75 mQ/EOD 25 mg/day
6 50mg/EOD 75mgJEOD 25 mg/day
8 50 mg/EOD 75 mQ/EOD 25 mg/day

DROMOSTANOLONE AND PROP
Dromostanolone and Test prop is a popular stack due to the fact that both steroids are injected every
one, two or three days depending on the preference of the user. One could also use them on
alternate days. Both steroids are known to provide lean mass gains with little bloating. Many will
use this stack while dieting as a "cutting stack". Both of these are painful injections depending on
the concentrations and the quantity injected. Androgenic side effects are a concern with this stack
with blood pressure, hair loss and acne common. The example stack is reasonably potent. Many
would opt for a higher testosterone dose but this would tend to cause bloating which is contrary to
the purpose of this stack, which is to "harden" the physique.
Examples:
Week Dromostanolone Testosterone Propionate

I 50 mg/dav 50 mg/dav

TREN AND WINSTROL
Tren and winstrol is an interesting cycle. Tren, of course, is a very strong androgen receptor binder
while winstrol is relatively weak. There is no conversion to estrogen with either compound but both
are known to have effects on glucocorticoids. This is a dry cycle with good strength gains and lean
mass gains. One might experience sore joints on this cycle due to the suppression of glucocorticoid
effects. The first example cycle utilizes tren acetate and the injectable version of winstro!. These are
moderate doses but are quite potent. Although tren is oil-based and winstrol is water based, these
injections can be given in the same syringe. Extra care must be taken to remove air bubbles as the
water bubbles can sometimes look like air
Examples:
Week Trenbolone Acetate Winstrol INJ

I 70 mg/EOD 50 mg/EOD
2 70 mg/EOD 50 mg/EOD
This variation of the stack utilizes the winstrol tabs with the longer acting enanthate ester of tren. Again, do
not associate the lower doses of this cycle with low potency. This is a high potency stack with the high
potential for androgenic side effects including altered blood lipids, hair loss, acne and increased aggression.
Week Trenbolone Enanthate Winstrol Tabs


TREN AND ANADROL
Similar to the test, tren, anadrol stack but without the test of course. This stack is still extremely
polent but without the added bloat that the added testosterone provides. Tren is a very good
glucocorticoid antagonist, which will result in increased glucocorticoid production. Oxymetholone,
on the other hand, has been shown to increases CBG levels, which will act to absorb the excess
cortisol produced. Blood pressure is still a major concern with this stack as is hair loss, acne,
aggression and blood lipid perturbations. The first example stack utilizes moderate doses of tren
with only 50 mg/day of anadrol. Theoretically, this cycle could be used for twelve weeks without
too much concern for the liver; however, most would choose to shorten this cycle to eight or even
six weeks to reduce the damage to the liver and kidneys.
Examples:
Week Trenbolone Enanthate Anadrol

I 200 m~ wk 50m~ day
2 200 m~ wk 50 mgt day
]1 200 mg/wk 50 mg/day
Switching to the acetate version of tren results in a higher weekly dosage but due to the shorten
duration, side effects will actually be somewhat reduced. The increase in the anadrol dosage further
increases the potency of this sample stack.
Week Trenbolone Acetate Anadrol

5 100 mglEOD ]00 mg/day
ANABOLlC PHARMACOLOGY 374

TREN AND ANAVAR
On the surface, this just looks like a weaker version of the tren/anadrol stack. On the contrary, it is
quite different. This would be a very dry stack as both tren and anavar act as glucocorticoid receptor
antagonists and neither converts to estrogen. Strength would increase rapidly with this stack. Side
effects would still be a concern, but not nearly as much as with the previous stack. One major
concern is that, once this cycle has ended, there is likely to be a severe cortisol rebound. For that
reason, it might be advisable to follow this cycle with replacement levels of test to provide some
anabolism as cortisol levels return to normal. The first example stack utilizes moderate doses of
both drugs. Again, this is still a potent stack
Examples:
Week Trenbolone Enanthate Anavar

5 200 mg/wk 25 mg/daY
Switching to the acetate ester of tren will increase the overall weakly dose combined with a
doubling of the anavar dose will increase the potency and decrease the duration of this sample stack.
Week Trenbolone Acetate Anayar

6 100 mg/EOD 50 mg) day
7 100 mg/EOD 50 mg! day

NANDROLONE AND WINSTROL
Many have attempted a winstrol only stack only to find out that their joints became horribly sore.
This is related to the fact that winstrol has potent anti-glucocorticoid effects. Anyone who has
received a cortisol injection into a sore joint knows how well cortisol relives inflammation. Since
winstrol blocks this effect, it is easy to see why the joints get sore. The answer was to add
nandrolone to the cycle since nandrolone is known to result in fluid retention. The first example
utilizes winstrol tabs at a dose of 100 mg per day with deca added at 200 mg per week. This is a
pretty mild stack that should result in modest gains with few side effects.
Examples:
Week Deca Winstrol Tabs

This second example utilizes the shorter acting durabolin with winstrol injectable. The injectable
version of winstrol is much more potent so even though this stack has a slightly lower weekly
dosage of winstrol, it is actually more potent. The shorter acting durabolin will load less fluid than
deca so a higher dose is required.
Week Durabolin Winstrol IN]

2 100 mg/EOD 100 mgfEOD
II 100 mg/EOD 100 mg/EOD

HALO AND TREN
A potent stack that would be used as a pre-contest stack for both bodybuilders and powerlifters.
This stack will increase strength and aggression dramatically as well as produce a dramatic
"hardening" of the physique. This would also be a dry stack resulting in little or no water retention.
Of course, this would also be a very toxic stack. Halotestin is a strong androgen with potent liver
toxicity. Both tren and halotestin act as anti-glucocorticoids so it is likely that there will be serious
cortisol rebound following this cycle. Blood pressure, acne, hair loss, altered blood lipids will all be
a concern with this cycle. The sample stack utilizes moderate doses oftren and halo but I have seen
these doses doubled. This is a dangerous stack with high likelihood for liver and kidney damage.
Examples:
Week Tren Acetate Halotestin

1 70 mg/EOD 20 mg/dav

EQUIPOISE AND WINSTROL
Eq and winstrol is an interesting stack. Both are relatively mild and produce decent lean mass
increases with a relatively low propensity for side effects. One could use winstroltabs as in the first
example or the injectable version as in the second example. The second example is a more potent
variation and may require an antiestrogen as the buildup of boldenone in the plasma may increase
its conversion to estrogen.
Examples:
Week Equipoise Winstrol Tabs

Week Equipoise Winstrol TN]


SUSTANON PYRAMID
Sustanon is a very popular steroid which contains a blend of testosterone esters which is meant to
supply even levels of testosterone over one month. Theoretically, one could take I to 2 mLs every
four weeks for replacement therapy. What many users do is to inject on a schedule much shorter
than the duration of action. This results in a buildup of testosterone levels over time without
increasing the dose. Commonly, people will inject one or two ml once a week although I have heard
of people injecting every two days to take advantage of the spike in levels that the propionate ester
provides. Sustanon does not produce the instant gratification of cypionate or enanthate because the
longer esters in sustanon provide a more gradual buildup in plasma levels. The sustanon pyramid is
an old cycle using just sustanon (which is often easy to obtain on the black market). Doses are
increased over four weeks and then decreased. This takes advantage of the self-tapering nature of
the drug. Nolvadex may be needed during weeks three to six as the cumulative dose of testosterone
is fairly high. Introduction of a low dose of an aromatase inhibitor and finasteride at week nine will
help to restore natural test levels more quickly. While many people would look down on this cycle
as being too week or not having enough different drugs "thrown" in, this cycle will produce good
solid lean mass gains with low incidence of side effects.
Examples:
Week Sustanon
1 250mg
2 500 mg
3 750mg
4 1000 mg
5 750 mg
6 500mg
7 250 mg
8
9 250 mg
10
I1 250 mg

THE STRING
The String is an interesting cycle that takes advantage of the different potencies ofdifferent AAS. If
one were to take a dose of a given steroid, say 300 mg per week of Testosterone cypionate, in a
relatively brief period of time, the effects would start to plateau. This is due to Illany factors
including downregulation of androgen receptors. This stack addresses the issue by using a week
androgen followed by a stronger androgen followed by a stronger androgen. Proviron is added to
reduce SHBG binding and provide some anti-estrogen activity. This is a potent stack that should
produce steady gains throughout its duration.
Examples:
Week Proviron Primobolan Equipoise Test Deca Tren

Enanthate Cyp Enanthate
I 25 400 mg
mg/day
2 25 300 mg
mg/day
3 25 200 mg 400 mg
mg/day
4 25 300 mg
mg/day
5 25 200 mg 400 mg
mg/day
6 25 300 mg
mg/day
7 25 200 mg 400 mg
mg/day
8 25 300 mg
mg/day
9 25 200 mg 400 mg
mg/day
10 25 300 mg
mg/day
1I 25 200 mg
mg/day

THE REVERSE STRING
The Reverse String is an interesting answer to the previous cycle. In this case, you start out with the
strongest androgen and move to progressively weaker androgens. The argument here is that you hit
the androgen receptors hardest before they have a chance to downregulate. Then, as you move to a
weaker androgen, the receptors will maintain their levels as the potency decreases. In this case, you
will see most of your gains early, but the gains should be more easily kept once the cycle ends.
Examples:
Week Proviron Primobolan Equipoise Test Deca Tren

Enanthate Cyp Enanthate
1 25 400 mg
mg/day
2 25 300 mg
mg/day
3 25 400mg 200 mg
mg/day
4 25 300 mg
mg/day
5 25 400 mg 200 mg
mg/day
6 25 300 mg
mg/day
7 25 400mg 200 mg
mg/day
8 25 300mg
mg/day
9 25 400mg 200mg
mg/day
10 25 300mg
mg/day
11 25 200mg
mg/day
1 381 ANABOLIC PHARMACOLOGY _

SECTION 11

POST-CYCLE THERAPY
The use of AAS results in suppression of natural androgen production through reductions in LH.
After a cycle has ended, the plasma level of AAS falls reducing stimulation of the androgen
receptor and natural androgens can stay low for some time resulting in a loss of gains, depression
and side effects. Athletes have attempted to combat this by utilizing post-cycle therapy (PCT). The
goal of PCT is to try to accelerate the return of normal androgen production as well as prevent any
side effects of an altered hormonal profile. Some have questioned the validity of trying to restore
natural hormone production through the addition of even more drugs but few are willing to suffer
through the post-cycle period without some form of PCT. There are a multitude of strategies that
athletes use in choosing their PCT with the subject as hotly debated (if not more so) as which cycle
to use. As an extension of PCT, most athletes will follow a similar approach while on-cycle (on-
cycle therapy or OCT) to reduce side effects as well as the severity of the post-cycle withdrawal.
The major components of PCT generally include antiestrogens, aromatase inhibitors, and HCG
either alone or in some combination. Antiestrogens such as clomid and nolvadex have traditionally
been major components of PCT. The thinking behind these is that LH is suppressed through
increased estrogens therefore, blocking the estrogen receptor will help to restore natural testosterone
production. Clomid has been used as a fertility drug in clinical practice for men and women for
quite some time while nolvadex is primarily used as an antiestrogen in breast cancer. Aromatase
inhibitors are also used to try to keep estrogen levels low and restore LH production. Some have
argued that since testosterone production is diminished that therefore, estrogen production will also
be reduced since estrogen is produced from testosterone. While this is true (especially with the use
of aromatase inhibitors), it also neglects the fact that estrogen is not only produced from
testosterone. Adrenal androgens, such as DHEA can be a source of estrogens as can estrone sulfate.
Estrone is produced along with estradiol from aromatizable androgens during a cycle. Estrone is
sulfated and binds to binding proteins such as SHBG and albumen. This bound estrone sulfate can
then be released post cycle as estrogen levels fall. It is then desulfated and converted to estradiol. In
this case, a SERM will help to reduce the action of this estrogen, while an aromatase inhibitor will
not.
Human chorionic gonadotropin (HCG) is a naturally produced hormone that is produced by

pregnant women and is excreted in the urine. Most pregnancy tests actually test for the presence of
HCG in urine for indication of a positive test. HCG is very similar in structure to LH and is used to
stimulate the endogenous production of testosterone. There is no definitive method to using HCG to
increase testosterone levels. Even in the scientific literature there is no consensus. One paper shows

that 250 IU administered intramuscularly every other day maintained intratesticular testosterone
levels on men who were given 250 mg per week of testosterone enanthate which should maintain
testicular size and testosterone production. Other regimens used in the literature include 1,000,
2500, 5000 or 10,000 IU twice per week with 2500 IU being common. Athletes vary in their usage
of HCG. Some recommend 1000 IU every day whereas others use 10,000 IU for just a single
injection. In any case, most realize that using too high of a dose for too long can result in
desensitization to LH. Of course, the choice of when to dose HCG and how much is a personal one
and will depend on the cycle in question and a person's individual physiology. Some will choose to
use HCG during a cycle at low doses as described above (250 IU every other day) and continue for
a month or so after the cycle has ended to allow for any injectables that were taken to clear. Others
will wait until after a cycle has ended, begin or continue using nolvadex or c10mid for two or three
weeks and then begin HCG therapy at 1000 IU twice a week for a month.
This brings me to an interesting discussion. At one time, athletes were fond of tapering their doses
at the end of a cycle. Doses of injectables and orals would be reduced each week for several weeks
to reduce the shock to the system. For example, if one was using 800 mg per week of testosterone
cypionate together with 100 mg per day of anadrol, the dose of testosterone might be reduced to
400mg in the first week then to 200 mg in the second week then to 100 mg in the third week. The
anadrol would be reduced to 50 mg per day in the first week then 50 mg every other day in the
second week and to nothing in the third week. Meanwhile, clomid and HCG therapy might begin in
the third week. Now, 100 mg is less than what would be necessary to maintain normal androgen
levels in males but it would allow for some androgenic stimulation. For some reason, tapering fell
out of favor. The argument is that any exogenous androgen will suppress natural testosterone
production. While this is true, it is not necessarily true that any amount of AAS will totally shut
down nalural production. For example, 100 mg per week of testosterone cypionate will not be
enough to maintain normal androgen levels so the body will produce some testosterone to make up
for the difference. If one were to taper down even lower, to say 50 mg then the body would produce
even more natural testosterone since 50 mg is quite a low dose. I use testosterone as the example
because stronger androgens like trenbolone or anadrol might be difficult to taper down because they
are very potent. Additionally, if you take a drug more frequently than its half-life would suggest,
then it might be necessary to increase the time between injections to taper. Some might argue that
injections are selt~tapering and this is also true but the drop-off still might be too severe for natural
testosterone production to adjust in time.
As you can see in the graph below, the dashed line represents the plasma level of nandrolone after
an injection of nandrolone decanoate while the solid black line represents plasma level of natural

testosterone. Natural testosterone starts to recover as the plasma level of steroid drops below the
269
level that would provide a normal level of androgenic stimulation Of course the longer and more
severely that natural testosterone production is suppressed; the slower will be the recovery.
25
20
15 "
... -- ... ,
10
\
,
\
5 ...
0
0 10
"'-
20
-- 30
As stated earlier, PCT is really an extension of on-cycle therapy (OCT) that athletes use to try to
prevent side effects during a cycle. Most athletes will take some form of antiestrogen, either a
SERM or an antiaromatase or both, during a cycle to help reduce the likelihood of estrogenic side
effects. Aromatase inhibition has been shown to adversely affect blood cholesterol which, combined
with androgens can be severe. There is some concern among steroid users that aromatase inhibition
may result in estrogen receptor upregulation or some other form of sensitization that could result in
post-cycle gynecomastia. It is possible that aromatase inhibition results in estrogen receptor
upregulation and it has been shown that the use of aromatase inhibitors in breast cancer patients can
be circumvented through the action of estrone sulfate. Tamoxifen and other antiestrogens have been
shown to be potent sulfatase inhibitors. This fact would argue for the use of tamoxifen over the use
of aromatase. Additionally, tamoxifen has been shown to have beneficial effects on cholesterol as
opposed to aromatase inhibitors.
Another component of OCT is the use of 5-alpha reductase inhibitors to reduce the loss of hair and
to prevent prostate enlargement. 5-alpha reductase inhibition will also help to normalize cholesterol
levels. One of the potential down sides is that inhibition of 5-alpha reductase can reduce androgen
levels to the point that it disrupts the androgen/estrogen ratio. This is especially harmful when
ending a cycle so many will stop the use of the 5-alpha reductase inhibitor a short time before
ending a cycle so that androgen levels can normalize.
OCT can become very complex with some athletes using anti-acne medications, antihypertensives,
fat loss medications, diuretics, anti-prolactin and thyroid medications. Any doctor would tell you
that this kind of polypharmacy is extremely dangerous, impossible to predict the outcome and may
put the athlete at greater risk than AAS themselves.

An example of an OCT/PCT regimen is listed below. 250 IU of HCG is administered on Monday,
Wednesday and Friday of the cycle to maintain testicular size and function. Tamoxifen is taken
every day at a dose of25 mg per day. This dose will antagonize the estrogen receptor and help keep
SHBG levels from dropping too low and causing an increase in free estrogen. Tamoxifen also acts
as a sulfotransferase inhibitor which will help to keep estrone sulfate levels low. Some may opt to
use an aromatase inhibitor in place of or in addition to tamoxifen. This often drives estrogen levels
too low while at the same time allowing SHBG levels to plummet which can result in any estradiol
or estrone or estrone sulfate that was bound to circulate in the free state. HDL levels will also drop
sharply with the addition of an aromatase inhibitor. Depending on the cycle, a small dose of a 5-
alpha reductase may be incorporated to help protect the prostate and reduce androgenic side effects
like hair loss. This will also reduce androgenic feedback to the hypothalamus. Once the cycle ends,
HCG is stopped, the timing of which depends on the components of the cycle. If a long lasting ester
is used, then the HCG should be stopped at the half-life. For example, if testosterone enanthate is
being used then then no I-ICG would be used 7 days after the last testosterone injection. Tamoxifen
could be continued or one could switch over to c10mid since some feel that c10mid is a linle bener at
stmulating the testes. Of course other on-cycle accessory medications may be used while on-cycle
such as a liver protectant when using orals.
Week Testosterone Dianabol HCG Clomid Tamoxifen

Enanthate
I 600 mg/week 50 mg/day 250 IU M,W,F 25 mg/day
2 600 mg/week 50 mg/day 250 IU M,W,F 25 mg/day
12 600 mg/week 50 mg/day 250 IU M,W,F 25 mg/day
13 250 IU M,W,F 25 mwday

14 100 mg/day
15 50 mg/day
16 50 mg/day

Although it has largely fallen out offaYor a similar OCT/PCT with a cycle that is tapered is shown
below:
Week Testosterone Dianabol HCG Clomid Tamoxifen

Enanthate
I 600 mg/week 50 mg/dav 250 IU M,W,F 25 mg/dav
2 600 mglweek 50 mg/day 250 IU M,W,F 25 mglday
12 600 mglweek 50 mg/day 250 IU M,W,F 25 mg/day
13 300 mglweek 250 IU M,W,F 25 mg/day

14 100 mglweek 250 IU M,W,F 25 mg/dav
15 50 mglweek 100 mg/dav
16 50 ma/daY
17 50 mg/dav
As you can see, after the first week at 300 mg the dose is then dropped below replacement levels to
100 mg/week. While this will still result in some suppression of natural testosterone production,
since plasma levels are dropping below a natural level, the body will start to initiate testosterone
production. The result of this is that plasma testosterone levels do not drop as quickly or as low with
a taper as they would without even though the time to recovery is about the same or slightly longer.
200 l
150 \
\
\
\
100 \
\
\ ,...
50 ... .... _--_ .. -~~
~~
12 14 16 18 20 22 24 26

PEPTIDE HORMONES
Peptide hormones are different from steroids in several ways. First of all, they do not have the
steroidal structure, but are composed of many amino acids linked together to form a protein.
Secondly, protein hormones generally do not enter the cell like steroid hormones and do not interact
directly with DNA. Protein hormones bind to receptors, which exist on the surface of the cell
membrane. When these receptors are activated, they activate "second messenger" systems which
carry out the actions of the peptide hormone. There are several second messengers including cyclic
AMP, cyclic GMP, inositol triphosphate and ion channels. The second messengers can produce a
variety of signals including transcription of new proteins, release of stored proteins, increased
degradation of proteins, increased cell permeability, etc ... There are several anabolic peptide
hormones, which are currently being used illicitly to increase skeletal muscle hypertrophy. I will
briefly discuss each of these hormones as well as a few additional peptide hormones, which may
find utility in the near future.
GROWTH HORMONE (SOMATOTROPIN)
Growth hormone (also known as Somatotropin) is a large peptide consisting of 191 amino acids 51 . It
is similar in structure to prolactin and is secreted from the pituitary in a pulsatile pattern as a result
of stimulation by growth hormone releasing hormone (GHRH). Somatostatin is a hormone that acts
51
to suppress the release of growth hormone from the pituitary and opposes the action of GHRH
GH secretion peaks during puberty and steadily declines in maturity. This increase in GH is largely
responsible for the accelerated growth rate experienced during adolescence. The secretion of GH
peaks during the night in the early stages of sleep. Exercise, stress, high levels of plasma amino
acids and hypoglycemia all increase the secretion of growth hormone. Hyperglycemia following a
meal elevated free fatty acids, obesity, hypo and hyperthyroidism and dopamine agonists decrease
the secretion ofGH 51
455
While GH has effects of its own, it also exerts many effects through IGFI and IGF2 GH alone
enhances Iypolysis and increases protein synthesis. Given to calorically restricted men for I to 3
456
weeks, GH significantly increases nitrogen retention, but these effects diminish after three weeks
GH has anti-insulin effects resulting in elevated blood glucose levels. Excess amounts of GH can
result in a condition known as acromegaly. This condition is characterized by local overgrowth of
bone especially the skull and jaw bones. Diabetes is also present in acromegaly, as is enlargement
of cartilage in the ears, nose, ribs and joints. Carpal tunnel syndrome is a common complaint of
those with excess growth hormone production. Internal organs, especially the heart and spleen as

well as enlargement of the hands and feet are also the result of excess GH stimulation. GH causes
the secretion of IGF-I, which feeds back to reduce growth hormone secretion which may be one of
the mechanisms of reduced efficacy with growth hormone over time.
GH use has become pretty widespread with everyone from bodybuilders to athletes to actors and
life extensionists using it for one purpose or another. GH alone is considered as not very effective
for increasing lean muscle mass, but is used largely for reducing body fat. More importantly, GH is
legal, therefore some are choosing to use GH and insulin over AAS because GH and insulin are
legal and easy to obtain while AAS are cheaper, more effective and generally safer to use.
The effects of GH are countered by the effects of another hormone known as somatostatin.
Somatostatin does not inhibit the effects ofGH but rather has an effect on the secretion ofGH from
the pituitary. Of course, when GH is administered exogenously, somatostatin will only inhibit the
release of endogenous GH. Somatostatin does have other effects, however. As GH levels increase
through exogenous administration, somatostatin is released resulting in decreased endogenous
production. In addition, somatostatin also decreases the secretion of insulin from the pancreas.
Another major action of somatostatin is the inhibition of thyrotropin releaseS]. Thyrotropin
stimulates the thyroid gland to produce thyroid hormones. With exogenous administration of GH,
the user experiences both decreased insulin response and decreased thyroid hormone production.
This has prompted some users to combine GH with insulin and thyroid hormone to correct these
deficits.
Though it was once common for users to inject 15 1U or more of G H per day, it seems that 4 to 6 1U
per day is more common of late. It seems that higher doses produced more side effects with rapidly
diminished results due to loss of efficacy. There have been recent attempts to schedule GH as a
controlled substance but as yet this has not happened. In any case, the illicit use of GH is not as
legally benign as some users think as a provision regarding distribution and intent to distribute for
illicit purposes was included in the steroid control act of 1990 was a 5 year felony.

INSULIN-LIKE GROWTH FACTORS
Insulin-like growth factors I and 2 (IGF-I, IGF-2) are peptides that are similar in amino acid
sequence and structure to insulin and can bind to the insulin receptor having the same glucose
lowering effect 51 . IGF-I and 2 also binds to the type I IGF receptor and are largely responsible for
the growth promoting effects of growth hormone. The Type I IGF receptor also binds insulin but
with lower affinity and is likely responsible for the anabolic effects of insulin beyond those of
glucose uptake. There is a type 2 receptor but it only binds IGF-2 and does not appear to be
involved with the anabolic effects of IGF-2. IGF-2 has largely been ignored as a promoter of
skeletal muscle anabolism but since it signals through the same receptor as IGF-I, it will produce
similar anabolic responses 5l .
IGF-I binds to the type-I receptor which acts through a cascade of transcription and differentiation
factors such as AKT, glycogen synthase kinase 3-beta (GSK-3b), mammalian target of rapamycin
(mTOR), myoD and others to increases amino acid uptake and protein synthesis and decreases
nitrogen excretion while stimulating the differentiation of satellite cells which can result in growth
not only of skeletal muscle but also of internal organs such as the spleen, liver and heart457
Circulating IGF-I is produced by the liver in response to stimulation by growth hormone. IGF-I in
skeletal muscle is produced locally and stimulates hypertrophy and hyperplasia locally in what is
referred to as a paracrine action 458 When produced locally, IGF-I is often modified to form a
slightly different protein called mechano-growth factor or MGF. Testosterone stimulation of the
androgen receptor has been shown to result in local production oflGF-1 in skeletal muscle.
IGF-I circulates in the plasma bound to a family of binding proteins 459,460,461. These binding
proteins extend the half-life of IGF-I, which is usually very short. They also transport IGF-I to
target cells and modulate the action of IGF-1. There are six known JGF binding proteins. Under
most conditions, IGF binding proteins seem to inhibit IGF-I activity, probably by reducing the free
concentrations available for binding. IGFBPs also inhibit IGF-I activity by competing with IGF-I
receptors for IGF-I binding, IGFBP3 can interact directly with cell membranes (possibly through a
receptor of its own) to inhibit the action of IGF-I and to exert effects of its own. IGFBP5 is widely
considered to be a potentiator of IGF-I action, probably by delivering IGF-I to its receptor.
Androgens increase IGFBP5 levels while reducing IGFBP3 levels which further suggests that
IGFBP3 is a negative regulator if IGF-I activity while IGFBP5 is a positive regulator462 IGFBP4
has been shown to be an inhibitor of IGF-J anabolic action in skeletal muscle.

It is no wonder that such a potent anabolic is being used illicitly to try to enhance muscle strength
and size. Recombinant IGF-I in various forms is available for research purposes and though it is not
intended for human consumption, users have been experimenting with it for quite some time. Some
have attempted to inject recombinant IGF-I subcutaneously but the quantities needed and the short
half-life result in minimal efficacy. Local intramuscular injections seem to produce some local
anabolic effect but again, the short half-life limits its utility463 A variant form oflGF-1 called Long
R3 IGF-I that has minimal binding to IGF binding proteins and a longer half-life has been used to
promote anabolism. The down side to this particular form oflGF-1 is that it circulates at high levels
in an unbound form. Circulating IGF-I has been shown to be associated with tumor progression
while IGF binding proteins (particularly binding protein 3) have been shown to protect against
tumor progression, likely through restricting the actions ofIGF_1 464 . Another form oflGF-1 that has
been proposed as an anabolic agent is des( 1-3)IGF-I. This shortened form of IGF-I is incapable of
being bound by IGF-I binding proteins and is much more potent in stimulating hyperplasia in
skeletal muscle. Injected locally, this peptide may have better growth promoting properties than
native IGF-1. The use of IGF-I, especially in a systemic fashion, will result in decreased natural
production ofGH.
The IGF system is complex with multiple ligands and binding proteins whose roles are not fully
understood. The IGF-I/AKT pathway has been demonstrated not just to promote growth in skeletal
muscle but also in internal organs and to playa role in the progression of cancer suggesting that this
465
pathway must be carefully regulated to prevent serious side effects The fact that these peptides
are not scheduled and are available in a pseudo-legal fashion makes them much more available than
AAS but with a potentially much higher liability profile. This is one of the unfortunate unintended
consequences of the criminalization of AAS.
INSULIN
Insulin is produced in the beta cells of the pancreas from a larger peptide called preproinsulin.
Endogenous insulin has a half-life of three to five minutes and the pancreas secretes about 40 to SO
units of insulin per day in normal adults. Insulin secretion is stimulated in response to feeding with
glucose being the strongest stimulator. Insulin binds to a cell surface receptor resulting in increased
glucose and amino acid transport through the cell membrane and glycogen and lipid synthesis and
storage. This is accomplished through the increased movement of Glut4 molecules to the surface of
the cell membrane. Glut4 is the main transporter of glucose across cell membranes into cells.
Insulin also binds to the type I IGF receptor which results in growth stimulating effects in muscle
cells.

Insulin is the main "storage" hormone and is very anabolic as well as anti-catabolic. In addition to
increasing glycogen and lipid synthesis and storage, insulin also promotes protein synthesis in
skeletal muscle and promotes glycogen storage by increasing glucose transport in skeletal muscle
cells466.467.468.
Insulin and insulin syringes are available in many states without a prescription making insulin a
more available anabolic hormone than AAS. That being said, the dangers of insulin are immediate
and potentially deadly. Insulin can produce in a state of severe hypoglycemia that can result in coma
or death with a maner of minutes. In addition, insulin resistance will occur over time in healthy
individuals using insulin. While this risk is down-played by users and on boards discussing insulin,
it should be considered a very real risk. Though insulin is highly anabolic in skeletal muscle, it is
also very anabolic in adipose tissue. This can result in increases in body fat, especially when used in
high doses on its own. Often insulin is combined with growth hormone to take advantage of growth
hormone's fat burning ability and to combat the decrease in insulin sensitivity with GH. IGF-I IS
sometimes combined with insulin (and GH) but this increases the risk of hypoglycemia.
INTERLEUKIN-15
Interleukin-15 is a peptide hormone that belongs to a class of related compounds known as

cytokines. Cytokines include a large number of similar peptides that regulate inflammation. IL-I 5 is
an unusual cytokine in that it has been shown to be anabolic in the skeletal muscle of rodents while
simultaneously decreasing fat mass469,470.471.472.473 Several other cytokines (such as IL-6, TNF-alpha
and IL-I) have been shown to be catabol ic. IL-I 5 was discovered fairly recently, therefore, Iinle is
known about the extent of its effects. IL-15 is produced in a paracrine or autocrine fashion, which is
difficult to simulate. Exogenous injections tend to raise whole body levels producing stimulation in
tissues, which could be detrimental. IL-I 5 has been shown to be a major player in the production of
white blood cells and mice that overproduce IL-IS die from leukemia474 . Although it is likely that
some are experimenting with this peptide, it is likely to be dangerous and unnecessary.

UROCORTIN II
Urocortin II is a recently discovered peptide hormone that acts at the CRF II receptor and is a
member of the CRF/urocortin family of peptide hormones. CRF is produced by the hypothalamus
and stimulates the release of ACTH which in turn stimulates the adrenal gland to produce
glucocorticoids and mineralocorticoids. CRF preferentially binds to the type I CRF receptor.
Urocortin II on the other hand acts through the type II receptor and has been shown to reduce food
intake but also to induce skeletal muscle hypertroph/ 7s Obviously, these effects are paradoxical
and have only been shown in rodents to date so it will be interesting to see how these effects will
translate into humans.
MYOSTATIN
Myostatin, for many, is the holy grail of skeletal muscle growth. It acts as a negative regulator of
muscle hypertrophy and hyperplasia which means that the more myostatin you have, the less muscle
growth occurs 477 .4 78 This is the opposite of AAS and IGF-I which are positive regulators of muscle
growth.
Myostatin is a member of the transforming growth factor beta superfamil/ 79 .4 80,481,482 Myostatin
has gotten a lot of press lately. It is a major inhibitor of muscle growth and animals that lack
myostatin have extraordinaty muscle growth, There has been a lot of speculation that inhibition of
myostatin in humans could result in the same spectacular muscle growth, While a case of myostatin
deficiency was recently documented in the scientific literature, there is a downside, Animals that
lack myostatin have a number of physiological problems including enlarged organs, cardiovascular
abnormalities and shortened lifespan, Mice deficient in myostatin have weak, brittle tendons48J
There are several dietary supplements available that claim to block myostatin resulting in
unrestrained muscle growth. Needless to say, these products do not work.
There are some potential leads in the scientific literature that might provide methods for blocking
myostatin activity, Myostatin is secreted in a larger form known as a propeptide, This propeptide
has been shown to inhibit myostatin activity. A vaccine against myostatin DNA has been shown to
increase muscle mass and endurance in mice476 , Follistatin is another protein that has also been
shown to inhibit myostatin activity. Finally, myostatin binds to the activin type liB receptor.
Injection of the soluble form of this receptor into mice has been shown to result in increased muscle
mass477 One or some combination of these methods would likely work in humans but the
consequences would be largely unknown. Myostatin comes from a large family of very important

proteins that share many receptor systems and pathways484,485.486 Using one of these methods to
inhibit myostatin activity could have severe negative side effects. Even the inhibition of myostatin
activity itself could have serious consequences. First of all, the inhibition of myostatin results in
growth of all muscles, including those which are not necessarily attractive when enlarged, such as
the abdominal muscles. Secondly, those animals with mutations of myostatin resulting in "double-
muscling" have maladies associated with the mutation.
It is unavoidable that myoslatin inhibition will be attempted (that IS, if someone is not already
attempting to do so through one of the above-mentioned methods). The question is not whether it
will work, but whether the muscle growth will be functional and if the user will suffer serious
adverse effects.

SECTION 12

HEALTH MONITORING
It is an unfortunate fact that most people, especially men, do not monitor their health closely
enough. It is even more important that steroid using athletes monitor their health, but most do not.
Many of the side effects of using anabolic steroids can be countered and their use can be made
much safer by paying attention to one's health. The simplest thing to do is to have your blood
pressure checked regularly. Automatic blood pressure cuffs can be purchased for home
measurement and are relatively inexpensive. High blood pressure is potentially one of the most
dangerous side effects of steroid use. Systolic (the top number) should stay below 120 and diastolic
(the bottom number) should stay below 80. ANY elevation should be brought to the attention of a
physician addressed through diet, aerobic exercise, reduction in androgen dose or antihypertensive
medications. Catching and treating blood pressure elevation early is very important for long-term
health.
Other monitoring is a bit more difficult in that blood tests are required. Blood tests can be expensive
and insurance companies can restrict the number that they will pay for. Also, insurance companies
have access to your medical records and too many blood tests showing negative results could
adversely affect you insurance status. People avoid this situation by using clinics and online
services such as www.directlabs.com, www.health-tests-direct.com/, www.bloodworksusa.com, or
www.lstlinkmedical.com/tests.asp. There are also home tests for cholesterol, PSA, hemoglobin etc.
however, the accuracy of these tests are largely unproven. Even if you only have blood tests
performed once a year, it is still an opportunity to make sure that the damage done from using AAS
is kept to a minimum.
The tests that can be done are CBC, Lipid Profile (HDL, LDL, TG), Liver Function (ALT, AST,
GGT, LH AP), Thyroid Panel (T4, T3 Free THY, TSH), Kidney Function (BUN, Creatinine), Blood
Chemistry and others as directed by a physician. It would also be wise to have your Total and Free
testosterone levels checked as well as FSH, LH and estradiol and estrone levels. This seems like a
lot, but most of it is pretty standard. You wi II need to speci fically ask for free and total testosterone
levels and estradiol and estrone levels as these are not normally done on an annual checkup.

BLOOD TESTS
Here you will find the reference ranges for different blood tests. These are the range of normal
values that normally occur. A test value outside these ranges can be indicative of a problem. In the
case of steroid using athletes, it is common for some values to be elevated or suppressed. This will
be explained with regard to each individual test. None of this information is meant to substitute for
the care of a licensed physician. Any lest that falls outside of normal ranges should be taken
seriously and discussed with your physician to determine the seriousness of the result.

Thyroid Panel:
Total Thyroxin (T4): 5-12 ~gldL in adults

Free Thyroxine (FT4): 0.9-2.4 ngldL
Total Triiodothyronine (T3): 70--195 ngldL
Free Triiodothyronine (FT3): 0.2-0.6 ng/dL
Free Thyroxine Index (FTI): 4-11
T3 Uptake: 24%-34%
Thyroid Stimulating Hormone (TSH): 0.4-4.5 mlUIL in adult
Summary:
As stated in the section on thyroid hormones, many androgens have the ability to alter thyroid
hormone balance by altering binding proteins and TSH production. This can lead to an initial
increase in circulating thyroid hormone levels and an increase in T3 uptake but an eventual decrease
in thyroid hormone production and secretion. Hypothyroid (low thyroid hormones) can result in
symptoms of tiredness, hair loss, weakness, muscle catabolism, constipation, fat gain, and others.
Hyperthyroid (too much thyroid) can result in symptoms such as nervousness, tremor, heart
palpitations, moodiness, sweating, diarrhea, hair loss, muscle catabolism, and weight loss.

Complete Blood Count (CBq:
White Blood Cell (WBC) Count: 4,000-10,000 WBCs per microliter (ilL)
Neutrophils: 47%-77%
Band Neutroph iIs: 00/0-3%
Lymphocytes: 160/0-43%
Monocytes: 0.50/0-10%
Eosinophils: 0.30/0-7%
Basophils: 0.30/0-2%
Red Blood Cell (RBC) Count: Men: 4.6-6.2 million RBCs per microliter (ilL)
Women: 4.2-5.4 million RBCs per ilL
Hematocrit (HCT): Men: 400/0-54%
Women: 37%-47%
Hemoglobin (Hgb): Men: 14-18 g/dL
Women: 12-16g/dL
Platelet (thrombocyte) count: 140,000-450,000 platelets per microliter (ilL)
Summary:
Androgens are known to increase red blood cell production, so it is not uncommon to see increased
RBC count as well as increased hematocrit and hemoglobin. While this is normally considered a
good thing, if hematocrit is elevated too much, it is an indication of increased blood viscosity. Since
most androgens also cause some water retention, hematocrit usually does not get out of range.
Proper hydration is also important since dehydration can cause these levels to be elevated as well.
Androgens are also known to affect bleeding times and may alter platelet counts. Heavy exercise
can cause WBC counts to be slightly elevated.

Lipid Profile:
Total Cholesterol: Less than 200 mgldL, (5.17 mmol/L)

HDL Cholesterol: Greater than 60 mgldL, (1.56 mmol/L)
LDL Cholesterol: Less than 130 mgldL
Triglycerides: Less than 150 mgldL
Summary:
It is well-known that androgens have a direct effect on lowering HDL and raising triglyceride
levels. However, it is becoming more apparent that these decreases in HDL are largely mediated by
conversion to dihydrotestosterone. Administration of finasteride tends to increase HDL levels in
men. This would also lead us to believe that steroids that are 5-alpha reduced to less potent forms
(such as nandrolone) would not be as detrimental to lipid levels. However, high doses of any
androgen will adversely affect lipid levels due to hyperstimulation of androgen receptors. It is
important to keep saturated fat at a reasonable level in the diet and to eat "clean". Altered lipid
levels are a risk factor for developing atherosclerosis and heart disease so it is important to try to
reduce the negative effects on lipid levels.

Liver Function:
Total protein: 5.5-9.0 g1dL

Albumin: 3.5-5.5 g1dL
Globulin: 2.0-3.5 g1dL
Albumin/globulin ratio: greater than 1.0
Total bilirubin: 0.3-1.0 mg/d L
Direct bilirubin: 0.1-0.3 mg/dL
Indirect bilirubin: 0.2-0.7 mgldL
Alkaline phosphatase: 38-126 lUlL
Aspartate aminotransferase(AST): 17-59 U/L
Alanine aminotransferase(ALT): 0-35 U/L
Total LDH (lactic dehydrogenase): 80-120 lUlL
Gamma-glutamyl transpeptidase (GGT): o to 51 lUlL
Summary:
An increase In serum albumin or globulin can indicate liver disease, kidney disease or severe
dehydration. It is not unusual for athletes and people using steroids to have high total protein levels
since they often consume large amounts of protein. While this is not dangerous necessarily, it is
important to rule out other causes of elevation. An elevation in albumin levels could result in greater
binding to AAS in a manner similar to SHBG.
High levels of AST usually indicate cellular damage of some kind. Levels can be elevated in cases
of liver toxicity, heart attack or kidney damage. High doses of vitamin A and heat exhaustion can
also cause elevated levels of AST. High levels of ALT can be caused by liver damage, excessive
alcohol consumption, excessive use of Tylenol, heart atlack and vigorous exercise. Elevated
alkaline phosphatase levels are another indicator of liver toxicity and elevated bilirubin can be
found when there is significant liver toxicity. It is the buildup of bilirubin in tissues giving it a
yellow color in jaundice.
Many diseases can cause elevation of lactic dehydrogenase including heart attack and liver toxicity.
GGT is another indicator of liver damage and can be elevated by consumption of alcohol or
Tylenol. The ingestion or injection of any foreign substance has the potential to damage the liver.
Everything that you put in your body has to be removed and excreted and the liver often bears the
brunt. Of course oral androgens have the most potential for liver damage; however, high doses of

injectable androgens can also raise liver enzyme levels. Accessory medications like tamoxifen as
well as alcohol consumption, vigorous exercise and consumption of large amounts of food,
especially protein, all put stress on the liver. Most of this stress is temporary and the incidence of
any lasting damage to the liver of anabolic steroid users is rare. In any case, it is important to take
steps to minimize this damage by drinking plenty of water and using things like milk thistle and
alpha-lipoic acid. Also, it is important to keep doses as low as reasonably possible and to keep the
duration of oral dosing as short as possible. As far as the tests go, any elevation should be taken
seriously and investigated, however, an elevation in more than one liver value is usually needed to
confirm some degree of liver toxicity.

Kidney Function:
Blood urea nitrogen (BUN): 8-20 mg/dL

Blood creatinine: 0.7-1.2 mg/dL
Creatinine clearance: 90-140 mLimin
BUN-to-creatinine ratio: 10:1-20:1
Summary:
A high BUN can indicate kidney damage or disease, which can be caused by high blood pressure.
BUN can also be elevated by a blockage of the urinary track (kidney stone) or by dehydration or a
high protein diet. High creatinine levels can indicate serious kidney damage or disease but
dehydration and muscle damage can also cause high levels. High creatinine clearance can be caused
by strenuous exercise and muscle damage. High Bun to creatinine ratios may indicate that there is
actual kidney damage and that elevated levels are not just due to exercise. In any case, it is
important to take the values seriously as androgens can cause kidney damage as well as high blood
pressure which can also damage the kidneys.

Blood Chemistry:
Potassium (K): 3.5-5.0 mEq/L or mmol/L

Sodium (Na): 135-145 mmol/L
Chloride (CI): 95-103 mEq/L
Calcium (Ca): 9.0-10.5 mg/dL
Phosphate: 2.5-4.5 mg/dL
Carbon dioxide: 23-29 mmol/L
Fasting Blood Glucose: less than 100 mg/dL (6.1 mmol/L)
Lactic Acid: 6-16 mg/dL
Uric Acid: Men: 3.5-7.2 mg/dL
Women: 2.6-6.0 mgldL
Summary:
Most of the synthetic androgens cause an increase in electrolyte levels. Methandrostenolone is

known to significantly increase potassium levels as is oxandrolone and nandrolone but not
testosterone. Testosterone is known to cause elevated sodium levels. Excessive retention of sodium
and potassium can cause water retention and high blood pressure. Lactic acid can be elevated with
strenuous exercise. Steroids have also been known to decrease fasting glucose levels. Altered
electrolyte levels, particularly potassium retention can be dangerous especially in potassium
supplements are taken concurrently.

Sex Hormones:
Total Testosterone: Men: 300-1,000 ng/dL

Women: less than 100 ng/dL
Free Testosterone: Men: 50-210 pg/mL
Women: less than 10 pg/mL
Bioavailable Testosterone: Male (> 18 yrs): 62-512 ng/dL
Female (> 18 yrs): 1-37 ng/dL
Prolactin: onpregnant women: less than 20 ng/mL
Men: less than 15 ng/mL
Estradiol: Women before menopause: 30-400 pg/mL or 110-1,468
pmol/L
Men: 10-50 pg/mL or 37-184 pmol/L
Estrone: Men: 10-50 pg/mL or 37-184 pmol/L
Women before menopause: 30-160 pg/mL or I I 1-592 pmol/L
Follicle Stimulating hormone (FSH): Men: 0.5-4.5 ng/mL or 2.25-20 lUlL
Women before menopause: 1.1-24ng/mL or 5-108 lUlL
Luteinizing Hormone (LH): Men: 0.4-1.9 ug/L or 3.6-17.1 lUlL
Women before menopause: 0.5-15.8 ug/L or 4.5-142 lUlL
Summary:
The use of any androgen other than testosterone will result in lowered testosterone levels. The use
of testosterone, of course, will cause testosterone levels to go very high. A fier a stack, testosterone
levels can remain low for months, or longer. People use accessory medications like clomid or HCG
to try to get testosterone production back to normal. Free testosterone is that portion of testosterone
that circulates in the blood unbound to S BG. Bioavailable testosterone is the free testosterone plus
the testosterone that is weakly bound to albumin. Estrogen and estrone levels can get very high
during a cycle ifaromatizable androgens are used and some people will combat this through the use
ofaromatase inhibitors or with tamoxifen. High estrogens can linger for some time after a cycle and
can cause problems such as gynecomastia quite easily when natural androgen levels are reduced. It
is important to keep estrogens in the normal range without suppressing them too much as they do
have important functions in men. Prolactin is often elevated as a result of increased estrogen.
Unfortunately, some people have resorted to using bromocriptine to reduce prolactin levels when it
would be more advisable to keep estrogen levels low and avoid the rise in prolactin. Even, worse,
some people associate prolactin with progesterone receptor action, or even think that prolactin and

progesterone are the same thing. This has led some to believe that using bromocriptine will stop
progesterone receptor induced gynecomastia. LH levels will decrease during a cycle as natural
testosterone levels are suppressed. FSH may decrease or may stay the same. This drop in LH is the
cause of reduced testosterone production and users will attempt to increase LH production though
the use of aromatase inhibitors or estrogen blockers like clomid.
THE ADDICT MENTALITY
After researching anabolic steroids for many years, it has become very clear that androgens have
addictive qualities. There is a very real psychological and physical dependency that develops when
a person begins to use these drugs. There are significant changes in brain chemistry with the use of
AAS that changes the behavior of the user and when the drugs are stopped, additional changes
occur in body chemistry which causes the user to experience negative feelings that lead them to
resume their usage of AAS. This makes it very difficult for even the most disciplined athlete to use
AAS reasonably and responsibly. I have seen many users take a very logical approach to the use of
AAS with very carefully planned cycles that, once started, the planned dosages were not high
enough, the duration of the cycle was not long enough or there were not enough drugs in the
"stack". As with any addictive substance, there does seem to be some variability in the degree to
which a person is affected. Some people just do not have the addictive mentality and can cycle
steroids responsibly without resorting to excess. Then, there are those that once they start, cannot
stop, and no amount of use or abuse is ever enough. What some users forget, or seem to ignore, is
that AAS are drugs with complex pharmacology and the potential for short term as well as long
term side-effects. There are so many steroid users that just WANT to be on, no matter what their
performance goals are. These are the people who will always argue that low doses do not work, that
a person must use at least two grams a week non-stop to see any results. They will argue that there
are different receptors so more drugs are needed in a cycle. They will maintain that the half-life of
testosterone cypionate is only three days instead of seven and therefore you need to inject more
often. These are the people that give AAS a bad name. It is very similar to comparing an alcoholic
to the casual drinker. These people will often be using recreational drugs along with their steroid
cycle as well as drinking alcohol (even with multiple oral steroids) and even smoking. It is no
longer about building a better physique, being a better competitor; it is simply about using the
drugs. If you are one of these people and you are reading this book, all I can say is, stop using and
get help.

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Deca-Durabolin, Durabolin, Sustanon@ and Andriol are registered trademarks of Organon Inc. DeEo-
testosterone, Halotestin, and Winstrol are registered trademarks of Phannacia Upjohn Inc. Oxandrin is
a registered trademark of BTG Pharmaceuticals. Nolvadex and Arimidex are registered trademarks of
Zeneca Pharmacuticals. Clomid is a registered trademark of Merell Dow Inc. Aldactone is a registered
trademark of Searle Inc. Dyazide is a registered trademark of Smithkline Beecham. Catapres is a
registered trademark of Boehringer Inc. Equipoise is a registered trademark of Solvay Veterinary Inc.
Finaplix is a registered trademark of Hoechst-Roussel Inc. Proscar and Propecia are registered
trademarks of Merck Inc. Periactin is a registered trademark of Merck & Co Inc. Mifeprix is a registered
trademark of Danco Laboratories, LLC. Parlodel is a registered trademark of Sandoz Phannaceuticals.
Dostinex, Aromasin, and Inspra are registered trademarks of Pfizer, Inc. Lasix is a registered trademark
of Sanofi Aventis. Accutane is a registered trademark of Hoffman-LaRoche, Inc. Avodart is a registered
trademark ofGlaxoSmithkline. Faslodex is a registered trademark of AstraZeneca. Femara and Cytadren
are registered trademarks ofNovartis. Evista is a registered trademark of Eli Lilly and Company. Fareston
is a registered trademark of GTx, Inc. Danocrine"" is a registered trademark of Sanofi Winthrop, Inc.
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III ANABOLIC PHARMACOLOGY

IN THE SENATE OF THE UNITED STATES

SEC. 3. SENTENCI G COMMISSIO GUIDELI ES.

The United States Sentencing Commission shall--

SEC. 4. PREVENTIO AND EDUCATlO PROGRAMS.

Wording from the DEA website also states that:

Alcohol (OH) Group

The basic steroid structure is a four-ring system:

PPAR (Peroxisome Proliferator-Activated Receptor)

glucocorticoid receptor activation and therefore decreased catabolism.

Progesterone is metabolized to 20-hydroxyprogesterone, 17-hydroxyprogesterone, allopregnenolone

Glucocorticoid secretion is stimulated by adrenocorticotropic hormone (ACTH), which is released

Cortisol is interconverted to cortisone and back again by enzymes referred to as II-beta

Thyroxine (T4) Tri iodothyroni ne(T3)

An interesting side effect of 5-alpha reductase inhibition is an increase in testosterone production

17-BETA HYDROXYSTEROID DEHYDROGENASES

17-beta hydroxysteroid dehydrogenase is responsible for the interconversion of C-17

Testosterone is also converted in small quantities to I I-hydroxytestosterone, which in tllrn converts

17-alpha Hydroxy Progesterone 11-Deoxycortisol

Inhibition of this enzyme results in decreased production of cortisol and mineralocorticoids

SEX HORMONE BINDING GLOBULIN

Androgens, glucocorticoids, hypothyroidism and growth hormone decrease SHBG concentrations,

THYROID HORMONE TRANSPORT

The injection procedure that a doctor will follow is as follows:

Superior Gluteal Artery

Benign Prostate Hypertrophy/Prostate Cancer

Blood Lipid Alterations

Bone Closure/Short Stature

FaciallBody Hair Growth

Lower Back Pain/Pumps

ANABOLIC PHARMACOLOGY 100

101 ANABOLIC PHARMACOLOGY

I: http://www.anabolex.com -- A hardcore site devoted to the discussion of anabolic steroids with

ANABOLIC PHARMACOLOGY 102

103 ANABOLIC PHARMACOLOGY

ANABOLIC PHARMACOLOGY 104

105 ANABOLIC PHARMACOLOGY

Name: (the most common name for the drug)

107 ANABOLIC PHARMACOLOGY

109 ANABOLIC PHARMACOLOGY

ANABOLIC PHARMACOLOGY 110

III ANABOLIC PHARMACOLOGY

Form ula: C2o HJ2 02

ANABOLIC PHARMACOLOGY 112

113 ANABOLIC PHARMACOLOGY

Formula: C2o HJ2 0

Ethylestrenol is an unusual derivative of nortestosterone. It lacks the double bonded oxygen at

ANABOLIC PHARMACOLOGY 114

115 ANABOLIC PHARMACOLOGY

ANABOLIC PHARMACOLOGY 116

117 ANABOLIC PHARMACOLOGY

ANABOLIC PHARMACOLOGY 118

119 ANABOLIC PHARMACOLOGY

Methenolone is a synthetic derivative of dihydrotestosterone. The acetate ester version is taken

ANABOLIC PHARMACOLOGY 120

121 ANABOLIC PHARMACOLOGY

Formula: C27 H42 03

ANABOLIC PHARMACOLOGY 122

123 ANABOLIC PHARMACOLOGY

Meslerolone is a simple derivative of dihydrotestosterone and is commonly known by its trade

ANABOLIC PHARMACOLOGY 124

125 ANABOLIC PHARMACOLOGY