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Association between circulating 25-hydroxyvitamin D and incident type 2 diabetes: a mendelian randomisation study
Zheng Ye1, Stephen J Sharp1, Stephen Burgess2
1MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Institute of Metabolic Science, Cambridge, UK.
The Lancet. Diabetes & Endocrinology
|October 5, 2014
Summary
Low vitamin D levels are not causally linked to increased type 2 diabetes risk. This mendelian randomization study suggests observational associations may be misleading, indicating vitamin D supplementation might not prevent type 2 diabetes.
Area of Science:
- Genetics and Human Health
- Metabolic Diseases
- Nutritional Epidemiology
Background:
- Low circulating 25-hydroxyvitamin D (25[OH]D) is linked to higher type 2 diabetes risk.
- Causality of this association remains uncertain.
Purpose of the Study:
- To estimate the unconfounded, causal association between 25[OH]D concentration and type 2 diabetes risk.
- Utilize a mendelian randomization approach to address confounding factors.
Main Methods:
- Mendelian randomization analysis using SNPs near genes involved in vitamin D metabolism (DHCR7, CYP2R1, DBP, CYP24A1).
- Assessed SNP associations with 25[OH]D, type 2 diabetes risk, and glycaemic traits.
- Compared findings with a meta-analysis of observational studies.
Main Results:
- All four SNPs significantly associated with 25[OH]D concentrations.
- Mendelian randomization showed no significant causal link between 25[OH]D and type 2 diabetes (OR 1.01, p=0.94 per 25.0 nmol/L lower 25[OH]D).
- Observational studies showed a significant association (RR 1.21, p<10(-19)).
Conclusions:
- The observed association between 25[OH]D and type 2 diabetes is unlikely to be causal.
- Increasing 25[OH]D may not reduce type 2 diabetes risk as suggested by observational data.
- Further research is needed to identify factors influencing both 25[OH]D and type 2 diabetes risk.
