Dr. Neil Binkley recently gave a presentation at the Southern Regional Conference of the ADA in May of 2010 that has made me rethink a lot of my previously held beliefs about vitamin supplementation and type 2 diabetes (T2DM). He reviewed the data on vitamin D and its potential association with diabetes in general and potential mechanisms of action. The role of vitamin D as a possible treatment for diabetes has been postulated for many years.
According to Binkley’s report, diabetes is one of many diseases/conditions associated with low vitamin D status. In fact, Binkley hypothesized that low vitamin D may play a potential role in the development of diabetes. Potential mechanisms underlying this association are supported by the following findings:
• Beta cells contain the vitamin D receptor and demonstrate activity of 1 alpha hydroxylase, an enzyme involved in vitamin D metabolism.
• Vitamin D improves beta cell function
- Direct effect on insulin secretion
- 1,25 (OH)2 D stimulates insulin release
- Vitamin D supplementation restores impaired insulin secretion in vitamin D deficient mice
- Indirect effect via calcium on insulin secretion—hypocalcemia is associated with impaired insulin secretion
• Vitamin D is known to improve insulin action
- Vitamin D stimulates expression of the insulin receptor
- Vitamin D enhances insulin responsiveness for glucose transport
Several authors and observational studies support Binkley’s hypothesis and suggest its clinical implications. In 1994, Kumar, Davies, Zakaria et al., for example, presented a case report titled, “Improvement in glucose tolerance and beta-cell function in patients with vitamin D deficiency during treatment with vitamin D."
In this report a vitamin D deficient patient with glucose intolerance had significant improvement in her glucose tolerance with the correction of vitamin D deficiency. Hypponen et al. also reported in the Lancet
a study of women in Finland who gave birth in 1996 in which the risk of type 1 diabetes was reduced by 80% in children who received vitamin D regularly.
In a similar study by Zipitis and Akobeng in 2008, a 29% reduction was reported.
Finally, the Nurses Health Study of 83,779 women with 20-year follow-up revealed 4,843 new cases of T2DM but showed that a “combined daily intake >1000 mg calcium and >800mg of vitamin D was associated with a 33% lower risk of type 2 diabetes.”
The debate will go on about what dose of vitamin D is necessary get some of these benefits. However, I now view vitamin D as a key component of a diabetes treatment plan and worthy of consideration for supplementation in deficient patients.
I encourage you to share your experience with vitamin D by leaving a comment below.
 Bland R, Markovic D, et al. Expression of 25-hydroxyvitamin D3-1 alpha hydroxylase in pancreatic islets. 2004 J Steroid Biochem Mol Bio 89-90:121-125. Vitamin D does not have significant biologic activity until it is metabolized to its hormonally active form, 1,25 dihydroxycholecalciferol. This occurs in a two step process, first in the liver by hydroxylation with the enzyme 25 hydroxylase and second in one of many tissues with the enzyme 1 alpha hydroxylase. See Gonzalez C. Vitamin D supplementation: an update. US Pharmacist. Medscape Today. Published 11/11/2010. http://www.medscape.com/viewarticle/731722?src=emailthis. Accessed 1/3/11.