title: Intake of antioxidant vitamins and trace elements during pregnancy and risk of advanced beta cell autoimmunity in the child.
abstract: BACKGROUND
  Type 1 diabetes may have its origins in the fetal period of life. Free radicals were implicated in the cause of type 1 diabetes. It was hypothesized that antioxidant nutrients could protect against type 1 diabetes.
  
  
  OBJECTIVE
  We assessed whether high maternal intake of selected dietary antioxidants during pregnancy is associated with a reduced risk of advanced beta cell autoimmunity in the child, defined as repeated positivity for islet cell antibodies plus >/=1 other antibody, overt type 1 diabetes, or both.
  
  
  METHODS
  The study was carried out as part of the population-based birth cohort of the Type 1 Diabetes Prediction and Prevention Project. The data comprised 4297 children with increased genetic susceptibility to type 1 diabetes, born at the University Hospital of Oulu or Tampere, Finland, between October 1997 and December 2002. The children were monitored for diabetes-associated autoantibodies from samples obtained at 3-12-mo intervals. Maternal antioxidant intake during pregnancy was assessed postnatally with a self-administered food-frequency questionnaire, which contained a question about consumption of dietary supplements.
  
  
  RESULTS
  Maternal intake of none of the studied antioxidant nutrients showed association with the risk of advanced beta cell autoimmunity in the child. The hazard ratios, indicating the change in risk per a 2-fold increase in the intake of each antioxidant, were nonsignificant and close to 1.
  
  
  CONCLUSIONS
  High maternal intake of retinol, beta-carotene, vitamin C, vitamin E, selenium, zinc, or manganese does not protect the child from development of advanced beta cell autoimmunity in early childhood.
authors.affiliation: Tampere School of Public Health, University of Tampere, Tampere, Finland.
authors.forename: Liisa
authors.initials: L
authors.lastname: Uusitalo
authors.forename: Mike G
authors.initials: MG
authors.lastname: Kenward
authors.forename: Suvi M
authors.initials: SM
authors.lastname: Virtanen
authors.forename: Ulla
authors.initials: U
authors.lastname: Uusitalo
authors.forename: Jaakko
authors.initials: J
authors.lastname: Nevalainen
authors.forename: Sari
authors.initials: S
authors.lastname: Niinistö
authors.forename: Carina
authors.initials: C
authors.lastname: Kronberg-Kippilä
authors.forename: Marja-Leena
authors.initials: ML
authors.lastname: Ovaskainen
authors.forename: Liisa
authors.initials: L
authors.lastname: Marjamäki
authors.forename: Olli
authors.initials: O
authors.lastname: Simell
authors.forename: Jorma
authors.initials: J
authors.lastname: Ilonen
authors.forename: Riitta
authors.initials: R
authors.lastname: Veijola
authors.forename: Mikael
authors.initials: M
authors.lastname: Knip
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000008:administration & dosage* / Q000378:metabolism; D001323:Autoantibodies / Q000097:blood; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D003922:Diabetes Mellitus, Type 1 / Q000453:epidemiology / Q000235:genetics / Q000517:prevention & control; D005260:Female; D005387:Finland / Q000453:epidemiology; D020022:Genetic Predisposition to Disease; D006683:HLA-DQ Antigens / Q000235:genetics; D059866:HLA-DQ beta-Chains; D006801:Humans; D007223:Infant; D007515:Islets of Langerhans / Q000276:immunology; D039382:Maternal Nutritional Physiological Phenomena / Q000502:physiology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D039401:Prenatal Nutritional Physiological Phenomena / Q000502:physiology*; D011446:Prospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D014131:Trace Elements / Q000008:administration & dosage* / Q000097:blood; D014815:Vitamins / Q000008:administration & dosage* / Q000097:blood
chemical_list: D000975:Antioxidants; D001323:Autoantibodies; D006683:HLA-DQ Antigens; D059866:HLA-DQ beta-Chains; C069051:HLA-DQB1 antigen; D014131:Trace Elements; D014815:Vitamins; C024211:islet cell antibody