Food Allergy — Causes, Symptoms, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Food allergy is an abnormal immune response to a food protein that is harmless to most people. When a sensitised individual ingests the allergen, their immune system mounts an IgE-mediated or cell-mediated reaction causing symptoms ranging from mild urticaria to life-threatening anaphylaxis. Food allergy affects approximately 8% of children and 2-3% of adults globally, with prevalence rising steadily over recent decades. The most common allergens in adults include peanuts, tree nuts, fish, and shellfish — collectively forming the 'Big Nine' alongside milk, eggs, wheat, soy, and sesame. Food allergy is distinct from food intolerance (e.g., lactose intolerance), which does not involve the immune system and is rarely life-threatening. Anaphylaxis from food allergy accounts for approximately 30,000 emergency department visits annually in the USA alone and remains a potentially fatal emergency if not treated promptly with epinephrine.

Food allergy involves sensitisation — upon first exposure, the immune system mistakenly produces IgE antibodies against food proteins. On subsequent exposures, these IgE antibodies trigger mast cell and basophil degranulation, releasing histamine, leukotrienes, and prostaglandins causing allergic symptoms. Risk factors include atopic conditions (eczema, asthma, allergic rhinitis — the 'atopic triad'), family history of food allergy, early childhood eczema (increases peanut allergy risk 6x), and delayed introduction of allergenic foods. The dual allergen exposure hypothesis proposes that early oral exposure to foods builds tolerance, while skin sensitisation through eczema-damaged skin promotes allergy — supporting early introduction of peanuts and eggs in infancy. Specific genes (HLA-DQ, FLG filaggrin mutations) confer genetic susceptibility. Western lifestyle, antibiotic use, and reduced microbial diversity (hygiene hypothesis) may contribute to rising prevalence.

Symptoms typically begin within minutes to 2 hours of ingesting the allergen. Skin: urticaria (hives), angioedema (swelling of lips, face, throat), flushing, and pruritus. Gastrointestinal: nausea, vomiting, abdominal cramping, and diarrhoea. Respiratory: rhinorrhoea, sneezing, bronchospasm, wheeze, and stridor. Anaphylaxis — the most severe reaction — involves two or more organ systems simultaneously, or isolated cardiovascular collapse: hypotension, tachycardia, dizziness, syncope, and potentially fatal respiratory and cardiovascular failure. The Sampson criteria define anaphylaxis when symptoms involve the skin plus respiratory or cardiovascular systems, or when two or more systems are affected after allergen exposure. Biphasic anaphylaxis (recurrence 4-12 hours later without re-exposure) occurs in 5-20% of cases, mandating 4-6 hours of observation after treatment. Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE form causing severe vomiting 1-4 hours after ingestion.

Clinical history is the cornerstone: allergen exposure, timing of symptoms, reproducibility, and response to prior reactions. Skin prick testing (SPT): positive wheal-and-flare response (wheal diameter 3 mm or more above negative control) within 15-20 minutes indicates sensitisation — high negative predictive value but does not confirm clinical allergy. Specific IgE blood testing (ImmunoCAP): serum IgE to specific food allergens; component-resolved diagnostics (CRD) distinguish genuine allergy from cross-reactivity (e.g., Ara h 2 for peanut, Ana o 3 for cashew). Oral food challenge (OFC): gold standard — double-blind placebo-controlled food challenge (DBPCFC) under medical supervision confirms or excludes allergy; used when history and tests are discordant. Serum tryptase (elevated in anaphylaxis — collected within 30 minutes to 3 hours) confirms mast cell activation in equivocal cases. Patch testing for suspected delayed food allergy (FPIES, eosinophilic oesophagitis).

Strict allergen avoidance remains the cornerstone of management: meticulous food label reading (EU 14 major allergens must be labelled; USA FALCPA covers Big Nine), disclosure when eating out, and avoidance of cross-contamination. Emergency treatment for anaphylaxis: intramuscular epinephrine (adrenaline) 0.3-0.5 mg (adults) or 0.01 mg/kg (children) to the anterolateral thigh — first-line, lifesaving, must not be delayed; followed by 999/911 emergency call, supine positioning (legs elevated), supplemental oxygen, IV antihistamines (chlorphenamine), and corticosteroids (hydrocortisone IV) to reduce biphasic reaction risk. All patients with moderate-severe or systemic reactions must carry two epinephrine auto-injectors (EpiPen, Jext, Emerade) at all times. Oral immunotherapy (OIT): peanut OIT (Palforzia — FDA approved 2020; NICE approved UK 2023) involves controlled incremental exposure to peanut protein to induce desensitisation — achieves ingestion of 600 mg peanut protein in 67% of patients; suitable for peanut-allergic children aged 4-17. Antihistamines and corticosteroids are adjunctive for mild-moderate reactions only — never replace epinephrine.

Fatal anaphylaxis from food allergy is the most severe consequence — approximately 100-200 food-allergy deaths occur annually in the USA, predominantly in adolescents and young adults with peanut or tree nut allergy who did not carry or delayed using epinephrine. Delayed epinephrine administration is the leading modifiable factor in fatal anaphylaxis. Biphasic anaphylaxis — a second severe reaction 1-72 hours after apparent recovery — occurs in 5-20% of food-triggered cases and can be more severe than the initial episode, making hospital observation mandatory. Chronic psychological burden is significant — food-allergic individuals and their families experience heightened anxiety, food avoidance behaviours, dietary restriction, and reduced quality of life; approximately 30-45% of teenagers with food allergy develop food-related anxiety or eating disorders. Nutritional deficiencies from overly restrictive exclusion diets are a recognised risk, particularly in children with multiple food allergies. Children with severe eczema and unmanaged food allergy are at high risk for developing asthma and perennial rhinitis as part of the atopic march.

LEAP (Learning Early About Peanut Allergy) trial established that early introduction of peanut protein from age 4-11 months in high-risk infants (severe eczema or known egg allergy) reduces peanut allergy by 86% compared to avoidance. Current BSACI and NIAID guidelines recommend early peanut introduction (around 6 months, once weaning is underway) for all infants including high-risk. For high-risk infants, allergy specialist assessment before introduction is recommended. Similarly, early introduction of egg, milk, wheat, and other allergenic foods during complementary feeding reduces sensitisation. Regular dietary exposure after introduction maintains tolerance. Emollient therapy and good eczema control in infancy may reduce transcutaneous sensitisation. Probiotics during pregnancy and infancy may modestly reduce atopic disease risk.

Call emergency services (999/911) immediately if: throat tightening, difficulty swallowing, or change in voice after eating; severe breathing difficulty, wheeze, or stridor; collapse, loss of consciousness, or sudden severe drop in blood pressure; rapidly spreading hives across the body combined with any other symptom. Use epinephrine auto-injector (EpiPen) immediately — do not wait for symptoms to worsen. See an allergist if: you have had any allergic reaction to food; a child has eczema plus a food trigger; reactions are uncertain in cause; existing food allergy needs annual review for natural resolution (milk and egg allergy often resolves in childhood). Do not attempt food challenges at home — always performed under medical supervision.