Role of Vitamin D in T1D and Glycemic Variability
Vitamin D is actually a steroid hormone that you generate from exposure to sunlight and normal food intake, including vitamin supplements. There are two forms of vitamin D: D2 (ergocalciferol) which is found in some edible plants like mushrooms and D3 (cholecalciferol) which is synthesized in our skin when exposed to ultra violet beta rays and consuming foods such as fatty fish, eggs, liver or fortified products such as milk and cereals. Studies have found vitamin D2 is much less potent than D3 in raising blood levels of vitamin D.
Neither form is biologically functional in the body until they undergo a two step metabolic process: first, conversion to 25-hydroxy vitamin D (25OHD) in the liver and final conversion to the active form within the kidney. The active form seeks out target tissues that have a vitamin D protein receptor (VDR) expressed by VDR genes. 25(OHD) is stable for weeks within the bloodstream serving diagnostically as a biomarker of the level of vitamin D uptake.
Vitamin D is an essential vitamin in calcium and bone metabolism. Deficiency of vitamin D leads to Rickets, a childhood disease characterized by a softening and weakening of the bones. In adults, such deficiency leads to osteomalacia.
Vitamin D deficiency has been implicated in other medical conditions: T1D, Insulin Resistance, obesity, osteoporosis, cancer, cardiovascular disease, hypertension, multiple sclerosis, impaired immunological functions, asthma, and higher infection rates. Common polymorphisms of the VDR gene have been reported to affect the risk of breast, colon and prostate cancer, in addition to bone mineral density and immune disorders including T1D.
Risk factors for low vitamin D levels within a given population include: age 50+, female, lack of sun exposure, winter seasons, excessive clothing, use of sunscreens, darker skin pigmentation, dietary habits, inability to absorb vitamin D from the intestines caused by celiac or crohn’s disease, kidney or liver disease which interrupts vitamin D production, the lack of vitamin D in most food sources and certain drugs such as anticonvulsants and corticosteroids.
As it relates to T1D, there were several difficulties encountered in writing this review:
Most of the earlier studies were observational meaning that one cannot come to any real conclusion as to whether vitamin D prevents or treats T1D nor does it serve to prove causality.
Research results were found contradictory, leading to caution regarding the value of Vitamin D as a form of treatment.
Health organizations, testing laboratories, researchers and physicians lacked agreement as to what constitutes deficiency, insufficiency or normal levels of vitamin D.
Studies on clinical practice revealed that physician treatment was haphazard. Some doctors over-prescribed, some under-prescribed and many did not treat for deficiency.
Studies were poorly designed, lacked controls, or contradicted other existing findings.
The difficulty in determining the impact vitamin D may have in long-term large population T1D studies, stems from an inability to control sun exposure, food intake, and vitamin supplementation on the part of the participants.
Diagnosis – The only way to be sure you’re vitamin D deficient is by blood tests. There have been many estimates but at least one out of every two USA residents have blood levels considered to be either deficient or insufficient.
Role of Vitamin D in pathogenesis and prevention of T1D.
Research suggests that there is a link between vitamin D and T1D:
Higher doses of vitamin D early in life appear to protect against type 1 much later in life.
There has been speculation that vitamin D supplementation during pregnancy may help prevent T1D later in life. Vitamin D deficiency during pregnancy may increase the incidence of autoimmune diseases such as T1D.
Vitamin D is known to influence gene transcription. It has been shown that vitamin D aids in DNA repair resulting in aiding metabolic processes.
It affects pancreatic B cell function. Vitamin D appears to be essential for normal insulin production.
Vitamin D is considered a modulator of the body’s immune system and helps regulate cellular growth and differentiation suggesting that it may play a role in preventing T1D. Glycemic Control in T1D. BDF found that for every research paper that suggested that vitamin D supplementation in type 1 and type 2 diabetics was effective, there was a paper that concluded the very opposite. Whether these contradictory findings can be attributed to the differences noted in experimental parameters such as concentration of D3 supplementation administered, length of study time, differences in data interpretation or methodology, country location where research was conducted taking into consideration latitude, dietary issues and factors that deal with sun exposure, we cannot say for sure.
Better designed clinical studies are required to ascertain whether raising 25OHD levels improves glycemic control in patients with type 1 diabetes. The Diabetes Control and Complication trial showed that improving glycemic control, as measured by HbA1C, significantly reduces the risk and/or the progression of all diabetic complications and reduces the mortality and morbidity due to cardiovascular diseases in T1D patients. Patients with elevated HbA1C levels should be evaluated for vitamin D deficiency.
Treatment: there does not appear to be any consensus on treatment regimens other than to employ supplements when vitamin D levels are considered low.
Vitamin D’s role in bone health is established but whether it prevents, treats or delays a wide variety of other health issues including T1D and glycemic variability remains debatable. There are several large vitamin D studies whose results will be forthcoming in 2017 through 2020 that may help resolve this issue once and for all.
Further research, including clinical trials to explore the mechanisms linking Vitamin D to both T1D and glucose variability, is needed.