Thirty-three studies (three randomized clinical trials, 11 cohort, 18 cross-sectional, and one non-randomized parallel clinical trial) were included in the systematic review (3879 participants; 1766 AAS users and 2113 non-AAS users). The majority of the participants were men; only six studies provided data for female athletes. A meta-analysis (11 studies) was conducted of studies evaluating serum gonadotropin and testosterone levels in male subjects: (1) prior to, and during AAS use (six studies, n = 65 AAS users; seven studies, n = 59, evaluating gonadotropin and testosterone levels respectively); (2) during AAS use and following AAS discontinuation (four studies, n = 35; six studies, n = 39, respectively); as well as (3) prior to AAS use and following AAS discontinuation (three studies, n = 17; five studies, n = 27, respectively). During AAS intake, significant reductions in luteinizing hormone [weighted mean difference (WMD) - IU/L, 95% confidence interval (CI) - to -, p < ], follicle-stimulating hormone (WMD - IU/L, 95% CI - to -, p < ), and endogenous testosterone levels (WMD - nmol/L, 95% CI - to -, p < ) were reported. Following AAS discontinuation, serum gonadotropin levels gradually returned to baseline values within 13-24 weeks, whereas serum testosterone levels remained lower as compared with baseline (WMD - nmol/L, 95% CI - to -, p < ). Serum testosterone levels remained reduced at 16 weeks following discontinuation of AAS. In addition, AAS abuse resulted in structural and functional sperm changes, a reduction in testicular volume, gynecomastia, as well as clitoromegaly, menstrual irregularities, and subfertility.
Evidence has accumulated over the pst several years which associates androgenic-anabolic steroid (AAS) use with sudden cardiac death, myocardial infarction, altered serum lipoproteins, and cardiac hypertrophy in humans who habitually use these drugs. Even though some experimental data obtained from animals correlate well with the human findings, the adverse cardiovascular effects of AAS use are poorly understood. The evidence presented in this review suggests that there are at least four hypothetical models of AAS-induced adverse cardiovascular effects: 1) an atherogenic model involving the effects of AAS on lipoprotein concentrations; 2) a thrombosis model involving the effects of AAS on clotting factors and platelets; 3) a vasospasm model involving the effects of AAS on the vascular nitric oxide system; and 4) a direct myocardial injury model involving the effects of AAS on individual myocardial cells. Future studies should be directed at determining the exact mechanisms responsible for AAS-induced adverse cardiovascular effects, at determining the relative contribution of each of these models, and at identifying other possible contributing factors such as metabolism of these steroids and the effects of potential metabolites on various target organs.