Evaluation of food allergies and sensitivities

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Theory 
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Last reviewed: 10 Apr 2025

Last updated: 13 Feb 2024

Food allergy is defined as an adverse immunologic response to a food protein.[1] Although approximately 19% of adults in the US have a perceived adverse reaction to food, only 10.8% have a convincing history of true food allergy, according to a cross-sectional survey study.[2] In a separate study of US households, approximately 11% of children were perceived by their parents to have a food allergy, but only 7.6% had a convincing history of true food allergy.[3]

People who believe they have a food allergy may suffer from a metabolic intolerance to a particular food; for example, lactose intolerance. Others may be sensitive to a particular pharmacologically active component of food such as caffeine or tyramine. Some people may mistake bacterial food poisoning as a reaction to a particular food.[1][4] Although all of these scenarios involve food, they do not result from an abnormal immune response to a particular food protein and therefore cannot be considered a true food allergy.[5] Rather, some of them, such as lactose intolerance and sucrase-isomaltase deficiency, are considered nonimmune food intolerances, and others, such as tyramine and sulfite reactions, are considered nonimmune food sensitivities.

It is important that people with suspected food allergy are investigated and followed up appropriately so that they do not unnecessarily avoid food and impair their quality of life.[2]

Pathophysiology

Food allergies can be classified into disorders that are IgE-mediated, cell-mediated, or a combination of the two.[6]

IgE-mediated food allergies result from abnormal sensitization to a food allergen that results in specific IgE production. However, a positive skin prick test or IgE test on its own does not indicate that a patient has a food allergy; it only means that they are sensitized to a food. Only the history or an oral food challenge can identify true food allergens. Once produced, food-specific IgE binds onto mast cells. When the particular food is subsequently ingested, the food is broken down and absorbed. The food antigen then binds to the IgE on the mast cells leading to mast-cell degranulation and release of mediators that cause the signs and symptoms of the allergic reaction.[6] IgE-mediated food disorders include anaphylaxis and oral allergy syndrome.

Cell-mediated reactions involve T cells and may occur several hours to days after ingesting the offending food.[6] Food protein-induced enterocolitis, enteropathy, proctocolitis, and celiac disease are examples of cell-mediated food-allergic diseases.

Mixed IgE- and cell-mediated food diseases include atopic dermatitis and the eosinophilic gastroenteropathies such as eosinophilic esophagitis.[6]

Nonimmune food intolerances often result from deficiencies in the enzyme that breaks down the food component into absorbable substrates in the small intestine.[7]

Nonimmune food sensitivities to biogenic amines (such as tyramine) or to food additives (such as monosodium glutamate) are more controversial and are debated vigorously in the literature.[8][9] However, sensitivities to sulfites found in foods such as red wine and dried fruit have been confirmed as a trigger of bronchospasm in sulfite-sensitive asthmatic patients.[10]

Differentials

Common

Oral allergy syndrome
Atopic dermatitis
Food protein-induced proctocolitis
Celiac disease
Lactose intolerance

Full details

Uncommon

Food-induced anaphylaxis
Food-dependent exercise-induced anaphylaxis
Eosinophilic esophagitis
Food protein-induced enterocolitis
Congenital sucrase isomaltase deficiency
Monosodium glutamate (MSG) reactions
Tyramine reactions
Sulfite sensitivity
Galactose-alpha-1,3-galactose (alpha-gal) allergy (tick borne)

Full details

Contributors

Authors

J. Andrew Bird, MD

Associate Professor

Department of Pediatrics

Division of Allergy and Immunology

University of Texas Southwestern Medical Center

Dallas

Disclosures

JAB has received grant funding from DBV Technologies, FARE, and Aimmune Therapeutics, and he has received advisory board fees from DBV Technologies, FARE, Pharm-Olam International Ltd, Aimmune Therapeutics, Pfizer Pharmaceuticals, Allergy Therapeutics Ltd, and AllerGenis. He has received speaking fees from Abbott, DBV Technologies, and Aimmune Therapeutics.

A. Wesley Burks, MD

Curnen Distinguished Professor and Chair

Department of Pediatrics

University of North Carolina

Chapel Hill

Disclosures

AWB receives grant support to his institution from the National Institutes of Health, Food Allergy Research & Education, and Allergen Research Corporation; royalties from UpToDate; consulting honorariums from Aravax, Astella Pharma Global Development, DBV Technologies and N-Fold, LLC, as well as Aimmune Therapeutics, Consortia TX, Inc., Intrommune Therapeutics, and Prota Therapeutics for his service on their respective Scientific Advisory Boards. AWB has consulted for the following companies (which are all now expired): Biomerica, Inc., Evelo Biosciences/Epiva, Genentech, Insys Therapeutics, PPD Development, Sanofi US Services, Valeant Pharmaceuticals North America, LLC, LEK Consulting, LLC, Hycor Biomedical. AWB has received payments for speaking at the Gordon Research Conferences, the Pediatric Allergy and Asthma Meeting, and the American College of Allergy Asthma and Immunology. AWB is a minority stockholder of both Allertein and Mastcell Pharmaceuticals stock. These interests do not directly relate to the article but are being shared for full disclosure. AWB is an author of references cited in this topic.

Acknowledgements

Dr J. Andrew Bird and Dr A. Wesley Burks would like to gratefully acknowledge Dr Alison Church, previous contributor to this topic.

Disclosures

AC declares that she has no competing interests.

Peer reviewers

Aaron Lerner, MD

Head of Pediatric Gastroenterology and Nutrition Unit

Carmel Medical Center

Haifa

Israel

Disclosures

AL declares that he has no competing interests.

Roy Gerth van Wijk, MD, PhD

Professor of Allergology

Head of Section of Allergology

Department of Internal Medicine

Erasmus Medical Center

Rotterdam

The Netherlands

Disclosures

RGvW declares that he has no competing interests.

References

Our in-house evidence and editorial teams collaborate with international expert contributors and peer reviewers to ensure that we provide access to the most clinically relevant information possible.

Key articles

Shaker MS, Wallace DV, Golden DBK, et al. Anaphylaxis-a 2020 practice parameter update, systematic review, and Grading of Recommendations, Assessment, Development and Evaluation (GRADE) analysis. J Allergy Clin Immunol. 2020 Apr;145(4):1082-123.Full text Abstract

Lieberman P, Nicklas RA, Randolph C, et al. Anaphylaxis - a practice parameter update 2015. Ann Allergy Asthma Immunol. 2015 Nov;115(5):341-84. Abstract

Golden DBK, Wang J, Waserman S, et al. Anaphylaxis: a 2023 practice parameter update. Ann Allergy Asthma Immunol. 2024 Feb;132(2):124-76.Full text Abstract

Rubio-Tapia A, Hill ID, Semrad C, et al. American College of Gastroenterology guidelines update: diagnosis and management of celiac disease. Am J Gastroenterol. 2023 Jan 1;118(1):59-76.Full text Abstract

Sampson HA, Aceves S, Bock SA, et al. Food allergy: a practice parameter update-2014. J Allergy Clin Immunol. 2014 Nov;134(5):1016-25.e43.Full text Abstract

Reference articles

A full list of sources referenced in this topic is available to users with access to all of BMJ Best Practice.

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Evaluation of food allergies and sensitivities

Summary

Pathophysiology

Differentials

Common

Uncommon

Contributors

Authors

J. Andrew Bird, MD

Disclosures

A. Wesley Burks, MD

Disclosures

Acknowledgements

Disclosures

Peer reviewers

Aaron Lerner, MD

Disclosures

Roy Gerth van Wijk, MD, PhD

Disclosures

References

Key articles

Reference articles

A full list of sources referenced in this topic is available to users with access to all of BMJ Best Practice.

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