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Fertil Steril. 1990 Jan;53(1):1-12.

Lipids, cardiovascular disease, and oral contraceptives: a practical perspective.

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  • 1Wyeth-Ayerst Research and Medical College of Pennsylvania, Philadelphia.


Figure 9 is an attempt to summate the influences of life-style on lipid parameters. Based on the work of Nikkila, it shows the source of the production of HDL and LDL, the factors that can affect these lipoprotein levels, and where in the cascade of lipoprotein metabolism these factors exert influence. The source of HDL production is the liver and the intestine. At this stage, diet, exercise, hormones, genetics, drugs, and certain disease states can affect HDL levels. Lecithin-cholesterol acyl transferase (LCAT) esterifies HDL-free cholesterol in plasma, and HDL3 is formed that in turn is transformed to HDL2. At the same time, VLDL from the gut and the liver will be converted, under the influence of LPL, to HDL2 and LDL. Thus HDL2 is being formed by the breakdown of VLDL and from the transformation of HDL3 to HDL2. Insulin, exercise, alcohol, fats, drugs, and diet affect lipoprotein lipase and consequently influence levels of LDL and HDL2 indirectly. Progestogens increase and estrogens decrease hepatic endothelial lipase, thus affecting the HDL2 concentration. It is at this point that combination OCs influence HDL2. The balance between estrogen and progestogen in a given contraceptive determines the extent and direction of HDL2 concentration. A separate pathway in the liver also catabolizes HDL2 and HDL3. LDL is generated partly from catabolism of VLDL and is partly secreted from the liver. The removal of LDL is mediated by receptors in both the liver and peripheral tissues. It is here that the Brown-Goldstein theory plays a major role. If LDL receptors are present in an insufficient number or are defective, then the C will accumulate and atherosclerosis may follow. Thus two key enzymes, LCAT and LPL, control the production of HDL2 and LDL, whereas a third enzyme, hepatic endothelial lipase, catabolizes HDL2.


A practical interpretation of the mass of literature on lipids, lipoproteins, oral contraceptives and cardiovascular disease is presented. 1st it is important to realize that lipoprotein values reported by researchers use ultracentrifugation and electrophoresis methods that make commercial laboratory results meaningless. 2nd, most epidemiological studies cited to claim that oral contraceptives cause cardiovascular disease are based on data from the early 1970s, when women took high dose pills and were not screened for risk factors or smoking. The effect of a combined pill on lipids is a summation of the estrogenic and androgenic, as well as antiestrogenic, and anabolic, effects of the respective steroids it contains. Thus, although levonorgestrel is said to be androgenic, when combined with ethinyl estradiol its effect is balanced, as shown by its anti-acne effects. Lipid changes during oral contraceptive use go through a cycle of enzyme induction that occurs for the 1st 3-6 months, after which many observed changes will return to normal. Possible adverse effects of estrogen- induced high triglycerides must be evaluated by the HDL-C level. It is likely that atherogenic risk factors, such as smoking, alcohol and lack of exercise, far outweigh adverse lipid effects of the pill itself.

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