The extensive literature on the effects of oral contraceptives on plasma lipoproteins is reviewed. The interpretation of various studies has been confounded by the diversity of contraceptive formulations and by the fact that estrogen and progestogen components in a given preparation may neutralize or potentiate each other's effects. Recent studies on contraceptive estrogens and progestogens administered alone have helped to reveal some of the mechanisms behind oral-contraceptive-induced changes in plasma lipoproteins. The introduction of modern low-dose oral contraceptives has resulted in a reduction in adverse effects on plasma lipoproteins and has decreased concern about the risk of arterial disease.
PIP: This article reviews the literature on the effects of oral contraceptives (OCs) on plasma lipoproteins. The diversity of OC formulations and the recent trend toward a lower steroid content have complicated examination of this relationship. Moreover, the estrogen and progestogen components in a given preparation may neutralize or potentiate each other's effects on lipoproteins. Combination OCs have been found to cause elevated serum triglyceride levels, a risk factor in cardiovascular disease. This effect increases with the estrogen dose and is counteracted more effectively by androgenic progestogens such as levonorgestrel than by nonandrogenic progestogens such as desogestrel. Modern low-estrogen OCs do not generally elevate serum triglyceride levels above the normal range. Combination OCs also may increase serum low density lipoprotein (LDL) levels and androgenic steroids appear to cause elevation of LDL cholesterol levels. Synthetic and natural estrogens increase high density lipoprotein (HDL) cholesterol levels, while nortestosterone-derived progestins lower such levels and progesterone derivatives have little effect on HDL. Although the acute, thrombogenic effects of OCs are unrelated to duration of use and disappear soon after discontinuation, the chronic, metabolic effects correlate positively with duration of use and persist. 3 possibilities are suggested to counteract the reduction in HDL cholesterol levels associated even with low-dose OCs: 1) use of progesterone-derived progestins, 2) use of nortestosterone derivatives that lack androgenic properties, and 3) increase the estrogen: progestogen ratio by developing multiphasic combinations.