Trial Lecture – time and place
See Trial Lecture.
- First opponent: Physician Daniel Agardh, Lund University, EXODIAB: Excellence in Diabetes Research in Sweden
- Second opponent: Associate Professor Lars Krogvold, Institute of Clinical Dentistry, Pediatric Dentistry and Behaviorial Science, University of Oslo
- Third member and chair of the evaluation committee: Associate Professor Anne-Marte Bakken Kran, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo
Chair of the Defence
Professor Knut Stavem, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo
Researcher Ketil Størdal, Norwegian Institute of Public Health
The large proportion of healthy people carrying the genotypes predisposing to celiac disease and exposed to gluten points to additional environmental factors to be involved in disease development. As celiac disease often develops at an early age, pregnancy and early childhood have been considered important windows of exposure. Emerging evidence is now pointing towards infections as potential triggers of celiac disease. This thesis aimed to investigate early life infectious exposures that so far have limited epidemiological findings with regard to celiac disease: maternal infections in pregnancy, infections in general during the first years of life and specific intestinal viruses. Infections and celiac disease may also affect growth. A secondary aim of this thesis was to study growth in the first years of life in relation to celiac disease.
We used data from two cohorts: 1) The Norwegian Mother and Child Cohort study (MoBa), a large-scale population-based pregnancy cohort which recruited pregnant women across Norway between 1999 and 2008: and 2) The MIDIA study, a birth cohort of Norwegian children carrying the HLA high-risk haplotype DQ-2/DQ-8 recruited during 2001-2007 and followed with monthly stool samples from 3 to 36 months and annual blood samples. All children still participating in MIDIA were screened for celiac disease during 2014-2016.
Maternal infections during pregnancy showed no clear association with offspring celiac disease. Children in MoBa who had frequent infections during 0-18 months had an increased risk of celiac disease. In MIDIA, enterovirus in monthly stool samples before development of celiac disease antibodies was associated with celiac disease. Finally, celiac children had lower mean height already at 12 months of age.
The findings suggest that viral infections early in life may induce celiac disease. However, gluten and predisposing genes are required, and corroboration of the potential role of different types of viruses is warranted.
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