A food allergy is an immune system reaction that occurs shortly after eating a certain food, where the body mistakenly identifies a harmless food protein as a threat, triggering the release of chemicals like histamine. This is distinct from a food intolerance, which does not involve the immune system. Food allergies are not inherited in a single, predictable pattern but result from a complex interaction between a person’s genetic makeup and various external factors that influence whether an allergy develops.
Genetic Basis for Food Allergies
The inheritance of food allergies is polygenic, meaning multiple genes work together to increase a person’s susceptibility rather than a single gene being responsible. Genetic predisposition sets a foundation for an overactive immune system, but it does not guarantee the development of an allergy.
One well-studied genetic marker is the FLG gene, which provides instructions for making filaggrin, a structural component of the skin barrier. Loss-of-function mutations in FLG are strongly associated with eczema, a condition that often precedes food allergy development. These mutations create a “leaky” skin barrier, allowing food proteins to enter the body through the skin and sensitize the immune system. Children with these FLG mutations have an approximately three-fold increased risk of developing a food allergy.
Another set of genes involved are the Human Leukocyte Antigen (HLA) genes, located on chromosome 6, which are fundamental to immune system function. HLA genes code for molecules that act as presenters, displaying foreign protein fragments to immune T-cells. Specific variants of HLA class II genes, such as HLA-DR and HLA-DQ, are associated with the risk of developing certain food allergies, most notably peanut allergy. These genetic differences dictate how the immune system recognizes a food protein, influencing whether it chooses tolerance or an allergic reaction.
Environmental Influences on Allergy Development
Since the prevalence of food allergies has risen dramatically, genetics alone cannot explain the increase, pointing to significant environmental influences that modify inherited risk. These external factors revolve around the development and function of the immune system in early life. A key area of research is the gut microbiome, the community of microorganisms living in the digestive tract, which is critical for training the immune system.
Factors like Cesarean section delivery and the use of antibiotics in infancy can disrupt the establishment of a diverse gut microbiome. This microbial imbalance, or dysbiosis, may impair the immune system’s ability to develop tolerance, shifting it toward an allergic response. Changes in dietary patterns, such as a shift toward processed foods low in fiber, further contribute to a less diverse gut environment.
Vitamin D status is another environmental factor that acts as an immunomodulator. Low levels of Vitamin D in infancy are linked to a higher risk of developing food allergies, particularly to eggs and peanuts. Vitamin D helps promote the development of T-regulatory cells, which suppress allergic overreactions. Deficiency may inhibit this regulatory mechanism, making the immune system more prone to attacking food proteins.
Understanding Risk in Families
The complex interaction of genes and environment translates into measurable statistical risks for families with a history of allergies. Children inherit a general tendency toward developing allergies, a state known as atopy, rather than the specific allergy itself. For instance, if a parent has a shellfish allergy, the child is predisposed to an increased overall risk for any allergic disease, such as asthma, eczema, or a different food allergy.
If one immediate family member has any form of allergy, the child’s risk of developing an allergy is estimated to be between 30% and 50%. This likelihood increases when both parents have allergies, with the risk rising to a range of 60% to 80%. Even when neither parent has a history of allergies, the chance for a child to develop one remains around 15%, highlighting the role of non-inherited, external triggers.