The Effects of Vitamin D-K-Calcium Co-Supplementation on Endocrine, Inflammation, and Oxidative Stress Biomarkers in Vitamin D-Deficient Women with Polycystic Ovary Syndrome: A Randomized, Double-Blind, Placebo-Controlled Trial.

The current study was conducted to assess the effects of vitamin D-K-calcium co-supplementation on endocrine, inflammation, and oxidative stress biomarkers in vitamin D-deficient women with polycystic ovary syndrome (PCOS). This randomized double-blind, placebo-controlled trial was performed on 60 vitamin D-deficient women diagnosed with PCOS aged 18-40 years old. Participants were randomly allocated into 2 groups to intake either 200 IU vitamin D, 90 mu g vitamin K plus, 500 mg calcium supplements (n = 30), or placebo (n = 30) twice a day for 8 weeks. Endocrine, inflammation, and oxidative stress biomarkers were quantified at the beginning and the end of the study. After 8 weeks of intervention, compared with the placebo, vitamin D-K-calcium co-supplementation resulted in a significant reduction in serum-free testosterone (-2.1 +/- 1.6 vs. + 0.1 +/- 1.0 pg/ml, p < 0.001) and dehydroepiandrosterone sulfate (DHEAS) levels (-0.8 +/- 1.0 vs. -0.1 +/- 0.5 mu g/ml, p = 0.006). In addition, a significant increase in plasma total antioxidant capacity (TAC) (+ 75.7 +/- 126.1 vs. -80.4 +/- 242.8 mmol/l, p = 0.005) and a significant difference in plasma malondialdehyde (MDA) concentrations (+ 0.03 +/- 0.6 vs. + 1.4 +/- 2.4 mu mol/l, p = 0.005) was observed following the supplementation with vitamin D-Kcalcium compared with the placebo. A trend toward a greater decrease in luteinizing hormone was observed in vitamin D-K-calcium co-supplement group compared to placebo group (-7.0 vs. -1.2 IU/l, p = 0.09). We did not find any significant effect of vitamin D-K-calcium co-supplementation on prolactin, follicle-stimulating hormone, 17-OH progesterone, inflammatory markers, and glutathione levels. Overall, vitamin D-K-calcium co-supplementation for 8 weeks among vitamin D-deficient women with PCOS had beneficial effects on serum DHEAS, free testosterone, plasma TAC, and MDA levels.