The existence of vitamin D receptors in activated T lymphocytes, antigen-presenting cells (macrophages and dendritic cells), and thymus tissue raised the idea that 1,25-dihydroxyvitamin D (1,25(OH)2D) might function as an immunomodulator.14
The fact that immune cells (activated macrophages and dendritic cells in particular) also contain the enzyme 1-alpha-hydroxylase, which is necessary for the final activating step in the conversion of 25-hydroxyvitamin D to the metabolically active molecule, shows that these cells are able to synthesize and secrete 1,25(OH)2D which is able to target the immune system.8
In order to provide evidence that vitamin D affects the risk of developing T1DM, several studies have been done using animal models such as nonobese diabetic (NOD) mice. A study conducted by Mathieu et al reported that 1,25(OH)2D has been shown to reduce T1DM onset in NOD mice. He administrated 5 μg/kg of 1,25(OH)2D in the NOD mice and found that diabetes incidence in NOD mice at 200 days was reduced to 8% in the 1,25(OH)2D-treated group vs 56% in the control group.17
A study conducted by Zella et al reported that a vitamin D deficient state alone can potentiate diabetic onset in the NOD mouse. The authors also found that daily dietary supplementation with 2000 IU of 1,25(OH)2D prevents diabetes over 200 days regardless of vitamin D status before the study.18
They suggested that oral administration of 1,25(OH)2D or preferably a nonhypercalcemic analog would be clinically relevant for the prevention of T1DM in humans.16
In our study we aimed to show that an increase in vitamin D serum level is correlated to an improvement in glycemic control as shown in a decrease in HbA1c
levels. Interestingly the vitamin D level was significantly higher at the end of the sunny season than in the summer season itself. The vitamin D levels reported by this study were taken in Lebanon at latitude 33°N and were lower than the ones reported by Greer in Australia (latitude 29°S) and by Littorin in Sweden (latitude 55–65°N).19
It seems that vitamin D levels in our study are affected by factors relevant to developing countries21
rather than purely on geographical/solar distribution considerations.22
In a national US study, it was found that the average American spent 93% of their 24-hour day indoors. Air conditioning, computers, video games, and extensive television programming are reasons behind the increasing time spent indoors with decrease in outdoor activities. Because of the current changes in lifestyles, humans are now more dependent on foods rich in vitamin D or oral vitamin D supplementation and less exposed to sunlight even in summer. 23
Remarkably in the sunniest areas of the world, vitamin D deficiency is also a major health problem. It was found that in Saudi Arabia, India, Turkey, New Zealand, Egypt, Hong Kong, China, Libya, Lebanon, Spain, Australia, San Diego, California, and the southeastern US 35%–80% of children are vitamin D deficient. We cannot always assume that just because there is more abundant sunlight outdoors vitamin D levels would be higher in summer season compared to winter.10
Nevertheless it is important to note that the study’s focus is not on the vitamin D absolute level but rather on its trend with seasonal change. Diabetes control as represented by HbA1c
seems to be affected by seasonality with a mean rise of 0.175% ± 1.46%. These results did not reach statistical significance in our study but showed a trend for better control of glycemia during the end of the cloudy months.
In this study, however, no correlation could be found between diabetes control and variation of vitamin D level in a population of Lebanese with T1DM. Moreover, vitamin D levels tend to significantly increase at the end of the summer season and this is associated with better blood sugar control.
Future studies are needed with a larger sample size and a standardized questionnaire for the level of exercise, accuracy of insulin dosing, and timing of insulin injection. Such studies will provide more data on any possible relationship between vitamin D and diabetes pathogenesis and control.