Vitamin D deficiency has been suggested to contribute to the high and rising worldwide prevalence of cardiovascular disease. Vitamin D is a hormone precursor, which before exerting its metabolic effects undergoes two successive hydroxylations. The first hydroxylation converts vitamin D to 25hydroxyvitamin D and the second to the main active hormonal form, 1,25-dihydroxyvitamin D. Hormonal vitamin D activity is found throughout human circulatory tissue and 1,25 2D production has been demonstrated in endothelial cells of blood vessels. Vitamin D receptors are expressed in endothelial cells, cardiomyocytes and vascular smooth muscle cells, including those in the coronary arteries. VDR knockout mice show signs of enhanced thrombogenicity. The strongest evidence for a relation between vitamin D metabolism and CVD risk has been obtained from clinical studies reporting a marked reduction in mortality following administration of vitamin D analogues to patients with end-stage renal disease. Evidence for an Soyasaponin-Bd association between vitamin D status and subsequent risk of CVD was found in recent prospective studies on myocardial infarction and cardiovascular mortality ; both of these studies reported a two-fold increase in the risk of CVD for vitamin D insufficient participants compared to others. Concentration of the active hormone has been related to the degree of arterial calcification in individuals at increased risk of myocardial infarction and an inverse association has been reported between serum 25 D concentration with carotid artery intima-media thickness, myocardial infarction, metabolic syndrome, and CVD. To date there is relatively little evidence from population-based studies on the associations of 25 D with indicators of inflammation or hemostasis, and to what extent possible covariation is affected by adiposity. Obesity is a key Rhein-8-O-beta-D-glucopyranoside determinant for the circulating 25 D concentrations and also an important cardiovascular risk factor. Consequently, it is difficult to separate the effects of vitamin D status and adiposity when evaluating their influences on cardiovascular risk.