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B iological sex and gender 1 * have emerged as prominent players in cardiovascular health. It is widely appreciated that male and female hearts are different both at baseline and in response to numerous stimuli (for a recent review see Llamas et al 2 ). In general, male hearts respond less well to pressure or volume overload, to myocardial infarction (MI), and to aging. In considering the mechanisms that underlie sexually dimorphic cardiac traits, estrogen is an obvious candidate. However, data in the literature conflict on this point. The findings that cardiovascular risk increases when estrogen production ceases and that ovariectomy prevents the more beneficial outcome of volume overload or aging in females argues in favor of a protective role of estrogen. In contrast, the finding that estradiol-treated female rodents have a greater post-MI rate of death argues against a protective role. Recent human studies on hormone replacement therapy similarly question the cardioprotective role of estrogen. learly, the role of estrogen in cardiovascular disease (CVD) is complex, and further study is necessary. More significantly, it seems unlikely that the male/female dimorphisms in CVD can be attributed to a single factor such as estrogen. This review will consider the impact of estrogen, estrogen receptors (ERs), and diet on heart disease. The relationship between diet and CVD has traditionally focused on the consumption of fat and its impact on blood triglycerides and cholesterol. 9 -11 This review will not focus on these well-studied nutritional factors but will focus instead on a group of nutritional factors, phytoestrogens, that can mimic the actions of endogenous estrogens and seem likely to have profound effects on CVD in a sex-specific manner.
Konhilas et al. (Mon,) studied this question.