CHD is a major cause of morbidity and mortality in women. The incidence of
CHD in premenopausal women is low but increases substantially after the men
opause, and this difference suggests that endogenous oestrogens are cardiop
rotective. Observational prospective studies have consistently shown that e
xogenous oestrogens also lower CHD risk. The biological mechanisms by which
endogenous and exogenous oestrogens exert their protective effect are mult
ifactorial, affecting lipids, carbohydrate metabolism, body fat distributio
n and blood pressure. The prevention of CHD with oestrogen therapy is there
fore aimed both at correction of the traditional risk factors and at direct
control of vessel structure and function. The wide international variation
in rates of CHD together with the lower mortality in sub-groups of the pop
ulation suggests that a considerable proportion of CHD may be prevented by
dietary modification. Since phytooestrogens are structually similar to oest
rogen, they have the potential to mimic its effects in vivo. The hypocholes
terolaemic effects of soyabean protein (rich in phyto-oestrogen precursors)
are well established, but the underlying mechanism and atherogenic potenti
al of these changes are unknown. One isoflavone, genistein, has been shown
in vitro to exert effects which may slow the development of atherosclerotic
disease. However, further studies are required to determine the dose-relat
ed changes induced by phyto-oestrogens on serum lipoproteins, haemostasis a
nd vascular function.