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Timing of initial cereal exposure in infancy and risk of islet autoimmunity.

Abstract

CONTEXT

Dietary exposures in infancy have been implicated, albeit inconsistently, in the etiology of type 1 diabetes mellitus (DM).

OBJECTIVE

To examine the association between cereal exposures in the infant diet and appearance of islet autoimmunity (IA).

DESIGN

Birth cohort study conducted from 1994 to 2002 with a mean follow-up of 4 years.

SETTING

Newborn screening for HLA was done at St Joseph's Hospital in Denver, Colo. First-degree relatives of type 1 DM individuals were recruited from the Denver metropolitan area.

PARTICIPANTS

We enrolled 1183 children at increased type 1 DM risk, defined as either HLA genotype or having a first-degree relative with type 1 DM, at birth and followed them prospectively. We obtained exposure and outcome measures for 76% of enrolled children. Participants had variable lengths of follow-up (9 months to 9 years).

MAIN OUTCOME MEASURES

Blood draws for the detection of insulin autoantibody, glutamic acid decarboxylase autoantibody, or IA-2 autoantibody were performed at 9, 15, and 24 months and annually thereafter. Children with IA (n = 34) were defined as those testing positive for at least 1 of the autoantibodies on 2 or more consecutive visits and who tested positive or had diabetes on their most recent visit.

RESULTS

Children initially exposed to cereals between ages 0 and 3 months (hazard ratio [HR], 4.32; 95% confidence interval [CI], 2.0-9.35) and those who were exposed at 7 months or older (HR, 5.36; 95% CI, 2.08-13.8) had increased hazard of IA compared with those who were exposed during the fourth through sixth month, after adjustment for HLA genotype, family history of type 1 DM, ethnicity, and maternal age. In children who were positive for the HLA-DRB1*03/04,DQB8 genotype, adjusted HRs were 5.55 (95% CI, 1.92-16.03) and 12.53 (95% CI, 3.19-49.23) for initial cereal exposure between ages 0 to 3 months and at 7 months or older, respectively.

CONCLUSION

There may be a window of exposure to cereals in infancy outside which initial exposure increases IA risk in susceptible children.

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  • Authors+Show Affiliations

    ,

    Department of Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver 80262, USA. jill.norris@uchsc.edu

    , , , , ,

    Source

    JAMA 290:13 2003 Oct 01 pg 1713-20

    MeSH

    Animals
    Autoantibodies
    Autoimmunity
    Child
    Child, Preschool
    Cohort Studies
    Diabetes Mellitus, Type 1
    Edible Grain
    Genetic Predisposition to Disease
    Genotype
    Glutamate Decarboxylase
    HLA-DR Antigens
    HLA-DRB1 Chains
    Humans
    Infant
    Infant Food
    Infant Nutritional Physiological Phenomena
    Infant, Newborn
    Insulin Antibodies
    Islets of Langerhans
    Milk
    Proportional Hazards Models
    Risk Factors
    Time Factors

    Pub Type(s)

    Journal Article
    Research Support, U.S. Gov't, P.H.S.

    Language

    eng

    PubMed ID

    14519705

    Citation

    Norris, Jill M., et al. "Timing of Initial Cereal Exposure in Infancy and Risk of Islet Autoimmunity." JAMA, vol. 290, no. 13, 2003, pp. 1713-20.
    Norris JM, Barriga K, Klingensmith G, et al. Timing of initial cereal exposure in infancy and risk of islet autoimmunity. JAMA. 2003;290(13):1713-20.
    Norris, J. M., Barriga, K., Klingensmith, G., Hoffman, M., Eisenbarth, G. S., Erlich, H. A., & Rewers, M. (2003). Timing of initial cereal exposure in infancy and risk of islet autoimmunity. JAMA, 290(13), pp. 1713-20.
    Norris JM, et al. Timing of Initial Cereal Exposure in Infancy and Risk of Islet Autoimmunity. JAMA. 2003 Oct 1;290(13):1713-20. PubMed PMID: 14519705.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Timing of initial cereal exposure in infancy and risk of islet autoimmunity. AU - Norris,Jill M, AU - Barriga,Katherine, AU - Klingensmith,Georgeanna, AU - Hoffman,Michelle, AU - Eisenbarth,George S, AU - Erlich,Henry A, AU - Rewers,Marian, PY - 2003/10/2/pubmed PY - 2003/10/8/medline PY - 2003/10/2/entrez SP - 1713 EP - 20 JF - JAMA JO - JAMA VL - 290 IS - 13 N2 - CONTEXT: Dietary exposures in infancy have been implicated, albeit inconsistently, in the etiology of type 1 diabetes mellitus (DM). OBJECTIVE: To examine the association between cereal exposures in the infant diet and appearance of islet autoimmunity (IA). DESIGN: Birth cohort study conducted from 1994 to 2002 with a mean follow-up of 4 years. SETTING: Newborn screening for HLA was done at St Joseph's Hospital in Denver, Colo. First-degree relatives of type 1 DM individuals were recruited from the Denver metropolitan area. PARTICIPANTS: We enrolled 1183 children at increased type 1 DM risk, defined as either HLA genotype or having a first-degree relative with type 1 DM, at birth and followed them prospectively. We obtained exposure and outcome measures for 76% of enrolled children. Participants had variable lengths of follow-up (9 months to 9 years). MAIN OUTCOME MEASURES: Blood draws for the detection of insulin autoantibody, glutamic acid decarboxylase autoantibody, or IA-2 autoantibody were performed at 9, 15, and 24 months and annually thereafter. Children with IA (n = 34) were defined as those testing positive for at least 1 of the autoantibodies on 2 or more consecutive visits and who tested positive or had diabetes on their most recent visit. RESULTS: Children initially exposed to cereals between ages 0 and 3 months (hazard ratio [HR], 4.32; 95% confidence interval [CI], 2.0-9.35) and those who were exposed at 7 months or older (HR, 5.36; 95% CI, 2.08-13.8) had increased hazard of IA compared with those who were exposed during the fourth through sixth month, after adjustment for HLA genotype, family history of type 1 DM, ethnicity, and maternal age. In children who were positive for the HLA-DRB1*03/04,DQB8 genotype, adjusted HRs were 5.55 (95% CI, 1.92-16.03) and 12.53 (95% CI, 3.19-49.23) for initial cereal exposure between ages 0 to 3 months and at 7 months or older, respectively. CONCLUSION: There may be a window of exposure to cereals in infancy outside which initial exposure increases IA risk in susceptible children. SN - 1538-3598 UR - https://www.unboundmedicine.com/medline/citation/14519705/full_citation L2 - https://jamanetwork.com/journals/jama/fullarticle/vol/290/pg/1713 DB - PRIME DP - Unbound Medicine ER -