Vitamin D₂ may help preserve honeymoon phase of type I diabetes

A team of medical researchers and doctors reports that administration of vitamin D2 to patients newly diagnosed with diabetes type 1 can prolong the so-called honeymoon phase of the disease.

The group conducted a clinical trial involving giving vitamin D2 supplements to children newly diagnosed with diabetes.

Prior research has shown that at the time of diagnosis, most diabetes type 1 patients still have approximately 30% to 50% function in pancreatic beta cells (diabetes occurs when such cells stop making insulin). Sometimes the beta cells continue to function for several months or even years. This time period is known as the honeymoon phase because it gives patients time to adjust to their disease and puts off the onset of damaging symptoms.

Most new research involving treatment or prevention of type 1 diabetes involves efforts to prevent beta cells from ceasing production of insulin. In this new effort, the research team has found evidence that giving newly diagnosed patients vitamin D2 can prolong the honeymoon phase.

The work involved carrying out a randomized clinical trial involving 36 young volunteer patients who had been newly diagnosed with type 1 diabetes. Some of the volunteers received vitamin D2 supplements every week for two months, while others received a placebo for the same time period.

The research team found that those volunteers given the vitamin D2 supplements saw improvements in insulin secretion capacity in beta cells—they observed decreases in the PI:C ratio compared to a placebo. They also found reductions in %ΔAUC of C-peptide that were slower in those given the vitamin supplements, which led to longer delays in loss of the C-peptide.

It is expected that the benefits derived from vitamin D2 during the honeymoon phase will vary by patient, though any delay in the onset of symptoms can have beneficial lifelong impacts.

“We previously reported1 that ergocalciferol significantly decreased circulating tumor necrosis factor (TNF)-α and temporal trends in both hemoglobin A1c (HbA1c) and insulin dose–adjusted A1c (IDAA1c), a marker of PR, compared with placebo.”

D2 seems an odd choice. D3 seems to also show promise:

“A relationship between type 1 diabetes mellitus and vitamin D deficiency has been reported.5,6 The prevalence of vitamin D deficiency in patients with type 1 diabetes was 15% to 90.6%.7–9 There is evidence that vitamin D is important in the prevention of islet cell death and might be useful in improving the survival of islet cell grafts, and it improves the production of insulin. Low vitamin D levels were shown to have a negative effect on beta-cell function.3,4 Regular doses of vitamin D early in life have been shown to reduce the risk of developing type 1 diabetes.5 Vitamin D treatment has also been shown to improve glycemic control and insulin sensitivity in people with type 1 and type 2 diabetes and in normal individuals. Increasing vitamin D levels from 25 to 75 nmol/L results in a 60% improvement in insulin sensitivity.3,4,10–12 These effects have been mainly attributed to the immunomodulatory actions of vitamin D.5...

...The patients in our study were repleted with vitamin D3, and using up to 4000 IU of vitamin D3 to reverse states of deficiency was found to be safe.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994161/

https://diabetes.org/food-nutrition/diabetes-vitamins-supplements/low-vitamin-d-insulin-resistance

“We describe here the cases of two young women who presented with positive glutamic acid decarboxylase (GAD) antibody and classic clinical manifestations of T1DM. Both patients had a prior history of Hashimoto’s thyroiditis. They were initially treated with a basal-bolus regimen of insulin (glargine and lispro/glulisine). Once their blood glucose levels were controlled, they were started on oral sitagliptin 100 mg and vitamin D3 5000 IU daily. After this therapy, both patients achieved clinical diabetes remission for 4 years, along with a decrease in anti-GAD antibody levels. These benefits were probably associated with immunological effects of these medications. Inhibition of dipeptidyl peptidase 4 (DPP-4) in animal models deregulates Th1 immune response, increases secretion of Th2 cytokines, activates CD4+CD25+FoxP3+ regulatory T-cells and prevents IL-17 production. Vitamin D3 also activates CD4+CD25+FoxP3+ regulatory T-cells, and these medications combined can improve the immune response in patients with new-onset T1DM and probably promote sustained clinical remission.”

https://edm.bioscientifica.com/view/journals/edm/2016/1/EDM16-0099.xml

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