The net effect of testosterone on cardiovascular risk is difficult to assess for at least six main reasons. First, the effects of testosterone on cardiovascular risk factors are contradictory depending on whether associations with endogenous testosterone or effects of exogenous testosterone have been investigated. Second, the associations between serum concentrations of endogenous testosterone and cardiovascular risk factors are confounded with mutual interactions between endogenous androgens, body fat distribution, and insulin sensitivity. Third, exogenous testosterone has profound effects on several risk factors, some of which at first sight appear beneficial, namely lipoprotein(a) (Lp(a)), insulin, fibrinogen, and plasminogen activator type 1 (PAI-1), while others are considered adverse, namely HDL-C. Fourth, the causal relationship between some of the aforementioned risk factors and atherosclerosis has not been proven. Of special importance are results of experimental and clinical studies indicating that therapeutically-induced changes in HDL-C may not necessarily be accompanied by changes in cardiovascular risk (Hersberger and von Eckardstein 2003). Fifth, testosterone can exert its metabolic effects directly or by its metabolites estradiol and dihydrotestosterone. The effects of testosterone and estradiol, in particular, can be either additive (for example on Lp(a)) or counteractive (for example on HDL-C). Sixth, polymorphisms in the genes of the androgen and estrogen receptors, sex hormone binding globulin (SHBG), 5a-reductase and aromatase, regulate genomic effects and the bioavailability of testosterone, dihy-drotestosterone and estradiol, respectively. Thus, at a given serum concentration the bioactivity and metabolic effects of testosterone can be diverse.
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