New trial suggests vitamin D supplementation does not improve blood sugar among patients with prediabetes

Posted on: October 28, 2016   by  Amber Tovey

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A recent randomized controlled trial published in the journal Diabetes, Obesity and Metabolism found that weekly vitamin D supplementation did not improve markers of glycemic status among patients with prediabetes.

Type 2 diabetes (T2D) is a common disease, accounting for approximately 90-95% of all cases of diabetes. The remainder is attributed to type 1 diabetes. Diabetes affects more than 10% of adults 20 years and older.

T2D, also known as noninsulin dependent diabetes, is a chronic condition that disrupts the way the body processes glucose (sugar). In T2D, the body either does not respond to insulin properly, a hormone that controls the movement of sugar into the cells, or does not produce enough insulin to maintain a normal glucose level.

Prediabetes develops, as the name implies, before T2D. The diagnosis of prediabetes occurs when blood sugar levels are higher than normal, but not quite high enough to be considered diabetes. When one is diagnosed with prediabetes, lifestyle and dietary changes are of the utmost importance to reduce one’s risk of developing T2D. In fact, research shows that individuals can lower their risk for T2D by nearly 60% by losing 7% of their body weight and exercising moderately 30 minutes a day, five days a week.

As the prevalence of T2D continues to rise, researchers and medical professionals have begun to strategize methods for prevention and intervention. Recently, studies have investigated the potential role of vitamin D in T2D. While observational studies have produced encouraging results, showing that healthy vitamin D levels are associated with an decreased risk of type II diabetes, clinical trials have yielded conflicting results. However, the inconsistent results could be attributed to a variety of factors, such as the metabolic status of the population, type of vitamin D (D2 vs D3), dosage, duration and baseline vitamin D status of the participants.

In an effort to provide clarity upon the effects of vitamin D supplementation on glucose levels and insulin resistance, researchers recently conducted a randomized controlled trial. A total of 71 patients considered pre-diabetic with vitamin D levels of 26 ng/ml or less (< 65 nmol/L) were included in the study.

The researchers randomly divided the patients into two groups: the vitamin D group and placebo group. The vitamin D group received 28,000 IU of vitamin D3 in cheese once weekly for 24 weeks; whereas, the placebo group received a dummy pill in cheese for the same frequency and duration.

The study’s primary outcome was change in two-hour postprandial glucose (2h-PPG). This test assesses how the body responds to sugar and starch after a meal. As one digests food, blood glucose levels sharply rises. This peak stimulates insulin to help move sugars into cells to be used as fuel. After two hours, blood glucose levels should return to normal. However, when one suffers from T2D or prediabetes, their blood glucose remains high. Secondary outcomes included fasting glucose, fasting insulin and indices of insulin sensitivity, among others.

After 24 weeks, here is what the researchers found:

  • The average vitamin D levels of the vitamin D group significantly increased from 19.2 ng/ml to 39.5 ng/ml (p < 0.0001).
  • The average vitamin D levels remained similar in the placebo group.
  • No significant differences were found in 2h-PPC glucose (p = 0.56), fasting glucose (p = 0.36) or other markers of glucose metabolism, including insulin sensitivity were observed.
  • A sub-group analysis of individuals with a baseline vitamin D status below 20 ng/ml and prediabetes did not change these results.
  • The vitamin D group’s LDL levels significantly declined (p = 0.03).

The researchers concluded,

“Vitamin D3 supplemented cheese significantly increased [vitamin D status] but had no effect on glycemia or indices of insulin sensitivity…in participants with sub-optimal vitamin D and at risk for type 2 diabetes.”

They went on to explain why the results are contrary to observational studies,

“One plausible explanation for these findings is that low [vitamin D status] is not related to glycemia at all but rather is an indicator of poor nutrition, physical inactivity, obesity and overall poor health. Another plausible explanation is that the studies conducted to date have not been large enough, long enough or conducted in the appropriate population needed in order to adequately determine whether there is a causal relationship between vitamin D deficiency and increased risk for type 2 diabetes.”

As the researchers pointed out, the good news is that a large clinical trial examining the effect of vitamin D supplementation on the progression to T2D is currently underway and should provide us with more answers.

Citation

Tovey, A. & Cannell, JJ. New trial suggests vitamin D supplementation does not improve blood sugar among patients with prediabetes. The Vitamin D Council Blog & Newsletter, 2016.

Source

Lucas. T, et al. Effect of vitamin D supplementation on oral glucose tolerance in individuals with low vitamin D status and increased risk for developing type 2 diabetes (EVIDENCE): a double-blind, randomized, placebo-controlled clinical trial. Diabetes, Obesity and Metabolism, 2016.

1 Response to New trial suggests vitamin D supplementation does not improve blood sugar among patients with prediabetes

  1. Ron Carmichael

    Once again a study is designed with a protocol which ignores the fundamental pharmacokinetics regarding how humans have historically acquired vitamin D: through daily exposure to sun. This study presumes a single dose that approximates in general what a person is capable of generating in a single day, and then depriving the test subjects of fresh raw D3 for 6 days. The half-life for D3 is under 24 hours, thus we can conclude the investigators fail to grasp fundamentals of what they sought to investigate. D3 is of significance due to absorption via osmosis in the bulk of the body’s tissues where it functions as an autocrine hormone. This study negates the clinical aspects of this to a very large and perhaps clinically significant degree. I do suspect, with little scientific data to support my notion, that when one FINALLY develops T2D it may be due to the damage of a life-long deficiency of D3 or even now, multi-generational deficiency and is not reversible in a short-term nature such as only 10 weeks of sub-optimal therapy, if ever. Obviously, more studies are called for with particular emphasis on formulation of a more competent protocol to increase the scientific legitimacy of the conclusions to be drawn.

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