The atherogenic index of plasma is increased by hormonal contraception

Abstract

The increased AIP and hs-CRP concentration after 9 months of hormonal contraception demonstrate that contraceptive-induced dyslipidemia has a proatherogenic nature, even when the TC/HDL-C and the apoB/apoA1 ratios are unchanged.

Adiponectin, leptin and lipid profiles evaluation in oral contraceptive pill consumers

“…As shown, our results are in good agreement with the result of Di Carlo et al regarding the NETA COC influence on adiponectin levels only. According to the results of present study, LD COCs affect the serum adiponectin, leptin and lipid levels, which is in agreement with some [23] but not all [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24] studies. The biological pathways underlying COC alteration of adiponectin, leptin, lipid and lipoprotein production are not clear, but could include effects on maturation or synthesis of new molecules or might be a result of an increased frequency of a particular allele of these molecules.…”

“…There was a nonsignificant decrease in the mean concentration of LDL-C during the study period. Soska et al [19] found that the contraceptive-induced dyslipidemia has a proatherogenic nature, when the TG/HDL-C ratio is unchanged. It was postulated that oral contraceptives with estrogen plus progestin are likely to influence apolipoprotein B (apoB)-containing lipoprotein metabolism by changing the expression of different enzymes or receptors that play a major role in this metabolism [20].…”

Positive Association Between 25-Hydroxyvitamin D and C-Reactive Protein is Confounded by Hormonal Contraceptive Use

“…HC use has also been associated with changes in numerous physiologic pathways, increased inflammation, and a poorer metabolic profile. 23,24,28,29,31 Our finding that adjustment for HC use attenuates a positive association between 25(OH)D and CRP might partly account for some of the unexpected results of previous studies.…”

“…In addition, use of HC and HRT has also been associated with deleterious health outcomes, such as increased risk of cardiovascular disease and cancer, as well as a worsened metabolic profile, thrombosis, and elevated inflammation. [23][24][25][26][27][28] A recent study examining the association between HC use and the plasma proteome identified a number of novel pathways that are affected by HC use, suggesting that the effects of HC on disease-associated metabolic pathways may be widespread. 29 Use of these medications may, therefore, confound the association between 25(OH)D and various health outcomes.…”

“…22 The use of HC in particular has been associated with elevated concentrations of CRP and other inflammatory biomarkers. 23,24,28,31 These effects are apparent after only 3 months of continued HC use, 24 and are thought to result from first-pass hepatic metabolism of estrogen-containing HC, which may affect hepatic production of CRP and other proinflammatory acute phase reactants. 31 However, despite these well-known effects on inflammation, no studies have directly investigated whether HC use, which is widespread among premenopausal women worldwide, modifies the association between 25(OH)D and inflammation.…”