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

Estrogens and androgens have opposing effects on lipoprotein lipids. P rogestins 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 co ncentrations, raise LDL and lower HDL concentrations. Apoprotein B and A-I levels change in parallel with alterations in LDL and HDL, respec tively. An exception is Lp(a), which decreases with estrogen or androg en. There are numerous examples of these effects. Male puberty is asso ciated 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 prog estin androgenicity. Lipoprotein changes in pregnancy are generally an estrogen dominant effect while in oral contraceptive use the lipoprot ein 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 fa t diet and fish oil. Postmenopausally, use of estrogens alone or with a low-dose low-androgenic progestin such as medroxyprogesterone acetat e reveal a predominantly estrogenic effect and beneficial effects on I DL and HDL. Advantage can be taken of these hormonal effects to manage hypercholesterolemia and Type III hyperlipidemia (''remnant removal d isease''). Rarely, androgens may be useful in treating intractable hyp ertriglyceridemia. Pending the outcome of ongoing studies, the prevent ion of coronary artery disease in women with estrogen may be feasible through favorable effects on lipid and carbohydrate metabolism and the artery wall.