Tufts-Harvard study builds vitamin D's anti-diabetes potential

By Stephen Daniells

- Last updated on GMT

Related tags Vitamin d3 Insulin

Tufts-Harvard study builds vitamin D's anti-diabetes potential
Daily supplements of vitamin D may boost the function of the cells in the pancreas that produce insulin, says a new study from Boston-based researchers that supports the potential role of the vitamin for pre-diabetics.

A daily 2,000 International Units (IU) dose of vitamin D3, also known as cholecalciferol, was associated with a 25 percent improvement in the functioning of beta cells in the pancreas, according to findings published in the American Journal of Clinical Nutrition​.

Low levels of beta cell function in the pancreas predict the risk of diabetes, said the researchers.

“These results suggested that vitamin D may have a role in delaying the progression to clinical diabetes in adults at high risk of type 2 diabetes,” ​wrote researchers led by Anastassios Pittas from Tufts Medical Center in Boston.

“Our results may also be relevant to patients with type-1 diabetes, which is characterized by beta-cell failure; however, a specific study in type-1 diabetes would be needed to test this hypothesis because the underlying defect (autoimmunity) is different from type-2 diabetes.”

Study details

The study included 92 people with an average age of 57 and an average BMI of 32 kg/m2. Participants were randomly assigned to receive vitamin D (2000 IU per day) or calcium carbonate (800 mg per day). Participants received either the vitamin D with or without calcium or calcium alone for 16 weeks.

At the end of the study, a measure of the function of beta-cells was improved in the people receiving vitamin D, with the so-called disposition index (a measure of beta cell function in the pancreas that includes measures of insulin secretion and insulin sensitivity) improved by about 26 percent, compared with a decline of about 14 percent in the no-vitamin D group.

“Vitamin D improved the disposition index and insulin secretion,”​ said the researchers, “but its effect on insulin sensitivity was not significant, which indicated a predominant effect of vitamin D on the pancreatic beta cell.”

The researchers added that there were no significant differences with calcium compared with no calcium for any of their measures.

Vitamin D

Vitamin D refers to two biologically inactive precursors - D3, also known as cholecalciferol, and D2, also known as ergocalciferol. Both D3 and D2 precursors are transformed in the liver and kidneys into 25- hydroxyvitamin D (25(OH)D), the non-active 'storage' form, and 1,25-dihydroxyvitamin D (1,25(OH)2D), the biologically active form that is tightly controlled by the body.

The science builds

The link between vitamin D and metabolic syndrome is plausible biologically. Vitamin D deficiency has previously been linked to impaired insulin secretion in animals and humans, and has also been linked to insulin resistance in healthy, glucose-tolerant subjects.

Commenting on the mechanism, the Boston-based scientists note: “Vitamin D may have a direct effect mediated by the binding of the active form 1,25 dihydroxyvitamin D to the vitamin D receptor, which is expressed in beta cells.

“The presence of the vitamin D response element in the human insulin gene promoter and transcriptional activation of the human insulin gene caused by 1,25 dihydroxyvitamin D further supported a direct effect of vitamin D on insulin synthesis and secretion.”

A role for supplements?

The results were welcomed by Harry Rice, PhD, director of regulatory & scientific affairs for the United Natural Products Alliance (UNPA), a trade association for dietary supplement and functional food manufacturers, as adding to our understanding the role of vitamin D in the development and progression in type-2 diabetes.

“The results from this study suggest that supplementation with vitamin D alone or with calcium may delay the progression of pre-diabetes to type-2 diabetes,”​ said Dr Rice.

“While we may be far from seeing a public health recommendation associated with taking vitamin D for the prevention of type-2 diabetes, the body of quality scientific evidence supporting a multitude of health benefits (above and beyond reducing the risk of developing type-2 diabetes) associated with vitamin D keeps growing.

“Given the number of health benefits associated with vitamin D, coupled with evidence that certain segments of the population are vitamin D deficient, those not supplementing their diet with vitamin D may want to rethink that decision,”​ he added.

“While there's been some high-quality research conducted to date in this area, to better elucidate the potential role of Vitamin D in type-2 diabetes, high-quality observational studies and randomized clinical trials measuring blood concentration of 25-hydroxyvitamin D and clinically relevant glycemic outcomes are necessary.”


According to the World Health Organisation (WHO), diabetes affects over 220 million people globally and the consequences of high blood sugar kill 3.4 million every year. If such statistics weren’t scary enough, the WHO is predicting deaths to double between 2005 and 2030.

The total costs associated with the condition in the US alone are thought to be as much as $174 billion, with $116 billion being direct costs from medication, according to 2005-2007 American Diabetes Association figures.

Beyond diabetes

Vitamin D deficiency in adults is reported to precipitate or exacerbate osteopenia, osteoporosis, muscle weakness, fractures, common cancers, autoimmune diseases, infectious diseases and cardiovascular diseases. There is also some evidence that the vitamin may reduce the incidence of several types of cancer and type-1 diabetes.

Source: American Journal of Clinical Nutrition
August 2011, Volume 94, Number 2, Pages 486-494
“Effects of vitamin D and calcium supplementation on pancreatic β cell function, insulin sensitivity, and glycemia in adults at high risk of diabetes: the Calcium and Vitamin D for Diabetes Mellitus (CaDDM) randomized controlled trial”
Authors: J. Mitri, B. Dawson-Hughes, F.B. Hu, A.G. Pittas

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