Food allergy in adults is usually mediated by IgE antibodies, with one or more immediate typical allergic symptoms (flushing, hives, itching, swelling, vomiting, diarrhoea, difficulty breathing) to trigger foods.1
The most common non-IgE-mediated food allergy in adults is eosinophilic oesophagitis, characterised by symptoms of reflux, dysphagia and food impaction, with eosinophilic infiltration provoking structural changes in the oesophagus.1 Food intolerance has no immune trigger. Sufferers may experience reactions due to pharmacological effects, an enzyme deficiency or gastro-intestinal disorder such as irritable bowel syndrome (IBS).2 If symptoms include hives and facial swelling, but their onset is not linked to any specific food, then a differential diagnosis of spontaneous urticaria/angio-oedema may need to be considered. A robust diagnosis is important to ensure the correct management is implemented and unnecessary food exclusion is avoided as there may be adverse nutritional consequences, especially if a major food group, such as milk, wheat or fruits/vegetables are excluded.3
IgE-mediated food allergy affects around 4% of adults, lower than in children but with a greater risk of fatal anaphylaxis.4,5 Milk, egg, wheat and soy allergy often resolves by the age of 18 years; despite this, milk and wheat are the foods most frequently suspected by adults to cause symptoms.6–8 A small number of adults can have a severe persisting milk allergy from childhood. Adults sensitised to, but tolerant of, milk (typically those with severe eczema), who exclude it for a long period then reintroduce it, risk developing a milk allergy due to subsequent non-recognition by the IgE antibodies.9 The most probable cause of symptoms to milk in adults is lactose intolerance although respiratory symptoms associated with milk are also frequently reported by those with asthma or other lung conditions.10,11
Wheat allergy is very rare, although wheat is one of the triggers of food-dependant exercise-induced anaphylaxis (FDEIA).12,13 This food allergy is characterised by a lack of reaction to the trigger food unless it is consumed in large quantities or in close proximity to a cofactor (exercise, aspirin, non-steroidal anti-inflammatory drugs, alcohol).14 Apart from wheat, other common trigger foods of FDEIA include shellfish, tomatoes, celery and nuts.15 Wheat-associated symptoms in adults are most often gastro-intestinal, thus a diagnosis of coeliac disease should first be excluded before considering other causes.16 Those suffering with IBS may be wheat intolerant due to poor digestion of the fermentable carbohydrates.17,18 Others may avoid wheat due to non-coeliac gluten sensitivity, although it has been demonstrated that less than 15% of those considered to be gluten intolerant are likely to have this condition.19,20
Peanut and tree nut allergy
Peanut and tree nut allergies usually start in childhood; peanut allergy resolves before adolescence in one third or more of sufferers, whereas only 10% of those allergic to tree nuts will experience resolution.21–25 A concomitant allergy to tree nuts is only likely in less than 40% of peanut allergic individuals, so it is important that sensitisation and allergy to tree nuts is individually assessed, especially since severe reactions to nuts are more frequent in teenagers and adults.26,27 New onset symptoms to tree nuts or peanuts in adults is usually due to a condition known as pollen-food syndrome (PFS) or oral allergy syndrome.28 Over 60% of birch-sensitised individuals are likely to develop PFS due to specific IgE antibodies against birch pollen recognising and reacting to similar proteins in plant foods, although grass and weed pollens are also involved.29,30 Consumption of the trigger food, usually raw tree nuts, apples, kiwifruit and stone fruits (peaches, plums, cherries), causes immediate mild to moderate localised oropharyngeal symptoms.31 Another plant food allergy which mainly occurs in adult life also involves cross-reactions between allergenic proteins in plant foods called lipid transfer proteins (LTP).32 Food triggers are often similar to those reported in PFS, but due to their high resistance to heating and digestion, LTP allergens cause reactions to both raw and cooked food especially in the presence of co-factors.33–35
Fish allergy usually starts in childhood, whereas shellfish allergy is a common new-onset food allergy manifesting in adult life.36,37 Reported reactions to shellfish are most often to crustaceans (shrimp, crab, lobster) rather than molluscs (mussels, scallops, clams, oyster, squid).38 The primary shellfish allergen, tropomyosin, is water soluble and heat stable, so allergic symptoms can be triggered by inhalation of cooking vapours or by the residue of prawns in cooking oils.39,40 The lack of similarity between tropomyosin and β-parvalbumin, the main allergen in fish, usually means cross-reactivity between fish and shellfish is unlikely, although this can occur possibly due to co-sensitisation to other allergenic proteins found in both.39,41–43 Scombroid poisoning, caused by an excessive level of histamine due to the bacterial decarboxylation of histidine, is a common differential diagnosis for seafood allergy.39 However, there are some adults who are sensitive to much smaller amounts of natural histamine in foods. Histamine intolerance is difficult to diagnose as there are no validated tests, so dietary exclusion and reintroduction is the only option. Foods likely to contain high levels of histamine include red/brown fish (mackerel, salmon, herring, sardines, tuna), shellfish, pork products, aged meat, mature or aged cheeses, and fermented foods such as wine.44
Allergy to food additives
Additives can cause food intolerance, but the best studied of these is sodium metabisulphite, an additive used to preserve foods and prevent browning. Sodium metabisulphite use was greatly reduced in the 1990s after many reported instances of severe adverse reactions, especially in those with asthma.44 Foods most often implicated include white and rose wine, sparkling wine, lager, cider, light coloured dried fruits, raw peeled potato products, light coloured fruit cordials and preserved lemon and lime juice. Should tests to the obvious foods not reveal the cause of a severe allergic reaction in adults, and food intolerance has been ruled out, it might be that a hidden allergen is the cause of the problem. This could be an LTP allergen or an allergy linked to co-factors, but other less obvious ‘hidden’ food allergens might need to be considered. These include buckwheat, legumes (soy, lupin, chick peas flour, pea protein, lentils, fenugreek, guar gum), pectin, mycoprotein, psyllium, mustard, celery and natural food colourings such as carmine (cochineal).45
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- Boyce JA et al. Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-sponsored expert panel. J Allergy Clin Immunol 2010;126(6 Suppl):S1–58.
- Skypala IJ, McKenzie R. Nutritional issues in food allergy. Clin Rev Allergy Immunol 2018;May 15:doi: 10.1007/s12016-018-8688-x.
- Burney P et al. Prevalence and distribution of sensitization to foods in the European Community Respiratory Health Survey: a EuroPrevall analysis. Allergy 2010;65:1182–8.
- Turner PJ et al. Increase in anaphylaxis-related hospitalizations but no increase in fatalities: an analysis of United Kingdom national anaphylaxis data, 1992–2012. J Allergy Clin Immunol 2015;135:956-9–63.
- Savage J, Sicherer S, Wood R. The natural history of food allergy. J Allergy Clin Immunol Pract 2016;4:196–203.
- Golley S et al. Motivations for avoiding wheat consumption in Australia: results from a population survey. Public Health Nutr 2015;18:490–9.
- van Gils T et al. Prevalence and characterization of self-reported gluten sensitivity in The Netherlands. Nutrients 2016;8(11).
- Nachshon L et al. Food allergy to previously tolerated foods: Course and patient characteristics. Ann Allergy Asthma Immunol 2018;121(1):77–81
- Deng Y et al. Lactose intolerance in adults: Biological mechanism and dietary management. Nutrients 2015;7:8020–35.
- Wuthrich B et al. Milk consumption does not lead to mucus production or occurrence of asthma. J Am Coll Nutr 2005;24:547S–555S
- Nwaru BI et al. Prevalence of common food allergies in Europe: a systematic review and meta-analysis. Allergy 2014;69:992–1007.
- Christensen MJ et al. Exercise lowers threshold and increases severity, but wheat-dependent, exercise-induced anaphylaxis can be elicited at rest. J Allergy Clin Immunol Pract 2018;6(2):514–20.
- Cardona V et al. Co-factor-enhanced food allergy. Allergy 2012 Oct;67(10):1316–8.
- Hompes S et al. Elicitors and co-factors in food-induced anaphylaxis in adults. Clin Transl Allergy 2013;3(1):38.
- Lebwohl B, Sanders DS, Green PHR. Coeliac disease. Lancet 2018 Jan 6;391(10115):70–81.
- Monsbakken KW, Vandvik PO, Farup PG. Perceived food intolerance in subjects with irritable bowel syndrome – aetiology, prevalence and consequences. Eur J Clin Nutr 2006;60:667–72.
- Gibson PR, Shepherd SJ. Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach. J Gastroenterol Hepatol 2010;25:252–8.
- Catassi C et al. Diagnosis of non-celiac gluten sensitivity (NCGS): The Salerno Experts’ Criteria. Nutrients 2015;7:4966–77.12.
- Elli L et al. Evidence for the presence of non-celiac gluten sensitivity in patients with functional gastrointestinal symptoms: Results from a multicenter randomized double-blind placebo-controlled gluten challenge. Nutrients 2016;8:84.7.
- Peters RL et al. Natural history of peanut allergy and predictors of resolution in the first 4 years of life: A population-based assessment. J Allergy Clin Immunol 2015;135:1257–66.
- Bégin P et al. Natural resolution of peanut allergy: a 12-year longitudinal follow-up study. J Allergy Clin Immunol Pract 2013;1:528–30.
- Neuman-Sunshine DL et al. The natural history of persistent peanut allergy. Ann Allergy Asthma Immunol 2012;108:326–31.
- Wainstein BK, Saad RA. Repeat oral food challenges in peanut and tree nut allergic children with a history of mild/moderate reactions. Asia Pac Allergy 2015;5:170–6.
- Fleischer D et al. The natural history of tree nut allergy. J Allergy Clin Immunol 2005;116:1087–93.
- Lomas JM, Järvinen KM. Managing nut-induced anaphylaxis: challenges and solutions. J Asthma Allergy 2015;8:115–23.
- Deschildre A et al. Peanut-allergic patients in the MIRABEL survey: characteristics, allergists’ dietary advice and lessons from real life. Clin Exp Allergy 2016;46:610–20.
- Skypala IJ et al. The prevalence of PFS and prevalence and characteristics of reported food allergy; a survey of UK adults aged 18-75 incorporating a validated PFS diagnostic questionnaire. Clin Exp Allergy 2013;43:928–40.
- Werfel T et al. Position paper of the EAACI: food allergy due to immunological cross-reactions with common inhalant allergens. Allergy 2015;70:1079–90.
- Skypala IJ et al. Development and validation of a structured questionnaire for the diagnosis of oral allergy syndrome in subjects with seasonal allergic rhinitis during the UK birch pollen season. Clin Exp Allergy 2011;41(7):1001–11.
- Gunawardana NC, Rey-Garcia H, Skypala IJ. Nutritional management of patients with pollen food syndrome: Is there a need? Curr Treat Options Allergy 2018;5(4):500–14.
- Asero R et al. Lipid transfer protein: a pan-allergen in plant-derived foods that is highly resistant to pepsin digestion. Int Arch Allergy Immunol 2001;124:67–69.31.
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