The interest in the potential health effects of dietary phytoestrogens has increased with the findings that hormone replacement therapy is not as safe or effective as previously thought. This review summarizes the dietary sources of the phytoestrogens; isoflavonoids, stilbenes, coumestans and lignans. It also examines 105 clinical studies related to effects of phytoestrogens on bone density, cardiovascular health, cancer prevention, cognitive ability and menopausal symptoms.
The interest in plant derived estrogens or phytoestrogens has recently been increased by the realization that hormone replacement therapy is not as safe or effective as previously thought (Hays et al., 2003). The prevalence of phytoestrogens in our diets and the biological effects that they may cause need to be fully examined. This review summarizes what is known about the distribution of phytoestrogens in the diet as well as some of the physiological activities of these compounds. Although this topic has been recently reviewed (Fitzpatrick, 2003; Rowland et al., 2003; Setchell and Lydeking-Olsen, 2003) this review examines 105 clinical studies related to the effects of phytoestrogens on bone density, cardiovascular health, cancerprevention, cognitive ability and menopausal symptoms.
Estrogens, produced in the ovaries and testis, have many biological effects in the body beyond the reproductive system. The estrogen receptors localized in the nucleus and form dimers when bound to an estrogen. The dimers then interact with the estrogen response element (ERE), which regulates transcription of estrogen responsive genes. A small percentage (2–3%) of estrogen receptors are located on the cell membrane and contribute to non genomic effects of estrogen (Norfleet et al., 1999; Razandi et al., 1999; Xu et al., 2003; Chen et al., 2004). There are two known estrogen receptors, ERa and ERb. Although the two estrogen receptors can be localized within the same cell, they vary in tissue distributions and can have different effects on mixed agonists and antagonists (Nilsson and Gustafsson, 2002). Both ERa and ERb function in normal ovarian follicular development, vascular endothelia cells, myocardial cells, smooth muscle, and breast tissue (Nilsson and Gustafsson, 2002). ERa is involved in bone maturation in both males and females, however, only ERb plays a role in bone maintenance in females (Nilsson and Gustafsson, 2002). ERa is more important in maintaining follicle stimulating and luteinizing hormone concentrations in blood, and ERb is involved in frontal lobe mediated learning and memory (Nilsson and Gustafsson, 2002). The dominant form of estrogen in the body is 17b estradiol (Fig. 1), although any compound that induces receptor dimerization and subsequent binding to the ERE, can be considered an estrogen. Antagonistic effects can occur when a compound is able to bind to the receptor but dimer formation either does not occur or the correct configuration to activate the ERE is not attained. Some compounds act as estrogen agonists and antagonists and are referred to as Selective Estrogen Receptor Modulators (SERMs). As an example, the antiestrogen tamoxifen acts as an estrogen antagonist in breast tissue but as an agonist in the uterus, bone and vascular system (Macgregor and Jordan, 1998). These agonist/antagonistic effects are believed to be responsible for the differential effects of phytoestrogens compared to estradiol. There are several recent reviews on estrogen receptors and SERMs (Nilsson and Gustafsson, 2002; Gustafsson, 2003; Meegan and Lloyd, 2003; Riggs and Hartmann, 2003).
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Dietary phytoestrogens and health
