Relationship between vitamin D deficiency, vitamin D receptor gene variants, and the risk of coronary artery disease among South Indians: A case-control study

Background & objectives Vitamin D deficiency (VDD) and variations in the vitamin D receptor ( VDR ) gene are implicated in the pathogenesis of coronary artery disease (CAD). This study investigated the association between VDD, VDR gene variants ( Apa I, Bsm I, Fok I, and Taq I), and CAD risk among South Indians. Methods The case-control study was conducted in 250 CAD patients and 260 matched controls. Serum vitamin D levels were measured by ELISA. Genotyping for VDR Apa I (A>C, rs7975232), Bsm I (A>G, rs1544410), Fok I (T>C, rs2228570), and Taq I (C>T, rs731236) was performed using the polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) method. Results VDD was significantly higher among CAD patients (90%) than in controls (63%). Individuals with vitamin D levels <20 ng/ml were 5.7 times more likely to have CAD when compared to those with vitamin D levels ≥ 20 ng/ml ( P< 0.001, OR=5.74, 95% CI=2.92-11.30). No correlation was observed between vitamin D levels and CAD risk factors, systolic and diastolic blood pressure (r=-0.105, P= 0.095, r=-0.049, P= 0.437), and blood glucose (r=-0.067, P= 0.304). A trend for negative correlation of vitamin D levels with cholesterol (r=-0.112, P= 0.094) and triglyceride levels (r=-0.133, P= 0.061) was observed. The VDR Taq I variant showed significant association with reduced CAD risk in the overall analysis (Model II, OR=0.60, 95% CI=0.39-0.90, P= 0.016). The Fok I variant was associated with an increased risk of CAD in males (Model III, OR=5.9, 95% CI=2.09-16.85, P= 0.001). However, combined analysis of VDD and VDR gene variants indicated that neither Fok I ‘ff’ ( P= 0.145) nor Taq I ‘tt’ ( P= 0.138) genotypes significantly altered CAD risk in vitamin D-deficient subjects. Interpretation & conclusions The findings of this study suggested that VDD was significantly higher among the CAD patients and increases the risk of CAD by 5.7-fold.This study revealed the differing roles of V DR gene variants in CAD susceptibility and the influence of gender and other covariates.