title: Dietary glycemic index, development of islet autoimmunity, and subsequent progression to type 1 diabetes in young children.
abstract: BACKGROUND
  Dietary factors may trigger or exacerbate the autoimmune disease process.
  
  
  OBJECTIVE
  Our objective was to examine dietary glycemic index (GI) and glycemic load (GL) for association with islet autoimmunity (IA) development, and progression from IA to type 1 diabetes.
  
  
  METHODS
  The Diabetes Autoimmunity Study in the Young follows children at increased genetic type 1 diabetes risk. Diet is collected prospectively via a parent-reported food frequency questionnaire.
  
  
  METHODS
  This was an observational study of children in the Denver area.
  
  
  METHODS
  A total of 1776 Diabetes Autoimmunity Study in the Young children younger than 11.5 yr was included in the study.
  
  
  METHODS
  There were no interventions.
  
  
  METHODS
  IA, defined as the presence of autoantibodies to insulin, glutamic acid decarboxylase, or protein tyrosine phosphatase at two consecutive visits, or the presence of autoantibodies at one visit and diabetic on the next consecutive visit was determined. Type 1 diabetes was diagnosed by a physician. A total of 89 subjects developed IA, and 17 subsequently developed type 1 diabetes during follow-up. Our hypothesis was formulated after data collection.
  
  
  RESULTS
  GI and GL were not associated with IA development. More rapid progression to type 1 diabetes in children with IA was associated with higher dietary GI (hazard ratio: 2.20; 95% confidence interval: 1.17-4.15) and marginally associated with GL (hazard ratio: 1.59; 95% confidence interval: 0.96-2.64) at the first IA-positive visit.
  
  
  CONCLUSIONS
  Higher dietary GI and GL are not associated with IA development, but higher GI is associated with more rapid progression to type 1 diabetes in children with IA, perhaps due to increased demand on the beta-cell to release insulin. Further study is needed to confirm this finding and identify the underlying biological mechanism.
authors.affiliation: University of Colorado, Denver, Colorado 80262, USA.
authors.forename: Molly M
authors.initials: MM
authors.lastname: Lamb
authors.forename: Xiang
authors.initials: X
authors.lastname: Yin
authors.forename: Katherine
authors.initials: K
authors.lastname: Barriga
authors.forename: Michelle R
authors.initials: MR
authors.lastname: Hoffman
authors.forename: Anna E
authors.initials: AE
authors.lastname: Barón
authors.forename: George S
authors.initials: GS
authors.lastname: Eisenbarth
authors.forename: Marian
authors.initials: M
authors.lastname: Rewers
authors.forename: Jill M
authors.initials: JM
authors.lastname: Norris
mesh_terms: D015551:Autoimmunity / Q000502:physiology; D001786:Blood Glucose / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000209:etiology* / Q000276:immunology; D004032:Diet / Q000009:adverse effects*; D018450:Disease Progression; D002149:Energy Intake / Q000502:physiology; D005192:Family Health; D005260:Female; D005500:Follow-Up Studies; D038321:Glycemic Index / Q000502:physiology*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007515:Islets of Langerhans / Q000276:immunology* / Q000473:pathology; D008297:Male
chemical_list: D001786:Blood Glucose