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Gaps, limitations and new insights on endogenous estrogen and follicle stimulating hormone as related to risk of cardiovascular disease in women traversing the menopause: A narrative review

•Previous reviews on endogenous estrogen and CVD risk mainly focused on postmenopausal women and could not come to a clear conclusion.•None of the previous reviews discussed role of follicle stimulating hormone (FSH) on CVD risk.•All previous studies assumed common trajectories of estradiol decline...

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Bibliographic Details
Published in:Maturitas 2017-10, Vol.104, p.44-53
Main Author: El Khoudary, Samar R.
Format: Article
Language:English
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Summary:•Previous reviews on endogenous estrogen and CVD risk mainly focused on postmenopausal women and could not come to a clear conclusion.•None of the previous reviews discussed role of follicle stimulating hormone (FSH) on CVD risk.•All previous studies assumed common trajectories of estradiol decline and FSH rise over the menopause transition.•Distinct trajectories of estradiol decline and FSH rise over midlife have been identified and linked to vascular health after menopause.•It is much more important to observe a woman over time rather than ascribe risk to a single determination at a single time point. While it is known that estrogen protects heart health in women prior to menopause, its role after menopause and during the menopause transition is far less apparent. Previous reviews summarizing the literature on the impact of endogenous estrogen on risk of cardiovascular disease (CVD) have focused on postmenopausal women and have not come to a clear conclusion. No previous review has summarized the associations between follicle stimulating hormone (FSH), a proxy measure of the menopause transition, and CVD risk. The main purpose of this narrative review is to highlight gaps and limitations in the literature on endogenous estrogen and FSH as related to CVD risk. Future directions are addressed in light of recent findings in the field. When studying the relationship of estrogen to cardiovascular risk, it is critical to separate endogenously produced estrogen from exogenously administered estrogen. Moreover, other reproductive hormones such as FSH should be assessed, since growing evidence suggests a potential contribution of this hormone. Evaluation of estrogen changes over time allows a separation of women based on their hormone trajectories. These individual trajectories correlate with subclinical CVD and thus indicate that it is much more important to observe a woman over time rather than ascribe risk to a single determination at a single time point. As women progress through menopause and the ovary stops producing estradiol, the nature of the relationship between estrogens and subclinical CVD markers also appears to undergo a switch. Studies are needed to examine the midlife course of endogenous estradiol, FSH and CVD risk. These studies should also consider other hormones, including androgens, with an eye towards helping women modify their cardiovascular risk in midlife, when prevention is most likely possible.
ISSN:0378-5122
1873-4111
DOI:10.1016/j.maturitas.2017.08.003