SEX-HORMONES AND LIPID INTERACTIONS - IMPLICATIONS FOR CARDIOVASCULAR-DISEASE IN WOMEN

Estrogens and androgens have opposing effects on lipoprotein lipids. Progestins fall in between depending on their androgenicity. Estrogens raise plasma triglyceride concentrations but lower remnant and LDL and raise HDL levels while progestins and androgens lower triglyceride concentrations, raise LDL and lower HDL concentrations. Apoprotein B and A-I levels change in parallel with alterations in LDL and HDL, respectively. An exception is Lp(a), which decreases with estrogen or androgen. There are numerous examples of these effects. Male puberty is associated with a testosterone-induced reduction in HDL. Estrogen appears to explain the lower LDL levels experienced by women premenopausally. Oral contraceptive effects reflect estrogen-progestin potency and progestin androgenicity. Lipoprotein changes in pregnancy are generally an estrogen dominant effect while in oral contraceptive use the lipoprotein changes are a balance of the estrogenic and progestogenic effects of the given formulation. The hypertriglyceridemia of pregnancy may be severe enough to cause pancreatitis and require treatment with low fat diet and fish oil. Postmenopausally, use of estrogens alone or with a low-dose low-androgenic progestin such as medroxyprogesterone acetate reveal a predominantly estrogenic effect and beneficial effects on IDL and HDL. Advantage can be taken of these hormonal effects to manage hypercholesterolemia and Type III hyperlipidemia (''remnant removal disease''). Rarely, androgens may be useful in treating intractable hypertriglyceridemia. Pending the outcome of ongoing studies, the prevention of coronary artery disease in women with estrogen may be feasible through favorable effects on lipid and carbohydrate metabolism and the artery wall.