Food Allergy in Colombia: Symptoms, Causes & Treatment | aihealz
Allergy & Immunologymoderate
Food Allergy.Care & specialists in Colombia
In Colombia, food Allergy is managed by allergy & immunologists. 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.
aliases · Food Allergy (IgE-mediated food hypersensitivity)· खाद्य एलर्जी (Khadya Allergy)· உணவு ஒவ்வாமை (Unavu Ovvamai)· Allergie alimentaire· reviewed May 12, 2026
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Reviewed by AIHealz Medical Editorial Board · Allergy & ImmunologyLast reviewed May 12, 2026
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.
key facts
Prevalence
10.8% of US adults and 7.6% of US children (Gupta 2019, JAMA Netw Open)
Demographics
Higher rates in non-Hispanic Black, Asian, and Hispanic children versus white children; female-skewed in adults
Avg. age
Onset typically before age 2 for milk, egg, wheat, soy; later for peanut, tree nut, shellfish (often lifelong)
Global cases
~220-250 million people worldwide; rising prevalence in industrialized countries over 20 years
Specialist
Allergy & Immunology
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How you might notice it
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..
01Hives (urticaria) and itching that appear within minutes of eating the trigger food, often starting around the mouth and spreading to the trunk and limbs.
02Swelling (angioedema) of the lips, tongue, eyelids, or face — sometimes severe enough to distort facial features within 10-30 minutes of exposure.
03Acute gastrointestinal symptoms including nausea, vomiting, cramping abdominal pain, and diarrhea, typically beginning 30 minutes to 2 hours after ingestion.
04
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How it’s diagnosed
diagnosis
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.
Key tests
01
Skin prick testingDetects food-specific IgE bound to skin mast cells. A wheal 3 mm or greater than the saline control indicates sensitization. Negative skin prick testing has a negative predictive value above 95% for IgE-mediated reactions and is useful for ruling out allergy.
✓Omalizumab (Xolair, 75-600 mg subcutaneous every 2-4 weeks)
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Causes & risk factors
known causes
IgE-mediated sensitization to a food protein
The immune system produces allergen-specific IgE antibodies after early exposure to a food protein, which bind to mast cell and basophil receptors. Subsequent exposure crosslinks the IgE, releasing histamine and other mediators within minutes.
Loss of oral tolerance during early life
Tolerance is the default immune response to ingested foods. Disruption — most often by delayed introduction, skin sensitization through eczematous skin, or altered gut microbiome — allows sensitization to occur. The LEAP trial (Du Toit 2015) showed early peanut introduction in high-risk infants reduces peanut allergy by 81%.
Skin barrier dysfunction and cutaneous sensitization
Loss-of-function variants in the filaggrin gene and active eczema allow food proteins from the environment to penetrate inflamed skin and prime allergen-specific IgE responses before the food has ever been eaten. This is the dual-allergen exposure hypothesis (Lack 2008).
Cross-reactive plant or tick-derived proteins
Pollen-food syndrome arises when IgE against birch pollen Bet v 1 cross-reacts with homologous proteins in apples, hazelnuts, and stone fruits. Alpha-gal syndrome is triggered by lone star tick saliva inducing IgE against a sugar (galactose-alpha-1,3-galactose) found in mammalian meat.
Non-IgE cellular immune responses to food protein
FPIES, food protein-induced proctocolitis, and eosinophilic esophagitis involve T-cell-driven inflammation rather than IgE. Symptoms are delayed, gastrointestinal-dominant, and not detected by skin prick or specific IgE testing.
Food-dependent exercise-induced anaphylaxis occurs when a food (commonly wheat) is tolerated at rest but causes anaphylaxis when followed by exercise within 2 hours. NSAIDs, alcohol, and acute infection lower the threshold for reaction in many sensitized patients.
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Living with it
01Introduce peanut-containing foods between 4 and 6 months of age in infants with severe eczema, egg allergy, or both — guided by the 2017 NIAID addendum based on the LEAP trial (Du Toit 2015 NEJM) which showed an 81% relative risk reduction
02Introduce common allergenic foods (egg, peanut, dairy, wheat, fish) into infant diet starting around 6 months alongside complementary foods, in line with EAT trial data (Perkin 2016 NEJM)
03Treat infantile eczema aggressively with topical emollients and corticosteroids to restore skin barrier function and reduce transcutaneous sensitization risk
04Exclusive breastfeeding for the first 4-6 months is recommended where feasible; routine maternal dietary restriction during pregnancy or lactation is not recommended
05Avoid unnecessary broad-spectrum antibiotics in the first year of life and support vaginal birth where clinically appropriate to preserve gut microbiome diversity
06Confirm vitamin D sufficiency in high-risk infants — supplement to maintain 25-hydroxyvitamin D above 50 nmol/L per pediatric guidelines
recommended foods
•Naturally allergen-free whole foods such as fresh fruit, vegetables, rice, quinoa, and meats (when tolerated)
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When to seek help
why see an allergy & immunology
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.
01Anaphylactic shock with airway obstruction, cardiovascular collapse, and death — preventable with prompt intramuscular epinephrine
02Biphasic anaphylaxis, occurring in approximately 5% of reactions 1-8 hours after apparent resolution, requiring extended emergency department observation
03Eosinophilic esophagitis presenting with dysphagia, food impaction, and chronic reflux, sometimes triggered or worsened by oral immunotherapy
04Nutritional deficiency and growth faltering in children with multiple food allergies, particularly milk, egg, wheat, and soy combined
05Anxiety, social isolation, and reduced quality of life — formal psychological support is recommended for children and parents struggling with restrictions
IgE-mediated food allergyClassic acute reaction within minutes to 2 hours of exposure. Includes urticaria, angioedema, vomiting, wheeze, and anaphylaxis. Confirmed by positive skin prick test or specific IgE plus a reproducible clinical history or oral food challenge.
Non-IgE-mediated food allergyCell-mediated reactions presenting hours to days after exposure. Includes food protein-induced enterocolitis syndrome (FPIES) with profuse vomiting 1-4 hours after ingestion, and food protein-induced proctocolitis with blood-streaked stools in breastfed infants.
Mixed IgE and cell-mediatedIncludes eosinophilic esophagitis and atopic dermatitis exacerbations. Symptoms are chronic and inflammatory rather than acute, and diagnosis often requires biopsy or supervised elimination diet.
Oral allergy syndrome (pollen-food syndrome)Localized itching and tingling of the lips, tongue, and palate after eating raw fruits or vegetables in patients with pollen allergy. Caused by cross-reactive proteins; usually mild and resolved by cooking the food.
Alpha-gal syndromeDelayed (3-6 hour) anaphylaxis to mammalian meat caused by IgE against galactose-alpha-1,3-galactose, triggered by lone star tick bites. Increasingly recognized in the southeastern US.
Living with Food Allergy
Timeline
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.
Lifestyle
01Carry two epinephrine auto-injectors at all times, with both kept at room temperature and replaced before expiry; teach family, school staff, and caregivers how to administer them
02Read every food label on every purchase — manufacturers reformulate without notice, and may-contain advisory statements vary by company and country
03Use a written, personalized anaphylaxis action plan reviewed annually with the allergist; share copies with school, childcare, and workplace
04Wear a medical alert bracelet or necklace listing food allergies and emergency contacts
05Inform restaurants of the allergy clearly and in writing where possible; favor establishments with documented allergen management training
06Avoid sharing utensils, plates, and lipsticks/lip balms with people who have recently eaten the trigger food
07Plan travel with extra epinephrine, medical letters, and translated allergy cards; identify nearby emergency facilities at destination
Complementary approaches
Probiotic-supplemented oral immunotherapyThe PPOIT trial (Tang 2015) combined peanut OIT with Lactobacillus rhamnosus and reported higher sustained unresponsiveness rates than OIT alone in a small pediatric cohort. Larger confirmatory trials are ongoing; not standard of care.
Chinese herbal Food Allergy Herbal Formula-2 (FAHF-2)An investigational herbal preparation studied at Mount Sinai. Phase II trials showed it is safe but did not significantly reduce reactivity threshold on its own. Mechanistic studies continue; not approved for clinical use.
Choosing a doctor
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.
Patient support resources
Food Allergy Research & Education (FARE) →Leading US patient advocacy and research organization, with anaphylaxis action plans, education, and a clinical network directory.
NIAID Food Allergy Guidelines →Official 2010 NIAID expert panel guidelines and the 2017 peanut-prevention addendum, with practical clinical summaries.
Anaphylaxis UK →UK patient charity offering helpline, training, school resources, and updates on regulation and product recalls.
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Frequently asked
What is the difference between food allergy and food intolerance?▾▴
Food allergy is an immune response, most often IgE-mediated, that triggers symptoms within minutes — hives, swelling, vomiting, or anaphylaxis — even after tiny exposures. Food intolerance, such as lactose intolerance, is a non-immune problem with digestion or absorption. It causes bloating, cramps, or diarrhea, is dose-related, and is never life-threatening. The two are confirmed with different tests and managed very differently.
Which foods cause most allergic reactions?▾▴
Nine foods cause more than 90% of reactions: peanut, tree nuts, cow's milk, hen's egg, wheat, soy, fish, crustacean shellfish, and sesame. Sesame was added in the US as the ninth recognized major allergen by the FASTER Act in 2021. The most common triggers in young children are milk, egg, and peanut; in adults, shellfish, peanut, tree nut, and fish predominate.
How soon after eating do food allergy symptoms appear?▾▴
IgE-mediated reactions typically start within 5-30 minutes of exposure and almost always within 2 hours. Non-IgE reactions such as FPIES or food protein-induced proctocolitis are delayed, often 1-4 hours for FPIES vomiting and up to 24-48 hours for skin or stool symptoms. Delayed anaphylaxis 3-6 hours after eating mammalian meat suggests alpha-gal syndrome.
How is food allergy diagnosed?▾▴
Diagnosis combines a detailed history with skin prick testing and specific IgE blood tests. Component-resolved diagnostics for proteins such as Ara h 2 improve accuracy for peanut. The gold standard is a supervised oral food challenge, used when testing and history disagree, to confirm a suspected allergy, or to confirm resolution of childhood allergy. IgG food panels, hair analysis, and applied kinesiology are not valid.
Can children outgrow food allergies?▾▴
Many children outgrow allergies to milk, egg, wheat, and soy by school age, with resolution rates of 50-80%. Peanut allergy is outgrown in roughly 20% and tree nut in 9-14%. Fish, shellfish, and sesame allergies are usually lifelong. Outgrowth should be confirmed by an oral food challenge in an allergist's office, not by home reintroduction.
What is the LEAP trial and why does it matter?▾▴
The LEAP trial (Du Toit 2015, NEJM) randomized 640 high-risk infants aged 4-11 months to early peanut introduction or avoidance. At age 5, peanut allergy was 81% less common in the early-introduction group. The result reversed earlier guidance and led to the 2017 NIAID addendum recommending peanut introduction at 4-6 months in high-risk infants. It is the foundation of modern food allergy prevention.
How is anaphylaxis treated?▾▴
Intramuscular epinephrine into the lateral thigh is the first-line treatment for anaphylaxis. The adult dose is 0.3 mg and the pediatric dose is 0.01 mg/kg up to 0.3 mg. Repeat at 5-15 minutes if symptoms persist. Antihistamines and steroids do not treat airway swelling or hypotension and must not substitute for epinephrine. After epinephrine, emergency department observation for at least 4-6 hours is needed.
When should I use an EpiPen?▾▴
Use the auto-injector at any sign of anaphylaxis: throat tightness, difficulty breathing, repeated coughing, hoarseness, dizziness, vomiting with hives, or rapid spread of symptoms beyond the skin. When in doubt, give epinephrine first and call emergency services. Underuse is the strongest predictor of fatal outcome. Epinephrine is safe in the rare patient who turned out not to be having a true reaction.
Is there a cure for food allergy?▾▴
No cure exists. Oral immunotherapy with peanut allergen powder (Palforzia, FDA-approved 2020) and the anti-IgE antibody omalizumab (FDA-approved February 2024) achieve desensitization — patients tolerate larger inadvertent exposures without severe reactions — but both typically require ongoing daily or regular dosing. Sustained off-treatment tolerance is achieved in a minority. Research into curative therapies is active.
What is oral immunotherapy (OIT)?▾▴
Oral immunotherapy is the daily ingestion of increasing doses of the allergen to raise the reaction threshold. The peanut OIT product Palforzia is given as a starting 0.5 mg dose escalated over 22 weeks to 300 mg daily maintenance. In the PALISADE trial, 67% of treated children tolerated 600 mg of peanut protein versus 4% on placebo. Side effects include abdominal pain and a small risk of eosinophilic esophagitis.
How is peanut allergy different from tree nut allergy?▾▴
Peanuts are legumes and tree nuts are botanically unrelated — almond, cashew, walnut, hazelnut, pistachio, and pecan are tree nuts. Cross-reactivity is variable: roughly 30-40% of peanut-allergic individuals also react to one or more tree nuts. Each food should be tested and challenged individually rather than assumed allergic. Avoiding all nuts unnecessarily worsens nutrition and quality of life.
Can adults develop food allergy?▾▴
Yes. Approximately 26-30% of US adults with food allergy developed it after age 18 (Gupta 2019, JAMA Netw Open). Shellfish is the most common adult-onset trigger. Adult-onset allergy rarely resolves and warrants prompt allergist referral, an action plan, and two epinephrine auto-injectors. Alpha-gal syndrome from lone star tick bites is a particularly important adult-onset cause of delayed anaphylaxis to mammalian meat.
Is food allergy hereditary?▾▴
There is a strong genetic component. A first-degree relative with food allergy, eczema, asthma, or hay fever roughly doubles personal risk. Twin studies estimate peanut allergy heritability at 82%. Filaggrin loss-of-function variants increase peanut allergy risk roughly 5-fold by impairing skin barrier function. Genes set susceptibility; early-life environment and feeding practices determine expression.
What is alpha-gal syndrome?▾▴
Alpha-gal syndrome is delayed anaphylaxis to mammalian meat (beef, pork, lamb) caused by IgE against galactose-alpha-1,3-galactose, a sugar found in mammals but not humans, fish, or birds. The trigger is a lone star tick bite, which sensitizes the immune system to the sugar. Reactions occur 3-6 hours after eating meat. Diagnosis is by specific IgE to alpha-gal. Strict mammalian meat avoidance is the main treatment.
Are food allergy tests reliable?▾▴
Skin prick testing and specific IgE blood tests are reliable when interpreted with clinical history. Negative tests rule out IgE-mediated allergy with over 95% confidence. Positive tests indicate sensitization, not necessarily clinical reactivity — about half of people with positive tests can eat the food without symptoms. This is why oral food challenges remain the gold standard. IgG food panels are not valid.
How can I prevent food allergies in my baby?▾▴
Current evidence supports introducing common allergenic foods, including peanut and egg, between 4 and 6 months alongside complementary feeding. In infants with severe eczema or egg allergy, introduce peanut between 4-6 months under guidance (per 2017 NIAID addendum). Treat eczema aggressively to restore skin barrier function. Avoid delaying allergen introduction and avoid restricting maternal diet during pregnancy or lactation.
Does cooking destroy food allergens?▾▴
Partly, depending on the food. Heat alters egg and milk proteins so that 70-80% of children with these allergies tolerate baked egg or baked milk in muffins and bread, supervised reintroduction can be considered. Peanut, tree nut, fish, and shellfish allergens largely survive cooking; roasting actually increases peanut allergenicity. Cooking does not make a true food allergy safe in general.
How much does food allergy treatment cost?▾▴
Epinephrine auto-injectors cost USD 110-700 per twin pack in the US depending on insurance and generic availability. Skin prick and specific IgE testing cost USD 100-500. Peanut OIT with Palforzia is approximately USD 4,200 per year before insurance. Omalizumab for food allergy is roughly USD 30,000-45,000 per year. Costs in India and other emerging markets are markedly lower, particularly for generic adrenaline and basic testing.
Can stress trigger a food allergy reaction?▾▴
Stress and acute illness do not cause new reactions, but they can lower the threshold at which a sensitized person reacts. Cofactors including exercise, NSAIDs, alcohol, menstruation, and febrile illness all amplify reaction severity to a known trigger. Patients should be especially careful about food choices during these periods and ensure epinephrine is immediately accessible.
Is food allergy linked to eczema and asthma?▾▴
Yes — these conditions are part of the atopic march. Infants with moderate-to-severe eczema have up to a 35% chance of developing food allergy. Roughly 30-40% of food-allergic children also have asthma, and uncontrolled asthma is the strongest predictor of fatal food-induced anaphylaxis. Allergic rhinitis is also common. Treating eczema early and controlling asthma reduce overall atopic morbidity.
When should I see an allergist?▾▴
See an allergist after any reaction suspicious for food allergy, particularly with respiratory or cardiovascular symptoms; when reactions are reproducible; when testing is needed to clarify a trigger; before starting oral immunotherapy or omalizumab; when an oral food challenge is needed to confirm resolution; for adult-onset reactions; and when multiple food allergies or co-existing asthma complicate management.
Respiratory involvement with throat tightness, hoarseness, repetitive coughing, wheeze, and shortness of breath — these features signal a more severe systemic reaction.
05Anaphylaxis with rapid-onset multi-system involvement: airway swelling, bronchospasm, hypotension, tachycardia, and loss of consciousness, usually within minutes to 1 hour of exposure.
06Oral 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.
07Eczema flares in infants and young children, particularly with milk, egg, peanut, or wheat exposure, occurring hours to days after ingestion rather than minutes.
08Repetitive projectile vomiting 1-4 hours after eating a trigger food in infants — the hallmark of food protein-induced enterocolitis syndrome (FPIES), often accompanied by pallor and lethargy.
09Blood-streaked or mucousy stools in otherwise well, breastfed infants — typical of food protein-induced proctocolitis, most commonly to cow's milk protein in maternal diet.
10Difficulty swallowing, food impaction, or persistent reflux symptoms suggesting eosinophilic esophagitis, which often shares triggers with classic food allergy.
early warning signs
•Tingling or itching of the lips, tongue, or palate within seconds of biting a food, even before swallowing
•Sudden hives or a flushed rash on the face or neck during or immediately after a meal
•Repeated coughing, throat-clearing, or a hoarse voice within 10-15 minutes of eating
•A sense of impending doom, dizziness, or rapid heartbeat after exposure to a known or suspected trigger
•Mild stomach upset, vomiting, or diarrhea consistently linked to the same food across multiple exposures
● emergency signs
•Difficulty breathing, throat tightness, hoarseness, or stridor — administer intramuscular epinephrine immediately and call emergency services
•Sudden dizziness, fainting, weak pulse, or pale clammy skin — signs of anaphylactic shock requiring epinephrine and supine positioning with legs elevated
•Hives or swelling combined with vomiting or any breathing change after eating — treat as anaphylaxis, do not wait for symptoms to worsen
•A return of symptoms 1-8 hours after initial improvement — biphasic anaphylaxis occurs in roughly 5% of cases and requires repeat epinephrine and emergency department observation
•Repetitive vomiting with profound lethargy in an infant after starting a new food — possible severe FPIES episode requiring IV fluids
Quantitative measurement of allergen-specific IgE in serum. Useful when extensive eczema, dermatographism, or required antihistamine use preclude skin testing. Higher values predict higher likelihood, not severity, of clinical reaction.
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Component-resolved diagnostics (e.g., Ara h 2 for peanut)Measures IgE to individual allergen proteins rather than whole-food extracts. Distinguishes true allergy from clinically silent cross-reactivity. Ara h 2 above 0.35 kU/L has a positive predictive value over 95% for peanut allergy.
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Oral food challenge (gold standard)Definitive test when history and testing disagree, to confirm or exclude allergy before introducing a food into the diet, or to confirm resolution of childhood allergy. Performed in a supervised allergy clinic with resuscitation equipment.
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Serum tryptase during acute reactionTryptase rises within 1-2 hours of mast cell activation and supports retrospective diagnosis of anaphylaxis. Particularly useful when the trigger is unclear or in fatal cases.
06
Endoscopy with esophageal biopsyRequired to diagnose eosinophilic esophagitis when food allergy presents with dysphagia or food impaction. Confirmation requires 15 or more eosinophils per high-power field on biopsy after 8 weeks of high-dose proton pump inhibitor therapy.
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Supervised elimination diet and reintroductionUsed for non-IgE conditions where laboratory testing is uninformative. Suspected foods are removed for 2-6 weeks; sustained improvement followed by symptom return on reintroduction confirms the trigger.
Outlook
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.
risk factors
Atopic dermatitis (eczema) in infancymodifiable
Moderate-to-severe infantile eczema is the strongest clinical predictor — up to 35% of these infants develop a food allergy. Disrupted skin barrier permits transcutaneous sensitization to environmental food proteins.
Family history of atopygenetic
A first-degree relative with food allergy, eczema, asthma, or allergic rhinitis roughly doubles risk. Twin studies estimate peanut allergy heritability at 82%.
Filaggrin gene loss-of-function variantsgenetic
Variants in FLG impair skin barrier and increase peanut allergy risk roughly 5-fold independent of eczema severity.
Delayed introduction of allergenic foodsmodifiable
Postponing peanut, egg, and other common allergens beyond 6-11 months in high-risk infants raises lifetime allergy risk. The 2017 NIAID addendum reversed prior guidance and now recommends introduction between 4-6 months in high-risk infants.
Non-Hispanic Black, Asian, or Hispanic ancestry (US data)non-modifiable
US childhood food allergy prevalence is highest in non-Hispanic Black (8.7%) and Asian (7.4%) children compared with non-Hispanic white (6.8%) — driven by a mix of genetic, environmental, and access factors.
Caesarean delivery and early-life antibiotic exposureenvironmental
Altered gut microbiome from C-section delivery and broad-spectrum antibiotics in the first year is associated with a 20-30% higher risk of food allergy in observational cohorts.
Vitamin D insufficiency in infancymodifiable
Lower 25-hydroxyvitamin D levels correlate with higher food allergy prevalence in some cohorts (HealthNuts study, Australia). Causality is unsettled but supplementation in deficient infants is reasonable.
Geographic latitude (higher latitudes, less UV exposure)environmental
EpiPen prescription rates and EpiPen-treated anaphylaxis rise with distance from the equator, suggesting a vitamin D and microbial exposure gradient.
Lone star tick bites (alpha-gal syndrome)environmental
Bites from Amblyomma americanum induce IgE against galactose-alpha-1,3-galactose, causing delayed anaphylaxis to mammalian meat. Endemic in southeastern and central US.
•Calcium-fortified plant milks (oat, rice, pea) for children with cow's milk allergy under dietetic supervision
•Alternative protein sources matched to the missing allergen — legumes (for non-legume allergic children), seeds, and well-tolerated meats
•Foods rich in vitamin D, omega-3, and zinc to support skin barrier and immune regulation
•Diverse complementary feeding in infants once allergens have been safely introduced, to maintain oral tolerance
foods to avoid
•The specific trigger food in any quantity, including hidden sources in processed foods and shared production lines
•Cross-contact in shared kitchens, fryers, ice cream scoops, and bakery surfaces — particularly relevant for peanut, tree nut, and shellfish
•Foods carrying may contain or processed in a facility advisory labels for the trigger allergen, in moderate-to-high-risk patients
•Buffets, family-style serving, and unlabelled bakery items where contamination risk is unpredictable
•Cosmetics, soaps, and topical products containing the allergen if there is a history of contact reactions
•Unproven IgG food intolerance panels and broad elimination diets without specialist supervision — they cause nutritional deficiency and unwarranted restriction
06Severe reactions during oral immunotherapy — 10-15% of patients withdraw because of recurrent gastrointestinal symptoms, anaphylaxis, or new eosinophilic esophagitis
08Stay current with annual allergist review for testing trends, immunotherapy options, and outgrowth assessment
Daily management
01Check epinephrine auto-injector expiry monthly and replace promptly; store at room temperature, never in a hot car or freezer
02Read every label at every grocery trip; verify ingredients with restaurant servers and chefs at every meal
03Keep a brief written symptom and exposure diary, particularly during oral immunotherapy or after accidental exposures, to share at allergist visits
04Coordinate with school or childcare on allergen-aware meal plans, emergency drills, and staff training every academic year
05Take maintenance OIT doses consistently — missed doses for more than a few days can cause loss of desensitization and the dose must then be re-escalated under supervision
Exercise
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.