Our understanding of the relationship between genetics and food allergies is continually evolving. Information on genetic research and its practical implications for the diagnosis and management of food allergies is provided by featured expert Edwin Kim, MD, MS.

At a big-picture level, we know that there is a genetic predisposition to becoming allergic or atopic. And we typically tell our pediatric patients that, if they have 1 parent who has an atopic allergic disease, then their chance of being allergic is approximately 50% to 60%. And if both parents have atopic disease, that number jumps even higher.

Again, we understand this on a big-picture level, but for specific allergic diseases such as allergic rhinitis or peanut allergies, I think that a patient’s genetic predisposition is less clear. When talking to my patients, I emphasize that this predisposition is clearly not 100% guaranteed. There are plenty of examples of 2 very allergic parents having nonallergic children and 2 seemingly nonallergic parents having allergic children. We also understand that it is not only genetics that plays a role but there is likely a strong and probably critically timed environmental component as well.

Patients who have allergic disease in early childhood often go through a sequence of allergic diseases starting with atopic dermatitis, with many of them then going on to develop food allergies followed by, ultimately, allergic rhinitis and asthma. Atopic dermatitis is thought to be the first step toward that allergic march process in a lot of cases. The FLG mutation was identified and investigated to see if it could predict some of the children who would have this sequence of diseases, also opening the door for identifying potential therapies that could specifically target this to try to reverse the skin barrier defects that the FLG mutation caused and somehow prevent these allergic diseases.

While FLG is the best-known genetic marker, researchers have been very interested in looking for other types of genetic markers that are similar to FLG. There are some candidate genes that are under consideration, and studies are starting to target some of these as well. Many of these genes are thought to be involved in the allergic inflammatory pathway.

There are 2 places where I see genetics as probably being most important and useful. The first is with regard to determining whether any of these genetic markers could potentially tell us if a patient is more likely to become allergic, as it does seem that early intervention with therapies such as oral immunotherapy and others can work better. So, that might be a nice way to screen early and then know who requires intervention, because, right now, the approach of trying to do early introduction across the entire population is difficult. It has been 9 years since the publication of the LEAP study, which suggested early peanut introduction—especially in high-risk individuals—and we are still struggling to find ways for groups of patients to be able to keep doing this.

The second way that genetics may be useful is in trying to understand the actual underlying mechanisms of a lot of these diseases. How do food allergies actually come to pass? How does someone become asthmatic or develop seasonal allergies? If we can find certain genes that are more commonly found in patients with food allergies, understanding what those genes actually do and what part of that allergic process they are involved in may open the door to understanding the diseases better, hopefully helping us, in that indirect way, to target therapies better.