What Makes These Hormones So Evil?
by John Williams
"Laws are like sausages. It's better not to see
them being made."
Otto von Bismarck (1815-1898)
Introduction
In the United States, anabolic-androgenic
steroids (AAS) have always been considered drugs.
Contrary to what today's young athletes may believe,
these substances were never stocked on the shelves
of the corner grocery store. However, only within
the last decade have these drugs been classified
as "controlled substances," thereby placing them
in the same general category as more infamous drugs,
including heroin, cocaine, LSD, and methamphetamine.
The purpose of this article is to examine some of
the social, medical and
legal
forces which have driven these changes and which
continue to influence the use, abuse, and prohibition
of anabolic-androgenic steroids.
What Led to the Classification of AAS as
Controlled Substances?
Historically, AAS were classified as prescription
drugs; they could be dispensed only upon the order
of a licensed medical practitioner, who could then
monitor their use and control individual dosages.1
Minors could not obtain prescriptions for AAS without
the informed consent of their parents or guardian.
Since medical practitioners knew that the administration
of hormones could affect the body's natural development,
particularly in adolescents, they rarely prescribed
AAS for minors, except in cases of a genuine medical
disorder. Thus, as we examine the history of AAS
and the progression toward their prohibition, we
should be mindful of the following:
- Anabolic-androgenic steroids were subject
to government regulation long before legislators
decided to criminalize their use;
- Prior to the criminalization of AAS, proper
dosages could be prescribed and potential side
effects could be monitored by trained medical
practitioners;
- Existing government regulation, a practitioner's
medical judgment, and the required consent of
legal guardians have always stood as natural
barriers between adolescents and their use of
AAS.
In June of 1889, Charles Édouard Brown-Séquard,
a 72-year-old physiology professor, announced at
the Société de Biologie that he had injected himself
with extracts of dog and guinea pig testicles, resulting
in an increase in his physical strength and health;
further research into these purported effects led
to the synthesis of
testosterone in 1935.2 During World
War II, German scientists began to synthesize other
anabolic steroids, experimenting with human prisoners,
as well as with German troops, whose aggressive
tendencies they hoped to increase.3 Adolph
Hitler's personal physician reported that Hitler
was given injections of testosterone derivatives
for various maladies.4 Ironically, one
of the initial therapeutic uses of AAS was treatment
of chronic wasting, such as was experienced by Nazi
concentration camp prisoners.5
As early as the 1950s, bodybuilders and strength
athletes began to experiment with AAS. Soviet weightlifters
demonstrated impressive strength gains from the
use of testosterone derivatives, and their secret
was passed on to the Americans at the 1954 World
Championship.6 By the 1960s, the medical
community was conducting controlled scientific studies
of the effects of AAS on strength and muscle mass.7
Early studies yielded promising results, but later
research concluded that no palpable strength or
muscle gains resulted from the use of AAS; recently,
this trend has reversed, with scientists again finding
that AAS promotes strength and muscle gains.8
This discrepancy in scientific findings leads one
to wonder if some researchers intentionally misrepresented
scientific findings in order to discourage the use
of AAS for physical enhancement.
By the late 1960s, the use of AAS had become
commonplace amongst bodybuilders and strength athletes,
a trend which was quite noticeable in Olympic competition;
the androgynous appearance of female athletes from
former Communist bloc nations was a regular source
of bawdy humor. In 1975, the Medical Commission
of the International Olympic Committee (IOC) added
anabolic steroids to
its list of banned substances, and testing began
at the 1976 Montreal Olympic Games.9
The most notorious violation of the IOC's drug policy
came in 1988, when Olympic sprinter Ben Johnson
was stripped of his gold medal in the 100-meter
after testing positive for the use of AAS; another
positive test in 1993 resulted in Johnson being
subject to a lifetime ban.10
Acting upon the lead of the IOC, the National
Collegiate Athletic Association (NCAA) followed
suit. Although the NCAA had, in principle, banned
the use of AAS in the college sports in 1973, it
was not until 1986 that it initiated an active testing
program.11 Likewise, the National Football
League (NFL) began testing professional football
players for AAS use during training camps in 1986,
and by 1990, the NFL's testing program included
random tests during the regular competitive season.12
The medical community was not blind to the fact
that AAS were regularly distributed outside legal
channels; in December of 1986, the American Medical
Association (AMA) published a report that endorsed
the efforts of law enforcement to curb illegal distribution
of AAS and promoted educational efforts to increase
public understanding of the issues surrounding the
use of AAS.13 Nevertheless, the AMA opposed
the criminalization of AAS because government regulation
of prescription drugs already existed, and because
AAS did not meet the traditional criteria for scheduling
drugs as controlled substances.14 Despite
this opposition, a few vocal practitioners published
studies and lobbied strenuously for AAS to be classified
as illicit drugs.15 As a result, the
Anabolic
Steroids Control Act was passed into law by
the federal legislature, and AAS were classified
as Schedule III controlled substances.16
Once AAS were classified as controlled substances
under federal law, mere possession could result
in penalties of imprisonment of up to one year for
a first offense, with enhanced penalties for subsequent
offenses.17 Manufacturing, distributing
or dispensing AAS, or possessing AAS with purpose
to do the same, could result in imprisonment up
to five years.18 However, the most onerous
burden under the new classification may have been
the one placed on medical practitioners by the Code
of Federal Regulations: if a practitioner prescribes
AAS for any purpose other than a "legitimate medical
purpose * * * in the usual course of his professional
practice," or for "authorized research," he or she
may be prosecuted as common drug dealer and subjected
to the same penalties.19
Although the general public presumes that federal
jurisdiction is without limit, it is not. Federal
authorities cannot possibly investigate and prosecute
all drug cases, nor do they have the universal jurisdiction
to do so. Approximately 92% of all drug trafficking
convictions are in state courts, as are nearly all
convictions of simple drug possession.20
Therefore, nearly all states have adopted the federal
classification of anabolic steroids as controlled
substances.21 Perhaps more interesting
are the specific limitations which some states have
placed on medical practitioners regarding prescriptions
for AAS. Ohio law specifically prohibits a licensed
health professional from prescribing, administering,
or personally furnishing "a schedule III
anabolic steroid for
the purpose of human muscle building or enhancing
human athletic performance."22 A Texas
statute prohibits a medical practitioner from dispensing,
prescribing, delivering, or administering AAS for
anything other than "a valid medical purpose," further
stating that "bodybuilding, muscle enhancement,
or increasing muscle bulk or strength through the
use of an anabolic steroid or human growth hormone
listed in Schedule III by a person who is in good
health is not a valid medical purpose."23
Statutes such as these are clearly intended to intimidate
medical practitioners and preclude any possibility
that AAS will ever be legally prescribed for physical
enhancement.
The attack on AAS did not end with their legal
prohibition. Passionate statements before Congress
continue to this day. On October 20, 1999, in a
statement before the Senate Committee on Commerce,
Science and Transportation, drug czar Barry McCaffrey
asserted that "the international sale of steroids
is becoming increasingly sophisticated and entrenched
in criminal networks."24 Furthermore,
McCaffrey has joined in the active movement to ban
prohormones, stating, "The DEA is engaged in a scientific
process to determine if Andro [androstenedione]
actually produces muscle growth -- and, in turn,
whether it should be classed as a steroid."25
As we stand at the turn of the millennium, AAS
have been
banned in sports, prohibited by law, and vilified
before the general public. But what is it that makes
anabolic-androgenic steroids so evil?
Why Should AAS Be Illicit Drugs?
Anabolic-androgenic steroids are clearly the
"bastard child" of controlled substances. A review
of federal and state drug schedules reveals that
nearly all controlled substances are listed in sub-classifications
which describe them in terms of their immediate
psychoactive effects: stimulants, depressants, hallucinogens,
and narcotics or opiates.26 Since AAS
appear to have no immediate mood-altering effects,
how did they come to be classified amongst this
collection of unlike drugs?
Numerous references have been made in popular
literature to the "serious side effects" of anabolic
steroids. But what substantial side effects are
well established by scientific evidence?
We know that certain AAS, when taken in substantial
amounts, are toxic to the liver; however, this applies
largely to 17-alpha-alkylated steroids, such as
methandrostenolone
(Dianabol) and
oxymethelone
(Anadrol®-50).27 There appears to
be no strong evidence of such hepatotoxicity in
orally-effective testosterone esters, such as
methenolone acetate (Primobolan) and
testosterone
undecanoate, nor in the many injectable testosterone
esters, including
testosterone cypionate (Depo-Testosterone) and
nandrolone decanoate (Deca-Durabolin).28
It has also been suggested that hepatocellular carcinoma
(liver cancer) may result from the long-term use
of 17-alpha-alkylated AAS, although a regression
of tumors has been noted when AAS use is discontinued.29
Liver toxicity alone can hardly justify the classification
of AAS as controlled substances. Paracetamol, also
known as acetaminophen (Tylenol®), is touted as
"the most trusted combination of strength and safety
in pain relief today,"30 yet liver damage,
even fatal hepatic necrosis, has been reported from
repeated therapeutic usage of this over-the-counter
drug, particularly from therapeutic usage
amongst alcoholics.31 Nevertheless, even
if the hepatotoxicity of 17-alpha-alkylated AAS
is a matter of great concern, the banning of less
toxic AAS contributes to the problem. A perfect
example is
stanozolol (Winstrol), a 17-alpha-alkylated
steroid that is toxic to the liver in both its oral
and injectable form, but which continues to be readily
available on the U.S. black market because of its
use as a veterinary drug (Winstrol®-V).32
One might logically speculate that the current use
of more toxic AAS is less a matter of choice than
one of accessibility, where the availability of
safer choices has been limited by a legal prohibition
that applies to all AAS, regardless of their
toxicity.
The negative psychological and behavioral effects
of AAS, commonly known as "'roid rage," seem to
be accepted as a proven fact in popular, nonscientific
literature;33 however, there is little
conclusive proof that supports this presumption.
Once again, such effects appear to occur in cases
involving 17-alpha-alkylated steroids, but not in
cases involving 17-beta-estrified steroids.34
Furthermore, the existing studies cannot account
for the pre-steroid tendencies of individual users
with respect to violence and aggression, nor can
they account for the psychological "placebo effect"
that may occur from an AAS user's expectations of
heightened aggression. A detailed critique of those
studies, and flaws in their methodology, can be
found in a recent
Meso-Rx article by Jack Darkes, an expert in
the psychology of drug use.35 At best,
we can conclude that "'roid rage," to the extent
that it exists, may be limited to specific varieties
of AAS, and that such hyper-aggressive states may
well be the result of preexisting tendencies or
predetermined expectations of the user.
There has been much criticism of AAS for their
effect on a user's cardiovascular health; however,
this research is also highly speculative. One study
involving bodybuilders who self-administered AAS
found that AAS users had a ratio of "bad" low-density
lipoprotein cholesterol (LDLC) to "good" high-density
lipoprotein cholesterol (HDLC) that was four times
that of non-users;36 however, other studies
have indicated that this effect is, once again,
limited to 17-alpha-alkylated steroids.37
Later studies have indicated that AAS users retained
substantial increases in lean body mass and muscle
size three months after withdrawal, but with lipoprotein
levels which were no different than those of non-users.38
Furthermore, a study involving controlled dosages
of a 17-beta-estrified steroid showed that a 22-27%
decrease in HDLC was almost completely reversed
six weeks after discontinuation.39 It
should also be noted that diet is also a substantial
factor in the analyses of lipoprotein levels and
ratios; decreases in the intake of saturated fats
and dietary cholesterol can reduce LDLC levels by
more than 33%.40 Simply put, there seems
to be no concrete evidence that the use of AAS leads
to permanent cardiovascular health risks.
The greatest disgrace amongst the anti-AAS medical
community may be its "code of silence" as to the
major health benefits of AAS use. Though
rarely mentioned by the medical practitioners, scientific
studies have concluded that "anabolic-androgenic
steroid use as practiced by contemporary athletes
is a potent modulator of immune responsiveness."41
This benefit to the human immune response is by
no means inconsequential, particularly to those
with whose immune systems have been damaged by disease
or congenital defects. The use of AAS is becoming
an important element in the
treatment
of AIDS patients, not only to prevent AIDS-related
"wasting," but also to boost a severely depressed
immune response. Further information on the use
of AAS in AIDS treatment may be found at the
Medibolics™
web site.42
Without question, AAS produce several minor side
effects which are not life-threatening. But are
these minor problems sufficient to warrant the classification
of AAS as illicit drugs? Are many of these side
effects nothing more than minor annoyances which
many people endure as a result of their own hormonal
balances?
Acne has long been associated with elevated levels
of
free testosterone, particularly amongst young
women.43 Since AAS are potent providers
of free testosterone, they are also recognized as
a cause of acne.44 But isn't acne, to
varying degrees, an inevitable consequence of adolescence?
Doesn't every teenager learn to contend with the
"zits" brought on by the raging hormonal imbalances
of puberty?
It is also well established that AAS use can
lead to gynecomastia, an abnormal expansion of the
mammary glands in human males.45 Although
this condition is generally undesirable amongst
men, it is far from life-threatening, and it appears
to be treatable by the use of antiestrogenic compounds
such as
tamoxifen
(Nolvadex®)46, or by simple cosmetic
surgical procedures which have been practiced for
approximately 500 years.47 In any event,
it is apparent that the negative effects of gynecomastia
are largely aesthetic and not a justification for
criminalization of AAS.
Continued use of AAS can lead to atrophy of the
testicles; this is due to the endocrine feedback
loop, whereby a male's body reacts to the introduction
of additional testosterone by reducing its own natural
production of both testosterone and sperm.48
However, this effect appears to be
reversible upon the cessation of AAS use, and
medical researchers have found it to be therapeutically
useful for birth control.49 A report
of the World Health Organization is particularly
interesting in this respect: after global trials
of AAS as a male contraceptive, they found only
minimal short-term physical side effects from doses
exceeding those which caused Ben Johnson's Olympic
disqualification!50
The minor side effects of AAS are naturally more
pronounced when they are used by women. Negative
side effects can include enlargement of the clitoris,
hirsutism (masculine hair growth), and deepening
of the voice, while the positive side effects may
include muscle growth and reduction of body fat.51
Although most women would wish to avoid the negative
aspects of AAS use, it appears that none of the
foregoing side effects are life-threatening, and
if AAS
use by women is strictly limited in time and
dosage, the positive effects of muscle growth and
fat reduction might prove to be an acceptable trade-off.
- Comparison to Other Medical Procedures
While the serious side effects of AAS use appear
to be mostly speculative, and the minor side effects
are largely limited and reversible, critics of AAS
use will often justify the
criminalization of these drugs by pointing to
the fact that their use is predominantly for cosmetic
purposes and to enhance athletic performance, not
for treatment of legitimate medical disorders. Therefore,
it seems fair that these criticisms be evaluated
by comparing AAS use to legal medical procedures
which are used solely for cosmetic and physical
enhancement.
Cosmetic surgery has become commonplace within
our society. For actors and models, whose physical
appearance is an essential element of their work,
it is often accepted as an absolute necessity. Yet
cosmetic surgery is far from risk-free. Serious
complications and at least one death have been reported
as a result of local infection from purely cosmetic
rhinoplasty ("nose jobs").52 Infection
has been reported in as much as 7% of all cases
of augmentation mammoplasty (breast enhancement
surgery),53 and various other complications
have been observed after cosmetic breast surgery,
including Mondor's disease (hardening and blockage
of veins underlying the breasts),54 fibromyalgia
(aching pain in muscles and connective tissues)
and chronic fatigue syndrome,55 and the
frequent hardening, leakage, or collapse of implants.56
Suction-assisted lipectomy or "liposuction" (the
surgical removal of body fat by suction) is now
the most common cosmetic surgical procedure in North
America, despite the fact that it has resulted in
significant incidences of blood vessel blockage
and death.57 Nevertheless, all of these
purely cosmetic surgical procedures remain legal
in the United States. Can it be said that these
invasive surgical procedures are somehow safer than
the controlled administration of AAS by a qualified
practitioner for the purpose of muscle and strength
enhancement?
Purely cosmetic pharmaceutical treatments are
also quite popular in the United States. America's
obsession with hair has led many men to develop
a severe phobia of male pattern baldness, and the
pharmaceutical companies have gleefully exploited
that fear.
Finasteride
(Propecia®) is an oral prescription drug originally
designed to treat benign prostate hyperplasia, but
which is now used to combat common male pattern
baldness by reducing the conversion of testosterone
into dihydrotestosterone (DHT), a primary cause
of common baldness.58 Since finasteride
operates by the manipulation of male hormones, as
do anabolic-androgenic steroids, its side effects
tend to be similar or converse to those of AAS.
Reported side effects include impotence, allergic
reactions, loss of sexual desire, and gynecomastia,
and pregnant women are warned not to even touch
broken tablets because of possible deformities to
the sexual organs of a male fetus.59
Tretinoin (Retin-A® or Renova®), is a topical prescription
drug used to treat acne, but its use has been expanded
to the removal of wrinkles and striae (stretch marks)
on skin;60 its possible side effects
include skin rashes and peeling and severe swelling
and burning sensations.61 Despite the
substantial side effects of these prescription drugs,
they remain legal for use in purely cosmetic therapy.
Those most extreme medical procedure for modification
of physical appearance is considered by many to
be an abomination: gender reassignment surgery,
i.e., "sex change operations." Despite the
horror that many people experience when confronted
with this subject, gender reassignment "is now an
established and accepted practice in many parts
of the world."62 Gender reassignment
involves extensive surgical alteration of the genitals,63
as well as hormonal therapy, which in female-to-male
transsexuals involves the administration of anabolic-androgenic
steroids.64 It is interesting to
note that in one study, the administration of these
androgens to female-to-male transsexuals resulted
in no serious morbidity (disease) in nearly 300
cases of long-term use,65 while in another
study, the mortality and morbidity of male-to-female
transsexuals treated with female hormones was far
beyond that of female-to-male transsexuals treated
with androgens.66 While the ethics of
gender reassignment are debatable on a case-by-case
basis, it is worthy of comment that in one study
involving 20 patients seeking gender reassignment,
more than half were found to exhibit psychotic trends.67
Nevertheless, gender reassignment is legal in the
United States, and it continues to be a legally
legitimate purpose for prescribing AAS!
The True Evil Revealed
If the comparative dangers of AAS use for physical
enhancement do not warrant their criminalization,
then what characteristic of these substances justifies
their classification as a controlled substance?
Perhaps a review of the legal definition would be
instructive.
In addition to naming specific substances, federal
law provides an inclusive, general definition of
"anabolic steroids"; identical or near-identical
definitions have been adopted by many states.68
The first portion of this definition refers directly
to the chemical nature of the substance:
"[A]ny drug or hormonal substance, chemically
and pharmacologically related to testosterone
(other than estrogens, progestins, and corticosteroids)
..."69
The most interesting aspects of this portion
of the definition are the exclusions. Nearly all
steroid compounds are "chemically and pharmacologically
related to testosterone," but certain steroid hormones
were not deemed appropriate for criminalization.
Estrogens and progestins, female hormones commonly
used in contraceptives, were specifically exempted
from status as illicit drugs, as were the predominantly
catabolic corticosteroids, which are commonly used
to treat inflammation. Thus, the chemical portion
of the general definition is of little help in determining
the reason for criminalization.
The true basis for banning AAS is revealed in
the latter portion of the general definition:
"... that promotes muscle growth,
and includes * * * any salt, ester, or isomer
of a drug substance described or listed in this
paragraph, if that salt, ester, or isomer
promotes muscle growth."70
By definition, the single characteristic of AAS
that makes them subject to classification as controlled
substances is the fact that they promote muscle
growth. The statutory definition does not refer
to dangerous side effects or potential for abuse,
only the promotion of muscle growth. This factor
is no mystery to those who support the criminalization
of these substances. In October 1999, drug czar
Barry McCaffrey clearly expressed his desire to
ban androstenedione by stating:
"The DEA is engaged in a scientific process
to determine if Andro [androstenedione] actually
produces muscle growth -- and, in turn,
whether it should be classed as a steroid."71
What conclusions can be drawn from this single,
defining characteristic of AAS? We are not faced
with a definition which would ban all steroids,
since many steroid drugs are exempted from that
definition. Nor are we faced with with a definition
that refers to specific dangers. Rather, we are
faced with a definition that seeming leads to only
one conclusion: muscle growth must be a bad thing!
Part II:
The Demonization of Anabolic Steroids: Modern
Society's Love-Hate Relationship with Strength and
Muscle
Footnotes
1Taylor WN. Macho Medicine: A History
of the Anabolic Steroid Epidemic. Jefferson,
N.C.: McFarland&Co.,1991.
2Hoberman JM; Yesalis CE. The history
of synthetic testosterone. Scientific American.,
Feb.1995;76,77.
3Taylor WN, Macho Medicine,
supra at 8.
4Id. at 8-9.
5Hoberman JM, et al., Synthetic
testosterone, supra at 80.
6Id. at 77.
7eg., Fowler WM Jr; Gardner
GW; Egstrom GH. Effect of an anabolic steroid on
physical performance of young men. J Appl Physiol.,
1965;20(5):1038-40.
8Compare Johnson LC; O'Shea
JP. Anabolic steroid: effects on strength development.
Science., 1969;164(882):957-9; Percy
EC. Athletic aids: fact or fiction? Can Med Assoc
J., 1977;117(6):601-5; Hartgens F; Kuipers H;
Wijnen JA; Keizer HA. Body composition, cardiovascular
risk factors and liver function in long-term androgenic-anabolic
steroids using bodybuilders three months after drug
withdrawal. Int J Sports Med., 1996;17(6):429-33.
9Yesalis C. Incidence of anabolic
steroid use: a discussion of methodological issues.
Anabolic Steroids in Sport and Exercise.
Champaign, IL: Human Kinetic Publishers, Inc.,1993.
10 Bilder R. Drug testing in sport.
[http://www.gemini.co.uk/gemini/biopages/article/art-drug.html]
Gemini Biopages. 1995.
11Yesalis C; Courson S; Wright J.
History of anabolic steroid use in sport and exercise.
Anabolic Steroids in Sport, supra.
12 Ferstle J. Evolution and politics
of drug testing. Anabolic Steroids in Sport,
supra.
13Taylor WN, Macho Medicine,
supra at 37.
14 Id. at 58.
15 Taylor WN. Synthetic anabolic-androgenic
steroids: a plea for controlled substance status,
commentary. Physician & Sportsmed., 1987;15(5):140-150.
16 Anabolic Steroids Control Act of
1990, Pub. L. 101-647, 1901, 104 Stat. 4851 (1990).
17 21 U.S.C. 844.
18 21 U.S.C. 841(b)(1)(D).
19 21 C.F.R. 1306.04(a).
20 Brown JM; Langan PA. Felony
Sentences in the United States, 1996. July 1999,
NCJ 175045. [http://www.ojp.usdoj.gov/bjs/pub/pdf/fsus96.pdf]
U.S. Dept. of Justice, July 1999.
21 e.g., Ohio Revised Code
3719.41; Florida Statutes 893.03; Texas Health &
Safety Code 481.104; and New York State Consolidated
Laws: Public Health 3306.
22 Ohio Revised Code 3719.06(B).
23 Texas Health & Safety Code 481.071(b),(c).
24 McCaffrey, Barry R. "Before the
Senate Committee on Commerce, Science, and Transportation"
[http://www.senate.gov/~commerce/hearings/1020mcc.pdf]
October 20, 1999.
25 Id.; see also, Collins R;
Williams JM. Banning prohormones: the threat and
the legal issues. [http://www.mesomorphosis.com/exclusive/collins/prohormones.htm]
Mesomorphosis, 23 Nov. 1999.
2621 U.S.C. 812; 21 C.F.R. 1308.01-1308.15;
R.C. 3719.41 (Ohio).
27Kopera H. Side effects of anabolic
steroids and contraindications. Wien Med Wochenschr.
1993;143:399.
28Id.; Kuipers H; Wijnen JA;
Hartgens F; Willems SM. Influence of anabolic steroids
on body composition, blood pressure, lipid profile
and liver functions in body builders. Int J Sports
Med. 1991;12:413.
29Falk H; Thomas LB; Popper H; Ishak
KG. Hepatic angiosarcoma associated with androgenic-anabolic
steroids. Lancet. 1979;2:1120; Farrell GC;
Joshua DE; Uren RF; Baird PJ; Perkins KW; Kronenberg
H. Androgen-induced hepatoma. Lancet. 1975;1:430.
30TYLENOL® ACETOMINOPHEN. [http://www.tylenol.com/products/adult/pain/index.htm]
McNeil Consumer Healthcare 1999.
31Prescott LF. Liver damage with non-narcotic
analgesics. Med Toxicol. 1986;1 Suppl 1:44;
Eriksson LS; Broome U; Kalin M; Lindholm M. Hepatotoxicity
due to repeated intake of low doses of paracetamol.
J Intern Med. 1992;231:567; Patel F. The
fatal paracetamol dosage--how low can you go?
Med Sci Law. 1992;32:303.
32Winstrol®-V Sterile Suspension and
Tablets [http://www.pnuanimalhealth.com/companimal/winstf.html]
Pharmacia & Upjohn 1999
33Taber A. 'Roid rage. [http://www.salon.com/health/feature/1999/11/18/steroids/print.html]
Salon.com. November 18, 1999.
34 Bahrke MS, Yesalis CE and Wright
JE. Psychological and behavioral effect of endogenous
testosterone levels and anabolic-androgenic steroids
among males. Sports Med. 1990;10(5):303-337.
35 Darkes J. Anabolic/androgenic steroid
use and aggression I: a review of the evidence.
[http://www.mesomorphosis.com/exclusive/vol02/aggression-01.htm]
Mesomorphosis. 23 Nov. 1999.
36 Lenders JW; Demacker PN; Vos JA;
Jansen PL; Hoitsma AJ; van 't Laar A; Thien T. Deleterious
effects of anabolic steroids on serum lipoproteins,
blood pressure, and liver function in amateur body
builders. Int J Sports Med. 1988;9(1):19-23.
37 Kopera H. Side effects of anabolic
steroids and contraindications, supra.
38 Hartgens F, et al. (1996)
Body composition, cardiovascular risk factors,
supra.
39 Kuipers H, et al. (1991)
Influence of anabolic steroids on body composition,
supra.
40 Lewis B. Diet and exercise as regulators
of lipid risk factors. Drugs. 1990;40 Suppl
1:19-24.
41 Calabrese LH; Kleiner SM; Barna
BP; Skibinski CI; Kirkendall DT; Lahita RG; Lombardo
JA. The effects of anabolic steroids and strength
training on the human immune response. Med Sci
Sports Exerc. 1989;21(4):386-92.
42 Mooney M; Brockman J; Vergel N.
Medibolics. [http://www.digiweb.com/~mmooney/toc2.htm]
15 Dec. 1999.
43 Schiavone FE; Rietschel RL; Sgoutas
D; Harris R. Elevated free testosterone levels in
women with acne. Arch Dermatol. 1983;119(10):799-802;
Yang XQ; Shen XL; Wu ER; Xia TA. Testosterone and
estradiol serum levels in acne. Chin Med J (Engl).
1989;102(3):236-8.
44 Kiraly CL; Alen M; Korvola J; Horsmanheimo
M. The effect of testosterone and anabolic steroids
on the skin surface lipids and the population of
Propionibacteria acnes in young postpubertal men.
Acta Derm Venereol. 1988;68(1):21-6; Scott
MJ 3d; Scott AM. Effects of anabolic-androgenic
steroids on the pilosebaceous unit. Cutis.
1992;50(2):113-6.
45 Pope HG Jr; Katz DL. Psychiatric
and medical effects of anabolic-androgenic steroid
use. Arch Gen Psychiatry. 1994;51(5):375-82;
Evans NA. Gym and tonic: a profile of 100 male steroid
users. Br J Sports Med. 1997;31(1):54-8.
46 Parker LN; Gray DR; Lai MK; Levin
ER. Treatment of gynecomastia with tamoxifen: a
double-blind crossover study. Metabolism.
1986;35(8):705-8.
47 Teimourian B; Perlman R. Surgery
for gynecomastia. Aesthetic Plast Surg. 1983;7(3):155-7;
Dogan T; Bayramicli M; Numanoglu A. Plastic surgical
techniques in the fifteenth century by Serafeddin
Sabuncuoglu. Plast Reconstr Surg. 1997;99(6):1775-9;
Colombo-Benkmann M; Buse B; Stern J; Herfarth C.
Indications for and results of surgical therapy
for male gynecomastia. Am J Surg. 1999;178(1):60-3.
48 Alen M; Hakkinen K. Physical health
and fitness of an elite bodybuilder during 1 year
of self-administration of testosterone and anabolic
steroids: a case study. Int J Sports Med.
1985;6(1):24-9; Hoberman JM, et al., Synthetic
testosterone, supra at 80.
49 Schurmeyer T; Knuth UA; Belkien
L; Nieschlag E. Reversible azoospermia induced by
the anabolic steroid 19-nortestosterone. Lancet.
1984;1(8374):417-20.
50 Hoberman JM, et al., Synthetic
testosterone, supra at 80.
51 Taylor WN, Macho Medicine,
supra at 55-56.
52 Cabouli JL; Guerrissi JO; Mileto
A; Cerisola JA. Local infection following aesthetic
rhinoplasty. Ann Plast Surg. 1986;17(4):306-9.
53 LeRoy J; Given KS. Wound infection
in breast augmentation: the role of prophylactic
perioperative antibiotics. Aesthetic Plast Surg.
1991;15(4):303-5.
54 Elsahy NI. Recurrent Mondor's disease
after augmentation mammoplasty. Aesthetic Plast
Surg. 1983;7(4):259-60.
55 Fenske TK; Davis P; Aaron SL. Human
adjuvant disease revisited: a review of eleven post-augmentation
mammoplasty patients. Clin Exp Rheumatol.
1994;12(5):477-81.
56 Ganott MA; Harris KM; Ilkhanipour
ZS; Costa-Greco MA. Augmentation mammoplasty: normal
and abnormal findings with mammography and US.
Radiographics. 1992;12(2):281-95.
57 Smith KA; Levine RH. Influence
of suction-assisted lipectomy on coagulation.
Aesthetic Plast Surg. 1992;16(4):299-302.
58 Propecia News. [http://www.hairmed.com/propecia.htm]
Ridgewood Dermatology & Hair Transplant Center,
PC. 12 Sep. 1999.
59 Id.; Patient information
about Propecia. [http://www.merck.com/product/usa/propecia/cns/ppi/ppi.html]
Merck & Co., Inc. Aug. 1999.
60 Bergfeld WF. A lifetime of healthy
skin: implications for women. Int J Fertil Womens
Med. 1999;44(2):83-95.
61 Experimental use of Retin-A. [http://www.fda.gov/bbs/topics/ANSWERS/ANS00263.html]
U.S. Food & Drug Admin. 4 Feb. 1988.
62 Snaith RP; Hohberger AD. Transsexualism
and gender reassignment. Br J Psychiatry.
1994;165(3):418-9.
63 Rehman J; Melman A. Formation of
neoclitoris from glans penis by reduction glansplasty
with preservation of neurovascular bundle in male-to-female
gender surgery: functional and cosmetic outcome.
J Urol. 1999;161(1):200-6.
64 Meyer WJ 3d; Finkelstein JW; Stuart
CA; Webb A; Smith ER; Payer AF; Walker PA. Physical
and hormonal evaluation of transsexual patients
during hormonal therapy. Arch Sex Behav.
1981;10(4):347-56.
65 van Kesteren PJ; Asscheman H; Megens
JA; Gooren LJ. Mortality and morbidity in transsexual
subjects treated with cross-sex hormones. Clin
Endocrinol (Oxf). 1997;47(3):337-42.
66 Asscheman H; Gooren LJ; Eklund
PL. Mortality and morbidity in transsexual patients
with cross-gender hormone treatment. Metabolism.
1989;38(9):869-73.
67 Finney JC; Brandsma JM; Tondow
M; Lemaistre G. A study of transsexuals seeking
gender reassignment. Am J Psychiatry. 1975;132(9):962-4.
68 21 U.S.C. 802(41)(A); Ohio Revised
Code 3919.41; Florida Statutes 893.03; Texas Health
& Safety Code 481.104; and New York State Consolidated
Laws: Public Health 3306.
69 21 U.S.C. 802(41)(A).
70 Id. (Emphasis added).
71 McCaffrey, Barry R. Before the
Senate Committee, supra. (Emphasis added).
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