Food intolerances. Metabolic Food Disorders. Anaphylactoid Reactions. Idiosyncratic Illnesses
As noted earlier, food intolerances involve nonimmunological mechanisms. Food intolerances can be divided into three categories: metabolic disorders, anaphylactoid reactions, and idiosyncratic illnesses. Like the food allergies, food intolerances are individualistic adverse reactions to foods; most consumers tolerate the offending foods, or ingredients, very well. In contrast to food allergies, individuals suffering from food intolerances can usually tolerate small amounts of the offending food in their diet.
A. Metabolic Food Disorders. Metabolic food disorders result from inherited defects in the ability to metabolize some component of food. Lactose intolerance is the most common example.
I. Lactose Intolerance. Lactose intolerance results from a deficiency of the enzyme lactase or B-galactosidase in the intestinal mucosa. As a result, lactose, the principal sugar in milk, cannot be properly digested into its constituent monosaccharides, galactose and glucose. Normally, lactose is hydrolyzed to galactose and glucose, which are absorbed through the intestinal mucosa into the blood and used as sources of energy. The disaccharide lactose cannot be absorbed without hydrolysis to galactose and glucose. In individuals lacking B-galactosidase, undigested lactose passes from the small intestine into the large intestine. The large intestine is teeming with bacteria that metabolize the lactose to carbon dioxide and water. The result is abdominal cramping, flatulence, and frothy diarrhea, the primary symptoms of lactose intolerance.
The prevalence of lactose intolerance increases with advancing age. Lactose intolerance can have its onset as early as the teenage years, but often develops later in life. The intestinal activity of B-galactosidase tends to diminish with age so the symptoms of lactose intolerances often worsen with increasing age. The prevalence of lactose intolerance varies with different ethnic groups. Though the prevalence among Caucasian Americans is only 6-12%, lactose intolerance occurs in 60-90% of some ethnic groups, including Greeks, Jews, Arabs, African-Americans, and many Asians.
The diagnosis of lactose intolerance is established by use of the lactose tolerance test. In this test, a fasting person is given an oral dose of 50 g of lactose. In normal individuals, this oral lactose challenge would result in an increase in blood glucose of at least 25 mg/dl over a few hours. In those individuals with lactose intolerance, the rise in blood glucose is less than 25 mg/dl.
The usual treatment for lactose intolerance is the avoidance of dairy products containing lactose. However, many individuals with lactose intolerance can tolerate some lactose in their diets, often as much as an 8-oz. glass of milk. The 50-g lactose challenge used in the lactose tolerance test is equivalent to the amount of lactose in a quart of milk, so it is possible to be clinically lactose intolerant but still able to ingest a glass of milk with no symptoms. Lactose-intolerant individuals can often consume yogurt and acidophilus milk that contain active microbial cultures with f3-galactosidase. Lactose-hydrolyzed milk is also sometimes available in the marketplace. The tolerance of lactose-intolerant individuals for lactose varies, so the development of a safe and effective avoidance diet must also be individual. Tolerance for lactose may decrease over time.
2. Favism. Some individuals experience acute hemolytic anemia following the ingestion of broad beans, also known as fava beans. This illness, known as favism, is manifested by pallor, fatigue, dyspnea, nausea, abdominal and/or back pain, fever, and chills. Occasionally, more severe symptoms occur, including hemoglobinuria, jaundice, and renal failure. Favism affects individuals with a deficiency of the enzyme glucose-6-phosphate dehydrogenase (G6PDH) in their red blood cells. The red blood cells of individuals with G6PDH deficiency are susceptible to oxidative damage by two substances, vicine and convicine, found in fava beans. G6PDH deficiency is the most common enzymatic defect affecting human populations worldwide, with perhaps 100 million affected individuals. The prevalence of this defect varies among ethnic groups and is highest among Asian Jews in Israel, Sardinians, Cypriot Greeks, African-Americans, and Africans. Favism would be extraordinarily common if fava beans were more widely consumed.
B. Anaphylactoid Reactions. Anaphylactoid reactions are caused by substances that can induce the spontaneous release of histamine and other mediators from mast cells and basophils without the intervention of IgE. The symptoms of an anaphylactoid reaction mimic those of IgE-mediated allergies, but it would not be possible to demonstrate the existence of allergen-specific IgE. The evidence for the involvement of anaphylactoid reactions in food sensitivities is circumstantial. No foodborne substances have been identified as mast cell-destabilizing agents, although several pharmaceuticals demonstrate such effects.
Strawberry “allergy” is considered the premier example of an anaphylactoid reaction, and they are well known to cause hives in some individuals. Strawberries contain little protein, no allergens have been found, and no evidence exists for strawberry-specific IgE. An anaphylactoid mechanism is a logical possibility, but more proof is required.
C. Idiosyncratic Illnesses. Idiosyncratic illnesses refer to adverse reactions to foods experienced by certain individuals for which the mechanism is unknown. Many such illnesses may exist, although the association with specific foods or food ingredients has often not been proven. Doubleblind, placebo-controlled challenge procedures are useful in the establishment of a cause-and-effect relationship to a specific food or ingredient, but such diagnostic procedures have not been widely employed. Obviously, examples of idiosyncratic illnesses abound, and the symptoms involved in these reactions range from very minor to life-threatening. The mechanisms, though unknown, are also likely to be quite variable. The best example of an idiosyncratic illness is sulfite-induced asthma, because the association with sulfite ingredients is well established but the mechanism is unknown. This illness is discussed separately in another article [see Sulfites in Foods]. Other idiosyncratic illnesses, though poorly documented, are caused by tartrazine, aspartame, and monosodium glutamate.
1. Tartrazine. Tartrazine is an azo dye, also known as FD&C Yellow #5, that is allowed as a colorant in foods, beverages, and pharmaceuticals. Tartazine has been alleged to elicit urticaria (hives) and asthma in sensitive individuals. However, the association of tartrazine in elicitation of these symptoms remains unproven. This additive is likely involved very rarely in urticaria and asthma.
2. Aspartame. Aspartame is an approved food additive that is used as a nonnutritive sweetener and sold under the trade name Nutrasweet®. Aspartame has been implicated as a causative agent in urticaria and headache. However, well-designed clinical studies have failed to confirm this relationship. Aspartame is unlikely to be involved in idiosyncratic illnesses.
3. Monosodium Glutamate. Monosodium glutamate (MSG) is a widely used food ingredient that has flavor-enhancing properties. MSG ingestion has been linked primarily with Chinese restaurant syndrome (CRS) and asthma. However, the evidence supporting a cause-and-effect relationship between MSG and these or other symptoms is rather weak. The conclusion from several large trials of MSG and its role in CRS is that MSG may affect a very small segment of the population, but only after very high levels of exposure.
CRS is characterized by headache, chest tightness, a burning sensation along the back of the neck, nausea, and diaphoresis occurring within minutes of the ingestion of a Chinese restaurant meal. CRS involves very subjective reactions, making it difficult to study objectively. CRS may be caused by some ingredient other than MSG. A few cases of MSG-induced asthma have been documented; high doses were necessary to provoke asthma in these few sensitive individuals. MSG-induced asthma appears to be, at worst, a rare phenomenon whose mechanism remains unknown.
Bibliography. Brostoff, J., and Challacombe, S. J. (eds.) (1987). “Food Allergy and Intolerance.” Bailliere Tindall, London.
Lemke, P. J., and Taylor, S. L. (1994). Allergic reactions and food intolerances. In “Nutritional Toxicology” (F. N. Kotsonis, M. Mackey, and J. Hjelle, eds.), p. 117. Raven, New York.
Metcalfe, D. D., Sampson, H. A., and Simon, R. A. (eds.) (1991). “Food Allergy-Adverse Reactions to Foods and Food Additives.” Blackwell, Boston.
Perkin, J. E. (ed.) (1990). “Food Allergies and Adverse Reactions.” Aspen Publishers, Gaithersburg, MD.
Schwartzstein, R. M. (1992). Pulmonary reactions to monosodium glutamate. Pediatr. Allergy Immunol. 3, 228. Simon, R. A. (1986). Adverse reactions to food additives. N. Engl. Reg. Allergy Proc. 7, 533. Strober, W. (1986). Gluten-sensitive enteropathy: A nonallergic immune hypersensitivity of the gastrointestinal tract. J. Allergy Clin. Immunol. 78, 202.
Zeiger, R. S., andPleller, S. (1995). The development and prediction of atopy in high-risk children: Follow-up at age seven years in a prospective randomized study of combined maternal and infant food allergen avoidance./. Allergy Clin. Immunol. 95, 1179.
Date added: 2022-12-11; views: 329;