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Invited Commentary
October 2016

Reproductive Health as a Marker of Subsequent Cardiovascular Disease: The Role of Estrogen

Author Affiliations
  • 1Connors Center for Women’s Health and Gender Biology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts
  • 2Division of Reproductive Science, the Oncofertility Consortium, Women’s Health Research Institute, Northwestern University, Chicago, Illinois
JAMA Cardiol. 2016;1(7):776-777. doi:10.1001/jamacardio.2016.2662

Cardiovascular disease (CVD) kills 1 in 3 women worldwide,1 and the risk of CVD increases markedly after the cessation of ovarian function at menopause.2 Although the dramatic decline in estrogen levels following menopause has been implicated in the loss of cardioprotection in women, the association between the decline in ovarian function and vascular disease may be even more complex.2 The menopausal transition is associated with significant changes in the vascular system, distribution of body fat, blood pressure, and blood lipid levels,3 all of which increase the risk of CVD. However, the possibility of shared risk factors, including genetic, lifestyle, and environmental, for both early menopause and elevated CVD risk warrants consideration. Key questions are whether early cessation of reproductive function etiologically increases risk of CVD or whether latent cardiovascular disease causes reproductive aging and accelerates the onset of menopause (or both).

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