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AASs increase muscle size and probably strength,^5,6 and athletes believe that they can enhance performance.^7,8 Performance enhancement is presumed by sporting bodies in their banning of these substances to ensure fair competition;⁹ performance enhancement is also supported by "underground" anabolic steroid guides and the media.¹⁰ Widespread and much-publicised AAS use continues at all levels of sport,⁵ having spread from elite athletes to recreational bodybuilders, adolescents and amateur athletes.¹¹ AAS use has been reported by 0.9%-7.6% of school-age males in the United States,^11-12 and 3.2% in young Australians.¹³ In the United States, 0.9% of adult males and 0.1% of females have reported AAS use;¹⁴ the prevalence in the Australian general population is not known. There is a very high reported prevalence (38%-58%) in particular subgroups worldwide, such as bodybuilders and weightlifters.¹⁵

Despite widespread AAS use, documentation of adverse effects in community users is usually based on questionnaires¹⁶ and case studies.² Clinical studies in which AASs are prescribed generally report a low rate of adverse effects.^6,17 This is a difficult area of research because the illicit status of AAS use impedes data collection. Further, those who use AASs to enhance their sporting performance should be compared with groups with similar dietary and exercise patterns rather than with population norms. Thus, we established a medical clinic which people taking AASs or considering taking them in the future could attend anonymously to undergo a medical assessment and laboratory investigations to provide data on adverse effects.

Each participant attended initial (90 minutes) and follow-up (30 minutes) consultations conducted by one practitioner (A O'S). A questionnaire was used to ask a series of open questions about medical history and history of AAS use. Participants underwent physical examination and investigations, including an electrocardiogram and blood tests. All results were discussed and follow-up of abnormal results was encouraged. Adverse effects of AAS use and the risks of parenteral drug use were discussed.

AASs were not prescribed, nor was their use supported. Participants were encouraged to enquire about adverse effects and information provided was based on published clinical research.

Participants were divided into three groups: past users were those who had ceased AAS use at least three weeks before being seen; present users, those who had used AASs within the past seven days; and potential users, those who reported they had never used AASs. The potential users (who formed our control group for the clinical, biochemical and hormonal parameters) were not asked questions about adverse effects of AASs.

Statistical analysis involved analysis of variance (ANOVA) for continuous variables, and all three groups were compared individually. For proportions, the ² test was used.

Forty-five participants (24 past, 13 present and 8 potential users) consented to blood tests. Thirteen participants reported male-to-male sexual activity.

After discussion of the adverse effects of AASs and of any abnormal findings, 30 participants (10 past, 13 present, 7 potential users) planned future AAS use, 11 (8 past, 0 present and 3 potential users) decided against further use and 17 (6 past, 4 present and 7 potential users) participants were undecided.

Mean testis volume was reduced and gonadotropins suppressed in the present users compared with the other groups and with population norms (Boxes 1 and 4). Gynaecomastia (usually tender) was detected in two present and 10 past users (P < 0.01 v. potential users), and varied from 5 mm to 50 mm in diameter. Six participants were referred for surgical review, five proceeding to bilateral excision. One past user had previously had surgery for gynaecomastia. Nineteen participants reported acne, usually involving the face and back, during AAS use.

We detected no significant difference in mean systolic and diastolic blood pressures (Box 1). Ten past users (37.0%; P = 0.02 v. potential users), five present users (29.4%) and one potential user (8.3%) were hypertensive (systolic pressure > 140 mmHg or diastolic pressure > 90 mmHg). Electrocardiograms (reported by M C K, who was blinded to AAS use) showed no evidence of myocardial ischaemia or previous myocardial infarction.

No participants had signs of chronic liver disease. Twenty participants declined serological testing for hepatitis B and C (10 past, 1 present and 9 potential users). Three present users and one potential user reported positive tests for hepatitis B, of whom one present and one potential user also reported positive tests for hepatitis C (excluded from the liver function analysis). No new cases of hepatitis B or C were detected among the 38 participants tested. There were no significant differences in the mean values of liver function tests in the three groups (Box 4). Twenty past (83.3%), eight present (61.5%) and five potential users (71.4%) had one or more abnormal liver function test results (P = 0.5). Creatine kinase levels were not significantly different between groups, but the increased values reflect increased muscle bulk and recent exercise.

Thirty-two of the 44 participants who consented to blood tests consented to HIV antibody testing; all results were negative. Of the 12 participants who declined HIV testing, seven gave no specific reason, and five reported a recent negative HIV antibody test.

AASs suppressed the hypothalamic-pituitary-gonadal axis, producing reversible suppression of gonadotropins and a reversible reduction in testis volume similar to that observed with androgens used for contraception.²¹ AAS use caused changes in libido, with decreased libido towards the end of a cycle or soon after cessation, presumably reflecting transient hypogonadism. Some participants reported erectile dysfunction, but psychological factors may have contributed.

Our finding of gynaecomastia in 12 participants (21%) was similar to proportions reported in some other studies (24%-31%;²⁰ 34%¹⁶). However, a proportion of 47% has been reported with chronic high-dose AAS use,²² and low prevalence (2%) has also been reported.¹⁷ Six of our participants were sufficiently worried about the cosmetic appearance to seek treatment, which involved surgical excision in five. Users took tamoxifen in combination with AASs in an attempt to resolve or prevent gynaecomastia.^17,23 One study reported resolution of gynaecomastia in three participants with tamoxifen.¹⁷

Time constraints precluded our attempting detailed psychological assessments. However, mood changes were reported in 48% of participants during AAS use, findings consistent with other reports.¹⁶ The psychological effects of AASs may represent an important public health problem.^20,24 One study of 41 AAS users reported that major psychiatric symptoms were common (44%),²⁵ while another reported no significant psychological side effects in AAS users taking moderate doses.²⁶ However, the dose and pattern of illicit AAS use differs from AAS use in a controlled clinical environment. On balance, it appears that these medications can have major psychological effects in some users which may be related to their prior psychological state.^20,24,26

Although mean blood pressure was not different between groups, we found that approximately a third of past and present users were hypertensive. The failure of blood pressure to return to normal after cessation of AAS use may relate to longer-term effects on vascular function.²⁷ Slight elevations in blood pressure have been reported previously following AAS use,²⁸ while other studies have reported no change in blood pressure.²⁷ Acute vascular events, including myocardial infarction and intracerebral haemorrhage, as well as cardiac arrhythmias, have been reported following AAS use.^27,29 The effects of AASs on cardiac function are discussed in a recent comprehensive review.²⁷

Abnormal results in liver function tests with AAS use have been reported previously,^2,4 although one study using weekly 600 mg intramuscular testosterone injections showed no change in liver function test results.⁶ Severe cholestasis, peliosis hepatis (blood-filled cysts in the liver⁴) and primary hepatocellular carcinoma have been reported after AAS use.² It is possible that hepatic damage may not manifest as elevated liver enzyme levels and that other means of hepatic assessment may be required.

Although all results and potential adverse effects were discussed with participants, only 11 were confident they would not start or recommence AAS use. Reasons for continuing to use AASs despite the presence and knowledge of risks are unknown, but may relate to self-esteem, body-image dissatisfaction,³⁰ or even opiate-like dependence.³¹ Compared with a control group, we found adverse effects on blood pressure and the development of gynaecomastia in AAS users, while results of liver function tests were not significantly different. Adverse effects may have been over-represented in our sample as participants may have presented because of symptoms. Long-term adverse effects may not have been identified in this study. More detailed investigations of AAS use on hypothalamic, hepatic, prostatic and cardiac function are required.

How best to approach the public health problem of AAS misuse is yet to be determined. Information about AASs should be made readily available to educate the general public and medical practitioners.³² Data obtained should aid further policy decision-making into methods of reducing AAS use. Further research into the reasons why people self-administer AASs, and into methods of reducing AAS use in the community, is required.

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St Vincent's Hospital, Sydney, NSW.
Michael C Kennedy, FRACP, MD, Consultant Physician,
Richard O Day, AM, FRACP, Professor of Clinical Pharmacology;
John H Casey, FRACP, PhD, Consultant Endocrinologist, Department of Endocrinology;
Alex D Wodak, FRACP, FAFPHM, Director, Department of Alcohol and Drug Services.

Institute of Sport, Concord Hospital, Sydney, NSW.
Brian Corrigan, AM, FRACP, Director.

Reprints will not be available from the author(s).
Correspondence: Dr A J O'Sullivan, Department of Medicine, St George Hospital, Belgrave Street, Kogarah, NSW, 2217.

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