Infants who are susceptible to diabetes and are first exposed to cereal before four months, or after six months of age, may have an increased risk of developing antibodies to islet cells - cells in the pancreas that produce insulin - a condition thought to precede the development of diabetes, according to two studies in the 1 October issue of The Journal of the American Medical Association (JAMA).
According to the first article, dietary exposures in infancy have been implicated, although not consistently, as a factor in type 1 diabetes mellitus (DM).
Jill M. Norris of the University of Colorado Health Sciences Center, Denver in the US, and colleagues examined the association between exposure to cereals in the infant diet and appearance of islet autoantibodies (IA) in a birth cohort of children at increased risk of type 1 DM, based on genotype and family history of DM. Islet autoantibodies are a type of antibodies associated with diabetes, and can be present for years prior to the diagnosis of type 1 DM.
The study included 1,183 children at increased risk of type 1 DM. The researchers obtained exposure and outcome measures on 76 per cent of enrolled children. The study was conducted from 1994 to 2002 with an average follow-up of four years.
After adjusting for covariates and confounders, the researchers found that compared with children who were exposed to cereal between ages 4 and 6 months - the recommended age - children exposed to any cereals before 4 months of age had a 4.32 times greater risk for IA, and those who were first exposed at 7 months or older had a 5.36 times increased risk for IA.
Gluten factor
In a related article in this week's JAMA, Anette-G. Ziegler, of the Diabetes Research Institute in Munich, Germany, and colleagues examined whether timing of exposures to breast milk, milk formula, solid foods, or gluten-containing foods is associated with an increased risk of developing antibodies to islet cells in children of parents with type 1 DM.
The autoimmunity that precedes type 1 DM can appear in the first years of life, suggesting that environmental agents encountered early in life, such as dietary factors, could be triggers of the disease process, according to the article.
The study followed 1,610 newborn children of parents with type 1 DM from 1989 to 2003 in inpatient/outpatient clinics in Germany. Blood samples were obtained at birth, age nine months, two, five, and eight years. Breastfeeding data were obtained by questionnaires and food supplementation data were obtained by family interview. Gluten-containing foods contain wheat, rye, barley, or oat, and include breads, biscuits, cakes, porridge, pasta, and flour products.
"Early introduction of gluten-containing foods was found to be a risk factor for the development of type 1 DM-associated autoantibodies in children of parents with type 1 DM," reported the authors. "Exposure to dietary gluten before age 3 months showed a five-fold higher risk for the development of islet autoantibodies than those who were exposed after age three months."
The researchers noted, however that islet autoantibody risk was not associated with reduced breastfeeding. Adding that these findings indicate that early introduction of gluten-containing foods should be avoided in children who are genetically predisposed to type 1 DM.
"The data suggest that the prevalence of islet autoimmunity could be reduced if all families complied with infant feeding guidelines and did not introduce gluten-containing and solid foods to infants until after age 3 months. A significant effect on type 1 DM incidence may be expected if the association also is found with type 1 DM risk and if it is found in children of parents without DM," concluded Ziegler.
Caution
However, in an accompanying editorial, Mark Atkinson of the University of Florida, Gainesville, and Edwin A.M. Gale of the University of Bristol, England, urged caution on the interpretation of these findings.
'Autoantibody positivity is used as the outcome measure, and, while this is a powerful predictive measure, the most critical outcome must be actual development of diabetes. A final concern with observational studies like these is the low number of end points-in this case islet autoimmunity with or without progression to diabetes,' they note.
'The reports do not present sufficient evidence to suggest that 'infant cereal causes diabetes', and hopefully will not be misinterpreted as such by parents and the public. Accordingly, given current knowledge, the current infant feeding guidelines should not be changed. In addition, further prospective cohorts must be examined to confirm and extend these findings,' they concluded.