Kelly Parcell, ND
So far, all studies examining the effects of hormone replacement therapy have shown no major reduction of cardiovascular risk. In fact, equine estrogens (Premarin) and progestins (Provera) appear to be associated with increased cardiovascular risk. Naturally occurring estrogen does not fully account for why women get heart disease later than men either. According to a BMJ study in 1995 of postmenopausal women, there was no relationship between estrogens—or any other measured sex steroid—to CAD risk. These results were consistent with those from previous studies that found no difference in estrogen levels in women with or without CAD.A trial by the Women’s Health Initiative (WHI) failed to show decreased risk of heart attack in women despite improvement in lipid levels. Estrogen can lower Lip (a) as well.
However, only non-bioidentical, horse-derived estrogen and synthetic progesterone were used. The WHI trial also did not demonstrate any overall benefit of estrogen alone (versus a placebo) for decreasing mortality caused by CAD, although there was a good suggestion of benefit in the 50- to 59-year-old group. Other recent studies have also failed to demonstrate the benefits of hormone replacement on CAD risk, coronary calcification, progression of carotid intima-medial wall thickness, and arterial obstruction among women with CAD. More women die from heart attacks than from cancer yet the public continues to regard heart attacks for women as a more remote problem.
The Atherosclerosis Risk in Communities (ARIC) study analyzed the traditional risks for CAD (i.e., age, cholesterol levels, blood pressure levels, smoking habit, and diabetes) of more than 15,000 middle-aged men and women with the goal of predicting the 10-year risk of a heart attack. The study determined that traditional risk factors are useful in predicting risk in women, but for men the nontraditional risk factors and measures of early plaque formation (carotid ultrasound) are better at predicting risk. It is likely that the gender difference in heart attack risk is caused by some combination of differences in nontraditional risk factors such as elevated blood viscosity, iron levels, hormones, and yet-to-be-discovered factors. Obviously, both men and women need to pay attention to all factors that increase risk of a heart attack, such as atherogenic lipids, inflammation, diet, and exercise. There is more to be learned about estrogen and CAD. It is possible that if a study were to be conducted using bioidentical estrogen that results would be more positive.