The cardiometabolic syndrome (MetS) is a clustering of related metabolic abnormalities including abdominal adiposity, insulin resistance, hypertension, dyslipidaemia and increased inflammatory and thrombotic markers, which is linked to increased risk of type 2 diabetes, CVD and overall mortality. Several cross-sectional and prospective studies have shown an association between low vitamin D status, as indicated by concentrations of serum 25-hydroxyvitamin D (s25(OH)D), and increased prevalence of the MetS and individual CVD risk factors. These epidemiological observations are supported by mechanistic studies but experimental data are limited. The available data from intervention studies are largely confounded as most vitamin D supplementation trials were mainly carried out to explore the role of Ca in CVD and include Ca in the treatment arms. Inadequate consideration of seasonal effects on s25(OH)D concentrations is also a common design flaw in most studies. Further complications arise from shared risk factors such as adiposity and ageing, which predispose individuals to exhibit both a more pronounced risk profile and relatively lower s25(OH)D concentrations. In conclusion, while epidemiological associations are promising and a rationale for low vitamin D status as a potentially modifiable risk factor for CVD is supported by mechanistic data, suitable experimental data from appropriately designed trials are just beginning to emerge. As yet, this body of literature is too immature to draw firm conclusions on the role of vitamin D in CVD prevention. Carefully controlled vitamin D trials in well-described population groups using intervention doses that are titrated against target s25(OH)D concentrations could yield potentially valuable outcomes that may have a positive impact on CVD risk modification.