Lack of Association Between Maternal or Neonatal Vitamin D Status and Risk of Childhood Type 1 Diabetes: A Scandinavian Case-Cohort Study
Author(s) -
S Thorsen,
Karl Mårild,
Sjúrður F. Olsen,
Klaus K. Holst,
German Tapia,
Charlotta Granström,
Þórhallur I. Halldórsson,
Arieh S. Cohen,
Margaretha Haugen,
Marika Lundqvist,
Torild Skrivarhaug,
Pål R. Njølstad,
Geir Joner,
Per Magnus,
Ketil Størdal,
Jannet Svensson,
Lars C. Stene
Publication year - 2017
Publication title -
american journal of epidemiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.33
H-Index - 256
eISSN - 1476-6256
pISSN - 0002-9262
DOI - 10.1093/aje/kwx361
Subject(s) - medicine , hazard ratio , pregnancy , cohort , vitamin d and neurology , proportional hazards model , cohort study , confidence interval , obstetrics , type 1 diabetes , confounding , diabetes mellitus , endocrinology , biology , genetics
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.
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