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The Role of Vitamin D and Calcium in Type 2 Diabetes. A Systematic Review and Meta-Analysis

Divisions of Endocrinology, Diabetes and Metabolism (A.G.P., B.D.-H.), and Clinical Research (J.L.), Tufts-New England Medical Center, Boston, Massachusetts 02111; Harvard School of Public Health and Channing Laboratory (F.B.H.), Boston, Massachusetts 02115; and Bone Metabolism Laboratory (B.D.-H.), Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts 02111

Address all correspondence and requests for reprints to: Anastassios G. Pittas, M.D., M.Sc., Division of Endocrinology, Diabetes and Metabolism, Tufts-New England Medical Center, 750 Washington Street, #268, Boston, Massachusetts 02111. E-mail: apittas{at}tufts-nemc.org.

Context: Altered vitamin D and calcium homeostasis may play a role in the development of type 2 diabetes mellitus (type 2 DM).

Evidence Acquisition and Analyses: MEDLINE review was conducted through January 2007 for observational studies and clinical trials in adults with outcomes related to glucose homeostasis. When data were available to combine, meta-analyses were performed, and summary odds ratios (OR) are presented.

Evidence Synthesis: Observational studies show a relatively consistent association between low vitamin D status, calcium or dairy intake, and prevalent type 2 DM or metabolic syndrome [OR (95% confidence interval): type 2 DM prevalence, 0.36 (0.16–0.80) among nonblacks for highest vs. lowest 25-hydroxyvitamin D; metabolic syndrome prevalence, 0.71 (0.57–0.89) for highest vs. lowest dairy intake]. There are also inverse associations with incident type 2 DM or metabolic syndrome [OR (95% confidence interval): type 2 DM incidence, 0.82 (0.72–0.93) for highest vs. lowest combined vitamin D and calcium intake; 0.86 (0.79–0.93) for highest vs. lowest dairy intake]. Evidence from trials with vitamin D and/or calcium supplementation suggests that combined vitamin D and calcium supplementation may have a role in the prevention of type 2 DM only in populations at high risk (i.e. glucose intolerance). The available evidence is limited because most observational studies are cross-sectional and did not adjust for important confounders, whereas intervention studies were short in duration, included few subjects, used a variety of formulations of vitamin D and calcium, or did post hoc analyses.

Conclusions: Vitamin D and calcium insufficiency may negatively influence glycemia, whereas combined supplementation with both nutrients may be beneficial in optimizing glucose metabolism.

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