title: Early childhood infections and the risk of islet autoimmunity: the Diabetes Autoimmunity Study in the Young (DAISY).
abstract: OBJECTIVE
  Type 1 diabetes is a common chronic childhood disease, and the incidence is increasing globally. Childhood infections are considered a potential environmental trigger of type 1 diabetes. Alternatively, improved hygiene and reduced childhood infections could explain the increase in type 1 diabetes in developed countries. The association of reported illnesses during infancy and later development of islet autoimmunity (IA) were examined in the Diabetes Autoimmunity Study in the Young.
  
  
  METHODS
  Complete illness interviews through 9 months of age were collected for 1,729 children-1,174 without a family history of type 1 diabetes and 555 with a first-degree relative with type 1 diabetes. Persistent IA was defined as positive antibodies to insulin, glutamic acid decarboxylase, or tyrosine phosphatase on at least two consecutive study visits.
  
  
  RESULTS
  There were 109 children with persistent IA among the 1,729 children with illness records. A greater number of gastrointestinal illnesses were associated with an increased risk of IA, but only among children who were exposed to gluten-containing grains (wheat or barley) either <4 months of age (hazard ratio 1.37 [95% CI 1.22-1.55]; P < 0.0001) or ≥7 months of age (1.12 [1.05-1.19]; P = 0.0005) compared with 4-6 months of age (P for interaction = 0.02). There were no associations of upper respiratory symptoms, respiratory illnesses, or fevers with IA.
  
  
  CONCLUSIONS
  Specific pathogens such as enteroviruses or rotavirus may increase the risk of IA in the presence of existing inflammation induced by diet.
authors.affiliation: Barbara Davis Center for Childhood Diabetes, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA. janet.snell-bergeon@ucdenver.edu
authors.forename: Janet K
authors.initials: JK
authors.lastname: Snell-Bergeon
authors.forename: Jennifer
authors.initials: J
authors.lastname: Smith
authors.forename: Fran
authors.initials: F
authors.lastname: Dong
authors.forename: Anna E
authors.initials: AE
authors.lastname: Barón
authors.forename: Kathy
authors.initials: K
authors.lastname: Barriga
authors.forename: Jill M
authors.initials: JM
authors.lastname: Norris
authors.forename: Marian
authors.initials: M
authors.lastname: Rewers
mesh_terms: D015551:Autoimmunity / Q000235:genetics / Q000276:immunology*; D003922:Diabetes Mellitus, Type 1 / Q000453:epidemiology* / Q000235:genetics / Q000276:immunology*; D005260:Female; D005767:Gastrointestinal Diseases / Q000150:complications / Q000821:virology; D005838:Genotype; D059866:HLA-DQ beta-Chains / Q000235:genetics; D015802:HLA-DR2 Antigen / Q000235:genetics; D059811:HLA-DRB1 Chains / Q000235:genetics; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D059866:HLA-DQ beta-Chains; C069051:HLA-DQB1 antigen; D015802:HLA-DR2 Antigen; D059811:HLA-DRB1 Chains