It should be noted that differences in prevalence rates or age of onset do not necessarily imply that genetic variation leads to different effects in males and females15, as many of these differences could be due to hormonal profiles, particularly with regard to sex steroids (Figure 1), or to behaviors that differ between the sexes (e.g., exposure to cigarette smoke)16. For example, the consistent associations between increased risk for disease among females during and following puberty (asthma), during the reproductive years (autoimmune disease), or post-menopausal (cardiovascular disease) have implicated sex hormones as important mediators of disease pathogenesis and contributors to sex differences in prevalence rates and progression.
