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Combined oral contraceptives have neutral impact on LDL levels
10 March 2010
MedWire News: Oral contraceptives containing both estrogen and progestin induce an increase in the production of apolipoprotein B (apoB)-containing lipoproteins, including low-density lipoprotein (LDL), a kinetic study has found.
But the overall effect is unlikely to be proatherogenic, say the researchers, because the increased production of apoB in LDL is counterbalanced by a higher LDL fractional catabolic rate, meaning that plasma LDL levels are unchanged.
For the study, Laurence Duvillard (Université de Bourgogne, Dijon, France) and colleagues examined the impact on lipoprotein kinetics of an oral contraceptive containing 30 µg ethinylestradiol and 75 µg gestodene (a low-androgenic-activity progestin).
The study participants were nine healthy nonobese women who underwent kinetic studies before and after 3 months’ treatment with the oral contraceptive.
The study, which is reported in the Journal of Clinical Endocrinology and Metabolism, found that the oral contraceptive treatment was associated with a 12% increase in serum triglycerides but no other changes in lipids or body weight.
However, kinetic studies revealed that the oral contraceptive increased the apoB production rates of very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and LDL by 49%, 55%, and 51%, respectively.
In addition, after the oral contraceptive treatment, LDL particles became increasingly enriched with triglycerides (7.5% vs 4.3% of total LDL mass).
Despite the higher production rate of apoB LDL, however, total plasma LDL concentrations were unchanged due to a 36% increase in the fractional catabolic rate (FCR). The same was true for VLDL and IDL.
Duvillard and co-authors say that the mechanism for the rise in LDL catabolism is most likely an increase in LDL receptor expression. This effect is of “major importance,” they say, because it counterbalances the increase in LDL production and contrasts with other circumstances, such as hypercholesterolemia or obesity, in which LDL serum levels rise.
“Moreover, the 36% increase in the LDL apoB FCR means that LDL residence is shorter, which may reduce the likelihood of atherogenic changes such as oxidation,” they add.