TEDDY - The Environmental Determinants of Diabetes in the Young

This study is ongoing, but not recruiting participants.
Sponsor:
Collaborators:
Juvenile Diabetes Research Foundation
Information provided by (Responsible Party):
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
ClinicalTrials.gov Identifier:
NCT00279318
First received: January 17, 2006
Last updated: July 17, 2013
Last verified: July 2013

January 17, 2006
July 17, 2013
September 2004
September 2025   (final data collection date for primary outcome measure)
Appearance of one or more islet cell autoantibodies: GADA, IAA, or IA-2A confirmed at two consecutive visits. [ Time Frame: September 2025 ] [ Designated as safety issue: No ]
Not Provided
Complete list of historical versions of study NCT00279318 on ClinicalTrials.gov Archive Site
Development of T1DM [ Time Frame: September 2025 ] [ Designated as safety issue: No ]
Not Provided
Not Provided
Not Provided
 
TEDDY - The Environmental Determinants of Diabetes in the Young
Consortium for Identification of Environmental Triggers of Type 1 Diabetes

The long-term goal of the TEDDY study is the identification of infectious agents, dietary factors, or other environmental agents, including psychosocial factors which trigger T1DM in genetically susceptible individuals or which protect against the disease. Identification of such factors will lead to a better understanding of disease pathogenesis and result in new strategies to prevent, delay or reverse T1DM.

Epidemiologic patterns suggest that viruses, nutrition, toxic agents or socioeconomic psychosocial factors may contribute to the etiology alone or in combination. Elucidation is confounded by the long interval between exposure and onset of clinical disease, as well as the interaction of multiple genes and/or insults, which appear to interact in a complex manner. Numerous studies have investigated environmental influences but have yielded conflicting results. This may be in part due to the failure to account for genetic susceptibility, begin observation at early ages or in utero, and/or monitor subjects long term and frequently.

Hypotheses:

  1. Initiation of persistent beta-cell autoimmunity and progression from beta-cell autoimmunity to diabetes is increased with:

    1. Exposure to a trigger factor during pregnancy, such as infections, preeclampsia, blood incompatibility, or birth weight.
    2. Differences in the timing of the introduction and/or the type of dietary constituents that include exposure to cereals or gluten, exposure to cow's milk during infancy and/or childhood, and short duration of breast- feeding;
    3. Lower intake of serum 25 hydroxyvitamin D in early infancy, vitamin E, anti-oxidants (e.g., carotenoids, ascorbic acid, selenium, or omega-3 fatty acids);
    4. Higher frequency of specific (e.g., enterovirus, rotavirus, or bacterial) infections, or non-specific childhood infections including those that exhibit molecular mimicry;
    5. Increased exposure to routine childhood immunizations and their timing;
    6. Environmental factors that may be contained in drinking water (e.g., low concentrations of zinc or high concentrations of nitrates, or lower pH levels);
    7. Exposure to household pets, and various allergies;
    8. Excessive weight gain;
    9. Increased psychological stress.
  2. The risk of persistent beta-cell autoimmunity is lower in children from the general population than in offspring or siblings of T1DM patients when stratifying for the HLA DR-DQ genotype and exposure to environmental triggers.
  3. The interaction of HLA DR-DQ genotype with exposure to dietary or infectious factors leads to increased incidence of beta-cell autoimmunity and T1DM.
  4. We expect that in some families study participation will be associated with affective (anxiety, depression) and behavioral responses (e.g. actions to prevent possible T1DM).
Observational
Observational Model: Cohort
Time Perspective: Prospective
Not Provided
Retention:   Samples With DNA
Description:

Serum, plasma, PBMCs, stool, urine, saliva, nasal swabs, nail clippings, water

Non-Probability Sample

Childen up to 4 months of age with specified HLA are enrolled and followed longitudnally until 15 years of age

Type 1 Diabetes Mellitus
Not Provided
General Population, First Degree Relative
Newborns with high risk HLA in the general population or having a first-degree relative affected with T1DM.
Hagopian WA, Erlich H, Lernmark A, Rewers M, Ziegler AG, Simell O, Akolkar B, Vogt R Jr, Blair A, Ilonen J, Krischer J, She J; TEDDY Study Group. The Environmental Determinants of Diabetes in the Young (TEDDY): genetic criteria and international diabetes risk screening of 421 000 infants. Pediatr Diabetes. 2011 Dec;12(8):733-43. doi: 10.1111/j.1399-5448.2011.00774.x. Epub 2011 May 12.

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Active, not recruiting
8668
September 2025
September 2025   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Newborns with high risk HLA in the general population or having a first- degree relative affected with T1DM
  • Newborns are less than 4 months of age

Exclusion Criteria:

  • Have an illness or birth defect that precludes long-term follow-up or involves use of treatment that may alter the natural history of diabetes (e.g. steroids or insulin)
  • Refuses to have blood and stool samples stored at the NIDDK Repository
Both
up to 4 Months
Yes
Contact information is only displayed when the study is recruiting subjects
United States,   Finland,   Germany,   Sweden
 
NCT00279318
DK63790, 5U01DK063790-04
Yes
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
  • National Institute of Allergy and Infectious Diseases (NIAID)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)
  • National Institute of Environmental Health Sciences (NIEHS)
  • Juvenile Diabetes Research Foundation
  • Centers for Disease Control and Prevention
Principal Investigator: Jeffrey P. Krischer, PhD University of South Florida
Principal Investigator: Marian J. Rewers, MD, PhD University of Colorado Health Science Center
Principal Investigator: William A. Hagopian, MD, PhD Pacific Northwest Diabetes Research Institute
Principal Investigator: Ake Lernmark, MD, PhD Lund University
Principal Investigator: Olli G. Simell, MD, PhD University of Turku
Principal Investigator: Jin-Xiong She, PhD Georgia Regents University
Principal Investigator: Anette G. Ziegler, MD University of Miami
Principal Investigator: Beena Akolkar, PhD National Institutes of Diabetes and Digestive Kidney Diseases
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
July 2013

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP