Exploring the Role of Vitamin B12 as an Anti-atherogenic and Anti-inflammatory Agent in Apparently Healthy Adults With Hypovitaminosis D

Vitamin B12 deficiency is associated with metabolic changes like methyl malonic acidemia and hyperhomocystinemia eventually leading to atherosclerosis. Dyslipidemia and vitamin D (vit D) deficiency are independent risk factors of CVD. This study aims to explore the interrelationship between inflammatory markers, adverse lipid profile and vitamin B12 in hypovitaminosis D. Since, atherosclerosis is an inflammatory condition we have investigated CRP and NLR as inflammatory markers along with lipid profile parameters and atherogenic indices in apparently healthy individuals with vitamin D deficiency. 90 apparently healthy subjects aged between 25-55 years were divided into 3 groups of 30 members each, as vit D sufficient (vit D ≥ 30 ng/ml), insufficient (vit D = 21-29 ng/ml) and deficient groups (vit D ≤ 20 ng/ml). Deficient group was further divided into moderately and severely deficient (vit D less than 20 and 10 ng/ml) groups respectively. Fasting lipid profile was estimated spectrophotometrically. Plasma vit D and B12 were determined by ECLIA. CRP was assayed by ELISA. Neutrophil Lymphocyte Ratio (NLR) was calculated manually. Vitamin B12 was significantly lower in vit D deficient group compared to insufficient (p<0.01) and sufficient groups (p<0.001). TC/HDL was significantly higher in insufficient group (p<0.01) compared to sufficient group. Further, both the atherogenic indices, TC/HDL and non -HDL increased drastically in severely deficient group where vitamin B12 was the least. Inflammatory markers CRP and NLR showed profound increase with vitamin B12 deficiency. The proposed mechanisms that underlie an abnormal lipid profile in vitamin B12 deficiency include increase in methyl malonyl CoA which inhibits oxidation of fatty acid and contributes to lipogenesis. Hyperhomocysteinemia interferes in VLDL secretion leading to dyslipidemia. Further, vitamin D modulates the expression of enzymes involved in homocysteine metabolism. While Vitamin B12 attenuates the expression of inflammatory cytokines, homocysteine induces the same. The observed abnormal lipid profile and elevated inflammatory markers in groups with lower vitamin B12 suggests its potential role in inflammatory reactions that precede subclinical atherosclerosis in hypovitaminosis D. The study also highlights synergistic action of both the vitamins in cardio protection which has not been previously reported.