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Sugar intake is associated with progression from islet autoimmunity to type 1 diabetes: the Diabetes Autoimmunity

Molly M Lamb1, Brittni Frederiksen, Jennifer A Seifert

  • 1Colorado School of Public Health, University of Colorado, 13001 E. 17th Place, Aurora, CO, 80045, USA.

Diabetologia
|June 7, 2015
PubMed

Insights

High sugar intake may worsen type 1 diabetes progression in children. Sugar-sweetened beverages are particularly risky for those with a high genetic predisposition to type 1 diabetes.

Area of Science:

  • Pediatric Endocrinology
  • Nutritional Science
  • Immunology

Background:

  • Dietary sugar intake is a potential risk factor for islet autoimmunity (IA) and type 1 diabetes.
  • Beta cell stress and increased insulin production are hypothesized mechanisms linking sugar to diabetes risk.

Purpose of the Study:

  • To investigate the association between dietary sugar intake and the risk of IA and type 1 diabetes development in children.
  • To examine if genetic predisposition modifies the effect of sugar intake on type 1 diabetes progression.

Main Methods:

  • Prospective cohort study (Diabetes Autoimmunity Study in the Young - DAISY) of 1,893 children at high genetic risk for type 1 diabetes.
  • Dietary intake (fructose, sucrose, total sugars, sugar-sweetened beverages) assessed via food frequency questionnaires.
  • Cox regression models adjusted for covariates, including HLA genotype, to analyze risk of IA and type 1 diabetes progression.

Main Results:

  • Total sugar intake was significantly associated with progression to type 1 diabetes in children who already had IA.
  • Sugar-sweetened beverage intake was linked to type 1 diabetes progression in children with high-risk HLA genotypes, but not in others.
  • No significant association was found between sugar intake variables and the initial risk of developing IA.

Conclusions:

  • Dietary sugar intake may exacerbate later stages of type 1 diabetes development.
  • Sugar-sweetened beverages may pose a greater risk for type 1 diabetes progression in genetically susceptible children.
Abstract

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