Type 1 Diabetes: Prospective Cohort Studies for Identification of the Environmental Trigger
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REVIEW
Type 1 Diabetes: Prospective Cohort Studies for Identification of the Environmental Trigger Kjersti S. Rønningen
Received: 10 September 2012 / Accepted: 5 August 2013 Ó L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2013
Abstract Type 1 diabetes (T1D) is one of the most common chronic diseases with childhood onset, and the disease incidence has increased two to fivefold over the past half century by as yet unknown means. T1D occurs when the body’s immune system turns against itself, destroying in a very specific and targeted way—the pancreatic b-cells. T1D results from poorly defined interactions between susceptibility genes and environmental determinants. In contrast to the rapid progress in finding T1D genes, identification and confirmation of environmental determinants remain a formidable challenge. This review article will give an overview of ongoing prospective cohort studies aiming to identify the environmental trigger(s) causing T1D. Keywords Autoimmunity Cohort studies Environmental factors Genetic factors Type 1 diabetes Abbreviations BMI Body mass index DAISY Diabetes Autoimmunity Study in the Young DIPP Diabetes Prediction and Prevention study FDR First-degree relatives HLA Human leukocyte antigen HR Hazard ratio MIDIA Norwegian acronym for: Environmental Triggers of T1D
K. S. Rønningen (&) Division for Women and Children, Department of Pediatric Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway e-mail: [email protected]
TEDDY T1D
The Environmental Determinants of Diabetes in the Young Type 1 diabetes
Introduction Type 1 Diabetes (T1D) is one of the most common chronic diseases with childhood onset. Its incidence has increased two to fivefold over the past half century by as yet unknown means (DIAMOND Project Group 2006; Harjutsalo et al. 2008). It was interpreted that if the present trend continues, the prevalence of children with the disease in Europe will increase by 50 % before year 2020, and by 70 % in children younger than 5 years of age (Patterson et al. 2009). Most recently European data were compared between the periods 1989–1998 and 1999–2008, and it was shown that the increase in T1D is not necessarily uniform; it has periods of less rapid and more rapid increase in incidence in different countries (Patterson et al. 2012). These patterns of change suggest that important risk exposures may differ over time in different European countries. T1D occurs when the body’s immune system turns against itself, destroying—in a very specific and targeted way—the pancreatic islet b cells, the only cells in the body that produce the vital hormone, insulin (Atkinson and Eisenbarth 2001; Eizirik et al. 2009). This autoimmune destruction is irreversible and the disease presently seems to be incurable. If pancreas or islets are transplanted they too are destroyed, unless heavy immunosuppression is applied (Natasha et al. 2011). T1D results from poorly defined interactions between susceptibility genes and environmental determina
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