Send to:

Choose Destination
See comment in PubMed Commons below
Am J Clin Nutr. 2010 May;91(5):1506S-1513S. doi: 10.3945/ajcn.2010.28701C. Epub 2010 Mar 24.

Infant feeding and the risk of type 1 diabetes.

Author information

  • 1Hospital for Children and Adolescents and Folkhälsan Research Center, University of Helsinki, Finland.


Type 1 diabetes is generally considered to be a chronic, immune-mediated disease with a subclinical prodrome during which beta cell autoimmunity becomes overt disease at a variable rate in genetically susceptible individuals. Accumulated evidence supports a critical role of environmental factors in its development. Prospective birth cohort studies show that the first signs of beta cell autoimmunity may be initiated during the first year of life. This implies that risk factors for beta cell autoimmunity and type 1 diabetes must be operative in infancy. Early nutrition provides essential exogenous exposures in that period. This article discusses the role of factors related to infant nutrition in the development of beta cell autoimmunity and type 1 diabetes and the potential mechanistic pathways involved. So far, no specific dietary factor has been shown to be an unequivocal risk factor for beta cell autoimmunity or type 1 diabetes, and there are a number of contradictory observations with regard to the effect of various foods. This may reflect geographic and cultural differences in infant-feeding practices. Most studies suggest that the early introduction of complex foreign proteins may be a risk factor for beta cell autoimmunity, and a pilot intervention trial has implied that weaning to a highly hydrolyzed formula may decrease the risk of beta cell autoimmunity. Lack of vitamin D supplementation and accelerated growth might increase the risk of type 1 diabetes. Additional work, which includes the application of modern approaches such as metabolomics and epigenomics, is needed to discern the contribution of dietary factors in infancy to the diabetic disease process.

[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Write to the Help Desk