Estrogen protection against coronary heart disease: are the relevant effects of estrogen mediated through its effects on uterus--such as the induction of menstruation, increased bleeding, and the facilitation of pregnancy?

Women in the age group of 20-50 are shown to have much less susceptibility to Coronary Heart Disease (CHD) and other atherosclerotic diseases as compared to men. Exact cause of which is not precisely known and estrogen is constantly shown to be associated with this phenomenon. Improvement of serum HDL concentration and improvement of endothelial functions are some of the proposed mechanisms through which estrogen is believed to mediate this effect. Estrogen therapy however has failed to protect women with bilateral oophorectomy and hysterectomy. Similarly inability of endogenous estrogen to protect women, who have undergone hysterectomy with functioning ovaries from CHD, questions the currently accepted mechanisms through which estrogen brings about these protective effects. Ineffectiveness of estrogen therapy as prophylaxis against CHD in men further questions the credibility of the currently accepted protective mechanisms of estrogen. Estrogen has variety of effects of on uterus, to induce menstruation, to induce bleeding, facilitative role in pregnancy, fetal growth and development. As these physiological effects either directly or indirectly result in loss of cholesterol from cardiovascular compartment, it is proposed that cholesterol-losing effects of estrogen are more important than its presently believed beneficial effects. The small amount that is lost causes movement of cholesterol from atheroma towards plasma and thereby retards the progress of atherosclerosis. These cholesterol-losing effects of estrogen enable women to enjoy freedom from CHD during their reproductive age, as compared to men of comparable age group. Statistical data obtained from blood donors indirectly support the proposed hypothesis.