title: Sugar intake is associated with progression from islet autoimmunity to type 1 diabetes: the Diabetes Autoimmunity Study in the Young.
abstract: OBJECTIVE
  Dietary sugar intake may increase insulin production, stress the beta cells and increase the risk for islet autoimmunity (IA) and subsequent type 1 diabetes.
  
  
  METHODS
  Since 1993, the Diabetes Autoimmunity Study in the Young (DAISY) has followed children at increased genetic risk for type 1 diabetes for the development of IA (autoantibodies to insulin, GAD or protein tyrosine phosphatase-like protein [IA2] twice or more in succession) and progression to type 1 diabetes. Information on intake of fructose, sucrose, total sugars, sugar-sweetened beverages, beverages with non-nutritive sweetener and juice was collected prospectively throughout childhood via food frequency questionnaires (FFQs). We examined diet records for 1,893 children (mean age at last follow-up 10.2 years); 142 developed IA and 42 progressed to type 1 diabetes. HLA genotype was dichotomised as high risk (HLA-DR3/4,DQB1*0302) or not. All Cox regression models were adjusted for total energy, FFQ type, type 1 diabetes family history, HLA genotype and ethnicity.
  
  
  RESULTS
  In children with IA, progression to type 1 diabetes was significantly associated with intake of total sugars (HR 1.75, 95% CI 1.07-2.85). Progression to type 1 diabetes was also associated with increased intake of sugar-sweetened beverages in those with the high-risk HLA genotype (HR 1.84, 95% CI 1.25-2.71), but not in children without it (interaction p value = 0.02). No sugar variables were associated with IA risk.
  
  
  CONCLUSIONS
  Sugar intake may exacerbate the later stage of type 1 diabetes development; sugar-sweetened beverages may be especially detrimental to children with the highest genetic risk of developing type 1 diabetes.
authors.affiliation: Colorado School of Public Health, University of Colorado, 13001 E. 17th Place, Aurora, CO, 80045, USA.
authors.forename: Molly M
authors.initials: MM
authors.lastname: Lamb
authors.forename: Brittni
authors.initials: B
authors.lastname: Frederiksen
authors.forename: Jennifer A
authors.initials: JA
authors.lastname: Seifert
authors.forename: Miranda
authors.initials: M
authors.lastname: Kroehl
authors.forename: Marian
authors.initials: M
authors.lastname: Rewers
authors.forename: Jill M
authors.initials: JM
authors.lastname: Norris
mesh_terms: D015551:Autoimmunity; D002241:Carbohydrates / Q000737:chemistry*; D002648:Child; D002675:Child, Preschool; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D004032:Diet; D004040:Dietary Carbohydrates / Q000009:adverse effects*; D018450:Disease Progression; D005192:Family Health; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D059866:HLA-DQ beta-Chains / Q000378:metabolism; D015803:HLA-DR3 Antigen / Q000378:metabolism; D015804:HLA-DR4 Antigen / Q000378:metabolism; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007328:Insulin / Q000737:chemistry; D008297:Male; D016016:Proportional Hazards Models; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D002241:Carbohydrates; D004040:Dietary Carbohydrates; D059866:HLA-DQ beta-Chains; C057615:HLA-DQbeta antigen; D015803:HLA-DR3 Antigen; D015804:HLA-DR4 Antigen; D007328:Insulin