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

Food allergy is a reproducible immune-mediated adverse reaction to specific food proteins, affecting approximately 250 million people globally — including 8% of children and 2–3% of adults in developed nations. The most common food allergens are the 'big nine' (USA labelling law): milk, eggs, peanuts, tree nuts, wheat, soy, fish, shellfish, and sesame; EU food law additionally requires labelling of celery, mustard, lupin, sulphites, and molluscs (the 'big 14'). The majority (75%) of IgE-mediated food allergy reactions are triggered by just four allergens: peanut, tree nuts, fish, and shellfish. Food allergy differs fundamentally from food intolerance (such as lactose intolerance) in that it involves immune system activation and can cause life-threatening reactions at microgram quantities of the food. IgE-mediated allergy — the most clinically significant form — causes immediate reactions within minutes to 2 hours via mast cell degranulation. Non-IgE-mediated allergy (e.g., food protein-induced enterocolitis syndrome — FPIES) involves T-cell pathways and causes delayed reactions. Reactions range from mild urticaria and oral tingling to life-threatening anaphylaxis with cardiovascular collapse, making accurate diagnosis via specialist allergy assessment, epinephrine auto-injector provision, and emergency preparedness education essential for all patients and families.

Food allergy occurs when the immune system develops specific IgE antibodies against normally harmless food proteins, establishing allergic sensitisation. On re-exposure, the allergen cross-links IgE bound to the surface of mast cells and basophils, triggering degranulation and release of histamine, prostaglandins, leukotrienes, and platelet-activating factor — producing the immediate allergic response. Non-IgE-mediated reactions (FPIES — food protein-induced enterocolitis syndrome; food protein-induced allergic proctocolitis; food protein-induced enteropathy) involve T-cell pathways and eosinophilic inflammation without IgE, causing delayed gastrointestinal symptoms (vomiting, diarrhoea) typically to milk, soy, or rice in infants. Risk factors include: personal or family history of atopic disease (eczema is the strongest predictor — sensitisation occurs through disrupted epidermal barrier, particularly in atopic dermatitis where food proteins penetrate inflamed skin); the 'dual-allergen exposure hypothesis' — oral introduction of foods leads to tolerance, while cutaneous sensitisation through eczematous skin promotes allergy; reduced gut microbial diversity in infancy (formula feeding, Caesarean section delivery, antibiotic exposure reduce colonisation with Bifidobacterium and Lactobacillus species, impairing regulatory T-cell development); filaggrin (FLG) gene loss-of-function mutations (present in 10% of European populations — causing skin barrier defects and eczema — are strongly associated with peanut and egg allergy); Vitamin D deficiency in infancy; living in urban environments with reduced microbial exposure ('hygiene hypothesis').

IgE-mediated food allergy symptoms typically appear within minutes to 2 hours of allergen ingestion and can affect multiple organ systems simultaneously. Cutaneous symptoms (the most common): urticaria (hives — raised, intensely itchy wheals with surrounding erythema), angioedema (deep tissue swelling, particularly of the face, lips, tongue, and periorbital area — alarming in appearance but not immediately life-threatening unless airway-compromising), flushing, and pruritus. Oral allergy syndrome (OAS/pollen-food allergy syndrome): immediate tingling, itching, and mild swelling of the lips, tongue, and palate after eating raw fruits, vegetables, or nuts — caused by IgE cross-reactivity between pollen proteins (e.g., birch pollen) and structurally homologous food proteins (e.g., apple, peach, hazelnut); OAS proteins are heat-labile and denatured by cooking — cooked apple is tolerated; OAS rarely causes systemic anaphylaxis. Gastrointestinal symptoms: nausea, vomiting, abdominal cramping, and diarrhoea — commonly accompany other allergic symptoms. Respiratory symptoms: rhinorrhoea, nasal congestion, bronchospasm, wheezing, and stridor (from laryngeal oedema) — present in moderate-to-severe reactions. Anaphylaxis — the most severe IgE-mediated reaction: involves two or more body systems simultaneously (or cardiovascular compromise alone after likely allergen exposure); features include hypotension (systolic below 90 mmHg), tachycardia, dizziness, collapse, loss of consciousness, and impending sense of doom; anaphylaxis carries a 1% fatality risk if epinephrine is delayed; biphasic anaphylaxis (recurrence 1–72 hours after apparent initial recovery without re-exposure) occurs in 5–20% of cases — mandating 4–6 hour observation post-epinephrine.

A comprehensive allergy assessment integrates clinical history, validated testing, and in selected cases supervised oral food challenge. Clinical history is the cornerstone: the allergist evaluates the specific food implicated, dose causing reaction (threshold dose — important for risk stratification), timing from ingestion to symptom onset (immediate versus delayed), symptoms produced, whether the reaction was reproducible on re-exposure, any cofactors present (exercise-induced food allergy — exercise within 4 hours of allergen ingestion triggers anaphylaxis; alcohol; NSAIDs; sleep deprivation), and tolerance history (whether previously tolerated food). Skin prick testing (SPT): a standardised allergy testing method — commercial food extracts are applied to the forearm skin, and a lancet creates a small puncture; a wheal diameter at 15 minutes above 3 mm greater than the negative control (saline) indicates sensitisation; sensitivity 70–90% but specificity 50–70% (positive SPT indicates sensitisation but not necessarily clinical allergy). Fresh food prick-to-prick testing — using the fresh food rather than commercial extract — is superior for unstable allergens (fresh fruits, vegetables). Serum specific IgE (ImmunoCAP/RAST): quantifies IgE antibody concentration against specific allergens; results reported in kUA/L; a higher specific IgE correlates with higher probability of clinical reactivity but not reaction severity. Component-resolved diagnostics (CRD): identifies specific protein components within a food allergen — for peanut: Ara h 2 specific IgE above 0.35 kUA/L is the best predictor of clinical peanut allergy; Ara h 8 (birch pollen cross-reactive protein) indicates OAS rather than systemic allergy. Oral food challenge (OFC): the diagnostic gold standard — performed by allergist in a hospital or clinic setting with resuscitation equipment; involves graded doses of the implicated food under direct observation; confirms or excludes clinical allergy and determines the threshold dose.

Strict, complete avoidance of the identified food allergen remains the primary management strategy — patients and families require structured education on allergen labelling regulations (EU and UK law requires the 14 major allergens to be declared in bold on pre-packaged foods and verbally communicated for non-packaged foods in food service settings), hidden allergen sources, cross-contamination risks, and how to read ingredient lists. Every patient with IgE-mediated food allergy at risk of anaphylaxis must be prescribed and trained to use an epinephrine auto-injector (EpiPen 0.3 mg for adults and children over 25 kg; EpiPen Junior 0.15 mg for 15–25 kg; Jext and Emerade are UK alternatives) — two auto-injectors should be carried at all times; intramuscular injection into the anterolateral thigh (through clothing if necessary) is the correct technique. A personalised written allergy action plan (provided by the allergist) specifies when to use epinephrine, when to call emergency services, and when oral antihistamines alone are appropriate for mild reactions. Oral immunotherapy (OIT): peanut OIT (Palforzia — FDA-approved January 2020; EMA-approved February 2020 for ages 4–17): a standardised peanut allergen powder escalated over months from 0.5 mg to 300 mg/day maintenance; reduces the risk of anaphylaxis from accidental peanut exposure — the Phase 3 PALISADE trial showed 67% of treated patients could tolerate 600 mg peanut protein versus 4% of controls; ongoing daily dosing is required to maintain desensitisation; mild GI reactions in 15% and systemic reactions requiring epinephrine in 2–5% during escalation. Dupilumab (anti-IL-4 receptor alpha monoclonal antibody — licensed for eczema and asthma): facilitates OIT by reducing background allergic inflammation during updosing in highly reactive patients. Omalizumab (anti-IgE): reduces IgE-mediated sensitisation — approved for multi-allergen OIT facilitation and food allergy treatment (FDA 2024 for multi-food allergy protection, ages 1+ years).

Anaphylaxis is the most serious and potentially fatal complication — mortality occurs from asphyxia (laryngeal oedema causing complete airway obstruction), cardiovascular collapse (profound distributive shock from massive vasodilatation), or both. Approximately 150–200 deaths per year occur from food anaphylaxis in the UK and USA combined, with peanut, tree nuts, fish, shellfish, and sesame responsible for the majority. Risk factors for fatal anaphylaxis include delayed or absent epinephrine administration, concomitant asthma (the primary independent risk factor — 90% of food anaphylaxis fatalities have a history of asthma), adolescent and young adult age group (risk-taking behaviours, not carrying medication), and beta-blocker use (reduces response to epinephrine). Accidental allergen exposure occurs in 20–50% of food-allergic individuals annually despite best efforts — hidden allergens in manufactured foods, cross-contamination in food service settings, and errors in allergen declaration contribute to exposure. Food allergy significantly impairs quality of life — validated measures show food-allergic children have quality-of-life scores comparable to children with type 1 diabetes; anxiety about accidental exposure is pervasive; 40–50% of adolescents with food allergy report food anxiety, social isolation, and food-related fear limiting participation in social and school activities.

The LEAP trial (Learning Early About Peanut allergy) definitively established that early introduction of peanut products (4–11 months of age) in high-risk infants (severe eczema or egg allergy, or both) reduces peanut allergy development by 80% — revolutionising infant feeding guidelines globally. Current NICE, BSACI, and AAP guidelines recommend: regular introduction of common allergenic foods (peanut, cooked egg, wheat, fish, sesame) from 4–6 months of age in all infants, including those with mild-to-moderate eczema; infants with severe eczema should have allergy assessment before peanut introduction (skin prick test or specific IgE to guide the setting of first introduction). Breastfeeding is recommended for at least 6 months — maternal diet does not need to exclude common allergens. Probiotic supplementation in infancy and early childhood shows emerging evidence for allergy prevention in high-risk infants. Label vigilance: read every food label on every purchase — manufacturers change ingredients without prominent announcement; 'may contain' advisory labelling (PAL — precautionary allergen labelling) is voluntary and not legally standardised but indicates a genuine cross-contamination risk that should be avoided by highly sensitive patients.

Call 999 and administer epinephrine (EpiPen) immediately for any anaphylaxis — throat tightening, difficulty breathing, rapid swelling of lips or tongue, loss of consciousness, or cardiovascular collapse after eating. Always call 999 even if epinephrine is given, as a biphasic reaction can occur up to 12 hours later. See a GP urgently for: a first-time allergic reaction to food with systemic symptoms (urticaria, vomiting, wheezing); any unexplained anaphylaxis; or a child with facial swelling after eating. Request referral to an allergist for: formal skin prick testing and specific IgE blood tests; oral food challenge under medical supervision; and consideration of oral immunotherapy for peanut allergy. Carry an epinephrine auto-injector and allergy action plan at all times once allergy is confirmed.