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Discover Supplement-Drug Interactions
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Last Updated: 3 years ago
Research Papers that Mention the Interaction
“Moreover, triglyceride and estradiol levels significantly decreased at V3 (p=0.001) and V2 (p=0.022), respectively, whereas total cholesterol (V2, p=0.008) and LDL cholesterol levels (V2, p=0.005; V3, p=0.026) significantly increased after vitamin D treatment.”
Effect of vitamin D3 treatment on glucose metabolism and menstrual frequency in polycystic ovary syndrome women: A pilot study“Furthermore, the beneficial effects of HRT on serum LDL cholesterol content were reduced when estradiol valerate was combined with vitamin D3.”
“Collectively, the present study demonstrated that vitamin D and 17β-estradiol could upregulate each other's receptors and regulate the AMPK/NF-κB pathway to relieve the OVX-induced depressive-like state.”
“Using the method of immunofluorescent staining and western blot, vitamin D and 17β-estradiol were demonstrated to upregulate each other's receptors, including VDR, ERα, and ERβ in the hippocampus of OVX rats.”
“Studies in both humans and animal disease models demonstrate a functional synergy for the immunomodulatory effects of Vitamin D3 and 17-β estradiol.”
“Moreover, vitamin D might influence steroidogenesis of sex hormones ( estradiol and progesterone) in healthy women and high 25(OH)D levels might be associated with endometriosis.”
“There are reports of possible beneficial interactions of vitamin D with other substances, such as quercetin, estradiol , some microelements, and other vitamins.”
“We find that women with lower vitamin D status (lower 25(OH)D or higher iPTH) have lower mean concentrations of estradiol across the menstrual cycle.”
“Insulin and vitamin D synergistically stimulate estradiol production.”
“ConclusionsHigher levels of vitamin D may reduce progesterone and estradiol , providing a potential mechanism for reduction in breast cancer risk from increased vitamin D exposure in young women.”
“In MCF-7 cells, vitamin D and vitamin D analogs have been shown to induce cell cycle arrest and apoptosis, to downregulate estrogen receptor expression, to limit responsiveness to the mitogenic effects of 17beta-estradiol , and to limit induction of the progesterone receptor.”
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