Abstract

ContextVitamin D has several effects on the immune system that might be of relevance for the pathogenesis of type 1 diabetes (T1D).ObjectiveTo evaluate whether umbilical cord serum concentrations of 25-hydroxy-vitamin D (25[OH]D) differ in children developing either islet autoimmunity (IA) or overt T1D during childhood and adolescence.DesignUmbilical cord serum samples from 764 children born from 1994 to 2004 with HLA-DQB1 conferred risk for T1D participating in the Type 1 Diabetes Prediction and Prevention Study were analyzed for 25(OH)D using an enzyme immunoassay.SettingDIPP clinics in Turku, Oulu, and Tampere University Hospitals, Finland.ParticipantsTwo hundred fifty children who developed T1D diabetes at a median age of 6.7 years (interquartile range [IQR] 4.0 to 10.1 years) and 132 additional case children who developed IA, i.e., positivity for multiple islet autoantibodies. Cases were matched for date of birth, gender, and area of birth with 382 control children who remained autoantibody negative. The median duration of follow up was 9.8 years (IQR 5.7 to 13.1 years).Main Outcome MeasureThe median 25(OH)D concentrations.ResultsThe median 25(OH)D concentration in cord serum was low [31.1 nmol/L (IQR 24.0 to 41.8); 88% <50 nmol/L], but not statistically different between children who developed T1D or IA and their control groups (P = 0.70). The levels were associated mainly with geographical location, year and month of birth, age of the mother, and maternal intake of vitamin D during pregnancy.ConclusionsThe 25(OH)D concentrations at birth are not associated with the development of T1D during childhood.

Highlights

  • Context: Vitamin D has several effects on the immune system that might be of relevance for the pathogenesis of type 1 diabetes (T1D)

  • We noticed an increase in 25hydroxyvitamin D (25[OH]D) concentrations in Finnish children after year 2003, when vitamin D fortification of milk started in Finland, which preceded the plateauing of the rapid increase in type 1 diabetes (T1D) incidence that had continued for more than 50 years [1]

  • We found no difference in median 25(OH)D concentration between children who developed T1D and healthy matched control children when the children were observed from the age of three months until the diagnosis of T1D [2]

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Summary

Methods

The study population comprised children (born between 1994 and 2004), who participated in DIPP in Finland. The children attend the study centers for follow-up visits at 3- to 12-month intervals and their serum samples are analyzed for T1D-related autoantibodies. If a child seroconverted to positivity for ICA, all the preceding and subsequent samples of this child were analyzed for insulin autoantibodies (IAA), antibodies to the 65 kDa isoform of glutamic acid decarboxylase (GADA), and to the tyrosine phosphatase-related islet antigen 2 (IA-2A). Data from the autoantibody-negative children participating in the follow-up were collected until they were 15 years of age or until the end point of this study (July 2016). Data from the autoantibodypositive children were collected until the follow-up for this study ended or until they were diagnosed with T1D according to the World Health Organization criteria, whichever came first

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