Technical Abstract: On the basis of evidence from animal and human studies, vitamin D has emerged as a potential risk modifier for type 1 and type 2 diabetes (t1DM and t2DM). Vitamin D is thought to have both direct (through activation of the vitamin D receptor) and indirect (via regulation of calcium homeostasis) effects on various mechanisms related to the pathophysiology of both types of diabetes, including pancreatic beta cell dysfunction), impaired insulin action and systemic inflammation. Observational case-control studies have shown that Vitamin D supplementation in pregnancy or early childhood is associated with reduced risk of incident t1DM. There are no trials on the effect of vitamin D on t1DM. An inverse association between vitamin D insufficiency and incident t2DM has been reported in longitudinal studies, but the association is not consistent. Post-hoc analyses of data from trials with vitamin D show no effect of vitamin D supplementation on glycemia in healthy adults but vitamin D may retard the progression to diabetes in adults with impaired glucose tolerance. Because vitamin D is an excellent marker of general health status, the positive results reported in the observational studies and post-hoc analyses of trials might reflect unmeasured and unaccounted confounding. Therefore, the hypothesis that vitamin D and calcium may modify diabetes risk needs to be confirmed in trials specifically designed for that purpose.