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Completed Not applicable Interventional

Nutritional Intervention to Prevent Diabetes

ClinicalTrials.gov ID: NCT00333554

Public ClinicalTrials.gov record NCT00333554. Field values are reproduced from the official study page; the official ClinicalTrials.gov record remains the source of truth for eligibility, enrollment, and contact information.

ClinicalTrials.gov public records Last synced Sep 8, 2026, 9:11 PM EDT

Data is sourced from official ClinicalTrials.gov public API records. Always review the official ClinicalTrials.gov record for the latest information.

Brief summary

Reproduced verbatim from the official ClinicalTrials.gov record. Not medical advice.

Type 1 Diabetes (T1D) is an autoimmune disease. This means that the immune system (the part of the body which helps fight infections) mistakenly attacks and destroys the cells that produce insulin (islet cells found in the pancreas). As these cells are destroyed, the body's ability to produce insulin decreases. The autoimmune process is thought to be initiated by a gene-environment interaction. The genetics involved in the development of T1D are fairly well understood. There is a higher risk of developing T1D with the presence of the human leukocyte antigen (HLA) DR3 or DR4. It is also known that not everyone with these genes actually develops T1D. Therefore, one or more environmental factors are thought to contribute to the process of developing T1D. The consumption of the anti-inflammatory fatty acids, the omega-3 fatty acids, has decreased significantly in the past 100 years. At the same time a rise in the incidence of T1D, especially in young children has occurred. Because of the warnings to eliminate fish during pregnancy, pregnant women are consuming even less omega-3 fatty acids during fetal development. Observations have been made that children who have received omega-3 fatty acid supplementation have a lower risk of T1D. Omega-3 fatty acids could have a protective effect that may occur during pregnancy, infancy, or both. The mechanism of this protection may be due to the DHA mediated suppression of the inflammatory response. Patients at higher risk for T1D have an increased pro-inflammatory environment. We hypothesize that DHA supplementation during pregnancy and early childhood will block the initial pro-inflammatory events and prevent development of islet cell autoimmunity in children at higher risk for T1D. This study is a feasibility study to determine if a full-scale DHA supplementation study will be implemented. If a full study is implemented, the primary outcome will be to determine if nutritional supplementation with omega-3 fatty acids during the last trimester of a mother's pregnancy and/or the first three years of life for children who are at higher risk of T1D will prevent the development of islet autoimmunity.

Study identification

NCT ID
NCT00333554
Recruitment status
Completed
Study type
Interventional
Phase
Not applicable
Enrollment
99 participants

Conditions and interventions

Interventions

Dietary Supplement

Eligibility (public fields only)

Age range
Up to 5 Months
Sex
All
Healthy volunteers
Healthy volunteers not accepted

This page does not interpret eligibility. Detailed inclusion and exclusion criteria are on the official ClinicalTrials.gov record.

Study timeline

Start date
May 31, 2006
Primary completion
Jan 31, 2008
Completion
Mar 31, 2013
Last update posted
Apr 28, 2020

2006 – 2013

United States locations

U.S. sites
9
U.S. states
7
U.S. cities
9
Facility City State ZIP Site status
Childrens Hospital of Los Angeles Los Angeles California 90027
Children's Hospital of Orange County Orange California 92868-3835
University of California, San Francisco San Francisco California 94143
Indiana University-Riley Hospital for Children Indianapolis Indiana 46202
University of Iowa Health Care Iowa City Iowa 52242
Joslin Diabetes Center Boston Massachusetts 02215
University of Minnesota Minneapolis Minnesota 55455
The Children's Mercy Hospital Kansas City Missouri 64108-9898
Utah Diabetes Center Salt Lake City Utah 84108

Site contact phone numbers, emails, and investigator names are intentionally not displayed here. Open the official ClinicalTrials.gov record for site contact information.

About this trial record page

What this page shows
Public field values for ClinicalTrials.gov record NCT00333554, including study identification, conditions, interventions, eligibility (age, sex, healthy volunteer), timeline, and U.S. site list.
What this page does not do
No medical advice, eligibility judgments, treatment recommendations, study quality scoring, or AI-generated medical summaries. No site contact phone numbers, emails, or investigator names.
Where the data comes from
Sourced from the official ClinicalTrials.gov public API. The official record is the source of truth.
Last refresh
Last update posted Apr 28, 2020 · Synced Sep 8, 2026

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The complete protocol, eligibility criteria, and contact information for NCT00333554 live on ClinicalTrials.gov.

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