Vitamin D deficiency is highly prevalent in the United States and worldwide. Low levels of 25-hydroxy-vitamin D (25-OH D), the principal circulating storage form of vitamin D, are present in as many as one third to one half of otherwise healthy middle-aged to elderly adults. Limited cutaneous synthesis due to inadequate sun exposure or pigmented skin and inadequate dietary intake are the principal causes of low 25-OH D levels.
Although the best-characterized sequelae of vitamin D deficiency involve the musculoskeletal system, a growing body of evidence suggests that low levels of vitamin D may adversely affect the cardiovascular system. Vitamin D receptors have a broad tissue distribution that includes vascular
smooth muscle, endothelium, and cardiomyocytes.In vitro, activated 1,25-dihydroxyvitamin D (1,25-OH D) directly suppresses renin gene expression, regulates the growth and proliferation of vascular smooth muscle cells and cardiomyocytes, and inhibits cytokine release from lymphocytes. Studies in knockout mice confirm that the absence of vitamin D receptor activation leads to tonic up regulation of the renin-angiotensin system, with the development of hypertension and left ventricular hypertrophy.
Clinical studies have reported cross-sectional associations between lower vitamin D levels and plasma rennin activity, blood pressure, coronary artery calcification, and prevalent cardiovascular disease. Additionally, ecological studies have reported higher rates of coronary heart disease and hypertension with increasing distance from the equator, a phenomenon that has been attributed to the higher prevalence of vitamin D deficiency in regions with less exposure to sunlight.
