Vitamin D is technically a hormone, since it is a chemical signal produced by the body and transported through the blood to other parts of the body. Vitamins cannot be made by the body, and must be obtained in other ways. When exposed to UV radiation, substances in the skin are converted to pre-vitamin D3, which slowly becomes vitamin D3. (Vitamin D can also be obtained via diet).
Vitamin D may be protective against diabetes, and vitamin D deficiency may increase the risk of the disease. Below is some of the evidence, organized by timing of exposure, from the womb through adulthood, since the timing of exposure may make a difference in the risk of diabetes.
Do a mother's vitamin D levels during pregnancy affect the later risk of type 1 diabetes or autoimmunity in her children?
Some studies say "yes:"
Others say "not really:"
So, in conclusion:
A meta-analysis of the data from 11 different studies found that there is not enough evidence to determine whether or not there is an association between on maternal intake of vitamin D and risk of type 1 diabetes in the offspring (Dong et al. 2013). While the jury is still out, it wouldn't hurt to get vitamin D levels checked during (or before) becoming pregnant, to make sure to avoid deficiency during pregnancy.
Do Vitamin D levels in infancy and early childhood affect the child's later risk of type 1 diabetes or autoimmunity?
Again, some say "yes:"
While others say "no:"
A review and meta-analysis of the data from five different studies found that type 1 diabetes risk was significantly reduced in people who had been given supplements of vitamin D in infancy. Higher doses appeared more protective (Zipitis and Akobeng 2008). Another meta-analysis of the data from 11 different studies also found that higher vitamin D intake during early life may in fact decrease the risk of type 1 diabetes (Dong et al. 2013). Another makes the point that supplementation at current recommended levels (400 IU per day) shows no benefit for type 1 diabetes prevention, but that some evidence supports that vitamin D sufficiency in pregnancy, or supplementation in early life, does decrease risk (Miller et al. 2016). So while not all studies agree, most do find that vitamin D supplements in infancy and early childhood-- enough to bring someone up to adequate vitamin D levels-- may be protective against later type 1 diabetes.
And yet it may be more complicated than that.
A long-term study of German children found that vitamin D levels were lower in children with multiple islet autoantibodies and in children with type 1 diabetes than in autoantibody-negative children. However, vitamin D deficiency was not associated with faster progression to type 1 diabetes in children with multiple islet autoantibodies (Raab et al. 2014). This finding suggests that low vitamin D levels may play more of a role in the development of autoimmunity than the subsequent development of type 1 diabetes. However, other evidence suggests the opposite: a study from Finland and Estonia found that there was no association between vitamin D levels and islet autoantibodies (Reinert-Hartwall et al. 2014). Thus the debate continues. There may be differences among populations that could also help to explain these differing findings.
Do people newly diagnosed with type 1 diabetes have lower Vitamin D levels than those without diabetes?
Many studies say "yes:"
One says "no:"
Yes, a number of studies have found that people with type 1 diabetes are often deficient in vitamin D:
Even in areas with abundant sunshine, people with type 1 diabetes (and often controls as well) have low vitamin D levels:
Other factors may combine to increase risk as well. Overweight and obese children with both celiac disease and type 1 diabetes had lower vitamin D levels than controls (Setty-Shah et al. 2014). Genetic background also may affect the risk; people with certain vitamin D receptor (VDR) genes have an increased risk of type 1 diabetes (Sahin et al. 2017).
Does adequate vitamin D facilitate blood glucose control and reduce the risk of complications in people with type 1 diabetes?
Perhaps! For example, a randomized, controlled trial for people with type 1 diabetes in Germany found that those given 4000 IU vitamin D per day for 3 months had a lower insulin requirement, better blood sugar control (lower HbA1c), and in six people, even a rising c-peptide (a marker of beta cell function). Men also had better immune system function (Bogdanou et al. 2016).
Beta cell function
Blood glucose control
Immune system function
Maybe! At least for a while...
In an animal model of type 1 diabetes (NOD mice), early, long-term, high doses of vitamin D can prevent diabetes (Takiishi et al. 2014). In a different animal model of type 1 diabetes (mice given the chemical STZ to kill beta cells), vitamin D improved diabetic kidney disease (Deng et al. 2015). In rats, animals who received both vitamin D and omega 3 fatty acids had lower blood sugar levels than untreated rats after islet transplantation (Gurol et al. 2016).
Vitamin D can affect the function of the immune system, and in this capacity may be protective against autoimmune diseases (Norris 2001). Vitamin D deficiency is also associated with an increased risk for other autoimmune diseases, including multiple sclerosis and inflammatory bowel disease (Lapillonne 2010). A prospective, population-wide study from Denmark found an increased risk of autoimmune diseases in people with lower vitamin D levels (Skaaby et al. 2015). Baeke et al. (2010) review how vitamin D affects the immune system, and its role in the development of autoimmune diseases.
Vitamin D can also protect beta cells from dysfunction caused by the immune system cells called cytokines (see the inflammation page for more on these cells). In fact, low vitamin D levels have been associated with various marker of inflammation in people with type 1 diabetes (Devaraj et al. 2011).
Mathieu et al. (2005) describe how vitamin D deficiency can impair insulin secretion from beta cells. Yet a study of black and white children without diabetes found that vitamin D levels did not affect insulin sensitivity, glucose levels, or beta cell function. However, this study did not examine children with diabetes, nor immune system markers (Rajakumar et al. 2012).
Other authors find that vitamin D promotes pancreatic islet cell function and survival, as well as modulates liver glucose and metabolism, both potentially protective against diabetes (type 1 or 2) (Leung 2016).
Blanton et al. (2011) found that people with type 1 diabetes have lower vitamin D-binding protein levels, a molecule important in the actions of vitamin D. These authors suggest that multiple factors may influence the vitamin D/type 1 diabetes risk, including genetic background, protein levels, and more.
One reason vitamin D was suspected of being protective against type 1 diabetes is that countries with high incidence of type 1 tend to be found near the polar regions (e.g., Finland, Sweden), where there is a lack of sunlight during long stretches of the year (see the incidence page). In northern Finland, there are only 2 hours of sun each day during December. In a study of 51 regions around the world, Mohr et al. (2008) found that lower levels of ultraviolet (UV) radiation (the main source of vitamin D in humans) was associated with higher incidence of type 1 diabetes.
Yet differences in vitamin D status do not explain all of the differences in type 1 diabetes incidence. For example, type 1 diabetes rates are six times higher than those in a neighboring section of Russia, despite similar genetic background (and similar latitudes). Vitamin D levels have been found to be essentially the same in both regions, in children and in pregnant women. More people in Russia, in fact, were deficient in vitamin D than in Finland. A number of Scandinavian researchers point out that vitamin D supplementation has long been common in these countries (Viskari et al. 2006). And yet vitamin D deficiency is still common in these countries, perhaps because the recommended supplementation dose has decreased over time.
Using historical data, Mohr et al. (2010) showed that in Finland, the incidence of type 1 diabetes rose gradually after the recommended daily dose of vitamin D was reduced from 4500 IU to 2000 IU, in 1964. In 1992, the recommended daily dose was lowered again, to 400 IU. This change was followed by a steep rise in type 1 diabetes incidence. And then, in 2003, vitamin D intake increased again, and by 2006 the incidence of type 1 diabetes had plateaued (Mäkinen et al. 2014). Is this an interesting coincidence or a causal correlation? That remains to be seen.
Vitamin D deficiency may also contribute to the development of type 2 diabetes (Palomer et al. 2008). A review and meta-analysis of 19 studies through Feb. 2011 found that people with the highest vitamin D levels had the lowest risk of type 2 diabetes (Mitri et al. 2011) . A more recent meta-analysis of 21 long-term prospective studies found a clear, statistically significant association between vitamin D levels and type 2 diabetes. Those with higher vitamin D levels had lower risk, across a broad range of vitamin D levels in diverse populations (Song et al. 2013). Another meta-analysis of 11 studies found that people with type 2 diabetes had lower vitamin D levels than those without diabetes (Shen et al. 2016).
And yet, a review of 39 studies on vitamin D and type 2 diabetes/insulin resistance concludes that "it is not possible to state that vitamin D supplementation has any effect on type 2 diabetes incidence or on insulin resistance" (Wallace et al. 2015). Yet the authors also point out that multiple randomized controlled trials of vitamin D supplementation will help to clarify the issue over the next few years. Now, if we look at a review of the four existing randomized controlled trials, we find that vitamin D supplementation had no effect on type 2 diabetes prevention (Seida et al. 2014). For more trial results, see below.
Genetic risk might also play a role in these associations. People with diabetes who had certain vitamin D-related genes were more susceptible to nephropathy than those without those genes (Liu et al. 2014).
A review finds that, "An increasing body of literature suggests a possible pathogenetic role of vitamin D in the long-term complications of diabetes and vitamin D deficiency may also exacerbate symptoms of painful diabetic peripheral neuropathy. It remains unknown if supplementation of vitamin D to normal or non-deficient levels alters pathogenetic processes related to diabetic microvascular complications." (Alam et al. 2016).
A review of cardiovascular disease and vitamin D finds that numerous studies have found links between low vitamin D levels and cardiovascular disease. However, as with diabetes, vitamin D's role has not been definitively established, due to the lack of large, randomized controlled trials. The authors argue that despite the lack of large trials, there is adequate evidence to promote treatment of low vitamin D levels (Mandarino et al. 2015).
Obesity is sometimes associated with vitamin D deficiency, probably because vitamin D can be deposited in fat stores and then not be available to the body (Holick 2004). A study of obese people found that those who were metabolically healthy had higher vitamin D levels than those who were metabolically unhealthy (Estghamati et al. 2014).
Low vitamin D levels have been associated with increased insulin resistance in people without diabetes (Forouhi et al. 2008), as well as higher fasting glucose levels, abdominal fat, and triglycerides (Sorkin et al. 2014). The latter authors found that there is a certain level of vitamin D in the blood below which these effects occur (about 26 μg/L); vitamin D levels above this amount were associated with normal blood sugar control. The people in this study were sedentary, obese or overweight, black and white post-menopausal women without diabetes.
A study of a sample of the general U.S. population found that abdominal obesity and vitamin D insufficiency interact to increase the risk of insulin resistance (Kabadi et al. 2012).
A study from Singapore found that if pregnant women were deficient in vitamin D, there was no effect on birth outcomes, growth, or weight gain in the offspring in the first 2 years of life (however, very few people in the study were deficient in vitamin D) (Ong et al. 2016).
Lower vitamin D levels in pregnant women were associated with lower birth weight but higher fat mass in offspring at 4 and 6 years of age (Crozier et al. 2012) and in another study, higher weight at 1 year but not at 4 years (Morales et al. 2015).
Trials: Can vitamin D supplements prevent type 2 diabetes and improve metabolism in people with pre-diabetes?
A literature review and meta-analysis found that vitamin D supplementation only led to small improvements in fasting blood sugar and insulin resistance in people with diabetes or impaired glucose tolerance (George et al. 2012). A trial of middle aged adults found that vitamin D and calcium supplementation reduced insulin resistance in people with pre-diabetes (Gagnon et al. 2014).
A 12 week trial of vitamin D supplementation in overweight/obese African Americans with pre-diabetes or early diabetes found that compared to a placebo, vitamin D improved insulin secretion and insulin resistance, but not glucose levels (Harris et al. 2012). However another trial of higher doses given to people with pre-diabetes for a year found that glucose, insulin secretion, insulin resistance, blood pressure, and lipid (cholesterol) levels did not improve in those given vitamin D compared to a placebo (note that vitamin D levels were higher to start with in this study though) (Sollid et al. 2014). Another trial also found that high dose vitamin D supplementation did not prevent the development of type 2 diabetes in people with pre-diabetes, over a 5 year time period. Again, however, the people in this trial started with normal average vitamin D levels, not deficient levels (Jorde et al. 2016). Yet another trial also found that high-dose vitamin D supplementation over 8 weeks did not affect insulin secretion, insulin resistance, or glucose levels in people who started at a lower vitamin D level (Wagner et al. 2016).
A trial of men deficient or insufficient in vitamin D without diabetes found that after a year of supplements, those on the placebo had increased levels of insulin resistance and insulin, but those who took vitamin D stayed the same. So, in other words, the vitamin D did help stop increasing insulin resistance (Tepper et al. 2016).
A trial of healthy Japanese adults found that one year of vitamin D supplementation improved fasting glucose levels and lowered insulin resistance (Sun et al. 2016).
A Canadian trial found that 24 weeks of high dose vitamin D supplementation did not affect glucose tolerance, insulin resistance, or other diabetes-related measures (Moreira-Lucas et al. 2016).
A trial that provided obese adolescents with vitamin D supplements found that compared to those who took a placebo, those who took 4000 IU vitamin D per day had lower insulin resistance after 6 months (Belenchia et al. 2013). Most studies of vitamin D in obese adolescents have found associations between low vitamin D levels and insulin resistance, and clinical trials have reported beneficial effects (Peterson et al. 2014). However, one trial of healthy children found no effects on glucose, insulin, or insulin resistance after 12 weeks of supplementation (Ferira et al. 2016).
In laboratory mice with chemically induced type 1 diabetes, vitamin D reduced the incidence of diabetes, enhanced insulin secretion, and reduced pancreatic inflammation. Vitamin D also decreased beta cell death (Wang et al. 2016).
Long-term ultra-violet radiation (which produces vitamin D in the skin) suppresses weight gain, glucose intolerance, and insulin resistance in mice fed a high-fat diet. However, many of these benefits did not appear with vitamin D supplementation-- perhaps other mechanisms are at work (Geldenhuys et al. 2014).
Rats with chemically induced beta cell destruction showed better cognitive function when given vitamin D (Calgaroto et al. 2014). They also showed better lipid levels, which may help prevent cardiovascular complications (Calgaroto et al. 2015). These rats given vitamin D also had lower inflammation, less liver damage, and lower insulin resistance (Liu et al. 2016).
Beta cells exposed to vitamin D show both increased and decreased insulin secretion, depending on the amount of glucose they were exposed to, and how long they were exposed to vitamin D (Jeddi et al. 2015).
Low vitamin D levels in mother mice led to offspring with modified pancreas development, leading to changes in beta cell mass and insulin secretion in adulthood (Maia-Ceciliano et al. 2016).
A meta-analysis that consolidated the data from seven different studies found that gestational diabetes was associated with vitamin D deficiency in pregnant women (Poel et al. 2012). A literature review also concluded that vitamin D deficiency and insufficiency is common in pregnant women, and is associated with gestational diabetes and poor glucose control (Senti et al. 2012). More recent meta-analyses of 20 studies found that vitamin D deficiency was associated with the development of gestational diabetes (although whether vitamin D can prevent gestational diabetes is still not known) (Lu et al. 2016; Zhang et al. 2015). While most studies have found a link between vitamin D deficiency and gestational diabetes (e.g., Arnold et al. 2015; Haidari et al. 2016; Wen et al. 2016), not all have (e.g., Makgoba et al. 2011). One found an association between low vitamin D levels and higher fasting blood glucose, but not gestational diabetes (Al-Shaikh et al. 2016).
Other factors may also play a role, for example, one study has found that the risk of gestational diabetes is higher in women who have low vitamin D levels and who also smoke during pregnancy (Dodds et al. 2016). Another found that genetic variations affect the relationship between vitamin D levels and gestational diabetes (Shi et al. 2016).
Among women with gestational diabetes, those with lower vitamin D levels had worse blood glucose control (El Lithy et al. 2014). A study of pregnant Australian women found that even in women with normal blood sugar and vitamin D levels, those with lower vitamin D levels had higher fasting blood sugar and lower beta cell function (but insulin resistance was not different) (McLeod et al. 2012).
Among pregnant women with type 1 diabetes, a UK study found that cord blood vitamin D levels correlate with those of the mothers, and that they tend to be low throughout pregnancy, delivery, and post-delivery. Women with low vitamin D levels had worse blood sugar control (higher HbA1c levels) (Bennett et al. 2014). A Czech study found that vitamin D levels tended to be lower post-partum in women who had had gestational diabetes (although levels during pregnancy did not differ in those with/without gestational diabetes) (Pleskačová et al. 2015).
Vitamin D levels, however, may not affect the later risk of developing diabetes following gestational diabetes. At least that is the finding of one study from Sweden. While low vitamin D levels were associated with beta cell dysfunction and insulin resistance in women with gestational diabetes, these levels were not associated with the later development of diabetes (Shaat et al. 2017).
Low vitamin D levels in pregnant women may also affect the offspring (bring us back to the topic at the top of this page, whether a mother's vitamin D levels can affect the risk of type 1 in the offspring). A Brazilian study found that vitamin D deficiency in women with gestational diabetes is associated with hypoglycemia in infants, and small for gestational age incidence (Weinert et al. 2016).
A randomized, placebo-controlled trial from Iran found that women with gestational diabetes who were given vitamin D and calcium supplements had lower fasting glucose levels, lower insulin levels, lower insulin resistance, and better cholesterol levels than those given a placebo (Asemi et al. 2014). Another study also found improved fasting glucose levels and long-term glucose levels in women with gestational diabetes (Yazdchi et al. 2016). Additional studies found that vitamin D supplements for women with gestational diabetes improved outcomes for both mother and child (Asemi et al. 2014; Karamali et al. 2015), and improved insulin resistance in these women (Zhang et al. 2016). In a study from India, pregnant women given vitamin D supplements had a lower risk of gestational diabetes (as well as other benefits) than those who took a placebo (Sablok et al. 2015). And, in another Iranian trial, women with gestational diabetes who took vitamin D and evening primrose oil for 6 weeks had better glucose and lipid levels, and lower insulin resistance (Jamilian et al. 2016). In a Chinese study, women with gestational diabetes who drank a yogurt drink enriched with vitamin D had lowered insulin resistance (Li and Xing 2016).
However, a review and meta-analysis of 13 randomized, controlled trials found that there was no association between vitamin D supplementation and gestational diabetes (there were other benefits however). As these studies were small and varied a lot in their design, this will not be the last word on the topic (Pérez-López et al. 2015).
Results may also depend on the type of supplementation. A randomized trial of Iranian women with low vitamin D levels found that those who received 50,000 IU vitamin D every two weeks had a lower incidence of gestational diabetes than those given 400 IU per day (Mojibian et al. 2015). Another Iranian trial of the high dose levels also found that women at risk of gestational diabetes who took vitamin D for the 1st and 2nd trimesters had a lower incidence of gestational diabetes (as compared to those who took a placebo) (Shahgheibi et al. 2016).
In Asian women with prior gestational diabetes, a double-blind randomized controlled trial showed that six months of supplementation with 4000 IU vitamin D safely restored vitamin D levels, improved beta cell function, and reduced blood glucose levels (HbA1c) (Yeow et al. 2015). An Iranian intervention trial of women with gestational diabetes found that while high dose supplementation with vitamin D raised vitamin D levels, it did not affect glucose levels in the short-term post-pregnancy (Valizadeh et al. 2016).
In guinea pigs, higher vitamin D levels before pregnancy were protective against gestational diabetes, however, vitamin D levels during pregnancy did not affect risk (Tabatabaei et al. 2014). In animals, maternal vitamin D deficiency during pregnancy leads to insulin resistance in the offspring (Zhang et al. 2014).
One surprising thing that most of the above studies have in common is the finding that many people have insufficient levels of vitamin D in their bodies-- even people who live in regions with adequate sunshine (e.g., in Florida (Bierschenk et al. 2009), or the Mediterranean region (Karras et al. 2016)). Ginde et al. (2009) found that based on a nation-wide sample, 77% of the U.S. population has insufficient vitamin D levels (including nearly all African Americans and almost all Mexican Americans). In addition, levels of vitamin D have declined in the U.S. population, comparing the periods 1988-1994 to 2001-2004. Even in the hot, sunny climate of Saudi Arabia, most people tested were vitamin D deficient (Al-Daghri et al. 2014). I just don't think sunshine is enough.
Mohr et al. (2008) suggest that children over age 1 who live more than 30 degrees from the equator (that includes almost all of the U.S.), take 1000-2000 IU vitamin D3 per day, especially during the winter, "to substantially reduce their risk of type 1 diabetes." The current U.S. recommendations are only 200 IU vitamin D per day, a level that is inadequate to address the growing epidemic of vitamin D deficiency (Ginde et al. 2009). During pregnancy, the current recommendations of 200-400 IU per day are also inadequate to maintain normal levels of vitamin D during pregnancy and lactation (Mulligan 2009). Parents of children at risk of developing type 1 might take note and supplement. And, during the sunnier months, parents might also try the "leave no child indoors" method of vitamin D "supplementation." Although, be aware that while the urban myth may argue that adequate vitamin D can be obtained from the sun, it appears that few US residents make adequate vitamin D even without sunscreen, at any time of the year (Godar et al. 2012).
Norris (2001) suggests that various public health initiatives may have acted together to reduce vitamin D exposure in children, including keeping babies out of the sun, using sunscreen on young children, and exclusive breastfeeding. Exclusively breastfed infants are at higher risk of vitamin D deficiency than are formula-fed infants (Kovacs 2008); each month of breastfeeding (without supplementation) increases the risk of vitamin D deficiency by 6% (Darmawikarta et al. 2016). This deficiency can be remedied however, with sufficient supplementation for pregnant and nursing mothers. During pregnancy, if the mother has sufficient levels of vitamin D (which may require supplementation), then the fetus should too. After birth, the mother may need up to 4000 IU per day to maintain sufficient levels in her and her exclusively breastfed baby (Kovacs 2008).
Vitamin D is known to improve the absorption of calcium (Norris 2001); adults with type 1 diabetes have lower bone mineral density and a higher risk of bone fractures (Carnevale et al. 2004).
In infants, vitamin D levels are associated with gut microbiota (Sordillo et al. 2016). Vitamin D levels also appear to affect the gut microbiota of mice (Jin et al. 2015). A review argues that the interactions between vitamin D and the gut microbiota may be critical factors in the increasing incidence of type 1 diabetes (Clark and Mach 2016). See the Diet and the gut page for more information on how the gut might be related to diabetes.
Unfortunately, some contaminants may be able to affect vitamin D levels, perhaps even causing or contributing to vitamin D deficiency. The first human study published on this topic found associations between vitamin D levels and persistent organic pollutants (POPs) in U.S. adults. That is, adults with higher levels of POPs in their blood had lower levels of vitamin D, especially people in old age, who were white, or who had chronic diseases (Yang et al. 2012). Another study, of pregnant women, found that women with high levels of some PCBs had lower vitamin D levels (Morales et al. 2013). In newborns, those whose mothers were exposed to higher levels of air pollutants during pregnancy (especially in the third trimester) had lower vitamin D levels than infants whose mothers were exposed to lower levels of air pollutants (Baïz et al. 2012). Likewise, children exposed to higher levels of air pollution (in Mexico City) had lower vitamin D levels than those exposed to lower levels (Calderón-Garcidueñas et al. 2015). And, a study from Korea found that a combination of vitamin D deficiency and arsenic exposure were associated with an increased risk of diabetes in adults (Lee and Kim 2013). In U.S. adults, higher phthalate and BPA levels (in women) are associated with lower vitamin D levels (Johns et al. 2016). Thus, a number of chemicals have been linked to lower vitamin D levels in humans.
However, not all human studies have found a link between chemical exposures and vitamin D levels. A study of adolescents from Mexico found that lead and cadmium levels were not associated with vitamin D levels, and that those with higher levels of molybdenum, thallium, uranium, and arsenic in fact had higher levels of vitamin D (Zamoiski et al. 2014).
Laboratory studies have also examined the possibility that chemicals may influence vitamin D levels. For example, early life exposure to the pesticide permethrin leads to low vitamin D levels in adult rats (Fedeli et al. 2013).
After vitamin D3 forms in the body, or is obtained via diet, it is then converted to other forms of vitamin D. In the liver, it is converted to 25-hydroxyvitamin D (25-D) and in the kidney to the more active form, 1,25 dihydroxycholecalciferol (1,25-D) (Norris 2001). Some chemicals may affect the conversion of one type of vitamin D to another. When researchers fed mother rats a mixture of PCBs similar to those found in human breastmilk, they found that the PCBs caused reductions in the levels of 1,25-D in the mothers at birth and weaning, and these reduction were dependent on PCB dosage. Levels of 1,25-D were also reduced in the offspring at higher exposure levels. Levels of 25-D were lower mothers at the time of delivery, and in the offspring at the highest dosage levels. In the mothers, levels of 1,25-D were reduced even at the lowest PCB treatment level, although this level was still higher than the PCB levels normally found in humans (Lilienthal et al. 2000). Rats given PCBs had lower vitamin D levels than unexposed controls (Alvarez-Lloret et al. 2009).
Another animal study found that POPs may disrupt vitamin D conversion processes in seals. It compared vitamin D levels in seals from the highly polluted Baltic Sea to seals from other less polluted waters. It found that while vitamin D3 levels in the liver were higher in the Baltic seals (probably due to sunlight or diet), levels of 1,25-D were lower. Both the contaminant levels and the hormone levels also varied by species. The authors suggest that these findings might explain the bone abnormalities found in gray seals in the Baltic Sea (Routti 2008).
Another study on bone toxicity examined the effects of dioxin, another POP, on vitamin D levels in mice. This study found that dioxin actually increased levels of 1,25-D in the mice, but also impaired bone mineralization (Nishimura et al. 2009). How exactly contaminants can affect vitamin D processes in animals, whether the same effects occur in humans, and whether these processes could be a factor in type 1 diabetes development all deserve further study.
Persistent organic pollutants, including PCBs, evaporate and migrate to the polar regions of the earth (Tanabe 2002). Perhaps exposure to environmental contaminants may also help explain the high and increasing incidence of type 1 diabetes in polar regions (especially high in some countries surrounding the Baltic Sea, as described on the diabetes incidence page), and why even many Floridians have low levels of vitamin D in their bodies. More research on these possibilities is necessary.
There is good evidence that having adequate vitamin D levels is protective against type 1 diabetes, and some evidence that vitamin D deficiency could contribute to the development of type 1 and type 2 diabetes. Further studies that include measurement of vitamin D levels in people before they develop diabetes, and intervention trials that involve ensuring adequate vitamin D levels could confirm these findings. In the meantime, vitamin D supplementation offers a safe way to protect against vitamin D deficiency, and perhaps protect against diabetes as well. Vitamin D deficiency is likely to be more of a factor in diabetes development in areas with less UV radiation, but the findings of widespread deficiency in other areas implies that this factor may play a role elsewhere as well.
Reviews of the evidence suggest that vitamin D may play a role in diabetes by influencing immune system function, inflammation, insulin secretion, and insulin resistance. Most (but not all) studies suggest that vitamin D is protective against diabetes, however, more evidence is needed from intervention studies to constitute conclusive proof (Al-Shoumer and Al-Essa, 2015; Harinarayan 2014; Papandreou and Hamid, 2015). In the meantime, it wouldn't hurt to make sure you are vitamin D sufficient. Vitamin D levels may be important for both diabetes prevention/development in people without diabetes, as well as for good blood glucose management in people with diabetes.
According to a comprehensive review, "Data from epidemiological and association studies clearly indicate a correlation between vitamin D deficiency and a higher prevalence of both forms of diabetes. In animal models, vitamin D deficiency predisposes to type 1 and type 2 diabetes, whereas high doses of vitamin D ... prevent disease. Large scale, randomized, blinded prospective studies however, remain lacking...We propose, in particular, to avoid vitamin D deficiency in individuals at risk of developing T1D or T2D. Applying international guidelines on supplementation of vitamin D using small daily doses of vitamin D (500-1000 IU) may contribute to reduce the burden of diabetes by preventing vitamin D deficiency" (Mathieu 2015). Another review states, "Data from observational studies correlated vitamin D deficiency with risk of type 1 and type 2 diabetes... The results to date generally satisfy Hill's criteria for causality regarding vitamin D and incidence of these pancreatic diseases [diabetes and pancreatic cancer]. However, large randomized, blinded, prospective studies are required to more fully evaluate the potential therapeutic role of vitamin D in preventing pancreatic diseases" (Altieri et al. 2016).
Pregnant women should also make sure they are sufficient in vitamin D. Vitamin D deficiency during pregnancy is linked not only to gestational diabetes but also preterm birth. Ensuring vitamin D sufficiency during pregnancy is safe, simple, and cost-effective (Genuis 2015).
One analysis calculates that if everyone in the UK took vitamin D supplements, 374 cases of type 1 diabetes (out of 1357 total predicted) could be prevented (Zipitis et al. 2016).
Further studies on the ability of environmental chemicals to influence vitamin D levels in animals and humans are in order.
To see or download the references cited on this page, as well as many others on this topic, see the collection Vitamin D and diabetes/obesity in Pubmed.