Sun, vitamin D, and cardiovascular disease

Abstract

Globally, cardiovascular disease (CVD) is the number one cause of death, being responsible for approximately 30% of deaths worldwide. Urbanization and a westernized lifestyle are thought to play a major role in the development of CVD. There is accumulating evidence that vitamin D is a nonclassical risk factor for CVD. The active vitamin D metabolite, 1,25-dihydroxyvitamin D, which is synthesized from its precursor 25-hydroxyvitamin D (25[OH]D), down-regulates several negative and up-regulates various protective pathways in the heart and vasculature. First randomized trials demonstrate that vitamin D supplementation leads to vasodilatation and suppresses cardiovascular risk markers such as triglycerides and the inflammation marker tumor necrosis factor-α. Solar UV-B radiation is the major source of vitamin D for humans. Consequently, the vitamin D status is largely influenced by season, geographic latitude, daily outdoor activities, and the percentage of body surface exposed to solar UV-B. A significant proportion of individuals in Europe and North America have vitamin D concentrations in the deficiency range (25[OH]D<25 nmol/l). Available data indicate that low solar UV-B exposure and/or low 25(OH)D concentrations are associated with an increased risk of CVD. Large nonrandomized studies indicate that CVD mortality is more than twice as high in older individuals with deficient 25(OH)D concentrations compared with those individuals who have adequate 25(OH)D concentrations (>75 nmol/l). Together, experimental and epidemiological evidence does support a plausible role for improving vitamin D status in CVD prevention in the population at large. Nevertheless, future randomised clinical trials are needed to evaluate whether vitamin D is effective with respect to primary, secondary, and/or tertiary prevention of CVD.