Abstract
The ovary ages uniquely to other organs and despite an increase in longevity and health, the age of menopause, cessation of ovarian reproductive function, has not changed for over 100 years. What causes the demise of such a vital organ and how does it impact fertility and health. So called “ovarian reserve”-the number of oocytes available in a single cycle – is a strong driver for assessing “ovarian age”. But does quantity equate to “quality” and fertility potential? We will discuss ovarian aging and its impact on fertility, spontaneous and assisted. Additionally, what do we know about how the process of ovarian aging impacts general health. Cardiovascular disease (CVD) is the leading cause of mortality in women in the United States. Compared with age-matched men, premenopausal women are protected against CVD, yet this difference dissipates after menopause. Hypogonadism underlies the shared increased CVD risk seen in menopause, primary ovarian insufficiency (POI), and hypogonadotropic hypogonadism. Early menarche and PCOS have also been associated with CVD risk factors, highlighting the importance of mediators other than deficient estrogen in the underlying etiology of this female-specific increased risk. And yet, women with PCOS present a unique population. Beginning early in life, these women have increased markers of cardiovascular risk. And yet, data regarding actual cardiovascular events, in this population, are mixed. If these individuals, with long-standing exposure to dyslipidemia and insulin resistance, are not at risk, is there some protective mechanism associated with PCOS? Might there be an underlying mechanism for prolongation of reproductive function and potential protection from long-standing exposure to cardiovascular risk factors. And might the converse be true so that women with accelerated loss of reproductive function, would be at increased long-term health risk. Identification of women at risk, and in need of early intervention, is critical to living healthy lives.
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