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Environmental triggers of type 1 diabetes.

Abstract

High risk HLA class II alleles account for 40% of the genetic susceptibility to type 1 diabetes in Caucasians, but the majority of the genetically predisposed do not develop the disease. This supports some environmental modification of the autoimmune destruction of beta cells that precedes type 1 diabetes. Identical twin studies and geographical variation in incidence also argue for a critical role of environmental factors. Attention has been directed to the possible harmful effect of cow's milk protein (or protective effect of breast-feeding) and enteric infections in early life. Natural history studies that follow children at increased risk of type 1 diabetes provide the best opportunity to study environmental triggers. The Australian Baby Diab Study has followed approximately 500 babies from birth who have a first-degree relative with type 1 diabetes. No prospective association between duration of breast-feeding or introduction of cow's milk and the development of islet autoimmunity was found. The same Australian cohort demonstrated a relationship between rotavirus infection and the first appearance or increase in islet antibodies. Enteroviral infection is seen more frequently in prediabetic children and prior to the onset of islet autoimmunity in Finnish cohorts. Environmental factors may interact. Breast milk protects against enteric infections; enteric infections in turn could increase immunity to dietary antigens by increasing intestinal permeability. It is also possible that an alteration in gut mucosal immune function in genetically susceptible individuals underlies any effect of dietary or viral proteins on the development of islet autoimmunity in early life.

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  • Publisher Full Text
  • Authors+Show Affiliations

    Department of Endocrinology, Women and Children's Hospital, North Adelaide, SA 5006, Australia. jcouper@medicine.adelaide.edu.au

    Source

    MeSH

    Animals
    Breast Feeding
    Diabetes Mellitus, Type 1
    Enterovirus Infections
    Environmental Exposure
    Gene Frequency
    Genetic Predisposition to Disease
    HLA Antigens
    Humans
    Infant
    Infant, Newborn
    Milk
    Rotavirus Infections
    Viral Proteins

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    11474705

    Citation

    Couper, J J.. "Environmental Triggers of Type 1 Diabetes." Journal of Paediatrics and Child Health, vol. 37, no. 3, 2001, pp. 218-20.
    Couper JJ. Environmental triggers of type 1 diabetes. J Paediatr Child Health. 2001;37(3):218-20.
    Couper, J. J. (2001). Environmental triggers of type 1 diabetes. Journal of Paediatrics and Child Health, 37(3), pp. 218-20.
    Couper JJ. Environmental Triggers of Type 1 Diabetes. J Paediatr Child Health. 2001;37(3):218-20. PubMed PMID: 11474705.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Environmental triggers of type 1 diabetes. A1 - Couper,J J, PY - 2001/7/28/pubmed PY - 2001/10/12/medline PY - 2001/7/28/entrez SP - 218 EP - 20 JF - Journal of paediatrics and child health JO - J Paediatr Child Health VL - 37 IS - 3 N2 - High risk HLA class II alleles account for 40% of the genetic susceptibility to type 1 diabetes in Caucasians, but the majority of the genetically predisposed do not develop the disease. This supports some environmental modification of the autoimmune destruction of beta cells that precedes type 1 diabetes. Identical twin studies and geographical variation in incidence also argue for a critical role of environmental factors. Attention has been directed to the possible harmful effect of cow's milk protein (or protective effect of breast-feeding) and enteric infections in early life. Natural history studies that follow children at increased risk of type 1 diabetes provide the best opportunity to study environmental triggers. The Australian Baby Diab Study has followed approximately 500 babies from birth who have a first-degree relative with type 1 diabetes. No prospective association between duration of breast-feeding or introduction of cow's milk and the development of islet autoimmunity was found. The same Australian cohort demonstrated a relationship between rotavirus infection and the first appearance or increase in islet antibodies. Enteroviral infection is seen more frequently in prediabetic children and prior to the onset of islet autoimmunity in Finnish cohorts. Environmental factors may interact. Breast milk protects against enteric infections; enteric infections in turn could increase immunity to dietary antigens by increasing intestinal permeability. It is also possible that an alteration in gut mucosal immune function in genetically susceptible individuals underlies any effect of dietary or viral proteins on the development of islet autoimmunity in early life. SN - 1034-4810 UR - https://www.unboundmedicine.com/medline/citation/11474705/Environmental_triggers_of_type_1_diabetes_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1034-4810&date=2001&volume=37&issue=3&spage=218 DB - PRIME DP - Unbound Medicine ER -