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Vitamin D levels likely have little impact on whether a person develops type 2 diabetes, according to results from a genetic study published in The Lancet.
Previous research has linked low circulating concentrations of 25-hydroxyvitamin D (25[OH]D) to an increased risk for type 2 diabetes, leading researchers to suggest a connection between vitamin D insufficiency and diabetes development.
A causal association, however, has not been established, potentially due to confounders often present in observational studies, Nita Forouhi, FFPHM, of the Medical Research Council (MRC) Epidemiology Unit at the University of Cambridge, and colleagues wrote.
To further investigate this possible relationship, the researchers conducted Mendelian randomization analysis using genetic variants, known as single nucleotide polymorphisms (SNPs), within or near four genes known to control 25(OH)D synthesis and metabolism: DHCR7, CYP2R1, DBP and CYP24A1.
They drew on data from studies that included type 2 diabetes cases and non-cases.
Each SNP underwent evaluation for an association with circulating 25(OH)D concentration (5,449 non-cases; two studies), risk for type 2 diabetes (28,144 cases and 76,344 non-cases; five studies) and glycemic traits, including fasting glucose concentrations, 2-hour glucose, fasting insulin and HbA1c (46,368 non-cases; study consortium).
The researchers then compared data from the Mendelian randomization analysis with those from a meta-analysis of observational studies (8,492 cases and 89,698 non-cases; 22 studies) on the relationship between 25(OH)D and type 2 diabetes.
The genetic variants associated with 25(OH)D levels did not appear to be linked to diabetes risk, with an OR of 0.93 (95% CI, 0.77-1.13) for type 2 diabetes per 25.0 nmol/L lower 25(OH)D concentration, according to the data. Further, relative risk from the meta-analysis was 1.22 (95% CI, 1.16-1.29), although the researchers noted that this result is subject to confounding.
The SNPs studied were also not related to physiological characteristics of type 2 diabetes, such as glucose and glycated hemoglobin (P>.25), with results also not demonstrating a causative link.
“Our findings suggest that interventions to reduce the risk of type 2 diabetes by increasing concentrations of vitamin D are not currently justified,” Dr. Forouhi said in a press release.
However, Dr. Forhouhi pointed out that these results do not offer a firm, final conclusion on the association between vitamin D and type 2 diabetes.
“While our current findings do not provide support for a causal role of vitamin D in the development of type 2 diabetes, we are far from done with this topic. Further research is yet needed with both better clinical trials and better observational studies with more precise measurement of important factors that may affect vitamin D and disease relationships,” Dr. Forouhi said.
“Until then, we need to be more cautious about vitamin D’s potential role in the prevention of type 2 diabetes and stick to things that are proven to work — diet and exercise.”
In a linked comment, Brian Buijsse, PhD, of the German Institute of Human Nutrition Potsdam-Rehbruecke in Nuthetal, also advised caution when considering these study findings.
“[These results] need careful interpretation, and long-term randomized trials of vitamin D supplementation, which are underway, remain important,” Dr. Buijsse wrote. “The results of a meta-analysis of 35 short-term trials, however, do not offer much hope that vitamin D supplementation can be used to prevent type 2 diabetes … The sky is becoming rather clouded for vitamin D in the context of preventing type 2 diabetes.”
