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
  Purpose

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.


Condition
Type 1 Diabetes Mellitus

Study Type: Observational
Study Design: Observational Model: Cohort
Time Perspective: Prospective
Official Title: Consortium for Identification of Environmental Triggers of Type 1 Diabetes

Resource links provided by NLM:


Further study details as provided by National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK):

Primary Outcome Measures:
  • 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 ]

Secondary Outcome Measures:
  • Development of T1DM [ Time Frame: September 2025 ] [ Designated as safety issue: No ]

Biospecimen Retention:   Samples With DNA

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


Enrollment: 8668
Study Start Date: September 2004
Estimated Study Completion Date: September 2025
Estimated Primary Completion Date: September 2025 (Final data collection date for primary outcome measure)
Groups/Cohorts
General Population, First Degree Relative
Newborns with high risk HLA in the general population or having a first-degree relative affected with T1DM.

Detailed Description:

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).
  Eligibility

Ages Eligible for Study:   up to 4 Months
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   Yes
Sampling Method:   Non-Probability Sample
Study Population

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

Criteria

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
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT00279318

Locations
United States, Colorado
University of Colorado Health Sciences Center
Denver, Colorado, United States, 80262
United States, Florida
Georgia Regents University
Gainesville, Florida, United States, 32608
United States, Georgia
Georgia Regents University
Atlanta, Georgia, United States, 30342
Georgia Regents University
Augusta, Georgia, United States, 30912
United States, Pennsylvania
Children's Hospital of Pittsburgh of UPMC (this site is only screening babies whose mother, father or full sibiling have type 1 diabetes)
Pittsburgh, Pennsylvania, United States, 15213
United States, Washington
Pacific Northwest Diabetes Research Institute
Seattle, Washington, United States, 98122
Finland
Turku University Central Hospital
Turku, Finland, 20520
Germany
Diabetes Research Institute
Munich, Germany, 80804
Sweden
Lund University
Malmo, Sweden, 20502
Sponsors and Collaborators
Juvenile Diabetes Research Foundation
Investigators
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
  More Information

Additional Information:
No publications provided by National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

Additional publications automatically indexed to this study by ClinicalTrials.gov Identifier (NCT Number):
Responsible Party: National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
ClinicalTrials.gov Identifier: NCT00279318     History of Changes
Other Study ID Numbers: DK63790, 5U01DK063790-04
Study First Received: January 17, 2006
Last Updated: July 17, 2013
Health Authority: United States: Federal Government
United States: Institutional Review Board

Keywords provided by National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK):
Environment
Exposures
Diet
Toxins
Psychosocial
Infectious Agents
Bacterial
Viral
Immunizations
Autoantibody

Additional relevant MeSH terms:
Diabetes Mellitus
Diabetes Mellitus, Type 1
Glucose Metabolism Disorders
Metabolic Diseases
Endocrine System Diseases
Autoimmune Diseases
Immune System Diseases

ClinicalTrials.gov processed this record on August 28, 2014