Misuse of supraphysiological doses of anabolic steroids is claimed to have serious side effects. The aim of the study was to determine the mortality, and the cause of premature deaths among a group of subjects who are strongly suspected to have used anabolic steroids for a non-medical purpose over several years. The mortality of 62 male powerlifters placed 1st-5th in weight series 82.5-125 kg in Finnish championships during 1977-1982 was compared with the mortality of population controls. The mortality during the 12-year follow-up was 12.9% for the powerlifters compared to 3.1% in the control population. By 1993 eight of 62 powerlifters and 34 of 1094 population controls had died, thus the risk of death among the powerlifters was 4.6 times higher (95% CI 2.04-10.45; p = 0.0002). The causes of premature death among the powerlifters were suicide (3), acute myocardial infarction (3), hepatic coma (1) and non-Hodgkin's lymphoma (1). These findings add to the growing amount of evidence of an association between anabolic steroid abuse and premature death, and support the view that measures to decrease AAS misuse among both competitive and amateur athletes are justified.

This article focuses on anabolic steroid adverse effects on the cardiovascular system and mental health issues as well as the possible increase in the incidence of neoplasms in anabolic steroid users. On the basis of findings in the literature, the authors consider these three issues as the most significant concerning morbidity and mortality among anabolic steroid users. A study by Pärssinen et al. (2000) has shown an increased incidence of premature mortality among power lifters. Anabolic steroids and other concomitantly used drugs are the probable cause of this increased mortality, as power training itself does not increase health risks and all types of physical activity promote health.

We examined the effect of supraphysiological doses of anabolic androgenic steroids (AAS) on collagen metabolism and whether the changes reflect the alterations in muscle, bone, and tendon collagen metabolism, possibly in a tissue-specific manner. Serum carboxyterminal propeptide of type I procollagen (PICP), carboxyterminal telopeptide of type I collagen (ICTP), aminoterminal propeptide of type III procollagen (PIIINP), urine hydroxylysylpyridinoline (HP), and lysylpyridinoline (LP) as well as urine creatinine were determined from 17 men abusing AAS. Measurements were made twice during the intake of AAS and twice during the subsequent withdrawal period. When the volunteers were on steroids, their serum PIIINP concentrations and urine HP/LP ratio were significantly higher and their serum ICTP concentrations were significantly lower than during the withdrawal period (p < 0.05). Serum PIIINP correlated with total cumulative doses of injectable intramuscular steroids, and serum ICTP correlated with the duration of the steroid intake period (p<0.05). The results suggest that high doses of AAS decrease the degradation and seem to increase the synthesis of type I collagen. Furthermore, high doses of AAS are suggested to enhance soft tissue collagen metabolism on the basis of increased type III collagen synthesis and elevated HP/LP ratio during the steroid administration period. Although the tissue-specific turnover of collagen of soft connective tissues remains unknown, the turnover of bone collagen seems not to change following the use of high doses of AAS, at least within the time interval of the present study.