Food allergy is an exaggerated immune response to dietary components, usually proteins. Manifestations vary widely and can include atopic dermatitis, gastrointestinal or respiratory symptoms, and anaphylaxis. Diagnosis is by history and sometimes allergen-specific serum IgE testing, skin testing, and/or elimination diets. Treatment is primarily preventive with elimination of the food that triggers the reaction. Treatment of mild reactions is usually with antihistamines and observation. Severe reactions may require treatment with epinephrine as for anaphylaxis. Oral immunotherapy and biologic therapies (eg, omalizumab) may also be used.
Food allergy should be distinguished from nonimmune reactions to food (eg, lactose intolerance, irritable bowel syndrome, infectious gastroenteritis) and reactions to additives (eg, monosodium glutamate, metabisulfite, tartrazine) or food contaminants (eg, latex dust in food handled by workers wearing latex gloves). Prevalence of true food allergy ranges from < 1 to 3% and varies by geography and method of ascertainment; variation may also reflect patients mistaking food intolerance for food allergy (1). (See also Overview of Allergic and Atopic Disorders.)
General reference
1. Warren CM, Sehgal S, Sicherer SH, Gupta RS. Epidemiology and the Growing Epidemic of Food Allergy in Children and Adults Across the Globe. Curr Allergy Asthma Rep. 2024;24(3):95-106. doi:10.1007/s11882-023-01120-y
Etiology of Food Allergy
Almost any food or food additive can cause an allergic reaction, but the most common triggers include:
In infants and young children: Milk, eggs, peanuts, soy, and wheat
In older children and adults: Nuts (peanuts and tree nuts) and seafood (fish and shellfish)
The allergenic foods shown here are (left to right):
Milk
Shellfish
Peanuts
Soy
Tree nuts
Egg
Wheat
Fish
SCIENCE PHOTO LIBRARY
Cross-reactivity between food and nonfood allergens exists, and sensitization may occur nonenterally. For example, children with peanut allergy may have been sensitized by topical creams containing peanut oil used to treat rashes. Patients who are primarily allergic to environmental aero-allergens such as tree pollen may cross-react to botanically related fruits, vegetables, and nuts.
Food allergies are more common among children whose parents have food allergies, allergic rhinitis, or allergic asthma. Many children outgrow certain food allergies over time. As they get older, earlier allergic manifestations (eg, atopic dermatitis, food allergies) may shift towards sensitization and increased reactions to inhaled allergens, with the development of asthma and rhinitis; this progression is referred to as the atopic march. By age 10 years, patients rarely have respiratory symptoms after the allergenic food is eaten, even though patients may remain sensitized on diagnostic testing.
In general, food allergy is mediated by IgE, T cells, or both:
IgE-mediated allergy (eg, urticaria, asthma, anaphylaxis) is acute in onset, usually develops during infancy, and occurs most often in people with a strong family history of atopy.
T-cell–mediated allergy (eg, dietary protein gastroenteropathies, celiac disease) manifests gradually and is chronic; it is most common among infants and children.
Allergies mediated by both IgE and T cells (eg, atopic dermatitis, eosinophilic gastroenteropathy) tend to be delayed in onset or chronic.
Oral allergy syndrome (pollen food allergy syndrome)
Oral allergy syndrome (pollen food allergy syndrome) is caused by proteins in pollens and foods that cross-react (frequently raw fruits and vegetables and nuts). Cross-reactivity between food and nonfood allergens exists, and sensitization may occur nonenterally. For example, patients with oral allergies (typically, pruritus, erythema, and edema of the mouth when fruits and vegetables are eaten) may have been sensitized by exposure to pollens that are antigenically similar to food antigens. When patients are allergic to a particular pollen protein, the immune system reacts to a similar protein in the food and generates an allergic response. Patients can usually tolerate the food if it is cooked or heated because the food protein is denatured, altering the structure of the proteins that cross-react.
The following pollens and foods are commonly associated:
Birch pollen: Apples, peaches, pears, plums, cherries, kiwi, carrots, celery, hazelnuts, and almonds
Grass pollen: Celery, melons, oranges, peaches, and tomatoes
Ragweed pollen: Bananas, cucumbers, melons, sunflower seeds, and zucchini
Many patients who are allergic to latex are also allergic to bananas, kiwis, avocados, potatoes, tomatoes, chestnuts, or a combination of these.
Typical symptoms include pruritus of the mouth and throat when the causative food is eaten. Although anaphylaxis is not common, it can occur (1).
The diagnosis of oral allergy syndrome is usually made clinically but can be confirmed by skin prick testing.
The treatment of oral allergy syndrome involves avoiding the food, thoroughly cooking the food to denature the protein, and carrying a prefilled, self-injecting epinephrine syringe (ie, autoinjector) in case of an anaphylactic reaction.
Desensitization to the pollen via allergen immunotherapy may occasionally also lead to a partial resolution of cross-reactive food allergy. For example, indirect desensitization via administration of allergen immunotherapy to some tree pollens such as birch may lead to a slightly improved ability to tolerate fruit such as apples (2, 3). However, such resolution is inconsistent, variable, and not routinely recommended as a primary treatment of oral allergy syndrome (4).
Eosinophilic gastroenteropathy
Eosinophilic gastroenteropathy is caused by eosinophilic infiltrates in different sections of the gut, which leads to pain, cramps, and diarrhea with blood eosinophilia, and protein-losing enteropathy; patients have a history of atopic disorders.
Eosinophilic esophagitis may accompany other eosinophilic gastric disorders or occur in isolation. Eosinophilic esophagitis is characterized by chronic inflammation of the esophagus and may cause dysphagia, nonacid-related dyspepsia, and dysmotility or, in children, feeding intolerance and abdominal pain. Eosinophilic esophagitis may cause strictures.
Red meat allergy (including Alpha-gal syndrome)
Alpha-gal syndrome is a form of allergy to red meat (5, 6). Alpha-gal is a carbohydrate moiety (galactose-alpha-1,3-galactose) that occurs in most mammals except for primates (including humans) (7). Alpha-gal does not occur in fish, birds, or reptiles.
At least one species of tick (lone star tick) has alpha-gal in its saliva. Evidence suggests that the bite (particularly multiple bites) from such ticks may sensitize a person to alpha-gal (8). Because alpha-gal is present in many red meats (eg, pork, beef, lamb, venison) and in food products derived from mammals (eg, dairy products, gelatin), affected people may develop an IgE-mediated allergic response to these food products.
Another example is pork-cat syndrome. This is a rare, immediate IgE-mediated meat allergy caused by primary sensitization to cat serum albumin, Fel d 2, with cross-reactivity to porcine serum albumin, Sus s 1. Sensitization usually occurs through primary respiratory exposure to cats and is subsequently followed by reactions when pork is eaten. Symptoms generally begin within 30 to 60 minutes of eating pork and present as oral pruritus, urticaria, angioedema, abdominal cramping, vomiting, wheezing, or anaphylaxis (9). Diagnosis is based on skin or blood testing to cat and porcine albumin allergens. Management is avoidance of all pork and products containing hidden porcine ingredients. An epinephrine autoinjector may be prescribed for the management of severe allergic reactions.
The lone star tick (A. americanum) is so named because the adult female is distinguished by a white dot or “lone star” on its back.
This tick transmits Ehrlichia chaffeensis, a causative agent of ehrlichiosis, and Francisella tularensis, the causative agent of tularemia. It also transmits the carbohydrate moiety alpha-gal in its saliva, leading to alpha-gal syndrome and subsequent red meat allergy.
CDC/ Lauren Bishop
Unlike the onset of occurrence of other typical food allergies, the symptoms of alpha-gal syndrome frequently do not occur until 3 to 8 hours after eating.
The allergic reactions can include a pruritic rash (typically urticarial), indigestion, constipation, nausea, and anaphylactic reactions.
The diagnosis is based on clinical history and detection of serum IgE to alpha-gal (also called alpha-gal sIgE) (10).
The management of alpha-gal syndrome requires strict avoidance of mammalian meat, dairy, and gelatin-containing products, along with diligent tick bite protective measures to prevent reactivation (10, 11).
Etiology references
1. Skypala IJ. Can patients with oral allergy syndrome be at risk of anaphylaxis? Curr Opin Allergy Clin Immunol. 2020 20 (5):459–464, 2020. doi:10.1097/ACI.0000000000000679
2. Nothegger B, Reider N, Covaciu CE, et al. Oral birch pollen immunotherapy with apples: Results of a phase II clinical pilot study. Immun Inflamm Dis. 2021;9(2):503-511. doi:10.1002/iid3.410
3. American Academy of Allergy, Asthma & Immunology. Ask the Expert. Does environmental immunotherapy help cross-reactive food allergy. May 18, 2023. Accessed June 16, 2026.
4. Al-Shaikhly T, Cox A, Nowak-Wegrzyn A, et al. An International Delphi Consensus on the Management of Pollen-Food Allergy Syndrome: A Work Group Report of the AAAAI Adverse Reactions to Foods Committee. J Allergy Clin Immunol Pract. 2024;12(12):3242-3249.e1. doi:10.1016/j.jaip.2024.09.037
5. Hashizume H, Fujiyama T, Umayahara T, et al. Repeated Amblyomma testudinarium tick bites are associated with increased galactose-α-1,3-galactose carbohydrate IgE antibody levels: A retrospective cohort study in a single institution. J Am Acad Dermatol. 2018;78 (6):1135-1141.e3. doi: 10.1016/j.jaad.2017.12.028
6. Centers for Disease Control and Prevention (CDC). Alpha-gal Syndrome. About Alpha-gal Syndrome. January 5, 2026. Accessed June 3, 2026.
7. Platts-Mills TAE, Gangwar RS, Workman L, Wilson JM. The Immunology of Alpha-Gal Syndrome: History, Tick Bites, IgE, and Delayed Anaphylaxis to Mammalian Meat. Immunol Rev. 2025;332(1):e70035. doi:10.1111/imr.70035
8. Maldonado-Ruiz LP, Reif KE, Ghosh A, Foré S, Johnson RL, Park Y. High levels of alpha-gal with large variation in the salivary glands of lone star ticks fed on human blood. Sci Rep. 2023;13(1):21409. doi:10.1038/s41598-023-48437-2
9. Kim C, Kim SW, Hwang YH. Recurrent urticaria caused by specific cat serum albumin IgE cross-reacting with pork serum albumin. Clin Exp Pediatr. 2020;63(11):451-453. doi:10.3345/cep.2019.01725
10. American Academy of Allergy, Asthma & Immunology (AAAAI). Alpha-gal, Red Meat Allergy and Tick Bites. May 12, 2026. Accessed June 3, 2026.
11. Centers for Disease Control and Prevention (CDC). Alpha-gal Syndrome. Managing Alpha-gal Syndrome. January 5, 2026. Accessed June 3, 2026.
Symptoms and Signs of Food Allergy
Symptoms and signs of food allergies vary by allergen, mechanism, and patient age.
The most common manifestation in infants is atopic dermatitis alone or with gastrointestinal (GI) symptoms (eg, nausea, vomiting, diarrhea). Children can outgrow some food allergies (eg, milk, eggs, soy) but typically remain allergic to others (eg, peanuts, tree nuts, fish, shellfish).
Food protein-induced enterocolitis syndrome (FPIES) is another food allergy manifestation that is characterized by delayed onset of severe vomiting and diarrhea, which typically occur > 2 hours after consumption of a trigger food. It can sometimes lead to severe lethargy, dehydration (because of hypovolemia), hypotension, and pallor.
When food allergy persists in older children and adults, the reactions are more severe (eg, explosive urticaria, angioedema, even anaphylaxis). In some patients, food (especially wheat and shrimp) triggers anaphylaxis only if they exercise soon afterward; this is called food-dependent exercise-induced anaphylaxis (FDEIA). Food may also trigger nonspecific symptoms (eg, light-headedness, syncope). Occasionally, cheilitis, aphthous ulcers, pylorospasm, spastic constipation, pruritus ani, and perianal eczema are attributed to food allergy.
Pearls & Pitfalls
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Diagnosis of Food Allergy
Allergen-specific serum IgE testing
Skin testing
Trial elimination diet (alone or after skin testing or allergen-specific serum IgE testing)
Severe food allergy is usually clinically evident in adults. When it is not or when it occurs in children (the most commonly affected age group), diagnosis may be difficult, and the disorder must be differentiated from other GI problems. Diagnosis of celiac disease is discussed elsewhere. The diagnosis of eosinophilic gastroenteropathy is suspected by the clinical presentation but requires confirmation by endoscopic biopsy, which on histopathologic examination will show ≥ 15 eosinophils per high power field (1, 2).
Testing (eg, allergen-specific serum IgE testing, skin testing) and elimination diets are most useful in diagnosing IgE-mediated reactions (3, 4). T-cell–mediated food reactions are challenging to diagnose. Patients should keep a food diary, meticulously listing everything they consume and any adverse effects they have (particularly timing in relation to food consumption), to help guide decisions regarding elimination of suspect foods.
It is recommended to test only to foods that have resulted in a significant clinical response with each and every exposure to the specific culprit food. Testing without a suggestive clinical history frequently leads to false-positive results, causing patients to unnecessarily eliminate tolerated foods from their diets, resulting in nutritional, behavioral and psychological harms (5). Therefore, broad panel testing to multiple foods or food groups is highly discouraged.
If a food reaction is suspected, one of the following is done:
In either case, a positive test does not confirm a clinically relevant allergy in the absence of a relevant positive clinical history. Both tests can have false-positive or false-negative results. Skin testing is generally more sensitive than the allergen-specific serum IgE test but is more likely to have to false-positive results (6). The skin test provides a result within 15 to 20 minutes, much more quickly than the allergen-specific serum IgE test. Component-resolved diagnostic testing (ie, serum antibody testing of a breakdown of component protein antigens for a given food allergen) may be performed for certain allergens (eg, milk, eggs, peanuts, tree nuts, sesame) and is characterized by high specificity (6).
If either skin or blood tests are positive, the tested food is eliminated from the diet. If eliminating the food relieves symptoms, the patient is reexposed to the food (preferably in a double-blind test) to see whether symptoms recur (oral food challenge).
If skin testing is not available to confirm food allergy or results are inconclusive, the next options may include one or both of the following:
Eliminating foods the patient suspects of causing symptoms based on the patient's food diary, then evaluating symptom resolution
Prescribing a diet that consists of relatively nonallergenic foods and that eliminates common food allergens (see table )
For the latter diet, no foods or fluids may be consumed other than those specified. Pure products must always be used. Many commercially prepared products and meals contain an undesired food in large amounts (eg, commercial rye bread contains wheat flour) or in traces as flavoring or thickeners, and determining whether an undesired food is present may be difficult.
A discussion with the patient and observations from the patient's food diary can help with the choice of the initial elimination diet. If no improvement occurs after 1 week of the initial diet, another diet should be tried; however, T-cell–mediated reactions may take weeks to resolve. If symptoms are relieved and if patients have less severe symptoms, one new food is added and eaten in large amounts for > 24 hours or until symptoms recur. But if patients have particularly severe symptoms, small amounts of the food to be tested are eaten in the clinician’s presence, and the patient’s reactions observed.
Aggravation or reemergence of symptoms after the addition of a new food is the best evidence of allergy.
Allowable Foods in Representative Elimination Diets*
Food | Diet No. 1 (No beef, pork, fowl, milk, rye, or corn) | Diet No. 2 (No beef, lamb, milk, or rice) | Diet No. 3 (No lamb, fowl, rye, rice, corn, or milk) |
|---|---|---|---|
Cereal | Rice products | Corn products | None |
Vegetables | Artichokes, beets, carrots, lettuce, spinach | Asparagus, corn, peas, squash, string beans, tomatoes | Beets, lima beans, potatoes (white and sweet), string beans, tomatoes |
Meats | Lamb | Bacon, chicken | Bacon, beef |
Flour (bread or biscuits) | Rice | Corn, 100% rye (ordinary rye bread contains wheat) | Lima bean, potato, soybean |
Fruits | Grapefruit, lemons, pears | Apricots, peaches, pineapple, prunes | Apricots, grapefruit, lemons, peaches |
Fat | Cottonseed oil, olive oil | Corn oil, cottonseed oil | Cottonseed oil, olive oil |
Beverages | Coffee (black), lemonade, tea | Coffee (black), lemonade, tea | Coffee (black), lemonade, juice from approved fruit, tea |
Miscellaneous | Cane sugar, gelatin, maple sugar, olives, salt, tapioca pudding | Cane sugar, corn syrup, gelatin, salt | Cane sugar, gelatin, maple sugar, olives, salt, tapioca pudding |
* Diet No. 4: If symptoms persist when patients are following any of the above 3 elimination diets and diet is still suspected, daily diet may be restricted to an elemental diet (using extensively hydrolyzed or amino acid–based formulas). | |||
Diagnosis references
1. Dellon ES, Muir AB, Katzka DA, et al. ACG Clinical Guideline: Diagnosis and Management of Eosinophilic Esophagitis. Am J Gastroenterol. 2025;120(1):31-59. doi:10.14309/ajg.0000000000003194
2. Hirano I, Chan ES, Rank MA, et al. AGA institute and the joint task force on allergy-immunology practice parameters clinical guidelines for the management of eosinophilic esophagitis. Ann Allergy Asthma Immunol. 2020;124(5):416-423. doi:10.1016/j.anai.2020.03.020
3. NIAID-Sponsored Expert Panel, Boyce JA, Assa'ad A, et al. Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-sponsored expert panel. J Allergy Clin Immunol. 2010;126(6 Suppl):S1-S58. doi:10.1016/j.jaci.2010.10.007
4. Sampson HA, Aceves S, Bock SA, et al. Food allergy: a practice parameter update-2014. J Allergy Clin Immunol. 2014;134(5):1016-25.e43. doi:10.1016/j.jaci.2014.05.013
5. Venkatesh S, Hsieh FH. The Harms of Inappropriate Food-Specific Immunoglobulin E Testing-Less Is More. JAMA Intern Med. 2025;185(12):1491-1492. doi:10.1001/jamainternmed.2025.5433
6. Riggioni C, Ricci C, Moya B, et al. Systematic review and meta-analyses on the accuracy of diagnostic tests for IgE-mediated food allergy. Allergy. 2024;79(2):324-352. doi:10.1111/all.15939
Treatment of Food Allergy
Food elimination
Sometimes glucocorticoids for eosinophilic enteropathy
Oral or sublingual immunotherapy for desensitization
Biologic therapies (eg, omalizumab)
The treatment of food allergies consists of eliminating the food that triggers the allergic reaction (1, 2). Thus, diagnosis and treatment overlap. When assessing an elimination diet’s effect, clinicians must take into consideration the fact that food sensitivities may disappear spontaneously.
Patients with severe food allergies should be advised to carry antihistamines to take immediately if a reaction starts and a prefilled, self-injecting syringe (autoinjector) of epinephrine to use when needed for severe reactions. Antihistamines are useful to abort urticaria and angioedema caused by an acute reaction.
Long-term glucocorticoid treatment is useful for symptomatic eosinophilic enteropathy. Treatment approaches for eosinophilic esophagitis include a combination of avoidance or elimination diets, oral proton pump inhibitors, swallowed topical glucocorticoids (ie, budesonide slurry or fluticasone inhaler [sprayed and swallowed]), and biologic therapies (eg, dupilumab) (3, 4).
For patients with eosinophilic esophagitis, an elemental diet or an empiric, 6-food elimination diet (ie, egg, milk, wheat, soy, peanut/tree nut, fish/shellfish) may be used (4, 5).
Omalizumab may be used to help prevent severe IgE mediated allergic reactions to foods and increase tolerance when a patient experiences an accidental exposure (6, 7).
Immunotherapy for desensitization
Oral immunotherapy for desensitization to several foods are available at specialized centers. Epicutaneous immunotherapy (patches placed on skin) has also been used. Oral immunotherapy for certain foods (eg, peanut, some tree nuts, milk, eggs, wheat) when used along with omalizumab may lead to desensitization of these foods. Oral desensitization protocols to various other foods are being investigated (8).
Sublingual immunotherapy for IgE-mediated food allergies involves placing drops of glycerinated allergen extracts under the tongue once a day. Allergens that have been studied include peanuts (mainly), hazelnuts, peaches, apples, and milk. Further studies are needed before sublingual immunotherapy to foods is broadly recommended in practice (9).
Biologic therapies
Omalizumab (a humanized recombinant monoclonal anti-IgE antibody) may be used for the treatment of IgE-mediated food allergies to reduce the risk of anaphylaxis from accidental exposures in patients age 1 year and older (10). Omalizumab dosing and frequency are typically based on body weight and serum IgE levels.
Data from successive phases of a multicenter randomized trial in the United States have demonstrated the efficacy of omalizumab compared to placebo and oral immunotherapy in increasing the reaction thresholds for patients aged 1 to 55 years (the majority of whom were aged 1 to 17) who were allergic to peanuts and at least 2 other specified foods (ie, cashew, milk, egg, walnut, wheat, hazelnut) (6, 7, 11). In the first phase, patients treated with omalizumab achieved significantly higher reaction thresholds to peanut as well as to cashew, egg, and milk compared with placebo. In the second phase, omalizumab demonstrated superior efficacy for inducing tolerance to allergenic foods when compared to omalizumab-facilitated oral immunotherapy in patients with multiple food allergies. In a third phase, evaluation of clinical outcomes assessed during a 12 month period after discontinuation of omalizumab showed that many participants retained sufficient tolerance for the continued incorporation of allergenic foods into their diets; however, consumption was noted to generally decline over time because of recurrent adverse effects or patient preference. The disease-modifying potential of omalizumab in multiple food allergies remains under investigation.
Treatment using other monoclonal antibodies, such as dupilumab (an anti-IL4R antibody), ligelizumab (a high potency anti-IgE antibody), anti-alarmins including etokimab (anti-IL-33), and tezepelumab (anti-TSLP) are also under investigation (12).
Treatment references
1. American College of Allergy, Asthma, & Immunology. Food allergy: a practice parameter. Ann Allergy Asthma Immunol. 2006;96(3 Suppl 2):S1-S68.
2. Sampson HA, Aceves S, Bock SA, et al. Food allergy: a practice parameter update-2014. J Allergy Clin Immunol. 2014;134(5):1016-25.e43. doi:10.1016/j.jaci.2014.05.013
3. Dellon ES, Muir AB, Katzka DA, et al. ACG Clinical Guideline: Diagnosis and Management of Eosinophilic Esophagitis. Am J Gastroenterol. 2025;120(1):31-59. doi:10.14309/ajg.0000000000003194
4. Hirano I, Chan ES, Rank MA, et al. AGA Institute and the Joint Task Force on Allergy-Immunology Practice Parameters Clinical Guidelines for the Management of Eosinophilic Esophagitis. Gastroenterology. 2020;158(6):1776-1786. doi:10.1053/j.gastro.2020.02.038
5. Kliewer KL, Gonsalves N, Dellon ES, et al. One-food versus six-food elimination diet therapy for the treatment of eosinophilic oesophagitis: a multicentre, randomised, open-label trial. Lancet Gastroenterol Hepatol. 2023;8(5):408-421. doi:10.1016/S2468-1253(23)00012-2
6. Wood RA, Togias A, Sicherer SH, et al. Omalizumab for the Treatment of Multiple Food Allergies. N Engl J Med. 2024;390(10):889-899. doi:10.1056/NEJMoa2312382
7. Wood RA, Togias A, Burk CM, et al. Treatment of Multifood Allergy With Omalizumab or Multiallergen Oral Immunotherapy: A Randomized Clinical Trial. JAMA Pediatr. Published online July 27, 2026. doi:10.1001/jamapediatrics.2026.2910
8. Anderson B, Wong L, Adlou B, et al. Oral immunotherapy in children: Clinical considerations and practical management. J Asthma Allergy. 2021;14:1497-1510. doi: 10.2147/JAA.S282696 eCollection 2021
9. Schworer SA, Edwin H Kim EH. Sublingual immunotherapy for food allergy and its future directions. Immunotherapy. 2020;12(12):921-931. doi: 10.2217/imt-2020-0123
10. Anagnostou A, Bird JA, Chinthrajah S, et al. The use and implementation of omalizumab as food allergy treatment: Consensus-based guidance and Work Group Report of the Adverse Reactions to Foods Committee of the American Academy of Allergy, Asthma & Immunology. J Allergy Clin Immunol. 2025;155(1):62-69.e1. doi:10.1016/j.jaci.2024.09.031
11. Dantzer J, Virkud Y, Wang J, et al. Introduction of allergenic foods after treatment with omalizumab. J Allergy Clin Immunol. 2025;156(2):394-405. doi:10.1016/j.jaci.2025.05.014
12. Schuetz JP, Anderson B, Sindher SB. New biologics for food allergy. Curr Opin Allergy Clin Immunol. 2024;24(3):147-152. doi:10.1097/ACI.0000000000000981
Prevention of Food Allergy
The avoidance of allergenic foods during infancy is no longer recommended for the primary prevention of food allergy. Various expert organizations have recommended that foods such as egg, peanuts and other allergenic foods be introduced at about age 4 to 6 months (1, 2, 3). In the seminal Learning Early About Peanut Allergy (LEAP) randomized trial, the early introduction and regular consumption of food that contains peanuts prevented the development of peanut allergy in infants at high risk (eg, infants with egg allergy and/or severe eczema) (4). The study enrolled 640 infants aged 4 to 11 months at high risk of peanut allergy who were randomized to consume peanuts several times a week until the age of 5 years and compared to an avoidance group. Among non-sensitized infants, peanut allergy developed in 1.9% of the peanut consumption group versus 13.7% of the avoidance group (absolute risk reduction of 11.8%). Among infants with early sensitization (ie, those at higher risk of allergy), peanut allergy developed in 10.6% of the peanut consumption group versus 35.3% of the avoidance group (absolute risk reduction of 24.7%).
To show the longevity of protection, a follow-up randomized trial (LEAP-On) showed persistent protection even after 12 months of avoidance in patients who had originally consumed peanuts (5). A third follow-up study (LEAP-Trio) established the role of early introduction of even longer-term tolerance; when outcomes were examined longitudinally, the prevalence of peanut allergy at age 12 years was 4.4% in the patients who had originally consumed peanuts compared to 15.4% in those who had avoided it (6).
The impact of early introduction to foods other than peanut have also been investigated. In the Enquiring About Tolerance (EAT) study, a randomized trial examining whether early introduction of 6 allergenic foods (ie, peanut, cooked egg, cow's milk, sesame, fish, and wheat) from 3 months of age in exclusively breastfed infants, there was no significantly reduced food allergy in the intention-to-treat analysis (7). However, in the per-protocol analysis, the prevalence of any food allergy was significantly lower in the early introduction group (2.4% vs. 7.3%), with the most pronounced effects noted for peanut (0% vs. 2.5%) and egg allergy (1.4% vs. 5.5%). The protective effects were found to be dose-dependent, with higher doses of consumed peanuts or eggs leading to lower allergy.
Finally, in one pooled analysis of the LEAP and EAT studies, early introduction to peanuts was associated with significantly reduced peanut allergy in both the intention-to-treat and per-protocol analyses across all risk groups (8).
Prevention references
1.Fleischer DM, Chan ES, Venter C, et al. A Consensus Approach to the Primary Prevention of Food Allergy Through Nutrition: Guidance from the American Academy of Allergy, Asthma, and Immunology; American College of Allergy, Asthma, and Immunology; and the Canadian Society for Allergy and Clinical Immunology. J Allergy Clin Immunol Pract. 2021;9(1):22-43.e4. doi:10.1016/j.jaip.2020.11.002
2. Sampson HA, Aceves S, Bock SA, et al. Food allergy: a practice parameter update-2014. J Allergy Clin Immunol. 2014;134(5):1016-25.e43. doi:10.1016/j.jaci.2014.05.013
3. Santos AF, Riggioni C, Agache I, et al. EAACI guidelines on the management of IgE-mediated food allergy. Allergy. 2025;80(1):14-36. doi:10.1111/all.16345
4. Du Toit G, Roberts G, Sayre PH, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. 2015;372(9):803-813. doi: 10.1056/NEJMoa1414850
5. Du Toit G, Sayre PH, Roberts G, et al. Effect of Avoidance on Peanut Allergy after Early Peanut Consumption. N Engl J Med. 2016;374(15):1435-1443. doi:10.1056/NEJMoa1514209
6. Du Toit G, Huffaker MF, Radulovic S, et al. Follow-up to Adolescence after Early Peanut Introduction for Allergy Prevention. NEJM Evid. 2024;3(6):EVIDoa2300311. doi:10.1056/EVIDoa2300311
7. Perkin MR, Logan K, Bahnson HT, et al. Efficacy of the Enquiring About Tolerance (EAT) study among infants at high risk of developing food allergy. J Allergy Clin Immunol. 2019;144(6):1606-1614.e2. doi:10.1016/j.jaci.2019.06.045
8. Logan K, Bahnson HT, Ylescupidez A, et al. Early introduction of peanut reduces peanut allergy across risk groups in pooled and causal inference analyses. Allergy. 2023;78(5):1307-1318. doi:10.1111/all.15597
Key Points
Food allergy is commonly mediated by IgE (typically resulting in acute systemic allergic reactions) or T cells (typically resulting in chronic gastrointestinal symptoms).
Distinguish food allergy from nonimmune reactions to food (eg, lactose intolerance, irritable bowel syndrome, infectious gastroenteritis) and reactions to additives (eg, monosodium glutamate, metabisulfite, tartrazine) or food contaminants.
If the diagnosis is not clinically obvious in adults or if children are being evaluated, do skin tests, an allergen-specific serum IgE test, or an elimination diet.
Make sure patients understand that in an elimination diet, they can eat only foods on the list and only pure foods (which excludes many commercially prepared foods).
Other treatments include immunotherapy for desensitization and monoclonal antibodies such as omalizumab.
Infants should be introduced to all foods, as culturally and regionally appropriate (including peanuts).
Drug Information for the Topic
