The correlation between estrogen loss and risk for osteoporosis and cardiovascular disease development has been strongly demonstrated by epidemiological data (Rosano and Panina, 1999). Sufficient experiments have been carried out to warrant the conclusion that dietary intake of soy protein, or specifically the soy isoflavones, results in estrogen-like protection against the development of the hormone-dependent breast and prostate cancers (Barnes, 1997; Lamartiniere and Fritz, 1998), as well as atherosclerosis (Anthony et al., 1996; Adlercreutz and Mazur, 1998; Setchell and Cassidy, 1999).
The mechanisms of protection against the cancers do not appear to be identical to those involved in cardioprotection, since the isoflavones only had effects against atherosclerosis when administered in a soy protein matrix (Clarkson et al., 1997), while breast cancer protection was measured with the soy isoflavone genistein, independent of soy protein (Murrill et al., 1996). Thus, these data foreshadowed our complex results, which suggested that the soy isoflavones and physiological estrogen have nonidentical actions in primate brain, although the end results in both cases may be beneficial, and similar behaviorally.
In terms of overall actions, it could be concluded that the soy isoflavones mimicked the effects of estrogen in protecting against the major chronic diseases that result from postmenopausal estrogen loss. These data added to the rationale for the hypothesis that dietary soy isoflavones might have neuroprotective actions in the primate model of menopause.
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