Food allergy is an IgE-mediated immune response in which the body mistakes a normally harmless food protein for a threat and triggers histamine release within minutes of exposure. Roughly 8% of US children and 10.8% of US adults are affected (Gupta 2019, JAMA Network Open), with peanut, tree nut, milk, egg, wheat, soy, fish, shellfish, and sesame accounting for over 90% of reactions.
Food allergy (ICD-10: T78.0 anaphylactic reaction due to adverse food reaction; T78.1 other adverse food reactions, not elsewhere classified) is an adverse health effect arising from a reproducible immune response on exposure to a specific food protein. The dominant mechanism is type I hypersensitivity, where allergen-specific IgE antibodies bound to mast cells and basophils crosslink on antigen contact and release histamine, tryptase, leukotrienes, and prostaglandins within minutes. Non-IgE-mediated forms exist — food protein-induced enterocolitis syndrome (FPIES), food protein-induced proctocolitis, and eosinophilic gastrointestinal disorders — and present with delayed gastrointestinal symptoms rather than acute systemic reactions. Mixed IgE and cell-mediated mechanisms underlie atopic dermatitis flares and eosinophilic esophagitis.
The key symptoms of Food Allergy are: Hives (urticaria) and itching that appear within minutes of eating the trigger food, often starting around the mouth and spreading to the trunk and limbs., Swelling (angioedema) of the lips, tongue, eyelids, or face — sometimes severe enough to distort facial features within 10-30 minutes of exposure., Acute gastrointestinal symptoms including nausea, vomiting, cramping abdominal pain, and diarrhea, typically beginning 30 minutes to 2 hours after ingestion., Respiratory involvement with throat tightness, hoarseness, repetitive coughing, wheeze, and shortness of breath — these features signal a more severe systemic reaction., Anaphylaxis with rapid-onset multi-system involvement: airway swelling, bronchospasm, hypotension, tachycardia, and loss of consciousness, usually within minutes to 1 hour of exposure., Oral allergy syndrome with localized itching and mild swelling of the lips, palate, and throat after eating raw apples, stone fruits, carrots, or other pollen-cross-reactive plants., Eczema flares in infants and young children, particularly with milk, egg, peanut, or wheat exposure, occurring hours to days after ingestion rather than minutes..
Diagnosis of food allergy starts with a detailed clinical history: which food, how soon symptoms began, what symptoms occurred, reproducibility across exposures, and whether cofactors such as exercise or NSAIDs were present. The 2010 NIAID food allergy guidelines and EAACI 2014 recommendations are explicit that no single laboratory test is diagnostic in isolation. Skin prick testing measures wheal size to standardized commercial extracts and to fresh food when relevant; a wheal 3 mm or greater than the negative control indicates sensitization but not necessarily clinical reactivity. Specific IgE (sIgE) by ImmunoCAP is the quantitative blood equivalent and useful when antihistamines or extensive eczema preclude skin testing. Levels correlate with likelihood, not severity, of clinical reaction. Component-resolved diagnostics measure IgE to individual allergen proteins — for peanut, Ara h 2 specific IgE above 0.35 kU/L carries a positive predictive value over 95% for clinical peanut allergy and helps separate true allergy from pollen cross-reactivity. The oral food challenge, performed under medical supervision with resuscitation available, remains the gold standard for confirmation or exclusion and is required when history and testing disagree. Skin and IgE testing for non-IgE conditions (FPIES, proctocolitis, eosinophilic esophagitis) is uninformative — these are diagnosed clinically and, for eosinophilic esophagitis, by endoscopic biopsy showing 15 or more eosinophils per high-power field. Unproven tests including IgG food panels, hair analysis, applied kinesiology, and electrodermal testing are not recommended by any major guideline and frequently mislead patients into unnecessary elimination diets.
Outlook depends heavily on the specific food and age at onset. Cow's milk, egg, wheat, and soy allergies that begin in infancy are outgrown by school age in 50-80% of children — confirmed by oral food challenge. Peanut allergy is outgrown in roughly 20%, tree nut in 9-14%, and shellfish, fish, and sesame allergies are usually lifelong. Adult-onset food allergy rarely resolves. Quality of life is comparable to that of children with chronic illnesses such as type 1 diabetes; food-allergic adolescents face heightened risk-taking, particularly in social and dining situations. Mortality from food-induced anaphylaxis is low — around 1 per million person-years in food-allergic populations — but every death is preventable with timely epinephrine. The strongest predictors of fatal outcome are coexisting asthma, peanut or tree nut as the trigger, adolescent or young adult age, and failure to use epinephrine promptly. With oral immunotherapy now in routine use for peanut and omalizumab approved across multiple allergens, the prognosis is shifting from passive avoidance to active disease modification, with measurable reductions in reaction severity for inadvertent exposures.
Refer to an Allergy and Immunology specialist after any reaction suspicious for food allergy, particularly if there was any respiratory or cardiovascular involvement, if symptoms were reproducible, or if testing is needed to clarify the trigger. Specialist input is essential before starting oral immunotherapy or omalizumab, when multiple food allergies or co-existing asthma complicate management, when an oral food challenge is needed to confirm resolution, and for adults with new-onset food allergy or suspected alpha-gal syndrome.
Find specialists →Acute IgE-mediated reactions begin within minutes, peak within 30-60 minutes, and typically resolve over 4-6 hours with appropriate treatment. Biphasic reactions, occurring in roughly 5% of cases, can recur 1-8 hours after initial improvement. Eczematous and gastrointestinal manifestations resolve over days to weeks of strict avoidance. Outgrowth of childhood allergies is gradual — milk and egg often resolve between ages 3 and 6, wheat by school entry, peanut by adolescence in 20%. Oral immunotherapy desensitization develops over 6-12 months of structured up-dosing and requires lifelong daily dosing to maintain.
Routine exercise is safe and encouraged in food allergy. Patients with food-dependent exercise-induced anaphylaxis (most often wheat) should avoid exercise for at least 4 hours after eating the trigger food, carry epinephrine during activity, and exercise with a companion who knows the action plan. Asthma — present in 30-40% of food-allergic patients — must be well-controlled before any high-intensity activity, because uncontrolled asthma is the strongest predictor of fatal food-induced anaphylaxis.
Look for board certification in allergy and immunology, active hospital privileges to manage food challenges with resuscitation backup, training in oral immunotherapy protocols, and routine use of component-resolved diagnostics. Practices that offer oral food challenges in-house, written anaphylaxis action plans, and dietitian support reflect the current standard of care. Continuity with the same allergist through a child's growth allows accurate retesting and outgrowth confirmation.
Medically reviewed by AIHealz Medical Editorial Board · May 12, 2026
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