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Food Intolerance and Food Allergy

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Some people have an adverse reaction on exposure to certain foods that can make them unwell. This can be a recurring reaction, happening each time that person ingests the food. Symptoms range from vomiting and diarrhoea to skin reactions, angioedema, respiratory distress and anaphylaxis.

A good way to classify adverse reactions to foods is as either:

  1. True food allergy
  2. Non-allergic food intolerance
The mechanism of food allergy

Food allergy occurs when the body's immune system mounts an exaggerated response against the offending food, which acts as an allergen. It is a type of hypersensitivity reaction. It can be either:

  • A type I, IgE-mediated reaction: this is the usual cause of food allergy. After initial sensitisation, the release of mediators such as histamine are triggered each time a person is exposed to the food. It is these mediators that cause the symptoms.
  • A delayed, type IV-mediated reaction: these reactions are mediated mainly by T cells. They typically affect the gastrointestinal tract or skin, for example exacerbation of eczema in children after milk ingestion.
The mechanism of food intolerance
  • Food intolerance includes any adverse physiological responses that can occur to foods that are not immunologically mediated.
  • It may be due to metabolic, toxic or pharmacological reactions to foods.1
  • If foods are contaminated by bacteria or toxins, this can lead to food intolerance in the form of 'food poisoning'. Eating tuna or mackerel that has gone off can lead to scombroid poisoning.
  • Monosodium glutamate can cause flushing, headache and abdominal symptoms.
  • Lactase deficiency, leading to lactose intolerance, is a metabolic non-allergic food intolerance that causes diarrhoea and abdominal symptoms after milk is ingested.
  • Coeliac disease is an autoimmune inflammatory disorder of the small intestine induced by exposure to gluten in genetically predisposed individuals.
Food aversion

Another important definition is that of food aversion. This refers to the dislike of, or an emotional response to, a particular food.2 The symptoms may be non-specific and do not occur when the person is faced with a blinded food challenge.

Epidemiology
  • Generally atopy seems to be rising worldwide and food allergy seems to be part of this trend.3
  • The prevalence of food allergies in children less than 3 years old is estimated at 8%.4
  • The prevalence in adults, confirmed by a double blind food challenge in one study, was 1.4%. However, in the same study, self-reported food intolerance had a 20% prevalence showing that a much higher number of people attribute symptoms to being caused by food than actually are.5
  • Estimated prevalence for peanut allergy is 0.5-0.6% in the UK and USA.6,7
  • That for egg is 2.6% by 2.5 years old.8
The foods commonly involved
  • Cows' milk
  • Hens' eggs
  • Cod
  • Shrimps and other shellfish
  • Peanuts
  • Tree nuts
  • Soy beans
  • Wheat
  • Food additives
Presentation

IgE mediated food allergy

Symptoms usually occur within minutes of food intake and the specific food causing the symptoms can usually be identified. The same food allergen can produce different symptoms in different people.

  • Swelling and itching of the lips, tongue, mouth and oropharynx (angio-oedema)
  • Exacerbation of asthma/wheezing
  • Urticaria
  • Nausea, vomiting and diarrhoea
  • Abdominal pain
  • Diarrhoea
  • Anaphylactic shock

Type IV mediated food allergy

  • Diarrhoea
  • Vomiting
  • Abdominal discomfort
  • Skin reactions such as eczema
Conditions associated with food allergy and intolerance
  • Asthma: asthma alone as a manifestation of food allergy is rare and atypical.4 In children with asthma, those with co-existing food allergy may have an increased asthma morbidity.9 Patients with asthma are also more likely to develop a fatal, or near fatal, food reaction.4
  • Atopic dermatitis: usually affects children. Common causes are cow's milk, eggs, soya, wheat. Approximately one third of children with moderate to severe atopic dermatitis have food allergy.10
  • Rhinitis: isolated rhinitis due to food allergy is extremely rare.11
  • Eosinophilic gastroenteropathies: features are dysphagia, weight loss, oedema, ascites, obstruction. Caused by multiple foods.
  • Dietary protein enteropathy: affects children. Features are malabsorption due to intestinal mucosa damage, vomiting, diarrhoea, failure to thrive. Cow's milk is a common cause.
  • Dietary protein enterocolitis/proctitis: affects children. Diarrhoea, failure to thrive, lethargy, vomiting, mucus and bloody stools in proctitis. Causes are cow's milk, soya, grains.
  • Coeliac disease: affects all ages. Malabsorption and diarrhoea caused by gluten intolerance. Please refer to the separate article on coeliac disease.
  • Dermatitis herpetiformis: associated with Coeliac disease. Affects all ages. Papulovesicular skin lesions caused by gluten intolerance. Please refer to the separate article on dermatitis herpetiformis.
  • Pulmonary haemosiderosis: affects children. Features are haemosiderosis, anaemia, pulmonary infiltrates and failure to thrive caused by intolerance to cow's milk. Rare.
  • Lactose intolerance: due to a deficiency in the intestinal enzyme lactase. The deficiency may be inherited or transient, due to intestinal mucosa damage by infection, allergy or inflammation. Features include bloating, abdominal pain and loose stools after exposure to lactose-containing substances such as milk. Please refer to the separate article on lactose intolerance.
Investigations
  • History: the most important diagnostic tool is good history taking. The suspected allergen may be easily identified from this. What does the patient mean by food allergy? Are they really describing a non-allergic food intolerance? What foods do they feel are implicated? What is the worst reaction that the person has had? Are they at risk of anaphylaxis? Is there a personal or family history of allergy? Is the diet nutritionally adequate?
  • Examination: especially in children, measure and plot/record height and weight. Look for signs of other atopic disease, e.g. eczema, asthma.
  • Skin prick testing: a drop of liquid or solid food is placed on the skin of the forearm. A lancet or needle is used to prick the skin through the allergen solution. A saline based control solution is also used at a separate site on the forearm. The reaction is 'read' after 15 minutes. A positive result is a skin weal >2 mm greater than that observed with the negative control solution.12 The result should be interpreted with referral to the history. Note that food extracts are not available, and skin-prick testing has not been validated, for all foods. There have been some cases of systemic reactions and anaphylaxis in food allergen testing.
  • Measurement of serum allergen-specific IgE: examples are the radioallergosorbent (RAST) test, enzyme linked immunosorbent assay (ELISA) and fluorescent-enzyme immunoassay (FEIA). Care must be taken as this may also highlight clinically insignificant cross reactions with other allergens so results must be interpreted with caution and always in conjunction with the clinical history. However, this test is safe and can be used in people who have widespread skin disease.
  • Elimination diet: this should be supervised by a dietician. The suspected problem food or foods are excluded from the diet and symptoms are reviewed. The foods are then reintroduced one-by-one to see if the symptoms recur. Ideally the food challenge involves the food, in a disguised form, and a placebo, given at separate times. Dietary elimination is easy in infants who are fed with formula milk but involves diet restriction for the mother in breastfed infants.
  • Food challenge: if diagnosis is in doubt, an oral food challenge can be undertaken by staff with specialist training and where full resuscitation equipment and drugs are available. The food is introduced in incremental doses and any reaction is observed. Ideally, the challenges should be double blind, placebo controlled. For non-IgE-mediated reactions, oral food challenges are usually the only way that a diagnosis can be reached. A food challenge should not be performed if the history suggests an anaphylactic reaction is possible.
Management

The management of an anaphylactic reaction is discussed in the article 'Anaphylaxis and its treatment'.

If an IgE-mediated food allergy is suspected, refer the patient to an allergy specialist. In the meantime, advise the patient to avoid the food trigger and consider prescription of injectable adrenaline, to be carried at all times, with full instructions for use.13

  • Food avoidance: the only treatment for food allergy and intolerance is food avoidance. This is particularly crucial in the case of a previous anaphylactic reaction to a food substance and can prove very difficult when eating out and when buying food as cross-contamination can occur. Food labelling is also an issue and laws on this are being tightened.
  • Dietician referral: this is helpful. Patients should be taught to read food labels carefully. Detailed written advice on avoidance strategies can be helpful. Dietary deficiencies can be anticipated and prevented. The possibility of allergen cross-reactivity should also be discussed, for example, > 90% of those allergic to cow's milk are allergic to goat's milk.14
  • Antihistamines: if symptoms are less severe, for example just pruritis or urticaria, antihistamines can be helpful. However, caution should be used as they may mask more serious reactions and the patient's degree of sensitivity can increase over time.
  • Adrenaline: if respiratory symptoms or severe anaphylactic reactions have occurred, or the allergy is to foods that commonly cause severe reactions such as peanuts, or there is a history of asthma, the need for stand by adrenaline should be considered.
  • Medic Alert bracelets or necklaces: these should be worn by people at risk of anaphylaxis.
  • Parents, relatives, schools and carer education: anyone closely involved with the person who has the food allergy or intolerance, particularly if there is risk of an anaphylactic reaction, should be informed and educated about what to do if a reaction occurs. A written emergency plan is helpful.
  • Support groups: there are many groups available for patients and their families. Please refer to the internet links below.
Complications

Severe anaphylactic reactions can result in cardiovascular collapse and death if not treated. However, death is rare and the risk of a child with food allergy dying is between 1 in 0.5 million and 1 in 1.5 million per year.15

Prognosis
  • About 85% of children 'grow out' of their allergy to most foods (eggs, milk, wheat, soya) by 3-5 years.16 This may be due to maturation of the gut or maturation of immune responses that are responsible for allergy.
  • Adults with food allergy can develop tolerance after appropriate food elimination diets have been implemented. One third of all adults and children lose their clinical reactivity to food allergens after 1-2 years of food elimination diets.14
  • Sensitivity to peanuts, seafood, fish and tree nuts is rarely lost.3
Prevention

Breast-feeding for 6-12 months is promoted as a way to prevent food allergy and atopy, however, there is some controversy surrounding this. Debate exists as to whether breast-feeding is protective against the development of allergies or is in fact sensitizing. However, in general, studies show that infants that are fed cow's milk or soy protein formula have a higher incidence of atopic dermatitis and wheezing illness in early childhood and support the fact that breast-feeding should be encouraged.17

There is also a school of thought suggesting that breast-feeding mothers should avoid allergenic foods such as peanuts and shellfish. In June 1998, the UK government advised that atopic pregnant and breast-feeding mothers and their infants should avoid peanuts. However, a study looking at the first school cohort to have been conceived after the advice was issued found that the cohort had an increased prevalence of peanut sensitisation. The study was unable to draw any conclusions from the impact of the government advice.18

Delayed introduction of solid foods until the child is 5 months old as an allergy prevention measure is also controversial.19 A systematic review published in 2006 showed that early solid feeding before 4 months may increase the risk of eczema but there was no evidence to show an association between early solid introduction and the development of food allergy. The review pointed out that the methods in most of the studies reviewed were flawed and that additional controlled trials are needed.20

There is also some controversy about at what age a child with a family history of atopy should be introduced to certain foods that are linked to food allergy such as milk, peanut, eggs, nuts and fish. The Isle of Wight prevention study looked at the prevention of allergic disease during childhood by allergen avoidance and concluded that allergic diseases can be reduced, for at least the first 8 years of life, by combined food and house dust mite allergen avoidance in infancy.21

Other considerations
  • Some vaccines are produced on egg-based media.
  • Current advice is that the measles-mumps-rubella vaccine can be given to all patients with egg allergy but this should be performed in a controlled environment with full resuscitation facilities available.22
  • The influenza vaccine is contraindicated if someone has has a proven systemic reaction to egg.23


Document references
  1. Bindslev-Jensen C; ABC of allergies: Food allergy; BMJ 1998 316:1299-1302.
  2. CORE (Digestive Disorders Foundation Charity); CORE Factsheet 8. Food intolerance. November 2005.
  3. Sicherer SH; Food allergy. Lancet. 2002 Aug 31;360(9334):701-10. [abstract]
  4. Beausoleil JL, Fiedler J, Spergel JM; Food Intolerance and childhood asthma: what is the link? Paediatr Drugs. 2007;9(3):157-63. [abstract]
  5. Young E, Stoneham MD, Petruckevitch A, et al; A population study of food intolerance. Lancet. 1994 May 7;343(8906):1127-30. [abstract]
  6. Sicherer SH, Munoz-Furlong A, Burks AW, et al; Prevalence of peanut and tree nut allergy in the US determined by a random digit dial telephone survey. J Allergy Clin Immunol. 1999 Apr;103(4):559-62. [abstract]
  7. Emmett SE, Angus FJ, Fry JS, et al; Perceived prevalence of peanut allergy in Great Britain and its association with other atopic conditions and with peanut allergy in other household members. Allergy. 1999 Apr;54(4):380-5. [abstract]
  8. Eggesbo M, Botten G, Halvorsen R, et al; The prevalence of allergy to egg: a population-based study in young children. Allergy. 2001 May;56(5):403-11. [abstract]
  9. Simpson AB, Glutting J, Yousef E; Food allergy and asthma morbidity in children. Pediatr Pulmonol. 2007 Jun;42(6):489-95. [abstract]
  10. Burks W; Skin manifestations of food allergy. Pediatrics. 2003 Jun;111(6 Pt 3):1617-24. [abstract]
  11. Malik V, Ghosh S, Woolford TJ; Rhinitis due to food allergies: fact or fiction? J Laryngol Otol. 2007 Jun;121(6):526-9. Epub 2006 Dec 8. [abstract]
  12. Cross S, Buck S, Hubbard J; ABC of allergies: Allergy in general practice; BMJ 1998 316:1584-1587.
  13. Sheikh A, Walker S; Food allergy. BMJ. 2002 Dec 7;325(7376):1337.
  14. Atkins D, James JM; Food Allergies. eMedicine. Updated June 13, 2006.
  15. ReFeR; Department of Health Research Findings Register. How dangerous is food allergy in childhood? A total population study in the United Kingdom and Ireland. Dr AF Colver. February 2001.
  16. Sampson HA, Scanlon SM; Natural history of food hypersensitivity in children with atopic dermatitis. J Pediatr. 1989 Jul;115(1):23-7. [abstract]
  17. Friedman NJ, Zeiger RS; The role of breast-feeding in the development of allergies and asthma. J Allergy Clin Immunol. 2005 Jun;115(6):1238-48. [abstract]
  18. Hourihane JO, Aiken R, Briggs R, et al; The impact of government advice to pregnant mothers regarding peanut avoidance on the prevalence of peanut allergy in United Kingdom children at school entry. J Allergy Clin Immunol. 2007 May;119(5):1197-202. Epub 2007 Mar 13. [abstract]
  19. Zutavern A, Brockow I, Schaaf B, et al; Timing of solid food introduction in relation to atopic dermatitis and atopic sensitization: results from a prospective birth cohort study. Pediatrics. 2006 Feb;117(2):401-11. [abstract]
  20. Tarini BA, Carroll AE, Sox CM, et al; Systematic review of the relationship between early introduction of solid foods to infants and the development of allergic disease. Arch Pediatr Adolesc Med. 2006 May;160(5):502-7. [abstract]
  21. Arshad SH, Bateman B, Sadeghnejad A, et al; Prevention of allergic disease during childhood by allergen avoidance: the Isle of Wight prevention study. J Allergy Clin Immunol. 2007 Feb;119(2):307-13. [abstract]
  22. NHS Immunisation Information; Measles, Mumps and Rubella Vaccine Factshhet 1
  23. NHS Immunisation Information; Influenza - The disease and vaccine.

Internet and further reading Acknowledgements EMIS is grateful to Dr M Preston for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2008.
DocID: 2158
Document Version: 21
DocRef: bgp1503
Last Updated: 4 Nov 2007
Review Date: 3 Nov 2009

The authors and editors of this article are employed to create accurate and up to date content reflecting reliable research evidence, guidance and best clinical practice. They are free from any commercial conflicts of interest. Find out more about updating.

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