Exposures to certain foods in the infant diet have been implicated in destruction of insulin-producing pancreatic cells, leading to type 1 diabetes. Autoantibodies to islet cells is also known as islet autoimmunity (IA). Studies have shown conflicting results in identifying cow's milk as a cause of IA. Similarly, in only some studies has early introduction of solid foods been associated with the development of type 1 diabetes. Exposure to cereals before six months of age was not associated with IA in children with a family history of type 1 diabetes in one study. Norris and colleagues examined the association between exposure to cow's milk and cereals in infant diets and the appearance of islet autoantibodies.
In the Diabetes Autoimmunity Study in the Young, high-risk and moderate-risk infants were identified by screening cord blood for diabetes susceptibility alleles. Further participants were recruited through a diabetes registry and newspaper publicity. The study population consisted of 841 HLA-screened children without a family history of type 1 diabetes and 342 children with a first-degree relative with type 1 diabetes. Children were tested for antibodies to pancreatic islet antigens at months 9, 15, and 24, and then annually, from birth to nine years of age. Dietary data were collected for the study cohort.
In the full cohort of 1,183 children, 85 percent were breastfed. Children who remained autoantibody positive on two or more consecutive visits were more likely than unaffected children to be non-Hispanic white and positive for specific HLA genotypes, and to have a first-degree relative with type 1 diabetes. The authors found that children first exposed to any cereals before four months or after six months of age were at increased risk of IA compared with those first exposed between four and six months. This association held whether or not there was any family history of type 1 diabetes. Neither cow's milk exposure at any age nor breastfeeding duration was associated with increased risk of IA.
The study data suggest that introducing cereals before four months of age may increase a child's risk of developing IA. However, waiting until seven months of age also seems to increase this risk. Early risk may suggest a mechanism involving an aberrant immune response to cereal antigens in an immature gut. Late exposure may be related to the quantity and frequency with which cereal is consumed at first exposure in older children. These results are valid for children at higher risk for type 1 diabetes but also may apply to the general population. Current recommendations for the timing of cereal introduction need not be changed from the four to six months of age that is generally recommended in this country.