title: Psychological stress may induce diabetes-related autoimmunity in infancy.
abstract: OBJECTIVE
  In retrospective studies, a number of disparate environmental factors (including experiences of serious life events) have been proposed as trigger mechanisms for type 1 diabetes or the autoimmune process behind the disease. Psychosocial stress in families may affect children negatively due to a link to hormonal levels and nervous signals that in turn influence both insulin sensitivity/insulin need and the immune system. Our aim was to investigate whether psychological stress, measured as psychosocial strain in families, is associated with diabetes-related autoimmunity during infancy.
  
  
  METHODS
  The first 4,400 consecutive 1-year-old children from a large prospective population-based project participated in the study. Parents completed questionnaires at birth and at 1 year, including various measures of psychosocial stress (e.g., parenting stress) and sociodemographic background. Blood samples drawn from the children at 1 year were analyzed for type 1 diabetes-associated autoantibodies toward tyrosine phosphatase and GAD. Antibodies toward tetanus toxoid were used as non-diabetes-related control antibodies.
  
  
  RESULTS
  Psychosocial factors, i.e., high parenting stress (odds ratio 1.8 [95% CI 1.2-2.9], P < 0.01), experiences of a serious life event (2.3 [1.3-4.0], P < 0.01), foreign origin of the mother (2.1 [1.3-3.3], P < 0.001), and low paternal education (1.6 [1.1-2.3], P < 0.01) were associated with diabetes-related autoimmunity in the child, independent of family history of diabetes.
  
  
  CONCLUSIONS
  Psychological stress, measured as psychosocial strain in the family, seems to be involved in the induction, or progression, of diabetes-related autoimmunity in the child during the 1st year of life.
authors.affiliation: Division of Paediatrics, Department of Molecular and Clinical Medicine, Linköping University, SE 581 85 Linköping, Sweden. anneli.sepa@imk.liu.se
authors.forename: Anneli
authors.initials: A
authors.lastname: Sepa
authors.forename: Jeanette
authors.initials: J
authors.lastname: Wahlberg
authors.forename: Outi
authors.initials: O
authors.lastname: Vaarala
authors.forename: Ann
authors.initials: A
authors.lastname: Frodi
authors.forename: Johnny
authors.initials: J
authors.lastname: Ludvigsson
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood; D015551:Autoimmunity / Q000502:physiology; D003922:Diabetes Mellitus, Type 1 / Q000453:epidemiology / Q000276:immunology / Q000523:psychology; D005192:Family Health; D005260:Female; D005968:Glutamate Decarboxylase / Q000276:immunology; D006801:Humans; D007223:Infant; D007515:Islets of Langerhans / Q000276:immunology; D008297:Male; D016487:Parenting / Q000523:psychology; D011446:Prospective Studies; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases / Q000276:immunology; D012307:Risk Factors; D013315:Stress, Psychological / Q000453:epidemiology* / Q000276:immunology*; D011795:Surveys and Questionnaires
chemical_list: D001323:Autoantibodies; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases; D005968:Glutamate Decarboxylase