Food allergy has been recognized since the time of Hippocrates. People with adverse reactions to food can be difficult to evaluate because an overlap exists between true food allergy and other chemical ingredients. The incidence of food allergy is increasing in the industrialized world, raising questions about the interactive effects of environmental and genetic factors. Society would be improved without the burden on society regarding the cost of treatment, death from anaphylactic reactions, and the anxiety produced by food allergies. Food avoidance is the current treatment, but new strategies are being developed.
Adverse reactions to the ingestion of food that can be reproduced are termed intolerance or hypersensitivity. Since this does not imply an underlying cause, it may encompass immune or nonimmune mechanisms. For example, chemicals like caffeine may cause reproducible symptoms, but the immune system does not mediate this.
True food allergy or food sensitivity is a reproducible adverse reaction to food caused by the immune system creating antibodies or cellular inflammation.
The classic example is an immediate anaphylactic reaction to food. In susceptible individuals, after exposure to the food, the immune system creates specific IgE antibodies to that food. IgE is produced by the immune system’s B-lymphocytes and is bound to receptors on the surface of mast cells. Mast cells reside in tissues at body surfaces such as the skin, eyes, nose, throat, lungs, and gastrointestinal tract. Mast cells are made up of granules containing chemicals, including histamine. When the food protein contacts and binds to adjacent specific IgE molecules at the mast cell surface, a cascade of events occurs, leading to degranulation of mast cells and the release of chemicals that cause the allergic reaction. This may include skin hives, airway swelling, wheezing, abdominal pain, vomiting, or diarrhea. This may progress to anaphylaxis, shock, and even death.
This reactivity to food can be demonstrated by skin-prick tests, which have been used to diagnose allergies since the 1870s. Food protein is placed on the skin, the skin is scratched or pricked, and a hive will develop in the presence of skin mast cells with IgE directed against the food. In the 1920s, Prausnitz and Kustner showed that a substance circulating in the blood of the allergic individual was responsible for a positive skin test because blood serum could be transferred to the skin of a nonallergic individual, resulting in a positive skin test.
IgE is that substance and food-specific IgE that can be measured directly in the blood by means of the IgE RAST (radioallergosorbent) test. Diagnosis of this immediate type of food allergy rests on the history of rapid onset of symptoms, demonstration of positive skin-prick test, or specific IgE RAST. Challenging an individual with the food is the ultimate way to prove a food allergy.
Other immune mechanisms can be responsible for allergic reactions to foods. The classic example is celiac disease (celiac sprue or gluten-induced enteropathy). This is an immune system reaction to wheat (gluten). Patients do not have IgE antibody directed against wheat, but exposure to gluten over a period of time causes inflammation of the intestine and a characteristic atrophy or flattening of the normal intestinal villous folds. The diagnosis rests on the characteristic biopsy of the small intestine coupled with another type of antibody (IgA) against wheat protein. Markedly more difficult is that any food may also cause a similar intestinal inflammation when defining different food allergies. This leads to varying symptoms and signs depending on the area of the intestine affected. Unlike IgE-mediated allergy or celiac disease, there are no readily available confirmatory tests for these other food allergies.
Food allergy is perceived as being common; however, large studies support the idea that true food allergy is less common than people think. A study of 480 infants from birth to age three revealed their parents suspected 28 percent as having food allergy. However, confirmation was in only 8 percent of this group. The prevalence then decreases with age. Twenty percent of adults suspect a food allergy, though allergy confirmation from a professional is only 1 to 2 percent of adults. Although defining different food allergies in adults tends to persist with age, many infants and children outgrow them with time.
Recently, interest has grown in the apparent increase in the prevalence and severity of food allergy. This has paralleled an increase in other atopic disorders such as asthma in industrialized nations compared with children of similar genetic backgrounds in developing countries (atopic refers to a tendency to develop allergic conditions such as hay fever, asthma, or food allergies). The “hygiene hypothesis” contends that through evolution, the human immune system has developed with a specific microbial environment, and reduced exposure to microbes in the developed world may lead to increased allergic response. Further study is needed.
Immediate hypersensitivity reactions to foods are most common in young children, with 50 percent of these reactions occurring in the first year of life. The majority is from cow’s milk and soy protein from infant formulas.
Other foods begin to predominate in older children, including eggs, fish, peanuts, wheat, milk, and soy. This accounts for over 90 percent of food allergies in children. Peanut, tree nut, and shellfish allergy predominate in adults. Exposures may occur inadvertently due to improper labeling, changes in product composition with time, and contamination of foods during processing. Symptoms from multiple organ systems may occur, beginning within minutes. Unfortunately, fatal anaphylactic reactions (shock) to food occur despite strict dietary avoidance and treatment of reactions. Families, caregivers, and individuals with a history of anaphylaxis to food require education in diet and the use of self-administered epinephrine. Individuals should get an observation in a hospital setting after a significant reaction.
Exercise-induced anaphylaxis to food occurs when the combination of ingesting the food followed by exercise leads to anaphylaxis. Oral allergy syndrome describes symptoms of itching of the mouth and throat, often attributable to eating fruit and typically does not progress.
Foods can cause chronic hives or urticaria. It is a common misconception that these conditions are caused by food exposure. In 1 to 2 percent of cases, it is urticaria or chronic hives, a reaction to food. Atopic dermatitis (AD) or eczema is a chronic skin condition in atopic individuals. Patients with AD have a 30 to 40 percent prevalence of food allergy.
The rapid onset of symptoms after ingestion correlates highly with positive skin-prick or IgE RAST tests to the offending food, making confirmation of immediate hypersensitivity straightforward. A good recommendation is to find a consultation with an allergist and dietitian.
Groups like Food Allergy and Anaphylaxis Network can provide support and educational materials. Established in 1991, when information about food allergies was scarce, the Food Allergy & Anaphylaxis Network (FAAN) is a nonprofit organization. They provide information, programs, and resources on food allergies.
The spectrum of non-IgE food allergy is quite varied, and the symptoms often parallel the area of inflammation in the gastrointestinal tract (see sidebar). Avoidance of the food will resolve symptoms and intestinal inflammation. Currently, the strategy is to re-challenge with the food, which will reproduce the injury. However, unlike IgE food allergy, symptoms may take days or weeks to resolve or reappear with elimination or exposure, making evaluation even more difficult.
Celiac disease or gluten-induced enteropathy is a chronic intestinal condition. The cause is the non-IgE mediated allergy to gluten, a protein in wheat and other grains. Chronic exposure to gluten causes inflammation and atrophy of small intestinal folds, leading to symptoms of malabsorption of food. Typically, patients have diarrhea, weight loss, and abdominal bloating.
There is a genetic predisposition to celiac disease. Still, onset may occur at any age, suggesting environmental factors. Even an infection may trigger a brand-new inflammatory process. The disease is more prevalent (up to 1 in 400-500) in individuals of Eastern European descent. Celiac disease has an association with certain skin conditions (dermatitis herpetiformis), thyroid disease, diabetes, and Down syndrome.
Allergic or eosinophilic colitis in infants commonly manifests as non-IgE food protein allergy. The condition has the characterization of diarrhea with blood and mucus. The cause is common milk or soy formulas and may occur in breastfed infants from dietary antigens, transmitted through breast milk. Specifically, colon biopsies show allergic inflammation.
Food protein-induced enterocolitis is a severe reaction to food, often delayed four to six hours, without evidence of IgE. Patients present with lethargy, vomiting, and diarrhea. Recovery is within six to eight hours after fluid resuscitation. For example, a careful study of the patient’s history reveals the offending food when multiple episodes occur.
Chronic enteropathy from food allergy can also lead to inflammation with villous atrophy, similar to celiac disease. Additionally, many patients suffer from diarrhea, weight loss, anemia, and low abdominal pain from protein loss from the intestine.
Allergic esophagitis has the characterization of intense eosinophilia of the esophagus on biopsy. Eventually, patients complain of pain and problems with swallowing, even to the point of having food impactions in the esophagus. Consequently, treatment with hypoallergenic formula shows to improve esophagitis in infants. However, older children and adults may require corticosteroid medication.
By definition, colic is a condition with an increasing crying behavior in infants for which no other cause has been specified. However, since allergy can potentially lead to inflammation and pain, formula allergy often has consideration.
Attempts are being made to associate various other conditions with food allergies. Specifically including joint disease, migraine, and behavioral and developmental disorders like autism. Many other conditions are possible, but breakthroughs come slowly. A causal relationship between food allergy and these disorders remains unproven.
Investigation and treatment of non-IgE-mediated food allergy. The diagnosis rests on the resolution of symptoms and/or biopsy findings on an elimination diet, with a return of symptoms on rechallenge. In contrast to the rapid response characteristic of IgE-mediated disease, a prolonged challenge may identify delayed reactions. Specifically, with predominantly gastrointestinal symptoms up to six days after exposure. In particular, elemental diets can eliminate dietary protein antigens, and then systematically re-challenge the patient with the suspect offending food.
As with IgE food allergies, avoiding the specific food remains the mainstay of therapy.
There are many exciting research areas into preventing and treating food allergies. Recent reports suggest that the allergic response can be altered by promoting beneficial gut flora (“probiotic therapy”). A recent discovery is that only a few sites (epitopes) on food protein molecules interact with the immune system to create an allergic reaction. Significantly, genetic engineering of foods makes it possible to alter these epitopes, creating nonallergic crops.” Currently, more studies are happening daily to ensure that altering food proteins does not lead to other health concerns or allergies. Other studies are underway to assess the effectiveness of promising new drug therapies for patients while they are defining different food allergies in themselves.
