Dietary factors modifying type 1 diabetes mellitus (DM) risk have been
proposed, but little is known if they trigger the islet autoimmunity that
precedes clinical disease.
To determine whether breastfeeding duration, food supplementation, or
age at introduction of gluten-containing foods influences the risk of developing
Design and Setting
Prospective natural history cohort study conducted from 1989 to 2003
in inpatient/outpatient clinics in Germany.
The BABYDIAB study follows newborn children of parents with type 1 DM.
Eligibility requirements were met in 1610 children. Blood samples were obtained
at birth, age 9 months, 2, 5, and 8 years. Dropout rate was 14.4% by age 5
years. Breastfeeding data were obtained by prospective questionnaires (91%
complete), and food supplementation data were obtained by family interview
(72% for food supplementation and 80% for age of gluten introduction).
Main Outcome Measure
Development of islet autoantibodies (insulin, glutamic acid decarboxylase,
or IA-2 antibodies) in 2 consecutive blood samples.
Life-table islet autoantibody frequency was 5.8% (SE, 0.6%) by age 5
years. Reduced total or exclusive breastfeeding duration did not significantly
increase the risk of developing islet autoantibodies. Food supplementation
with gluten-containing foods before age 3 months, however, was associated
with significantly increased islet autoantibody risk (adjusted hazard ratio,
4.0; 95% confidence interval, 1.4-11.5; P = .01 vs
children who received only breast milk until age 3 months). Four of 17 children
who received gluten foods before age 3 months developed islet autoantibodies
(life-table 5-year risk, 24%; SE, 10%). All 4 children had the high-risk DRB1*03/04,DQB1*0302
genotype. Early exposure to gluten did not significantly increase the risk
of developing celiac disease–associated autoantibodies. Children who
first received gluten foods after age 6 months did not have increased risks
for islet or celiac disease autoantibodies.
Ensuring compliance to infant feeding guidelines is a possible way to
reduce the risk of development of type 1 DM autoantibodies.