Vitamin D insufficiency and diabetes risks.
Diabetes is an increasing epidemic; hyperglycemia results from lack of insulin or inadequate insulin secretion following increases in insulin resistance. Huge costs are placed upon sufferers and health providers, aggravated as serious and disabling complications develop. Thus, measures to reduce the diabetic burden are public health concerns. Vitamin D, identified ≈100 years ago, promotes calcium absorption and utilization, preventing and curing rickets & osteomalacia. Calcium is necessary for insulin secretion, suggesting vitamin D may contribute to maintaining insulin secretion. Vitamin D, formed in skin in bright sunshine, is scarce in foodstuffs. Data linking hypovitaminosis D to hyperglycemia, type 2 diabetes (T2DM) and metabolic disorders increasing cardiovascular risk [metabolic 'syndrome'] has accumulated over ≈40 years. Many mechanisms are known whereby hypovitaminosis D could be causal, e.g. by increasing insulin resistance, reducing insulin secretion and increasing autoimmune or inflammatory damage to pancreatic islets. Major questions still to be answered are whether increasing vitamin D status to the maximum seen in healthy people would reduce the risk of diabetes, the severity of the disease or of its complications, including cardiovascular disease. These questions urgently require answers. If on-going/ planned RCTs confirm causality, maintenance of adequate vitamin D status at the population level by food-fortification or supplementation would be cost-effective measures likely to reduce the burden and costs of diabetes to individuals and health services. Additionally, vitamin D(2/3) supplementation is cheap but whether some non-hypercalcemia-inducing analogue may prove safer has not yet been addressed at the population level.
Boucher
Barbara J
BJ
Centre for Diabetes, Barts & The London School of Medicine and Dentistry, Queen Mary University of London, Blizard Institute of Cell and Molecular Science, Newart Street, London, E1 2AT, UK. bboucher@doctors.org.uk
D000375:Aging / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D015415:Biomarkers; D048909:Diabetes Complications / Q000188:drug therapy; D003920:Diabetes Mellitus / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D019587:Dietary Supplements; D005234:Fatty Liver / Q000150:complications / Q000188:drug therapy; D005527:Food, Fortified; D006801:Humans; D007333:Insulin Resistance; D024821:Metabolic Syndrome / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D018673:Nutrition Policy; D009751:Nutritional Requirements; D012306:Risk; D014807:Vitamin D / Q000009:adverse effects / Q000031:analogs & derivatives / Q000378:metabolism / Q000627:therapeutic use; D014808:Vitamin D Deficiency / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*
D015415:Biomarkers; D014807:Vitamin D