[IgE] and eosinophil count) were significantly and inversely associated with vitamin D status. These lower quality observational studies largely support the associations with symptoms of asthma identified in the larger cohort studies but do not support an association between 25OHD level in blood and diagnosed asthma.
Although genetic studies support a possible biological mechanism for a functional role of vitamin D in development of asthma there are no RCTs to demonstrate a causal role.
Autoimmune diseases such as multiple sclerosis (MS), rheumatoid arthritis (RA), inflammatory bowel disease (IBD), and lupus are characterized by abnormal T cell response to self, resulting in inflammatory reactions in peripheral tissues. Models of autoimmune diseases support a role for vitamin D in regulating the T helper 1 (Th1) immune response, an integral component of immune tolerance with regard to recognition of self (reviewed in Cantorna and Mahon, 2005; Szodoray et al., 2008). Recent genomic analyses for polymorphisms in the Vdr gene suggest that single nucleotide polymorphisms identified in individuals with type 1 diabetes could negatively modulate calcitriol synthesis and thereby play a detrimental role in autoimmune response and subsequent manifestation of the disease (Israni et al., 2009).
Diabetes (type 1) Type 1 diabetes is a chronic disease resulting from loss of β-cell function in the pancreas. The disease is characterized by diminished or absent insulin production and loss of control of blood glucose. Emerging evidence for an association between low vitamin D status and increased risk for type 1 diabetes comes from experimental animal, ecological, and observational studies; however, no intervention trials using supplemental vitamin D (not analogues) were identified to provide causal support for a relationship.
Biological plausibility Experimental animal, ecological, and observational evidence support a relationship between vitamin D status and risk for type 1 diabetes, although treatment protocols and dosages vary. Ecological evidence has suggested a link between type 1 diabetes risk and limited erythemal UVB exposure in Newfoundland (Sloka et al., 2009, 2010). Mohr et al. (2008) plotted incidence rates for type 1 diabetes by latitude in an ecologic study comparing geographical distribution, estimated UVB exposure and disease incidence and, using a polynomial analysis to best fit the data points, determined that the incidence of type 1 diabetes was greater at higher latitudes.