COMMENTARY

Food Allergy: What You Need to Know

Stephanie A. Leonard, MD

Disclosures

November 15, 2010

In This Article

The High and Increasing Prevalence of Food Allergy

Demographics. Food allergies affect up to 8% of children and 3%-4% of adults.[2,3] Food allergies account for 29%-50% of all cases of anaphylaxis, [4,5] which in turn cause 150-200 deaths annually[6] (6-7 times more than deaths from insect stings).[7] 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.[8]

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.[9] Peanut allergy now affects 0.6% of the population and is the most common cause of fatal food-induced anaphylaxis.[9,10] Adverse reactions to food additives, such as coloring or preservatives, are rare and estimated to affect be between 0.01% and 0.23% of the general population.[11,12,13]

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.[2,14] 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.[15,16,17,18] Only 20% of peanut-allergic children eventually outgrow this allergy and are able to tolerate peanut in their diets.[19] 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 sensitized (have a positive skin test or elevated specific IgE) to food or aeroallergens.[20,21]

In children with moderate-severe atopic dermatitis, 40% have clinical food allergy,[22,23] most commonly egg.[24] Food allergies have also been found to be a risk factor for life-threatening asthma.[25]

The Pathophysiology of Food Allergy

A Type I immediate hypersensitivity reaction is precipitated by the presentation of antigen (in this case, food peptides), by antigen-presenting cells (APCs) to T cells, which direct B cells to produce IgE.[26] The IgE antibodies then bind to tissue mast cells and basophils, the effector cells in an allergic reaction. Upon re-exposure, the antigen binds to and crosslinks IgE on mast cells and basophils, triggering degranulation and the release of preformed contents, such as histamine, tryptase, and proteoglycans. Activated mast cells and basophils also produce prostaglandins, leukotrienes, platelet-activating factor, and cytokines. These mediators act directly on tissue and recruit inflammatory cells. Histamine, the primary mediator, induces vascular permeability, mucus production, vasodilation, and airway and intestinal smooth muscle contraction; and affects cardiac function.[27,28] These actions result in the flushing, hives, edema, bronchoconstriction, abdominal cramping, vomiting, hypotension, and dysrhythmias typically seen in acute allergic reactions and anaphylaxis. It is possible to react on first known exposure. Some speculate that exposure in the environment, through breastfeeding, or in utero might be the priming event.[29]

Food allergy is viewed as a Th2-mediated condition.[30] Th2 CD4+ T cells produce cytokines interleukin (IL)-4, IL-5, and IL-13 and generate a humoral immune response that is classically used to fight off parasites but also inappropriately causes allergies. In contrast, Th1 CD4+ T cells produce IL-2 and IFN-gamma and generate cell-mediated immune responses.

Proposed Explanations for the Rise in Allergic Disease

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 westernized 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.[31] 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 moisturizers, which may favor sensitivity as opposed to tolerance.[32,33,34,35,36,37]

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