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The Longitudinal Evaluation of Ovarian Aging and Cardiovascular Risk
agingcardiovascular-diseasecardiovascular-disease-riskcardiovascular-risk-factorfertilityhealthinfertilityreproductive-health
Despite significant improvements in prevention and treatment of cardiovascular disease (CVD), the growing aging population suggests CVD will continue to pose a significant public health burden. Women are a special group where microvascular disease is more common and traditional risk factors may not fully identify risk. Women's reproductive history (e.g. menarcheal age, menstrual cycles, infertility, pregnancy, menopause) may pose unique risk and suggests an opportunity for new approaches. The investigators propose a women-centered approach for early identification of women at risk that investigates the unique loss of reproductive function at an age long before other vital systems fail. Despite its importance, little is known about the determinants or correlates of ovarian aging, or the health implications, especially in diverse communities. Only recently have reliable biomarkers of the remaining oocyte pool been available for use in normally cycling women. This availability gives us a unique opportunity to characterize the association between "ovarian age" (cross-sectional) and the rate of "ovarian aging" or oocyte decline over time (longitudinal) and the health implications of accelerated oocyte loss. The investigators hypothesize ovarian age/aging provides a window onto the general health of women. The investigators suggest it is not the progressive deficiency of estrogen with menopause that increases risk, but common underlying cellular aging mechanisms first evident in young populations as lower ovarian reserve (follicle number) due to the unique sensitivity of the ovary. Studies of cellular aging focused on mitochondrial dysfunction, oxidative stress, inflammation, and telomere length have identified correlations with CVD risk. Improved understanding of the mechanisms of cellular aging suggests telomere shortening and dysfunction may drive mitochondrial dysfunction and potentially the parallel between cellular aging and CVD. The oocyte is particularly sensitiv
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