Peanut allergy has been in the headlines recently in a major way, with widespread coverage about groundbreaking research that shows early introduction of peanut-containing foods to infants may help prevent peanut allergy. The recent annual meeting of the American Academy of Allergy, Asthma & Immunology also coincided with the release of promising, yet preliminary, results of studies that aim to prevent those with food allergies from experiencing potentially life-threatening reactions to peanut.
But scientists still don’t know for certain why some people develop peanut allergy and others do not. New findings recently published in the journal Nature Communications, however, suggest that genes may play a role in peanut allergy.
Led by Xiaobin Wang, MD, researchers at the Johns Hopkins Bloomberg School of Public Health in Baltimore identified a region in the human genome associated with peanut allergy in U.S. children.
“We always suspected it, but this is the first genome-wide association study (GWAS) that identified a genetic link to well-defined peanut allergy,” Wang said in a news release from the Bloomberg School of Public Health.
Other studies seeking to identify genetic risks have used skin prick or blood tests, which do not definitively diagnose a clinical food allergy. Announcing the results of the study, which was partially funded by FARE, the Bloomberg School of Public Health described the methodology and findings in its news release:
“In their study, Wang and her colleagues analyzed DNA samples from 2,759 participants (1,315 children and 1,444 of their biological parents) enrolled in the Chicago Food Allergy Study. Most of the children had some kind of food allergy. They scanned approximately 1 million genetic markers across the human genome, searching for clues to which genes might contribute to increased risk of developing food allergies, including peanut. They found that a genomic region harboring genes such as HLA-DQ and HLA-DR and located on chromosome six is linked to peanut allergy. This study suggests that the HLA-DR and -DQ gene region probably poses significant genetic risk for peanut allergy as it accounted for about 20 percent of peanut allergy in the study population.
Not everyone with these mutations, however, develops peanut allergy, and researchers wondered why. One possible reason, they determined, was that epigenetic changes may also play a role. Epigenetic changes, in which a methyl group attaches itself to the DNA, alter the expression of a gene without altering its underlying code. The levels of DNA methylation regulate whether people with genetic susceptibility to the peanut allergy actually developed it.”
Further exploration of these findings is needed, the authors noted. This research could potentially lead to new approaches in prevention and treatment of peanut allergy.
“Hopefully, one day, we can manage or prevent food allergies in a safe, simple, effective way,” Wang says. “We might be able to use pharmaceutical treatment, but if we can figure out whether a lifestyle, nutrition or environmental change could reduce allergies, that would be even better.”
This study was funded by the National Institute of Allergy and Infectious Diseases, FARE and the Bunning family and their family foundations.
“One in 13 children in the U.S. have food allergies, and peanut is the most common food allergen among children,” said James R. Baker, Jr., MD, CEO of FARE. “This important study adds critical insights that will help us understand the rise in the prevalence of peanut allergy, and we look forward to further exploration of these findings.”