Babies who are first exposed to solid food before the age of 4 months or at age 6 months or older are significantly more likely to develop type 1 diabetes mellitus than those with a first exposure at 4-5 months of age, findings from a longitudinal observational study have shown.
Of 1,835 children at increased genetic risk for type 1 diabetes mellitus (T1DM) who were included in the Diabetes Autoimmunity Study in the Young (DAISY), 53 developed the disease during follow-up. After adjustment for the human leukocyte antigen (HLA)-DR genotype, a first-degree relative with T1DM, maternal education, and delivery type, both the early and late first solid food exposures significantly predicted T1DM development (adjusted hazard ratios, 1.91 and 3.02, respectively), Brittni Frederiksen of the University of Colorado, Aurora, and her colleagues reported online on July 8 in JAMA Pediatrics.
Specifically, babies with early exposure to fruit and those with late exposure to rice/oat (non–gluten-containing foods) were at increased risk of T1DM development (HR, 2.23 and 2.88, respectively), the investigators found (JAMA Pediatr. July [doi:10.1001/jamapediatrics.2013.317]).
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Infants with a first exposure to solid food at 4-5 months of age may have a lower risk of developing diabetes than those who are exposed earlier or later.
Of note, babies who were still breastfeeding at the time of introduction to wheat/barley (gluten-containing food) had a significantly reduced risk of T1DM development (HR, 0.47), suggesting that breastfeeding confers some protection against the disease, they said.
The timing of the introduction of vegetables and meat did not predict T1DM in the DAISY cohort.
DAISY participants included two groups of children at increased genetic risk for developing T1DM – a group found to have diabetes-susceptibility alleles in the HLA region on cord blood screening, and a group of unaffected children with a first-degree relative with T1DM. Children included in the current analysis were those followed from birth, who completed clinic visits at 9, 15, and 24 months, and annually thereafter.
The findings, which support those from an earlier DAISY report demonstrating "a window of time for introduction of cereals, 4-6 months, outside of which the risk for development of islet autoimmunity (preclinical T1DM) increased." are important given the increasing worldwide incidence of T1DM. That increase is most rapid among children younger than age 5 years, the investigators noted.
As for the mechanisms of associations between early and late food exposures and T1DM development, the risk predicted by early exposure "might suggest a mechanism involving an abnormal immune response to solid food antigens in an immature gut immune system in susceptible individuals," and the increased risk predicted by late exposures "may be related to the larger amounts given at initial exposure to older children," the investigators said.
Also, the late introduction of solid foods, when breast milk no longer meets energy and nutrient needs, could lead to nutrient deficiencies that could increase T1DM risk. Similarly, late solid food exposures may be related to the cessation of breastfeeding before solid food introduction, resulting in the loss of the protective effects of breast milk in that setting, they suggested.
Although the findings require confirmation in a larger cohort, they provide some guidance for the introduction of solid foods.
"While much of the focus of infant diet and T1DM research has been on the timing of the introduction of a single antigen (i.e., milk or gluten), our data suggest multiple foods/antigens play a role and that there is a complex relationship between the timing and type of infant food exposures and T1DM risk. In summary, there appears to be a safe window in which to introduce solid foods between 4 and 5 months of age; solid foods should be introduced while continuing to breastfeed to minimize T1DM risk in genetically susceptible children," the investigators concluded.
This study was supported by a National Institutes of Health grant and a Diabetes Endocrine Research Center Clinical Investigation and Bioinformatics Core grant. The authors reported having no relevant financial disclosures.