Menopause is recognized as a period of increased risk for coronary heart disease (CHD) and osteoporosis. Vulnerability to these conditions is often attributed to the naturally occurring estrogen deficiency characteristic of this part of the life cycle. Premenopausal reductions in endogenous estrogen occasioned by functional ovarian abnormalities or failure are hypothesized to be similarly pathogenic and to accelerate development of CHD and osteoporosis prematurely, thereby increasing the health burden of older women. These functional abnormalities, which occur along a continuum from mild, luteal phase progesterone deficiency to amenorrhea, are relatively common and are often attributed to psychogenic factors (stress, anxiety, depression, or other emotional disturbance), exercise, or energy imbalance. Although numerous investigators have commented on these functional deficits, the abnormalities can be difficult to diagnose and are generally unappreciated for the contribution they may make to postmenopausal disease. Studies in nonhuman primates confirm that these deficits are easily induced by psychological stress and exercise, and that they accelerate the development of cardiovascular disease and perhaps bone loss in the presence of a typical North American diet. However, functional reproductive deficits are also reversible and are thus potentially amenable to environmental or behavioral intervention. Data from both women and nonhuman primates support the hypothesis that functional reproductive deficits are adaptive when triggered appropriately but are detrimental when activated in an environment (e.g., sedentary lifestyle, high-fat diet) permissive to the development of chronic disease.