AIMS: The onset and progression of the autoimmune process leading to type 1 diabetes is partly dependent on genetic predisposition and partly on environmental factors. We have implemented a study design where 1-year-old children, from two equally sized, neighbouring but socioeconomically different cities, were compared for the induction of beta-cell autoantibodies. METHODS: This study comprises 2448 newborn infants, all living in the urban parts of the twin cities, followed prospectively with regular biological samples and questionnaires in a major population-based study. Of these, a random sample of 1497 children were tested for tyrosine phosphatase (IA-2A) and 1409 children for glutamic acid decarboxylase (GADA). Other documented risk factors of beta-cell autoimmunity and type 1 diabetes, such as family characteristics, dietary factors, and psychosocial factors were also included in the analysis. RESULTS: The risk for diabetes-related autoantibodies, both against GADA and IA-2A (>95% cut off), was significantly higher (p<0.0001) among children from the blue-collar than from the white-collar city. This difference persisted still after adjustment for other previously documented risk factors. Some of these previously known risk factors remained significant in the multivariate analysis as independent explanatory factors, in addition to living in a blue-collar city. CONCLUSIONS: Factors in the social environment could trigger the induction of diabetes-related autoantibodies in 1-year-old children. These results point out that our present knowledge of factors influencing the autoimmune process might be widen to also include factors in the social environment of the community.
AIMS: The onset and progression of the autoimmune process leading to type 1 diabetes is partly dependent on genetic predisposition and partly on environmental factors. We have implemented a study design where 1-year-old children, from two equally sized, neighbouring but socioeconomically different cities, were compared for the induction of beta-cell autoantibodies. METHODS: This study comprises 2448 newborn infants, all living in the urban parts of the twin cities, followed prospectively with regular biological samples and questionnaires in a major population-based study. Of these, a random sample of 1497 children were tested for tyrosine phosphatase (IA-2A) and 1409 children for glutamic acid decarboxylase (GADA). Other documented risk factors of beta-cell autoimmunity and type 1 diabetes, such as family characteristics, dietary factors, and psychosocial factors were also included in the analysis. RESULTS: The risk for diabetes-related autoantibodies, both against GADA and IA-2A (>95% cut off), was significantly higher (p<0.0001) among children from the blue-collar than from the white-collar city. This difference persisted still after adjustment for other previously documented risk factors. Some of these previously known risk factors remained significant in the multivariate analysis as independent explanatory factors, in addition to living in a blue-collar city. CONCLUSIONS: Factors in the social environment could trigger the induction of diabetes-related autoantibodies in 1-year-old children. These results point out that our present knowledge of factors influencing the autoimmune process might be widen to also include factors in the social environment of the community.