title: Cardiovascular effects of endogenous and exogenous sex hormones over a woman's lifetime.
abstract: Natural fluctuations in concentrations of physiologic sex hormones over the course of a woman's lifetime affect lipoprotein levels; such effects may be compared with those induced by exogenous hormone therapy. During the progesterone-dominated luteal phase of the menstrual cycle, high-density lipoprotein (HDL) concentrations do not fall, but low-density lipoprotein (LDL) concentrations usually decline. During pregnancy both estrogen and progesterone levels are extremely high; LDL concentration gradually increases to a maximum value at term of 50% above the nonpregnant level. Total HDL and HDL2 concentrations also increase, reaching a maximal 30% increase at 20 weeks' gestation. These physiological fluctuations have not been associated with increased arteriosclerosis. Oral contraceptives that combine C21 progestins and certain C19 progestin derivatives with estrogen have little or no effect on HDL2; however, those with a marked progestogenic or androgenic effect are more likely to lower HDL and HDL2. Increases in LDL concentration during oral contraceptive use are not consistently proportional to estrogen/progestin ratio and may reflect progestin androgenicity or a progestin-estrogen interaction. In postmenopausal women estrogen alone benefits lipoproteins, whereas cyclical administration of progestin with estrogen appears to lower HDL2-cholesterol proportionate to progestin dose. These exogenous hormone-induced changes are associated with the expected changes in arteriosclerosis risk when they have been looked for. In summary, estrogen-progestin regimens that do not affect LDL- and HDL2-cholesterol concentrations are most desirable in terms of long-term cardiovascular risk.
authors.affiliation: Northwest Lipid Research Clinic, Seattle, WA 98104.
authors.forename: R H
authors.initials: RH
authors.lastname: Knopp
mesh_terms: D001161:Arteriosclerosis / Q000209:etiology; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology* / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003278:Contraceptives, Oral, Hormonal / Q000494:pharmacology; D004347:Drug Interactions; D004967:Estrogens / Q000097:blood / Q000378:metabolism*; D005069:Evaluation Studies as Topic; D005260:Female; D006801:Humans; D008074:Lipoproteins / Q000097:blood / Q000378:metabolism*; D008297:Male; D008593:Menopause / Q000097:blood; D008597:Menstrual Cycle; D011247:Pregnancy / Q000097:blood / Q000378:metabolism; D011374:Progesterone / Q000097:blood / Q000378:metabolism*; D011627:Puberty / Q000378:metabolism; D012307:Risk Factors
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D003278:Contraceptives, Oral, Hormonal; D004967:Estrogens; D008074:Lipoproteins; D011374:Progesterone