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From the Faculity of Medicine and Lipid Research Clinic, University of Toronto, Toronto, and G. D. Searle & Co of Canada, Limited, Oakville, Canada.
One hundred sixty-nine healthy women, aged 17 to 29 years, nonsmokers or light smokers (fewer than ten cigarettes per day), were assigned randomly to take one of five oral contraceptives: 1) 100 µg mestranol plus 0.5 mg ethynodiol diacetate (100 M + 0.5 ED); 2) 100 µg mestranol plus 1.0 mg ethynodiol diacetate (100 M + 1.0 ED); 3) 50 µg ethinyl estradiol plus 1.0 mg ethynodiol diacetate (50 EE + 1.0 ED); 4) 30 µg ethinyl estradiol plus 2.0 mg ethynodiol diacetate (30 EE + 2.0 ED); or 5) 30 µg ethinyl estradiol plus 0.15 mg levonorgestrel (30 EE + 0.15 NG). One hundred forty-seven women completed the study. When assessed for within-group differences, all preparations caused a statistically significant increase in total triglyceride (from 17.0 to 46.4 mg/dL), total cholesterol (from 6.3 to 24.4 mg/dL), and low density lipoprotein (LDL) cholesterol (from 7.0 to 10.3 mg/ dL). Effects on high-density lipoprotein (HDL) cholesterol varied widely. The product 100 M + 0.5 ED markedly increased (9.9 mg/dL) HDL cholesterol. Neither 100 M + 1.0 ED nor 50 EE + 1.0 ED altered HDL cholesterol levels, whereas both preparations containing 30 µg estrogen showed decreases: the preparation containing 2.0 mg ethynodiol diacetate lowered HDL cholesterol by 3.6 mg/dL and that containing 0.15 mg levonorgestrel lowered it by 6.9 mg/dL. Specific between-group comparisons revealed no statistically significant differences between differing amounts of estrogen (50 EE + 1.0 ED versus 100 M + 1.0 ED). Women receiving less progestogen (100 M + 0.5 ED). however, had significantly higher total cholesterol, HDL cholesterol, and HDL triglyceride when compared with 100 M + 1.0 ED, containing more progestogen. As there was less variation from baseline in the 100 M + 1.0 ED group, the higher dose of progestogen in this group more closely balanced the effects of 100 µg of mestranol. Although the differences between 30 EE + 2.0 ED and 30 EE + 0.15 NG were not statistically significant, the adjusted mean HDL cholesterol levels in the 30 EE + 2.0 ED group were higher (57.6 mg/dL) than in the 30 EE + 0.15 NG group (54.0 mg/dL). Thus, oral contraceptives should be regarded as differing in their potential for altering lipoprotein lipid levels, and the absolute steroid content of an oral contraceptive is not the only indicator of its effects upon lipid metabolism.
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