Assessment of food allergies and sensitivities

Last reviewed:December 2019

Last updated:July 2019

Summary

Food allergy is defined as an adverse immunological 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 non-immune food intolerances, and others such as tyramine and sulfite reactions are considered non-immune 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 sensitisation 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 sensitised to a food. Only the history, or an oral food challenge, can identify true food allergens. Once produced, food-specific IgE binds on to 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 coeliac 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 oesophagitis.[6]

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

Non-immune 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
Coeliac disease
Lactose intolerance

Full details

Uncommon

Food-induced anaphylaxis
Food-dependent exercise-induced anaphylaxis
Eosinophilic oesophagitis
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

AuthorsVIEW ALL

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.

Peer reviewersVIEW ALL

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.

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Summary

Pathophysiology

Differentials

Common

Uncommon

Contributors

AuthorsVIEW ALL

J. Andrew Bird, MD

Disclosures

A. Wesley Burks, MD

Disclosures

Acknowledgements

Peer reviewersVIEW ALL

Aaron Lerner, MD

Disclosures

Roy Gerth van Wijk, MD, PhD

Disclosures

Guidelines

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