Vitamin D deficiency does not increase risk of inflammatory bowel disease
Vitamin D deficiency does not appear to have any role in the development of inflammatory bowel disease (IBD), reports a recent study.
In observational studies, higher 25-hydroxyvitamin D (25[OH]D) levels are associated with a higher risk of ulcerative colitis (UC) but not of Crohn’s disease (CD), but genetically high plasma 25(OH)D level is not associated with UC or CD.
Multivariable-adjusted hazard ratios (HRs) for 10 nmol/L higher 25(OH)D level were 1.04 (95 percent CI, 0.93–1.16) and 1.13 (1.06–1.21) for CD and UC, respectively. A combined 25(OH)D allele score correlated with a 1.4-nmol/L increase in plasma 25(OH)D level and HRs of 0.98 (0.94–1.03) and 1.01 (0.97–1.05) for CD and UC, respectively.
Combined genetic data from the Copenhagen studies and the UK Biobank revealed that genetically determined vitamin D appeared to have no impact on the risk of CD or UC.
To determine whether plasma 25(OH)D levels are causally linked to risks of CD and UC, the authors conducted a Mendelian randomization study on 120,013 individuals from the Copenhagen City Heart Study, the Copenhagen General Population Study and a Copenhagen-based cohort of patients with IBD.
Of the participants, 35,558 had plasma 25(OH)D measurements available, and 115,110 were genotyped for rs7944926 and rs11234027 in DHCR7 and rs10741657 and rs12794714 in CYP2R1. All variants were associated with plasma 25(OH)D levels.
The authors identified 653 cases of CD and 1,265 cases of UC, of which 58 and 113 had 25(OH)D measurement available, respectively. Genetic data from 408,455 individuals from the UK Biobank, including 1,707 CD cases and 3,147 UC cases, were included.