 I didn't think I would be deficient in vitamin D due to my habit of exercising outdoors every day. I was wrong. A number of studies have found vitamin D to be protective against type 1 diabetes or the development of type 1-related autoantibodies. For example:
An analysis of the data from five 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, and the timing may also be important (Zipitis and Akobeng 2008). 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. 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.
And yet not all studies have confirmed that supplementation is protective; a Finnish study has found that maternal intake of vitamin D via food or supplements during pregnancy was not associated with the development of type 1 diabetes or related autoimmunity in their offspring (Marjamäki et al. 2010). Another Finnish study found no difference between the pregnant women's vitamin D levels and their children's later risk of type 1 diabetes (Miettinen et al. 2012). And, US researchers who followed type 1 development over time found that vitamin D intake and vitamin D levels during childhood were not associated with the development of either autoantibodies or type 1 diabetes in genetically at-risk children (Simpson et al. 2011).
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 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).
An epidemic of vitamin D deficiencyVitamin 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 via diet (Alberts et al. 1998). 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 D3 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). Ideally, studies should measure the levels of 25-D or 1,25-D to accurately determine vitamin D exposure (Norris 2001). Since vitamin D appears to be protective against type 1 diabetes, we might expect vitamin D deficiency to contribute to disease development. Indeed, one Swedish study has found that at the time of diagnosis, levels of 25-D were lower in people with type 1 diabetes than in people without the disease. Fifty-four percent of people with diabetes had insufficient levels of vitamin D, especially men (Littorin et al. 2006). A Swiss study has found that children and adolescents with type 1 diabetes had high levels of vitamin D deficiency, a finding similar to studies of Italian, U.S., and Australian children with type 1 diabetes (Janner et al. 2010).
In the U.S., one study in Florida did not find an association between vitamin D levels and type 1 diabetes, although they did find that all groups had lower than the recommended level of 25-D in their bodies, despite living in the sunshine state (Bierschenk et al. 2009). Ginde et al. (2009) found that based on a nation-wide sample, 77% of the U.S. population has insufficient 25-D levels (including nearly all African Americans and almost all Mexican Americans). Also, levels of vitamin D have declined in the U.S. population, comparing the periods 1988-1994 to 2001-2004.
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. 2011).
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). 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). Vitamin D deficiency has also been associated with preeclampsia during pregnancy (Mulligan et al. 2009), a risk factor for type 1 diabetes in the offspring (see the gestation and birth page).
Vitamin D deficiency may also contribute to the development of type 2 diabetes (Palomer et al. 2008). A study of U.S. adults found that people with lower levels of 25-D had higher hemoglobin A1c (HA1c) levels (a measure of long-term blood glucose levels), including people who did not have diabetes (Kositsawat et al. 2010). However, another study of healthy children found that vitamin D levels did not affect insulin sensitivity or beta cell function (Rajakumar et al. 2012). In people with type 2 diabetes, daily consumption of a yogurt drink enriched with vitamin D improved blood glucose control (Nikyooeh et al. 2011).
Pittas and Dawson-Hughes (2010) review the human studies on both type 1 and type 2 diabetes in relation to vitamin D. So far, there have not been any intervention trials to see if vitamin D supplementation actually prevents type 1 diabetes, and studies of type 2 have been inconclusive. On the basis of existing studies, these trials should be conducted.
Potential mechanismsWhy might vitamin D be protective against type 1 diabetes? 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). Baeke et al. (2010) review how vitamin D affects the immune system, and its role in the development of autoimmune diseases. A double-blind, placebo controlled trial found that adults given high doses of vitamin D for 3 months had enhanced levels of immune cells that are thought to be protective against autoimmunity (beta cell function was not affected) (Bock et al. 2011). As for diabetes in particular, Mathieu et al. (2005) describe a number of ways that vitamin D deficiency may contribute to the development of both types of diabetes. For example, vitamin D deficiency can impair insulin secretion from beta cells (see the beta cell stress page). And, vitamin D can 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).
Vitamin D may also interact with other factors to influence diabetes development. 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) (see the height and weight page for information on increased weight as a risk factor for type 1 diabetes). Low vitamin D levels have been associated with increased insulin resistance in people without diabetes (Forouhi et al. 2008) (see the insulin resistance page for information on the potential role of increased insulin resistance in type 1 diabetes). Vitamin D may also be involved in controlling gut permeability, which may be a factor in type 1 diabetes development (see the diet and the gut page) (Vaarala 2008).
Environmental contaminants and vitamin DUnfortunately, 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 US adults (Yang et al. 2012). One study fed mother rats a mixture of PCBs similar to that found in human breastmilk. Exposure to 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). The authors hypothesized that since PCBs can affect other hormones (see the endocrine (hormone) disruptors page), it might make sense that they could interfere with vitamin D levels.
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 type 1 diabetes incidence page), and why even many Floridians have low levels of 25-D in their bodies. More research on these possibilities is necessary.
The bottom lineThere is good evidence that vitamin D 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.
Further studies on the ability of environmental contaminants to influence vitamin D levels in animals and humans are in order. |