Background-The problem of anabolic-androgenic steroid (AAS) abuse has recently generated widespread public and media attention. Most AAS abusers, however, are not elite athletes like those portrayed in the media, and many are not competitive athletes at all. This larger but less visible population of ordinary AAS users began to emerge in about 1980. The senior members of this population are now entering middle age; they represent the leading wave of a new type of aging former substance abusers, with specific medical and psychiatric risks. Methods-We reviewed the evolving literature on long-term psychiatric and medical consequences of AAS abuse.Results-Long-term use of supraphysiologic doses of AAS may cause irreversible cardiovascular toxicity, especially atherosclerotic effects and cardiomyopathy. In other organ systems, evidence of persistent toxicity is more modest, and interestingly, there is little evidence for an increased risk of prostate cancer. High concentrations of AAS, comparable to those likely sustained by many AAS abusers, produce apoptotic effects on various cell types, including neuronal cells -raising the specter of possibly irreversible neuropsychiatric toxicity. Finally, AAS abuse appears to be associated with a range of potentially prolonged psychiatric effects, including dependence syndromes, mood syndromes, and progression to other forms of substance abuse. However, the prevalence and severity of these various effects remains poorly understood.Conclusions-As the first large wave of former AAS users now moves into middle age, it will be important to obtain more systematic data on the long-term psychiatric and medical consequences of this form of substance abuse.

Aims-Anabolic-androgenic steroids (AAS) are widely used illicitly to gain muscle and lose body fat. Here we review the accumulating human and animal evidence showing that AAS may cause a distinct dependence syndrome, often associated with adverse psychiatric and medical effects.Method-We present an illustrative case of AAS dependence, followed by a summary of the human and animal literature on this topic, based on publications known to us or obtained by searching the PubMed database.Results-About 30% of AAS users appear to develop a dependence syndrome, characterized by chronic AAS use despite adverse effects on physical, psychosocial, or occupational functioning. AAS dependence shares many features with classical drug dependence. For example, hamsters will self-administer AAS, even to the point of death, and both humans and animals exhibit a welldocumented AAS withdrawal syndrome, mediated by neuroendocrine and cortical neurotransmitter systems. AAS dependence may particularly involve opioidergic mechanisms. However, AAS differ from classical drugs in that they produce little immediate reward of acute intoxication, but instead a delayed effect of muscle gains. Thus standard diagnostic criteria for substance dependence, usually crafted for acutely intoxicating drugs, must be slightly adapted for cumulatively acting drugs such as AAS.Conclusions-AAS dependence is a valid diagnostic entity, and likely a growing public health problem. AAS dependence may share brain mechanisms with other forms of substance dependence, especially opioid dependence. Future studies are needed to better characterize AAS dependence, identify risk factors for this syndrome, and develop treatment strategies.The anabolic-androgenic steroids (AAS) are a family of lipophilic hormones derived from cholesterol that includes the natural male hormone, testosterone, together with numerous synthetic testosterone derivatives (1). By ingesting supraphysiological doses of these hormones, in combination with intensive weight lifting and appropriate nutrition, AAS users can greatly increase their muscle mass, often well beyond the limits attainable by natural means (2). For decades, elite athletes have used AAS to improve performance (3). Today, however, most AAS users are not competitive athletes, but simply individuals who want to look leaner and more muscular (1,4-8). As we have explained in detail elsewhere (9), this Correspondence should be addressed to Dr. Pope at McLean Hospital, Belmont, MA 02178; hpope@mclean.harvard.edu. NIH Public Access Author ManuscriptAddiction. Author manuscript; available in PMC 2010 December 1.Published in final edited form as: Addiction. 2009 December ; 104(12): 1966-1978. doi:10.1111/j.1360-0443.2009.02734.x. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript much larger but less visible population of illicit AAS users began to emerge in the 1980s -a trend stimulated in part by the appearance of progressively more sophisticated underground guides on how to self-administer AAS (10-14). We...

Background Millions of individuals have used illicit anabolic-androgenic steroids (AAS), but the long-term cardiovascular associations of these drugs remains incompletely understood. Methods Employing a cross-sectional cohort design, we recruited 140 experienced male weightlifters aged 34–54 years, comprising 86 men reporting at least 2 years of cumulative lifetime AAS use and 54 non-using men. Using transthoracic echocardiography and coronary computed tomography angiography, we assessed 3 primary outcome measures: left ventricular (LV) systolic function (left ventricular ejection fraction [LVEF]), LV diastolic function (early relaxation velocity [E´]), and coronary atherosclerosis (coronary artery plaque volume). Results Compared to non-users, AAS users demonstrated relatively reduced LV systolic function (mean±SD LVEF = 52±11% vs. 63±8%; P<0.001) and diastolic function (E´ = 9.3±2.4 cm/s vs. 11.1±2.0 cm/s; P<0.001). Users currently taking AAS at the time of evaluation (N = 58) showed significantly reduced LV systolic (LVEF = 49±10% vs. 58±10%; P<0.001) and diastolic function (E´ = 8.9±2.4 cm/s vs. 10.1±2.4 cm/s; P=0.035) compared to users currently off-drug (N = 28). Additionally, AAS users demonstrated higher coronary artery plaque volume then nonusers (median [interquartile range] 3 [0, 174] mL3 vs. 0 [0, 69] mL3, P = 0.012). Lifetime AAS dose was strongly associated with coronary atherosclerotic burden (increase [95% confidence interval] in rank of plaque volume for each 10-year increase in cumulative duration of AAS use: 0.60 SD units [0.16 to 1.03 SD units]; P = 0.008). Conclusions Long-term AAS use appears to be associated with myocardial dysfunction and accelerated coronary atherosclerosis. These forms of AAS-associated adverse cardiovascular phenotypes may represent a previously under-recognized public-health problem.