A food allergy occurs when the immune system mistakenly identifies a harmless food protein (allergen) as a threat. This reaction is mediated by Immunoglobulin E (IgE), which triggers chemicals like histamine, causing symptoms from mild hives to life-threatening anaphylaxis. Food allergies are not inherited in a straightforward dominant or recessive Mendelian pattern. Susceptibility is a complex, multifactorial trait resulting from the interplay of multiple genes and external environmental factors.
Why Food Allergies Defy Simple Mendelian Rules
Food allergies do not conform to dominant or recessive inheritance patterns. The condition is polygenic, meaning many different genes, each contributing a small effect, combine to confer risk. The genetic tendency to develop any allergic disease, including asthma, eczema, and food allergies, is known as atopy. This broad predisposition is what is passed down, not the specific allergy itself.
The inheritance is also categorized as multifactorial, acknowledging that genetics only provides susceptibility. External influences determine if and how that susceptibility is expressed. Studies comparing identical twins show a concordance rate of approximately 65% for peanut allergy. This high rate suggests a strong genetic component, but since it is not 100%, environmental factors play a significant role in triggering the condition.
Key Immune Genes That Increase Susceptibility
The genes contributing to food allergy risk primarily involve immune system regulation and the integrity of protective barriers. Many genetic variations affect T-helper (Th) cell function, skewing the immune response toward a Th2 profile. This Th2 profile is associated with allergic reactions and IgE production.
Specific gene complexes are strongly implicated, notably the Human Leukocyte Antigen (HLA) region. Variations within the HLA-DR and HLA-DQ regions increase genetic susceptibility to peanut allergy. Genes that maintain the epithelial barrier, such as Filaggrin (FLG), are also relevant. Mutations in FLG are strongly associated with eczema, and a compromised skin or gut barrier increases the likelihood of allergen sensitization.
Environmental Factors That Trigger Genetic Predisposition
Genetic susceptibility requires an environmental trigger to manifest as a food allergy. One major hypothesis is the hygiene hypothesis, suggesting that reduced exposure to diverse microbes in early life may prevent the immune system from developing tolerance. Alterations in the gut microbiome, known as dysbiosis, are factors, as an imbalance of gut bacteria can impair immune regulation.
The timing of allergen introduction during infancy is another environmental influence. Studies suggest that introducing common allergenic foods like peanuts and eggs early in life, rather than delaying, can help guide the immune system toward tolerance. Exposure to environmental pollutants, such as air pollution or tobacco smoke, influences the allergic cascade and modifies gene expression through epigenetic changes.
Practical Assessment of Hereditary Risk
The hereditary risk of a child developing a food allergy can be assessed based on parental history. A child with no immediate family members who have allergic diseases has the lowest baseline risk.
Risk Based on Parental History
If one parent has an allergy, the child’s likelihood of developing an allergy increases substantially, typically falling within a range of 30% to 50%. The risk is significantly higher when both parents have allergic disease, potentially rising to between 60% and 80%. Having two or more immediate family members with an allergic disease increases the child’s food allergy risk by approximately 1.8-fold compared to having no family history. The highest observed risk, reaching up to 20%, is seen in children who have both parents with allergies and an allergic sibling.