New Study Pinpoints the Genetic Roots of Common Food Allergies

Researchers have taken a major step forward in understanding the biological roots of food allergies, whose incidence has skyrocketed over the last few decades. In a large new study published in the Journal of Allergy and Clinical Immunology (JACI), researchers identified 37 genetic “clues”—known as risk variants—that may determine whether a person is likely to develop an allergy to certain foods. Although food allergies are known to be immune-mediated reactions often triggered by immunoglobulin E (IgE), the exact “genetic architecture of food allergy” remains incompletely understood, making this new data a vital piece of the puzzle.

To uncover these links, an international team conducted a genome-wide association meta-analysis, essentially a deep dive into the DNA of a large group of people. The study included data from over 229,000 adults and 14,000 children across 16 groups of European ancestry. By examining such a large population, researchers were able to overcome the “modest sample sizes and inconsistent definitions” that have limited similar studies in the past, providing a much clearer picture of how our genes influence our immune responses.

One of the most significant breakthroughs was the discovery of two specific genetic variants in adults that reached a high level of statistical significance. The first, a variant called rs116936231 located in the FGL1 gene, was strongly linked to cases in which a patient had both a doctor-diagnosed food allergy and a confirmed sensitivity on blood tests. Interestingly, this association remained strong even after the researchers accounted for other factors such as hay fever, suggesting this gene plays a unique and specific role in how the body reacts to food.

A second major finding involved a region of DNA known as AKAP6–NPAS3. A variant in this region, rs8022829, also showed a strong association with food allergy risk, particularly after adjustment for other allergic conditions. Beyond these new discoveries, the study confirmed three previously known genetic markers shared between food allergies and other “atopic” or allergic diseases, “reinforcing shared genetic pathways” that link food allergies to conditions such as eczema and asthma.

The researchers also highlighted a tricky aspect of allergy science: how we define an allergy shapes what we find in our DNA. The study showed that the genetic signals shifted depending on whether they were looking at self-reported allergies, doctor-diagnosed cases, or blood test results. This “demonstrated genetic differences across food allergy phenotypes,” proving that the way doctors and patients describe these conditions can influence the genetic associations scientists observe in the lab.

Because of these variations, the team emphasized that the medical community needs to get on the same page. The findings “underscored the need for harmonized diagnostic criteria” in future research. If scientists worldwide use the same standards to define what counts as a food allergy, they will be much more successful in pinpointing the exact genes responsible for the condition across different populations and age groups.

Looking ahead, this research paves the way for a future in which a simple genetic test could help predict a child’s risk of developing a life-threatening allergy before they take their first bite of peanut butter. The authors concluded that “larger, multi-ethnic studies using consistent, gold-standard phenotyping” will be the next essential step. By expanding this research, scientists hope to turn these genetic clues into “risk prediction tools and targeted prevention strategies” that can protect patients and improve lives.