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Are menstruating women protected from heart disease because of, or in spite of, estrogen? Relevance to the iron hypothesis

Editorial Jerome L. Sullivan, MD, PhD Winter Park, Fla Healthy premenopausal women are largely protected from ischemic heart disease, but, remarkably, so are women with heterozygous familial hypercholesterolemia (FH) (Figure 1).1,2 Thirty-year-old men with heterozygous FH have an excess of cardiovascular events in comparison with unaffected men. In sharp contrast, their 30-year-old sisters who have heterozygous FH have disease rates that are not readily distinguishable from those of unaffected women (Figure 2). In Figure 2, women younger than 40 years with FH had slightly lower incidences than unaffected women. After menopausal age, women with FH demonstrate susceptibility to heart disease, with an incidence increase that quickly surpasses that of their unaffected male relatives. Other than a delayed onset of clinical disease, women who have heterozygous FH have a life-long lipid phenotype identical to or, perhaps, slightly more severe than that of men with heterozygous FH. According to the estrogen hypothesis, this impressive protection is lost because healthy women, and women with FH, become estrogen-deficient after menopause. It follows that replacement of the missing protective element with hormone-replacement therapy (HRT) should eliminate susceptibility to cardiovascular disease. However, HRT did not reduce cardiovascular events or atherosclerosis in randomized trials. The http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Heart Journal Elsevier
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