Studies on vitamin D status during pregnancy and risk of type 1 diabetes mellitus (T1D) lack consistency and are limited by small sample sizes or single measures of 25-hydroxyvitamin D (25(OH)D). We investigated whether average maternal 25(OH)D plasma concentrations during pregnancy are associated with risk of childhood T1D. In a case-cohort design, we identified 459 children with T1D and a random sample (n = 1,561) from the Danish National Birth Cohort (n = 97,127) and Norwegian Mother and Child Cohort Study (n = 113,053). Participants were born between 1996 and 2009. The primary exposure was the estimated average 25(OH)D concentration, based on serial samples from the first trimester until delivery and on umbilical cord plasma. We estimated hazard ratios using weighted Cox regression adjusting for multiple confounders. The adjusted hazard ratio for T1D per 10-nmol/L increase in the estimated average 25(OH)D concentration was 1.00 (95% confidence interval: 0.90, 1.10). Results were consistent in both cohorts, in multiple sensitivity analyses, and when we analyzed mid-pregnancy or cord blood separately. In conclusion, our large study demonstrated that normal variation in maternal or neonatal 25(OH)D is unlikely to have a clinically important effect on risk of childhood T1D.

Background Vitamin D, certain single nucleotide polymorphisms (SNPs) in the vitamin D‐receptor (VDR) gene and vitamin D metabolism genes have been associated with type 1 diabetes (T1D). Objective We wanted to examine if the most widely studied SNPs in genes important for production, transport, and action of vitamin D were associated with T1D or to circulating levels of vitamin D 25‐hydroxyvitamin D [25(OH)D] in a juvenile Danish population. Methods We genotyped eight SNPs in five vitamin D metabolism genes in 1467 trios. 25(OH)D status were analyzed in 1803 children (907 patients and 896 siblings). Results We did not demonstrate association with T1D for SNPs in the following genes: CYP27B1, VDR, GC, CYP2R1, DHCR7, and CYP24A1. Though, variants in the GC gene were significantly associated with 25(OH)D levels in the joint model. Conclusion Some of the most examined SNPs in vitamin D metabolism genes were not confirmed to be associated with T1D, though 25(OH) levels were associated with variants in the GC gene.

The causes of the worldwide increase in type 1 diabetes (T1D) in children are still largely unknown. In Denmark, the increase in incidence is steep at 3.4% annually and does not appear to be leveling out (1). Lower levels of 25-hydroxyvitamin D [25(OH)D] have been found in patients with newly diagnosed T1D compared with healthy control subjects, implying that 25(OH)D might play a role in the pathogenesis of T1D (2,3). We aimed to elucidate the possible association between low levels of 25(OH)D and T1D by measuring 25(OH)D levels in children with newly diagnosed T1D and their healthy siblings in Denmark across a 13-year study period (1997–2009). We included 1,803 children (907 T1D patients and 896 siblings) in the data analyses. The children were aged 0–18 years (mean …

Background: Iron overload has been associated with diabetes. Studies on iron exposure during pregnancy and in early life and risk of childhood type 1 diabetes (T1D) are sparse. We investigated whether iron supplementation during pregnancy and early in life were associated with risk of childhood T1D. Methods: In a case-cohort design, we identified up to 257 children with T1D (prevalence 0.37%) from the Danish National Birth Cohort through linkage with the Danish Childhood Diabetes Register. The primary exposure was maternal pure iron supplementation (yes/no) during pregnancy as reported in interview two at 30 weeks of gestation (n = 68,497 with iron supplement data). We estimated hazard ratios (HRs) using weighted Cox regression adjusting for multiple confounders. We also examined if offspring supplementation during the first 18 months of life was associated with later risk of T1D. Results: Maternal iron supplementation was not associated with later risk of T1D in the offspring HR 1.05 (95% CI: 0.76–1.45). Offspring intake of iron droplets during the first 18 months of life was inversely associated with risk of T1D HR 0.74 (95% CI: 0.55–1.00) (p_trend = 0.03). Conclusions: Our large-scale prospective study demonstrated no harmful effects of iron supplementation during pregnancy and in early life in regard to later risk of childhood T1D in the offspring.