Original articleHyperhomocysteinemia in bodybuilders taking anabolic steroids
Introduction
The use of anabolic steroids has been linked to acute vascular events. Over the last decade, several case reports on sudden death, myocardial infarction, pulmonary embolism, stroke, sinus thrombosis, and other atherosclerotic/atherothrombotic events in bodybuilders taking anabolic steroids have appeared in the literature [1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11].
Homocysteine (HCY), a thiol-containing amino acid, is produced by intracellular demethylation of methionine and, after entering the plasma stream, circulates bound to plasma proteins [12], [13]. Severely elevated concentrations of total HCY are found in patients with homocystinuria. These patients exhibit mental retardation, early atherosclerosis, and arterial and venous thromboembolism [14].
Several epidemiological studies and meta-analyses have shown that even mildly elevated plasma concentrations of HCY constitute an independent risk factor for atherosclerosis and atherothrombosis [15]. Mild hyperhomocysteinemia occurs in approximately 5–7% of the general population [16] and leads to premature coronary artery disease, as well as to arterial and venous thrombosis in the third to fourth decade of life [17], [18], [19], [20].
Men have a higher risk of developing cardiovascular disease (CVD) than premenopausal women. In postmenopausal women, the risk of CVD increases rapidly and may be ameliorated by hormone replacement therapy [21]. HCY levels differ in a gender-specific manner [22]. Men have 10–15% higher levels of HCY than women. There is evidence that HCY levels are influenced by sex hormones. Plasma levels of HCY were found to be low during pregnancy, a state characterized by high levels of endogenous estrogens [23]. Hormone replacement therapy in postmenopausal women reduced plasma HCY levels by 11% after a half year of treatment [24]. In a crossover study, supraphysiological doses of testosterone did not alter HCY levels after a treatment period of 3 weeks [25]. In transsexuals, however, HCY decreased in male-to-female transsexuals after a combined estrogen and antiandrogen treatment, whereas HCY levels increased in female-to-male transsexuals after androgen treatment [26].
Because of the reported association between intake of anabolic steroids and high vascular risk in bodybuilders, we investigated whether intake of anabolic steroids is associated with hyperhomocysteinemia.
Section snippets
Study population
Twenty-three male bodybuilders and six male age- and body mass index-matched control athletes (all Caucasian) were recruited from training centers in western Austria, Italy, and Switzerland. Bodybuilders using such centers follow a training cycle consisting typically of a work-out phase, a build-up phase, and a competition phase. In the work-out phase (‘non-steroid phase’), the bodybuilders perform muscle training and do not take anabolic steroids, yet they have a history of taking such
Baseline characteristics
The baseline characteristics of the bodybuilders and control athletes are given in Table 1. Competition phase bodybuilders displayed a higher average body weight.
Hormonal status
In order to group the study subjects correctly and to confirm the history of intake of anabolic steroids in the bodybuilder groups and in the control athletes, the hormonal status was determined.
Levels of testosterone did not differ between work-out phase bodybuilders, build-up phase bodybuilders, competition phase bodybuilders, and
Discussion
In the present study, we investigated whether elevated plasma levels of HCY could contribute to the high risk of cardiovascular events associated with the intake of anabolic steroids in male bodybuilders. We took a cross-sectional, non-randomized approach as the only option available to us because of a reluctance of bodybuilders to participate in a prospective study design. According to the usual training cycle typically followed by bodybuilders in this area, bodybuilders were either in the
Acknowledgments
This study was supported by grant P 11693-Med of the Austrian FWF and by grant number 6442 of the Österreichische Nationalbank. We would like to thank M. Speckbacher and U. Stanzl for their expert technical assistance.
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