Abstract

Vitamin D is a fat-soluble secosteroid produced in the skin as a result of sunlight exposure, and its circulating levels are reduced in a wide variety of chronic illnesses and obesity. Observational studies clearly demonstrate a higher incidence of cardiovascular events in individuals with low circulating 25-hydroxyvitamin D [25(OH)D]. This relationship can potentially be explained by confounding, because individuals with low 25(OH)D are generally older, frailer, heavier, and have more comorbidities and higher estimated cardiovascular risk than individuals with higher 25(OH)D. The vitamin D receptor appears to be widely distributed, including in cardiovascular tissue, although this has recently been contested. Despite these epidemiological and laboratory findings, meta-analyses of clinical trials have not shown evidence of beneficial effects of vitamin D supplementation on cardiovascular endpoints. Trials are underway to assess these possibilities further. At present, there is insufficient evidence to support vitamin D supplementation for improving cardiovascular outcomes.