Low circulating concentrations of 25-hydroxyvitamin D (25[OH]D), a marker of vitamin D status, are associated with an increased risk of type 2 diabetes, but whether this association is causal remains equivocal.

A Mendelian randomization approach has been used to estimate the, causal association between 25(OH)D concentration and risk of type 2 diabetes by analysis using single nucleotide polymorphisms (SNPs) within or near four genes related to 25(OH)D synthesis and metabolism.

Scientists at the University of Cambridge (UK) used several data sources from populations of European descent. Associations of SNPs with risk of type 2 diabetes were based on 28,144 cases of type 2 diabetes and 76,344 non-cases from a case-cohort study. Apart from a few studies, all studies ascertained type 2 diabetes cases through biochemical testing, such as concentrations of fasting glucose, two-hour glucose, or HbA1c.

SNPs were assayed by the Illumina 660 quad-chip or the Metabochip (Illumina; Little Chesterford, UK). The assays used 10 ng of genomic DNA in a 2.5 μL reaction volume, 384-well plate with a G-Storm GS4 Thermal Cycler (Genetic Research Instrumentation (GRI); Rayne, UK). Endpoint detection and allele calling were done with an ABI PRISM 7900HT Sequence Detection System (Applied Biosystems; Paisley, UK). The authors also used circulating 25(OH)D levels, considered the best indicator of vitamin D status, as the measure for vitamin D. Insufficiency was defined as having blood levels of 25(OH)D under 50 nmol/L.

The scientists found no evidence of a link between the risk of developing type 2 diabetes and the different gene variants that control blood levels of vitamin D. They also found no links between varying levels of vitamin D and several features of type 2 diabetes, such as glucose and glycated hemoglobin, and neither did they find evidence that low vitamin D causes the disease. The authors concluded that their findings suggest that interventions to reduce the risk of type 2 diabetes by increasing concentrations of 25(OH)D are not currently justified. The study was published on October 1, 2014, in the journal the Lancet Diabetes & Endocrinology.

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