Abstract

The purpose of this review is to summarize important aspects of lipoprotein physiology and how abnormalities in this process can lead to accelerated atherosclerosis. The effects of various oral contraceptive formulations on lipoprotein lipid concentrations will then be examined followed by consideration of the epidemiologic experience associating oral contraceptive use, progestin dose, and arteriosclerotic disease in premenopausal women. This experience will be contrasted with postmenopausal estrogen use and its association with arteriosclerotic heart disease. To determine if oral contraceptives produce changes in lipoprotein lipids that are different from a physiological elevation of estrogen and progestin, comparisons will be made between oral contraceptive use and pregnancy. The question of whether oral contraceptive preparations can be successfully evaluated for their potential risk for arteriosclerosis causation in animal models will be discussed and contrasted with the alternative option of carefully examining lipoprotein physiology in human subjects in the earliest stages of oral contraceptive evaluation. Regardless of the approach taken, the conclusion will be drawn that better and more definitive approaches are required to evaluate the potential significance of long-term oral contraceptive use on arteriosclerotic disease.

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