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Sci Rep. 2018 Jun 13;8(1):9067. doi: 10.1038/s41598-018-27391-4.

Prenatal iron exposure and childhood type 1 diabetes.

Author information

1
Department of non-communicable diseases, Norwegian Institute of Public Health, Oslo, Norway. ketil.stordal@fhi.no.
2
Pediatric Department, Ostfold Hospital Trust, Fredrikstad, Norway. ketil.stordal@fhi.no.
3
The Rowett Institute of Nutrition and Health, University of Aberdeen, Foresterhill, Aberdeen, Scotland, UK.
4
Department of non-communicable diseases, Norwegian Institute of Public Health, Oslo, Norway.
5
Department of Medical Genetics, University of Oslo, Oslo University Hospital, Ullevål, Oslo, Norway.
6
Department of Immunology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
7
Department of Paediatric and Adolescent Medicine, Oslo University Hospital, Oslo, Norway.
8
Department of Environmental Exposure and Epidemiology, Norwegian Institute of Public Health, Oslo, Norway.
9
Department of Paediatrics and Adolescent Medicine, Haukeland University Hospital, Bergen, Norway.
10
KG Jebsen Center for Diabetes Research, Department of Clinical Science, University of Bergen, Bergen, Norway.
11
Centre for Biostatistics and Epidemiology, Oslo University Hospital, Oslo, Norway.
12
National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, Durham, NC, 27709, USA.

Abstract

Iron overload due to environmental or genetic causes have been associated diabetes. We hypothesized that prenatal iron exposure is associated with higher risk of childhood type 1 diabetes. In the Norwegian Mother and Child cohort study (n = 94,209 pregnancies, n = 373 developed type 1 diabetes) the incidence of type 1 diabetes was higher in children exposed to maternal iron supplementation than unexposed (36.8/100,000/year compared to 28.6/100,000/year, adjusted hazard ratio 1.33, 95%CI: 1.06-1.67). Cord plasma biomarkers of high iron status were non-significantly associated with higher risk of type 1 diabetes (ferritin OR = 1.05 [95%CI: 0.99-1.13] per 50 mg/L increase; soluble transferrin receptor: OR = 0.91 [95%CI: 0.81-1.01] per 0.5 mg/L increase). Maternal but not fetal HFE genotypes causing high/intermediate iron stores were associated with offspring diabetes (odds ratio: 1.45, 95%CI: 1.04, 2.02). Maternal anaemia or non-iron dietary supplements did not significantly predict type 1 diabetes. Perinatal iron exposures were not associated with cord blood DNA genome-wide methylation, but fetal HFE genotype was associated with differential fetal methylation near HFE. Maternal cytokines in mid-pregnancy of the pro-inflammatory M1 pathway differed by maternal iron supplements and HFE genotype. Our results suggest that exposure to iron during pregnancy may be a risk factor for type 1 diabetes in the offspring.

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