Search

In this study we partition the phenotypic correlations between body fat measures and serum levels of hormones with known, or suspected, lipolytic effects into their genetic and environmental components. Using variance decomposition techniques, we are able to estimate the pleiotropic effects of genes and/or shared environmental factors that give rise to the phenotypic correlations previously reported between these traits. We used data from a large sample of randomly ascertained Mexican-American families living in San Antonio, TX. Data were available for 582 individuals in 26 pedigrees. Levels of sex hormone-binding globulin, dehydroepiandrosterone sulfate, insulin, insulin-like growth factor I, total T4, and total T3 were assayed. The measures of body fat accumulation and topography included body mass index, subscapular/triceps ratio, and relative fat patterning index. The results of this analysis demonstrate that significant phenotypic correlations among these traits can arise from three underlying conditions: 1) entirely from shared genetic effects (pleiotropy), 2) entirely from shared random environmental effects, or 3) a combination of both effects. However, we also show that it is possible for significant genetic and environmental correlations to interact in such a way as to produce a phenotypic correlation that itself would not be considered significant.

Sex hormones may play a role in the determination of cardiovascular disease. Recently lipoprotein(a) (Lp[a]) has been recognized as a risk factor for coronary heart disease. Estrogens and anabolic steroids have been reported to alter Lp(a) levels, yet no data are available on the association between in vivo concentrations of sex hormones and Lp(a) concentrations. We examined the possible associations of sex hormone-binding globulin, total and free testosterone, estradiol, and dehydroepiandrosterone sulfate to Lp(a) concentrations in men in two population-based studies (San Antonio Heart Study [n = 178] and a Finnish study on the association between insulin resistance and atherosclerosis [n = 87]). In neither study were sex hormones significantly related to Lp(a) concentrations. In addition, Lp(a) was significantly related to apolipoprotein(a) molecular weight (which was measured in the Finnish study only). These results were unchanged when Lp(a) concentrations were adjusted for apolipoprotein(a) molecular weight (a strong correlate of Lp[a] concentrations). We conclude that in vivo concentrations of sex hormones are unlikely to be associated with Lp(a) concentrations in men.