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The role of vitamin D for obese patients in reversing the type 2 diabetes pandemic
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Due to an increased prevalence of obesity, the incidence and prevalence of type 2 diabetes is increasing dramatically at both a national and international level.
At this time, other than bariatric surgery, we have very few effective tools with which to treat obesity. However, one of the consequences of obesity, vitamin D insufficiency (25-OH vitamin D below 30 ng/mL) and deficiency (below 20 ng/mL) can easily be corrected with oral vitamin D therapy.
Could vitamin D supplementation also decelerate the epidemic of type 2 diabetes?
Presumably, due to sequestration of vitamin D in adipose tissue, obesity is associated with low vitamin D levels and low vitamin D levels have been associated with both insulin resistance and beta cell dysfunction.
Insulin resistance is an inflammatory state associated with elevated cytokine levels which through oxidative stress cause endothelial dysfunction. With vitamin D supplementation, markers of this inflammatory state such as hsC-reactive protein are lowered. Furthermore, a recent study of patients with type 2 diabetes showed that vitamin D supplementation improved endothelial function. Therefore, by lowering insulin resistance vitamin D supplementation should have the potential of not only preventing type 2 diabetes but also of preventing cardiac events.
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Of more importance is that type 2 diabetes is clearly a disease of insulin deficiency. Vitamin D has been shown to be associated with both preservation of pancreatic beta cells and improved insulin release. While metabolic factors such as glucotoxicity and lipotoxicity play a prominent role in apoptosis of the pancreatic beta cell that is characteristic of type 2 diabetes, it has now been well documented that inflammation is also a significant promoter of apoptosis. Because of this, studies of the role of anti-inflammatory agents in preserving of beta-cell function in patients with type 2 diabetes are being preformed. Vitamin D through its anti-inflammatory effect has been shown to reversibly protect isolated human pancreatic islet cells against cytokine-induced apoptosis through down regulation of the Fas receptor. Vitamin D deficiency has also been shown to decrease insulin release from the beta cell without having a significant effect on glucagon secretion. That vitamin D plays an important role in beta cell function is further evidenced by the demonstration that vitamin D receptors are present in the nucleus of the beta cell.
Since inflammation also plays a major role in pancreatic beta cell apoptosis in autoimmune diabetes, it is of interest that in 10,336 Finish children who were given 2,000 IU of vitamin D per day during their first year of life, there was a 78% reduced risk of developing type 1 diabetes after 31 years of follow-up.
Therefore, it is possible that utilizing vitamin D supplements in the obese vitamin D insufficient or deficient subject would prevent the development of type 2 diabetes. To prove this hypothesis, obese subjects at high risk for type 2 diabetes (ie, with a family history in at least one first degree relative) should be screened for vitamin D deficiency or insufficiency. To avoid ethical issues, these subjects should be randomized to either a group where a 25-OH-vitamin D level of 30 ng/mL is obtained or to a group where an ideal level of 100 ng/mL is achieved. In this way it could be established if vitamin D supplementation in the obese would avoid the development of type 2 diabetes.
If vitamin D hypothesis were proven a simple solution and inexpensive to a catastrophic pandemic would be available. Since this study would have no entrepreneurial interest, it would need to be funded by a government agency. However, if the results were positive, through a decrease in health care costs, governments would obviously benefit. Is this hypothesis too simplistic or too good to be true? There is only one way to find out.
David S. H. Bell, MB, FACE, is a Professor of Medicine at the University of Alabama School of Medicine, Birmingham, and a member of the Endocrine Today Editorial Board.
For more information:
- Hyppönen E, Läärä E, Reunanen A, et al. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001;358:1500-1503.
- Norman AW, Frankel JB, Heldt AM, Grodsky GM. Vitamin D deficiency inhibits pancreatic secretion of insulin. Science. 1980;209:823-825.
- Riachy R, Vandewalle B, Moerman E, et al. 1,25-Dihydroxyvitamin D3 protects human pancreatic islets against cytokine-induced apoptosis via down-regulation of the Fas receptor. Apoptosis. 2006;11:151-159.
- Sugden JA, Davies JI, Witham MD, et al. Vitamin D improves endothelial function in patients with Type 2 diabetes mellitus and low vitamin D levels. Diabet Med. 2008;25:320-325.