The Demonization of Anabolic Steroids, Part 1 – What Makes These Hormones So Evil?

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?

Serious Side Effects

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

Minor Side Effects

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!

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://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://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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Captopril, Alpha-2 Receptors and Fat Loss

The Permissive Substance Angiotensin II is a polypeptide which is required for the expression of some (but not all) alpha-2...

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