“…Some data suggested that vitamin D may reduce or prevent the disease progression and cardiovascular risk in T2D patients by decreasing oxidative stress and platelet-mediated inflammation (IL-18, TNF-α, IFN-γ, CXCL-10, CXCL-12, CCL-2, CCL-5, CCL-11, and PF-4), as well as blood vitamin D supplementation (2000 IU/day for six months) in T2D patients having vitamin D < 20 ng/mL resulted associated to a significant decrease in OxLDL, hsCRP, IL-6, PAI-1, and fibrinogen levels and a significant increase in FRAP, (although other studies failed to evidence any significant effect on different biomarkers of oxidative stress and inflammation in these type of patients) [ 191 , 192 , 193 , 194 ]. Furthermore, in patients with CAD, there are controversial data on the effects of vitamin D supplementation on oxidative or inflammatory biomarkers related to cardiovascular health [ 195 , 196 , 197 ]. A recent meta-analysis aiming to assess the effect of vitamin D supplementation on cardiac outcomes in patients with CAD did not evidence any significant effects on hs-CRP mean difference (−0.04, p = 0.25), although included a limited number of studies, with small sample size and short duration of interventions [ 198 ].…”