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Vitamin D deficiency, type 2 diabetes development lack causal relation
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The relationship between 25-hydroxyvitamin D concentration and type 2 diabetes does not appear to be causal, challenging prior observational evidence that increasing the vitamin could reduce disease risk, according to research published in The Lancet Diabetes & Endocrinology.
The findings from a Mendelian randomization study, however, warrant further investigation to determine which underlying factors may increase 25-(OH)D concentration and decrease type 2 diabetes risk, according to researchers in the United Kingdom.
“While the role of vitamin D for bone health is well established from other research, we found no support for its role in the prevention of type 2 diabetes,” Nita Forouhi, MRCP, PhD, FFPHM, of the University of Cambridge School of Clinical Medicine, told Endocrine Today. “On the other hand, we do have high-quality research evidence showing that the maintenance of a healthy weight and healthy lifestyle, including a healthy diet and physical activity, are the main ways to prevent the onset of type 2 diabetes.”
Nita Forouhi
Forouhi, along with Zheng Ye, PhD, and colleagues from the university, analyzed single nucleotide polymorphisms (SNPs) within or near genes related to 25-(OH)D synthesis and metabolism using data from populations of European descent, comprising type 2 diabetes cases and non-cases.
The four genes included: DHCR7, related to vitamin D synthesis; CYP2R1, related to hepatic
25-hydroxylation; DBP, also known as GC, related to transport; and CYP24A1, related to catabolism.
The scientists assessed associations between each SNP and circulating 25-(OH)D concentration (5,449 noncases; two studies), risk for type 2 diabetes (28,144 cases; 76,344 noncases; five studies) and glycemic traits (concentrations of fasting glucose, 2-hour glucose, fasting insulin and HbA1c; 46,368 noncases; study consortium).
Merging these associations in a likelihood-based Mendelian randomization analysis, the researchers estimated the causal relationships of 25-(OH)D concentration with type 2 diabetes and glycemic traits. These were compared with relationships from a meta-analysis of data from observational studies (8,492 cases; 89,698 noncases; 22 studies) that looked at the association between 25-(OH)D concentration and type 2 diabetes.
All four SNPs showed association with 25-(OH)D concentrations (P<10–⁶). The unconfounded OR for type 2 diabetes resulting from Mendelian randomization was 0.93 (95% CI, 0.77-1.13) per 25 nmol/L lower 25-(OH)D concentration. The potentially confounded corresponding RR resulting from the meta-analysis of observational studies was 1.22 (95% CI, 1.16-1.29). Estimates for glycemic traits derived from Mendelian randomization was not significant (P>.25).
Forouhi noted inadequate control for distorting or confounding factors, such as physical activity, could have influenced results in past observational studies.
“There has been confusion among the public, patients as well as clinicians, based on observational findings, for testing blood vitamin D levels and considering vitamin D supplements for the prevention of conditions like type 2 diabetes,” Forouhi said.
Despite lacking causal evidence for type 2 diabetes development, “there are guidelines from respected medical agencies that recommend vitamin D supplementation for good bone health when there is vitamin D deficiency, and these should be adhered to regardless of risk for type 2 diabetes,” Forouhi said.
In an accompanying commentary, Brian Buijsse, PhD, of the German Institute of Human Nutrition Potsdam-Rehbruecke, advised careful interpretation of data due to potential pleiotropic effects of Mendelian randomization.
“Long-term randomized trials of vitamin D supplementation, which are underway, remain important,” 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.” – by Allegra Tiver
Disclosure: This study was funded by the UK Medical Research Council Epidemiology Unit and European Union Sixth Framework Programme.
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