Steroid Use and Long-Term Health Risks in Former Athletes :

Reliable data are scanty on the incidence of chronic diseases and life expectancy (LE) of highly trained athletes. We therefore studied Finnish male world class athletes to estimate the LE of athletes. Finnish team members in the Olympic games, World or European championships or intercountry competitions during 1920-1965 in track and field athletics, cross-country skiing, soccer, ice hockey, basketball, boxing, wrestling, weight lifting, and shooting were included (N = 2613 men). The reference cohort, 1712 men, was selected from the Finnish Defence Forces conscription register matched on age and area of residence. All referents were classified completely healthy at the time of induction to military service. The stratified Kaplan-Meier product limit method and the Cox proportional hazards model were used to estimate the life expectancies and the mortality odds ratios (OR) and their confidence limits. The mean LE adjusted for occupational group, marital status, and the age at entry to the cohort (and its 95% confidence limits) was in endurance sports (long distance running and cross-country skiing) 75.6 (73.6, 77.5) yr; in team games (soccer, ice hockey, basketball, as well as jumpers and short-distance runners from track and field (73.9 (72.7, 75.1) yr; in power sports (boxing, wrestling, weight lifting, and throwers from field athletics) 71.5 (70.4, 72.2) yr; and in the reference group 69.9 (69.0, 70.9) yr. The increased mean life expectancies were mainly explained by decreased cardiovascular mortality (endurance sports mortality odds ratio OR = 0.49 (95% CL 0.26, 0.93), team sports OR = 0.61 (0.41, 0.92) compared with referents). For maximum life span no differences between the groups were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

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.