Is vitamin D status relevant to metabolic syndrome?

Abstract

Review of the evidence on hypovitaminosis D as a risk factor for metabolic syndrome and its sequelae, T2DM and CVD, suggests long-term vitamin D repletion could reduce these risks. There is mechanistic evidence for protective effects for MetS and the balance of evidence, (cross-sectional and prospective), supports this postulate. Much of the data so far available from randomized controlled trials is weakened by inadequate power, low vitamin D dosages, starting supplementation too late in life or after MetS disorders have developed or, most importantly, by non-inclusion of many recognizable confounders. On balance, therefore, maintenance of US 2010 recommended intakes for bone protection has the potential to prove protective for MetS. Supplementation has been shown to increase survival in patients with cardiac disorders; whether higher doses would provide useful protection for apparently healthy people in the general population awaits the outcomes of ongoing randomized-controlled trials that, it is hoped, will prove or disprove causality for hypovitaminosis D in MetS and its long-term ill-effects.

Keywords: cardiovascular disease; metabolic syndrome; syndrome “X”; type 2 diabetes; vitamin D.

Figure 1.

Response of serum 25-hydroxyvitamin D [25(OH)D] level to total intake of vitamin D in northern latitudes in Europe (0.49·58N) and Antarctica (788S) during their respective winter seasons, when effective sun exposure for endogenous vitamin D synthesis is minimal. Mean responses (white lines) with 95% CI using a weighted linear meta-regression model following either a natural logarithmic transformation (dark gray shading, curvilinear model) or no transformation (pale gray shading, linear model) of total vitamin D intake data. The maximum total intake data point in the linear model was 1400 IU/d (35 mg/d). A line is plotted at 50 nmol/l serum 25(OH)D for illustrative purposes” (from ref. with permission).