Cesarean section and interferon-induced helicase gene polymorphisms combine to increase childhood type 1 diabetes risk

Diabetes. 2011 Dec;60(12):3300-6. doi: 10.2337/db11-0729.

Abstract

Objective: The incidence of type 1 diabetes is increasing. Delivery by cesarean section is also more prevalent, and it is suggested that cesarean section is associated with type 1 diabetes risk. We examine associations between cesarean delivery, islet autoimmunity and type 1 diabetes, and genes involved in type 1 diabetes susceptibility.

Research design and methods: Cesarean section was examined as a risk factor in 1,650 children born to a parent with type 1 diabetes and followed from birth for the development of islet autoantibodies and type 1 diabetes.

Results: Children delivered by cesarean section (n = 495) had more than twofold higher risk for type 1 diabetes than children born by vaginal delivery (hazard ratio [HR] 2.5; 95% CI 1.4-4.3; P = 0.001). Cesarean section did not increase the risk for islet autoantibodies (P = 0.6) but was associated with a faster progression to diabetes after the appearance of autoimmunity (P = 0.015). Cesarean section-associated risk was independent of potential confounder variables (adjusted HR 2.7;1.5-5.0; P = 0.001) and observed in children with and without high-risk HLA genotypes. Interestingly, cesarean section appeared to interact with immune response genes, including CD25 and in particular the interferon-induced helicase 1 gene, where increased risk for type 1 diabetes was only seen in children who were delivered by cesarean section and had type 1 diabetes-susceptible IFIH1 genotypes (12-year risk, 9.1 vs. <3% for all other combinations; P < 0.0001).

Conclusions: These findings suggest that type 1 diabetes risk modification by cesarean section may be linked to viral responses in the preclinical autoantibody-positive disease phase.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Autoantibodies / immunology
  • Cesarean Section / adverse effects*
  • DEAD-box RNA Helicases / genetics
  • DNA Helicases / genetics*
  • Diabetes Mellitus, Type 1 / epidemiology*
  • Diabetes Mellitus, Type 1 / etiology
  • Diabetes Mellitus, Type 1 / genetics*
  • Diabetes Mellitus, Type 1 / immunology
  • Female
  • Humans
  • Infant, Newborn
  • Interferon-Induced Helicase, IFIH1
  • Interferons
  • Interleukin-2 Receptor alpha Subunit / genetics
  • Polymorphism, Genetic / genetics*
  • Pregnancy
  • Protein Tyrosine Phosphatase, Non-Receptor Type 22 / genetics
  • Risk Factors

Substances

  • Autoantibodies
  • Interleukin-2 Receptor alpha Subunit
  • Interferons
  • PTPN22 protein, human
  • Protein Tyrosine Phosphatase, Non-Receptor Type 22
  • IFIH1 protein, human
  • DNA Helicases
  • DEAD-box RNA Helicases
  • Interferon-Induced Helicase, IFIH1