Low serum 25-hydroxyvitamin D levels may increase the detrimental effect of VDR variants on the risk of essential hypertension.
Eur J Clin Nutr. 2019 Dec 11. doi: 10.1038/s41430-019-0543-5.
Shen F1, Guo C2, Wang Y1, Yu F1, Zhang D1, Liu X3, Ba Y4, Wang C3, Li W5, Li X6.
Hypertension category listing contains the following
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Overview Cardiovascular and vitamin D
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160% increase per decade (women, age adjusted)
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The present cross-sectional study evaluated the association of vitamin D receptor (VDR) variants with serum 25(OH)D3 levels and their interaction on essential hypertension (EH) risk.
1539 patients were eligible in the study population. Two loci in VDR gene (rs2239179, rs2189480) were genotyped by TaqMan probe assays. Logistic regression, Kruskal-Wallis rank test and Chi-square test were used to determine the association among VDR polymorphisms, serum vitamin D metabolites, and the risk of EH. Interaction plots were performed to explain the interaction effects of circulating 25(OH)D3 levels and VDR variants on EH susceptibility.
After potential confounding adjustment, we observed that the mutations of VDR (rs2239179/rs2189480) were associated with the increased risk of EH (P < 0.05). Moreover, plasma 25(OH)D3 levels were inversely associated with EH, However, we did not find the association between serum 25(OH)D3 and VDR variants. When comparing with wild-type homozygous and heterozygous genotype carriers with vitamin D sufficiency, hypovitaminosis D and insufficient participants carrying homozygous variant genotype of rs2239179 showed a higher risk of EH, increased by 113% (OR = 2.13, 95% CI: 1.20, 3.80); Notably, the detrimental effect of rs2239179 homozygous variant on EH became stronger in the case of serum 25(OH)D3 <30 ng/ml. However, we did not find the interaction effect between rs2189480 variants and serum 25(OH)D3 levels on the risk of EH.
Our results suggested that the mutations of VDR may accelerate the progression of EH etiology, especially when suffering hypovitaminnosis D and insufficiency.
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