Judy Perkin. Cambridge World History of Food. Editor: Kenneth F Kiple & Kriemhild Conee Ornelas. Volume 1. Cambridge, UK: Cambridge University Press, 2000.
Foods and beverages contain nutrients that are essential to human life, but they also contain elements that, for some individuals, may be harmful to health or even life-threatening. Foods and beverages may cause adverse reactions when ingested, but humans also can have adverse reactions to foods through inhalation (Edwards, McConnochie, and Davies 1985; Kemp, Van Asperen, and Douglas 1988), skin contact (Mathias 1983), or injection (Flu Shots and Egg Allergy 1992; Schwartz 1992).
Sensitivity to foods may be caused by immuno-logic abnormalities or by other mechanisms, such as host enzyme deficiency. Food sensitivities caused by immunologic abnormalities are commonly referred to as food allergies, whereas food sensitivities caused by nonimmunologic mechanisms are referred to as food intolerances (Anderson 1990; Beaudette 1991). This chapter reviews major considerations with regard to both classifications of food sensitivities. It should also be noted that a disorder called “pseudo-food allergy syndrome” exists. This syndrome is a psychological disorder in which the sufferer believes in the existence of a food allergy that cannot be confirmed by clinical testing (Pearson and Rix 1983, Pearson 1988).
Allergic, or immunologically based, reactions to food most commonly involve a Type I or IgE mediated reaction (Anderson, 1990) as classified by R. R. A. Coombs and P. G. H. Gell (1975). It has been theorized that IgE mediated reactions to food may be related to a reduction in the need to produce IgE in response to intestinal parasitic infection. This theory, known as the “mast cell saturation hypothesis,” speculates that when the majority of IgE antibodies are bound to intestinal parasites, fewer antibodies are available to bind with food antigens. Production of high levels of IgE to fight parasitism would be protective, whereas production of high levels of IgE specific for food antigens is counterproductive to health (Godfrey 1975; Merrett, Merrett, and Cookson 1976; Lieberman and Barnes 1990).
In food allergy, the Type I reaction involves production of IgE antibodies that are tailored to food allergens. Food allergens are most commonly proteins but also may be glycoproteins or glycolipids (Bindels and Verwimp 1990). In order for a food allergen to stimulate IgE production, it must be absorbed and be of the appropriate size and shape to bridge IgE antibodies on the mast cell surface (Perkin 1990; Taylor 1990). Although most individuals are able to digest food proteins without eliciting an allergic response, individual who are atopic seem to absorb food antigens in a form that causes their cells to produce IgE. When food allergens are of the appropriate size, they are capable of binding with IgE and triggering the release of chemicals that cause the clinical manifestations of food allergy. Chemicals commonly implicated in the allergic process include histamine, leukotriences and cytokines (Metcalfe, 1991).
In some individuals, exercise may play a role in stimulating the food allergy response (Sheffer et al. 1983). Food-dependent anaphylaxis related to exercise is thought to be associated with chemical mediator release from mast cells in conjunction with an abnormal functioning autonomic nervous system, specifically increased parasympathetic activity and decreased sympathetic activity (Fukutomi et al. 1992). Abnormalities of IgE synthesis associated with other disorders may result in the secondary appearance of food allergy. D. S. Mazza, M. O’Sullivan, and M. H. Grieco (1991) have published a case report of food allergy that developed secondary to infection with the human immunodeficiency virus.
There are types of food-related immunologic reactions that are not believed to be Type I. Heiner’s syndrome (a bovine milk-associated respiratory disorder) and celiac sprue are two examples of adverse food reactions believed to be associated with other types of immunologic reactions (Anderson 1990).
Food allergy is more common in children than adults although food allergy can develop at any age. One study that surveyed physicians estimated that allergy prevalence was 7 percent for adults and 13 percent for children (Anderson 1991). Another often-cited study estimates the prevalence of allergy in children to be from 0.3 to 7.5 percent, with adults having a lower prevalence (Buckley and Metcalfe 1982). One theory used to explain the relatively higher level of allergy prevalence in children relates to infancy-associated intestinal immaturity, which, some believe, results in greater passage of larger proteins across the gut with resultant stimulation of IgE production (Walker 1975; Udall et al. 1981). But the primacy of a more permeable intestine in terms of allergy causation has recently been questioned by T. Jalonen (1991), who has postulated that greater intestinal permeability is a secondary phenomena for food allergy rather than an initiating event.
Infants may become sensitized to food allergens in utero since IgE can be synthesized before birth and large food proteins can cross the placenta. It should be noted, however, that although prenatal sensitization occurs, it is a relatively rare event (Strimas and Chi 1988). P. G. Calkhoven, M. Aalbers,V. L. Koshte, and colleagues (1991) have postulated the existence of a “high food responder phenotype” based on their findings that certain children seem to demonstrate allergic responses to a wide variety of foods. High cord IgE levels or high levels of serum IgE measured seven days after birth are considered to be predictive of subsequent food allergy development in an infant (Chandra, Puri, and Cheema 1985; Strimas and Chi 1988; Ruiz et al. 1991). A low level of CD8+ suppressor cells in the neonatal period is also predictive of the potential for allergy development (Chandra and Prasad 1991).
Breast feeding is often cited as being allergy protective, but this is an extremely controversial subject (Kramer 1988; Perkin 1990). Certainly there are physiological reasons to suggest that breast feeding may be protective against food allergies or at least may delay food allergy development. These reasons include (1) the relative lack of exposure to food antigens associated with breast feeding; (2) the presence of secretory IgA in breast milk, which is believed to aid in reducing the intestinal entry of large food protein molecules; (3) the stimulation of infantile IgA production by breast milk; (4) the opportunity for less intestinal antigen uptake because of the decreased incidence of gastrointestinal infections associated with breast feeding; (5) the presence in breast milk of anti-inflammatory properties, such as histaminase and arylsulfatase, and (6) the provision of IgG antibodies in breast milk that are targeted at food antigens (Pittard and Bill 1979;Atherton 1983; Businco et al. 1983 ; Ogra et al. 1984; Goldman et al. 1986; Michael et al. 1986). Low breast milk IgA levels have been associated with an increased likelihood of developing infantile cow’s milk allergy (Savilahti et al. 1991).
Clinical studies that have examined breast feeding in relation to food allergy have not demonstrated a clear-cut protective or delaying effect (Kramer 1988; Perkin 1990), perhaps because of numerous methodological problems involved in this type of research. If breast feeding is protective, it is generally believed that exclusive breast feeding (no solid foods and no formula) should be practiced for at least six months (Bahna 1991; Kajosaari 1991). Since this is seldom done in the United States, the measurement of any allergy-prevention benefits of breast feeding is difficult.
Food allergies may disappear over time. Young age at food allergy onset coupled with a mild clinical reaction may mean that an individual will ultimately develop tolerance for an offending food. A more severe clinical reaction profile and older age of food allergy onset are associated with greater likelihood of allergy persistence. Allergies to certain foods, such as peanuts or crustacea, also tend to be allergies that persist through time (Anderson 1991). Food allergy developing in adulthood may be related to occupational exposure to food antigens (Anderson 1991; Metcalfe 1991). Baker’s asthma, caused by allergic reactions to several wheat proteins, is one of the most studied occupational allergies (Prichard et al. 1985; Anderson 1991).
Certain foods have been commonly identified as implicated in the causation of food allergies. Among these are cow’s milk, soybeans, wheat, eggs, nuts, and seeds (including cottonseed, which can be highly allergenic), crustacea (shrimp, lobster, crawfish), and fish. Also implicated are noncitrus fruits and vegetables (for example, tomato, celery, watermelon, pear, cherry, apple), citrus fruits, and spices (Perkin 1990). Table IV.E.5.2 outlines currently identified food allergens in some of the major food categories linked to allergy (Perkin 1990). Food types linked to allergy reflect cultural dietary patterns (Esteban 1992;Walker 1992).
The literature continues to identify new food categories that may cause allergic reactions in some individuals. Foods recently identified include squid (Carrillo et al. 1992), grand keyhole limpet and abalone (Morikawa et al. 1990), annatto dye (Nish et al. 1991), jícama (Fine 1991), and Swiss chard (de la Hoz et al. 1991). Progress has also been made in terms of identifying other factors, such as mites, that may be related to food allergies. For example, A. Armentia, J. Tapias, D. Barber, and colleagues (1992) have demonstrated that an allergic reaction may be precipitated by exposure to the wheat flour storage mite Lepidoglyphus destructor. Foods or beverages used as folk remedies may also elicit allergic reactions. J. Subiza, J. L. Subiza, M. Alonzo, and co-workers (1990) have described allergic responses that were initiated by washing the eyes with chamomile tea. Even human breast milk may contain allergenic food proteins (Gerrard and Shenassa 1983; Kilshaw and Cant 1984; Gerrard and Perelmutter 1986).
The determination of the extent to which foods related to one another in botanically defined plant families trigger allergies has long been of interest. When such a reaction occurs, it is called cross-reactivity. Legumes (Barnett, Bonham, and Howden 1987) and crustacea (Sachs and O’Connell 1988) are often studied in this regard. Cross-reaction between environmental and food allergens has also been reported. Birch pollen has been noted to be cross-reactive with the carrot and apple (Ortolani et al. 1988), and banana and latex have recently been reported as cross-reactive (M’Raihi et al. 1991).The phenomenon of cross-reactivity is one that is currently ill defined and is a subject of debate in terms of its clinical relevance.
Clinical signs and symptoms of food allergy are numerous, and diagnosis of food allergy is a complex process. Clinical manifestations may occur in selected body systems, such as the respiratory system or the skin, or may be a more generalized phenomenon, such as anaphylaxis. There are also specific syndrome symptom complexes that have been linked to food allergy.
Skin symptoms of food allergy may include hives, angioedema, eczema, and itching and/or redness (Anderson 1991). Eczema is particularly common in children and usually occurs on the elbows, knees, and perhaps the face (Burks 1992). Respiratory symptoms may include rhinitis, wheezing, and asthma.
Certain food allergies also produce gastrointestinal symptoms, such as nausea, vomiting, and diarrhea (Anderson 1991; Beaudette 1991; Metcalfe 1991). Cow’s milk allergy is particularly noted for its association with gastrointestinal symptoms. It may also be associated with low-grade gastrointestinal bleeding and, thus, may be a cause of anemia (Wilson and Hamburger 1988).
Anaphylaxis is a systemic manifestation of food allergy. It is also potentially deadly, although it may be mild and simply characterized by simultaneous allergic manifestations in several organ systems. But the term is commonly used to refer to the more serious form of multiorgan system reaction that includes the development of cardiovascular shock, severe respiratory distress, and even death (Anderson 1990). Symptoms of classic food allergy generally appear within one to two hours after ingestion of the offending food, although in some cases, symptoms can appear as much as 12 hours following consumption (Anderson 1990).
Several clinical syndromes have also been associated with food allergy. These include oral allergy syndrome, eosinophilic gastroenteritis, food protein-induced enterocolitis syndromes, and hypersensitive furrowed mouth (Anderson 1991; Metcalfe 1991).
Oral allergy syndrome, as described by C. Ortolani, M. Ispano, E. Pastorello, and colleagues (1988), is initially manifested by irritation and swelling of the lips, which is then followed by hives, respiratory problems, and, in some cases, the development of anaphylactic shock. The oral allergy syndrome is associated with allergies to certain fruits and vegetables, notably celery (Ortolani et al. 1988; Pauli et al. 1988). J. A. Anderson (1991) has estimated that 0.1 to 0.2 percent of the general population may experience oral allergy syndrome. The syndrome is more frequently seen in persons who are sensitive to ragweed pollen.
Eosinophilic gastroenteritis associated with food allergy is characterized clinically by gastrointestinal disturbance, elevated levels of eosinophils, the presence of eosinophils in the stomach and intestine, and elevated levels of IgE (Anderson 1991; Metcalfe 1991).The syndrome of food protein-induced enterocolitis is seen in infants and is characterized by diarrhea, malabsorption, and high levels of eosinophils (Metcalfe 1991).
Hypersensitive furrowed mouth syndrome is characterized by mouth swelling and the development of cracks and furrows in the mouth. Anderson (1991), who described this problem, has associated it with consumption of large amounts of foods rich in protein.
Diagnosis of food allergy can be complex. It involves analysis of the clinical history, epicutaneous skin testing, and/or the use of in vitro assays, such as the radioallergosorbent test (RAST) or the enzyme-linked immunosorbent assay (ELISA) (Anderson 1990).
Elimination diets and the analysis of diet-symptom diaries may also be used in the diagnostic effort (Olejer 1990; Burks and Sampson 1992). The “gold” standard for diagnosis of food allergy is the double blind placebo-controlled food challenge (Olejer 1990). In children under the age of three years, skin testing is not a reliable indicator of food allergy, and single blind food challenge is more commonly employed to determine foods to which a child has an adverse reaction (Olejer 1990; Beaudette 1991). Diagnostic procedures used for research purposes are being studied for potential clinical application. These include basophil histamine release assay and assay of intestinal mast cell histamine release (Burks and Sampson 1992).
Once a food allergy is diagnosed, treatment primarily involves instructing the patient to eliminate the offending substance from the diet. This requires that the allergic individual pay careful attention to food preparation techniques and food labeling. Unfortunately, food labels are not always helpful and can even be misleading. A label of kosher-parve, for example, generally denotes a milk-free product, but a recent report indicated that a dessert labeled as kosher-parve was found to contain milk protein (Jones, Squillace, and Yunginger 1992). In this instance, the milk proteins were present in the product as the result of a faulty production process that permitted milk contamination from previous use of the equipment.
In some cases, individuals may not understand the wording on food labels. R. N. Hamburger (1992) noted that one of his patients did not recognize that the term “calcium caseinate” meant the presence of milk protein. Eating outside of the home also presents special problems. The National Restaurant Association has recently launched an allergy awareness program and is attempting to make restaurant owners more aware of the needs of patrons with food allergies (Restaurant Food Allergy Awareness 1992).
Special attention must be paid to the nutritional adequacy of diets when foods are eliminated. Nutritional deficits, such as insufficiencies of calories, protein, and calcium, have been noted in children following restricted diets for food allergies (Lloyd-Still 1979; Sinatra and Merritt 1981; David, Waddington, and Stanton 1984).
For limited periods of time, elemental diet formulas may be useful for managing food allergies. These formulas contain protein that has been extensively hydrolyzed. However, the relatively poor taste and high cost of these products generally make them a poor long-term solution for food allergies. They can, however, help symptoms resolve and can bring relief prior to the development of a restricted dietary program of traditional foods.
Formula-fed infants who are allergic to cow’s milk protein are placed on alternative formulas. These may include a soy-based formula or one of casein hydrolysate (Olejer 1990). The use of soy formulas, however, to treat infants with cow’s milk allergy is controversial, and whey hydrolysate formulas are currently not recommended as treatment for such infants (American Academy of Pediatrics 1983; Businco et al. 1992).
Hypoallergenic formulas are defined as those that can be tolerated by children with cow’s milk allergy, such that 90 percent will experience no symptoms at a 95 percent level of confidence (Sampson 1992). Casein hydrolysate formulas are currently regarded as hypoallergenic (Oldaeus et al. 1992; Rugo, Wahl, and Wahn 1992). Breast-fed infants who are allergic to food proteins transferred through breast milk may be treated by the mother’s restriction of the offending foods from her diet (Perkin 1990).
Traditionally, pharmacological approaches have had limited application in the treatment of food allergies. Epinephrine is used as an antianaphylactic agent, and antihistamines and corticosteroids are employed to alleviate allergy symptoms (Doering 1990). Oral cromolyn is effective in some cases for treating food allergy or other food-related problems, such as migraine (Doering 1990; Knottnerus and Pelikan 1993). Injection treatment with peanut extract is currently being investigated (Oppenheimer et al. 1992), as are such drugs as loratadine (Molkhou and Czarlewski 1993) and pancreatic enzyme supplements (Bahna and McCann 1993).
Research efforts are attempting to find ways that food allergies can be prevented or delayed. One thrust of the research is to examine infant formulas for those types that can delay or prevent allergies. Although not currently recommended for cow’s milk allergy treatment, whey hydrolysates have been demonstrated by some studies to be protective (Chandra and Prasad 1991; Vandenplas et al. 1992); other studies have found that casein hydrolysate formula can decrease the occurrence of atopic dermatitis (Bahna 1991) and eczema (Mallet and Henocq 1992).
The majority of food allergy prevention focuses on alterations of both maternal and infant diet. As early as 1983, Hamburger, S. Heller, M. H. Mellon, and colleagues began testing the efficacy of a maternal elimination diet (no eggs, peanuts, and milk during the last trimester of pregnancy and during lactation) in conjunction with modifications in the infant’s diet, such as delayed introduction of solids and breast feeding supplemented only by casein hydrolysate formula. But this type of regimen has yet to prove successful even though it may help to delay allergy appearance (Zeiger et al. 1986; Zeiger et al.1989). Preventive strategies, such as the restrictive regimen just described, are used with infants who are considered at high allergy risk as determined by cord blood IgE levels (greater than 2 micrograms per liter) and a positive family history of allergy (Beaudette 1991). M. Kajosaari (1991) has demonstrated that delay of solid feeding until the age of six months can help prevent food allergy, and such a delay is currently standard dietary advice.
Some individuals experience adverse reactions to foods that cannot be explained by an immunologic mechanism. Several substances seem to elicit clinical problems through these alternative pathways that include enzyme deficiencies and pharmacological mechanisms (Schwartz 1992). Examples of food components associated with intolerance include lactose, histamine, gliadin, aspartame, sulfites, tartrazine, and monosodium glutamate. Some of these components are naturally present in foods, whereas others occur as food additives.
Lactose (or milk sugar) consumption causes problems because of inadequate amounts of intestinal lactase activity (MacDonald 1988). Symptoms of lactose intolerance include diarrhea, pain, and abdominal bloating (Scrimshaw and Murray 1988). The most common type of lactose intolerance is termed primary lactase deficiency. It occurs sometime following weaning and is found in varying degrees from mild to severe. It is a common condition among the majority of the world’s populations (Savaiano and Kotz 1988). Lactose intolerance can also occur as a secondary event subsequent to intestinal damage (Penny and Brown 1992).
Histamine, a preformed chemical mediator for allergic reactions, is naturally present in some foods and wines (Malone and Metcalfe 1986; Anderson 1990). Most of the time, histamine in foods does not cause problems because it is quickly broken down by enzymes in the digestive process. Some individuals do experience symptoms of histamine sensitivity, which include headache and reddening of various body parts, such as the eyes, face, and hands. Histamine sensitivity problems may also be seen when histidine is degraded to become histamine in fish and cheeses (Burnett 1990). Scombroid fish poisoning is the name given to the clinical complex (headache, flushing, and neck pain) caused by eating dark fish meat in which histidine has broken down to histamine because of improper storage and high temperatures. This syndrome can be treated with histamine antagonist drugs (Morrow et al. 1991).
Gliadin, a component of gluten, is a natural food substance that can cause adverse reactions in some individuals. It occurs in grain products such as wheat, rye, and barley. Celiac sprue, an intestinal disorder, and dermatitis herpetiformis, a skin disorder, are the clinical manifestations of intolerance to gliadin. A transient, rare form of gluten hypersensitivity, similar to celiac sprue, has also been reported in very young children (Iacono et al. 1991).
Celiac sprue, the intestinal form of gliadin intolerance, is characterized by iron deficiency, weight loss, diarrhea, malabsorption, abdominal distension, and altered mental capabilities. Persons suffering chronically from celiac sprue appear to be at increased risk for the development of cancer (Holmes et al. 1989) and osteoporosis later in life (Mora et al. 1993). Recent work has focused on identifying and describing peptides of gliadin that cause the damage in celiac sprue (Cornell, Weiser, and Belitz 1992). The disease may have an immunologic basis, but this has not been fully described; and for the moment at least, celiac sprue is classified as a food intolerance rather than a food allergy.
Dermatitis herpetiformis, the skin form of gliadin intolerance, is characterized by a rash with itching and blistering. Granular deposits of the immunoglobulin IgA between skin layers are also characteristic of dermatitis herpetiformis (Beaudette 1991).
Aspartame is a nutritive artificial sweetener added to a variety of foods. It was introduced into the marketplace in 1981 (Tollefson and Barnard 1992). Adverse reactions reported in conjunction with aspartame ingestion include headache, memory loss, depression, dizziness, changes in vision, and seizures (Bradstock et al. 1986; Roberts 1990). L. Tollefson and R. J. Barnard (1992) have indicated, however, that an analysis by the United States Food and Drug Administration does not support the assertion that aspartame causes seizures. The postulated mechanism for aspartame’s link to headache is via increasing serum tyrosine levels (Schiffman et al. 1987). One study has cited an immune basis for aspartame sensitivity manifested by hives (Kulczycki 1986). Aspartame, however, has not been shown to degranulate basophils or mast cells (Garriga and Metcalfe 1988). Therefore, in general, adverse reactions in conjunction with aspartame tend to be reported under food intolerance because of an unknown mechanism or mechanisms. After failing to reproduce hypersensitivity reactions to aspartame, M. M. Garriga, C. Berkebile, and D. D. Metcalfe (1991) noted that aspartame should not induce an IgE mediated response because it is easily broken down in the brush border of the intestine.
Sulfites are another category of food additive associated with adverse reactions in selected individuals. About one percent of the general United States population is estimated to be sulfite sensitive (Folkenberg 1988); this figure rises to about 5 percent of the asthmatic population (Nagy et al. 1993).As in the case of aspartame, most sulfite-associated adverse reactions cannot be linked to an immune mechanism, although an immune abnormality may be responsible for a reaction in a small number of individuals. W. N. Sokol and I. B. Hydick (1990) demonstrated basophil histamine release and obtained a positive skin test in a patient who had symptoms of angioedema, nasal congestion, and hives. Examples of clinical problems seen in conjunction with sulfite sensitivity include low blood pressure, hives, angioedema, intestinal cramping and chest tightness (Perkin 1990).
Sulfite sensitivity seems to have different clinical manifestations with asthmatics, where it is manifested by bronchial dysfunction (spasm or constriction), dizziness, flushing, wheezing, and perhaps anaphylaxis (Perkin 1990). Recently, sodium bisulfite has also been linked to genetic damage in lymphocytes (Meng and Zhang 1992). One postulated mechanism for sulfite sensitivity is the initiation of a cholinergic reflex by sulfur dioxide’s action upon tracheobronchial receptors (Anibarro et al. 1992). With some individuals, it is believed that a deficiency of sulfate oxidase may be responsible (Simon 1987; Perkin 1990). Deaths and severe reactions related to sulfite sensitivity have resulted in strict labeling regulations when sulfites are present in foods in excess of 10 parts per million (ppm) (Schultz 1986). Experimentation is also under way to determine if the use of cyanocobalamin can prevent sulfite-induced respiratory distress (Anibarro et al. 1992).
Tartrazine, or FD…C Yellow 5, is another food additive cited as causing adverse reactions in susceptible individuals.Tartrazine is used to produce various food colors including yellow, green, and maroon (Dong 1984; Schneider and Codispoti 1988), and more than half of the daily food dye consumption in the United States is in the form of tartrazine (Beaudette 1991). Clinical symptoms indicating an adverse reaction to this food additive include hives, asthma, angioedema, photosensitivity, eczema, purpura, and anaphylaxis (Michaelsson, Petterson, and Juhlin 1974; Desmond and Trautlein 1981; Pereyo 1987; Perkin 1990; Devlin and David 1992). J. Devlin and T. J. David (1992) recently indicated that they could confirm tartrazine intolerance in only 1 of 12 children whose parents reported that tartrazine consumption worsened their child’s eczema. Although the mechanism of tartrazine sensitivity is unknown, the cause has been postulated as an excess of bradykinin production (Neuman et al. 1978). There is a link between aspirin sensitivity and tartrazine sensitivity with a cross-reactivity of 5 to 25 percent reported (Settipane and Pudupakkam 1975; Condemi 1981).
Monosodium glutamate (MSG) as the cause of adverse food reaction has been a source of great controversy. It is used as a food additive because of its ability to enhance flavors (Beaudette 1991).The most often cited potential adverse reaction to MSG is Chinese Restaurant Syndrome characterized by such symptoms as development of tears in the eyes, facial flushing, tightness and burning, nausea, sweating, headache, and vascular abnormalities (Ghadimi and Kumar 1972; Gann 1977; Goldberg 1982; Zautcke, Schwartz, and Mueller 1986).
Symptoms of this syndrome usually occur shortly after consumption of an MSG-containing food, and problems generally resolve in less than one hour (Beaudette 1991). Some scientists suggest that the role of MSG as the causative agent of the Chinese Restaurant Syndrome remains unproven because of a lack of a demonstrated dose-response effect (Beaudette 1991), and histamine has been proposed as an alternative culprit (Chin, Garriga, and Metcalfe 1989). In addition to Chinese Restaurant Syndrome, other potential adverse reactions to MSG consumption have been reported. These include headache, angioedema, and asthma (Diamond, Prager, and Freitag 1986; Allen, Delohery, and Baker 1987; Squire 1987). It has also been suggested that there may be a subset of the population for whom the potential excitotoxicity of glutamate could be a problem (Barinaga 1990).
Prevention and treatment of food intolerance involves avoidance of the foods and beverages that contain the offending substances. Careful reading of food labels is critical. In the case of lactose intolerance, some individuals can consume small amounts of milk or dairy products, such as yogurt or cheese, which have a low lactose content. In addition, some find it beneficial to employ special dairy products in which the lactose has been partially hydrolyzed or broken down or to use tablets that serve to break down lactose in foods and beverages. Celiac sprue and dermatitis herpetiformis are treated with a gluten-restricted, gliadin-free diet (Beaudette 1991), sometimes referred to as a gluten-free diet. The gluten-free diet has recently been shown to relieve the primary symptoms of these conditions, and also to aid in protecting against bone loss (Mora et al. 1993) and cancer (Holmes et al 1989). Some have advocated the use of a low gluten diet for the treatment of celiac sprue (Kumar et al. 1985; Montgomery et al. 1988), but at present this is in the exploration stage as a potential treatment alternative.
Foods and beverages may cause clinical problems through immunologic or physiological mechanisms. When immunologic mechanisms are confirmed, the condition is called a food allergy. The term food intolerance is used to denote clinical problems associated with food when an immunologic mechanism cannot be confirmed.
Common food allergens in the United States include cow’s milk, soybeans, wheat, eggs, nuts, seeds, and crustacea. Food allergies are more common in children than adults. Most food allergies are of the Type I IgE mediated variety. Avoidance of the foods that cause problems is the mainstay of current prevention and treatment efforts.
Food intolerance may be associated with natural food components or with food additives. Natural food components that cause clinical problems include lactose (milk sugar), histamine, and gliadin. Food additives linked to intolerance include aspartame, sulfites, monosodium glutamate, and tartrazine. Here again, dietary avoidance is the key to preventing and treating food intolerances, although pharmacological agents may be useful in treating symptoms associated with food allergies or intolerances. Several new pharmacological approaches are now being investigated.
Research in the area of food intolerances continues to look at immune mechanisms (particularly those in addition to Type I) and other physiological mechanisms that cause clinical problems related to exposure to foods and beverages. Research efforts are also underway to characterize the specific components that cause food allergies and to find new ways of treating them. In addition, testing of potential preventive or delaying approaches will continue to be a research focus in future years.