From a medical perspective food allergy is an immunoglobulin (Ig)E- or non-IgE-mediated immune response to food protein. This small review will look at the IgE mediated food represented by immediate hypersensitivity (Gell-Coombs Type I), which can include anaphylaxis and can be life-threatening.
Food or environmental exposures that result in non-IgE-mediated reactions are thought to be cell mediated (allergic eosinophilic esophagitis/gastroenteritis, food protein-induced proctocolitis, food protein-induced enterocolitis syndrome, food protein-induced enteropathy; including coeliac disease).
Many practitioners and even more patients can sometimes confuse adverse reactions to foods as food allergies, but these reactions are nonimmunologic. Nonimmunologic food reactions can be metabolic (lactose intolerance), pharmacologic (chemical migraine triggers such as tyramine, aspartame, monosodium glutamate, nitrates/nitrites, alcohol, coffee, and chocolate), or toxic (food poisoning) in origin. Lactose intolerance can be managed with replacement of the enzyme lactase.
The High and Increasing Prevalence of Food Allergy
Demographics. Food allergies affect up to:
- 8% of children and
- 3%-4% of adults.[1],[2]
- Food allergies account for 29%-50% of all cases of anaphylaxis,[3]
- which in turn cause 150-200 deaths annually[4] (6-7 times more than deaths from insect stings).[5]
- No gender or racial disparities have been noted in food allergy, except for Hispanic children, who have a lower rate of food allergy than white or black children.[6]
Prevalence.
Food allergy is growing. From 1997 to 2007,
- The prevalence of reported food allergy increased 18% in children under the age of 18 years.8
- Peanut allergy has tripled in children under the age of 18 years in a similar time frame, from 0.4% in 1997 to 1.4% in 2008.[7][9] Peanut allergy is the most common cause of fatal food-induced anaphylaxis.
- Adverse reactions to food additives, such as colouring or preservatives, remain statistically rare and estimated to affect be between 0.01% and 0.23% of the general population.[8]
Virtually any food can cause an allergic reaction. The most common allergens in childhood are:
- cow’s milk (2.5%),
- egg (1.6%),
- peanut,
- soy,
- wheat,
- tree nuts,
- fish,
- and shellfish.
In adults, the most common allergens are:
- peanut,
- tree nuts,
- fish,
- and shellfish.
Associated conditions.
About 80% of children outgrow their milk and egg allergies; however, recent studies suggest that children now require more time to outgrow these allergies than in the past.[9] Only 20% of peanut-allergic children eventually outgrow this allergy and are able to tolerate peanut in their diets.
Children who have a food allergy are more likely to have other atopic conditions such as atopic dermatitis, allergic rhinitis, and asthma compared with children who do not have a food allergy.8 Most children with atopic dermatitis are sensitised (have a positive skin test or elevated specific IgE) to food or aeroallergens.[10]
In children with moderate-severe atopic dermatitis, 40% have clinical food allergy, most commonly egg. Food allergies have also been found to be a risk factor for life-threatening asthma.[11]
Why IgE antibody is inappropriately formed against benign food protein is not fully understood. One well-known hypothesis for the apparent Th2 shift and increase in allergic diseases in westernised countries is the hygiene hypothesis. This hypothesis postulates that because of our improved hygiene and vaccinations, our immune systems are not overburdened with disease or parasites, so instead we develop immunity against benign antigens that we are commonly exposed to, such as food.[12]
Other hypotheses for the increase in food allergies involve how we grow and process our food, how and when we introduce foods to infants and toddlers, dietary fat content, reduction in dietary antioxidants, vitamin D insufficiency, and environmental exposures to allergens, such as peanut oil in skin moisturisers, which may favour sensitivity as opposed to tolerance.
References
[1] Sicherer SH, Sampson HA. 9. Food allergy. J Allergy Clin Immunol. 2006;117(2 suppl):S470-S475 View Abstract
[2] Jansen JJ, Kardinaal AF, Huijbers G, Vlieg-Boerstra BJ, Martens BP, Ockhuizen T. Prevalence of food allergy and intolerance in the adult Dutch population. J Allergy Clin Immunol. 1994;93:446-456. View Abstract
[3] Lieberman P, Kemp SF, Oppenheimer J. The diagnosis and management of anaphylaxis: an updated practice parameter. J Allergy Clin Immunol. 2005;115 (3 suppl 2):S483-523. No Abstract
[4] Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol. 2001;107:191-193. View Abstract
[5] Moffitt JE, Golden DB, Reisman RE, et al, Stinging insect hypersensitivity: a practice parameter update. J Allergy Clin Immunol. 2004;114:869-886. No Abstract
[6] Branum AM, Lukacs SL. Food allergy among US children: trends in prevalence and hospitalizations. NCHS Data Brief. 2008:1-8. View Abstract
[7] Sicherer SH, Muñoz-Furlong A, Godbold JH, Sampson HA. US prevalence of self-reported peanut, tree nut, and sesame allergy: 11-year follow-up. J Allergy Clin Immunol. 2010;125:1322-1326. View Abstract
[8] Fuglsang G, Madsen C, Saval P, Osterballe O. Prevalence of intolerance to food additives among Danish school children. Pediatr Allergy Immunol. 1993;4:123-129. View Abstract
[9] Wood RA. The natural history of food allergy. Pediatrics. 2003;111(6 Pt 3):1631-1637. View Abstract
[10] Sampson HA. Atopic dermatitis. Ann Allergy. 1992;69:469-479 No Abstract
[11] Sampson HA. Food sensitivity and the pathogenesis of atopic dermatitis. J R Soc Med. 1997;90 (suppl 30):2-8. View Abstract
[12] Lack G. Epidemiologic risks for food allergy. J Allergy Clin Immunol. 2008;121:1331-1366. View Abstract
