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Diagnosis of Food Allergy: Tests
The desire for simple, definitive tests for food allergy is easy to understand, but difficult to fulfill. Food interacts complexly and sequentially with many different consequences. It is unlikely that food allergy occurs in a consistent manner; there are too many variables. No single test will ever reveal the complex and variable nature of this reactivity. The lack of specific tests for food allergy have hindered progress in this field.
The difficulty in diagnosing food allergy and other food-related problems in clinical medicine and disputes within the allergy community have left many patients suffering, frustrated and confused. At the same time as physicians default in the diagnosis and treatment of food-related illnesses, many non-medical practitioners have launched careers in the food and chemical "sensitivity" business, using diverse, sometimes curious and bizarre methods, dubious tests and questionable treatments. Also unfortunate, has been the insistence of some allergists on the skin test as definitive in food allergy. The skin test is a limited exploration of immune reactivity, mostly useful in the investigation of hay fever and other inhalant allergy. Some labs offer other tests for food allergy, including IgG RAST, and immune complex assays. While these tests produce interesting results, they are expensive and do not answer the main question - what should the patient eat?
This review addresses, briefly, some of the testing and treatment issues and confusions about food allergy.Even well-intentioned efforts to diagnose and treat allergy are often based on faulty premises and fail to deliver proper results.
The following questions must be asked about every proposed test:
What is the test simulating? Is the simulation related to eating real food in real time, by real people, exposed to many other influences? Does this test do a credible job of simulating digestion and absorption? Are the testing substances representative of foods, actually eaten? Are the results reproducible? Are the test results just spot samples or do they represent the sequential interaction of food with body systems? Does the test simulate problem with GIT permeability and does it demonstrate the different responses to varying doses and frequency of food ingestion?
The only test that answers all the simulation criteria, is to actually eat the food as meals over days to weeks and observe what happens.
When the simple model of linear IgE-mediated reactions dominate thinking, some unreasonable demands for "proof of food allergy" are placed on physicians and patients alike. The notion that double blind food challenge is essential for the diagnosis and before diet revision is prescribed is among the most impractical, and sometimes refractory ideas. Food allergy research should include studies of people who are evaluated by supervised challenge with food materials in a variety of circumstances. But, very limited conclusions can be drawn from these isolated experiments. MDs should never learn to discredit the evidence that patients bring during their forays in the real-world.
The Alpha Nutrition Program is both a diagnostic and a treatment procedure. This standardized method of diet revision can be conducted at home and spare the patient the inconvenience and cost of hospitalization or frequent office visits. In the era of cost-containment and increased patient responsibility for self-care, a well-constructed diet revision program empowers the patient to resolve health problems with a minimum of medical interventions.
Delayed Food Allergy
The concept of delayed patterns of immune response ("food allergy") to food materials provides both a theoretic and practical basis for interpreting symptoms of patients with both specific diseases and non-specific syndromes. The presence of food allergy ( as a pathophysiological mechanism) is concealed in a variety of nosological diagnoses such as migraine headaches, asthma, eczema, irritable bowel syndrome, Crohn's disease, celiac disease, chronic fatigue, Fibromyalgia, depression, panic disorder, and arthritis. Patients with these problems tend to have two or more syndromes concurrently in a matrix of non-specific symptoms. The grand theory of hypersensitivity disease attempts to explain these illness complexes as expressions of reactive immune networks, responding to food and airborne antigens.
Food allergy is diagnosed by physicians who understand the multisystem, polysymptomatic patterns of illness involved. These patterns are revealed by a careful history, and the diagnosis made on clinical grounds. The pattern of food-related illness, the sequence of symptom production, and the distribution of disturbances in the body can be explained if complex causation is assumed. The temporal order of sequential immune responses may be appreciated by thinking in terms of simultaneous immunologic, physiological and biochemical mechanisms, and followed clinically by careful recording of each individual's symptom production in response to food challenges.
Without a well-equipped research laboratory it will not be possible to actually measure the pathophysiological events. The patient's symptom reports and a general understanding of pathophysiology will usually suffice to construct an adequate theory (diagnosis) and prescribe effective intervention. Often a burst of symptoms, emerging over hours or days, can be explained by antigenic material from food entering the circulation from GIT and triggering a variety of alarm and defense procedures.
Allergy Skin Tests
Skin tests can reveal some of the immediate-type hypersensitivities to food materials and are always of interest, when distinctly positive. If a food extract produces a wheal > 10 mm, the food probably should not be eaten. However, the skin test does an enormous disservice if it is used to deny food allergy. A negative skin test for food is meaningless. The entire spectrum of delayed pattern food allergy lies beyond the predictive abilities of this elementary form of immunological testing.
Provocation Tests: by Injection
Provocation tests by needle injection of food proteins into the skin have also been used. The intradermal (ID) injection test will occasionally show a delayed, cell-mediated response in 24-48 hours. Symptoms may develop as injected antigen reacts with skin mast cells, or reaches circulating basophils and triggers an amplified, immediate alarm-response. There is no question that injected antigen can sometimes demonstrate symptom-production in the allergic patient. Indeed every allergist is concerned about triggering life-threatening anaphylactic reactions with any injection. If major symptoms do occur to one injected antigen, further testing is invalid for several days.
Clinical ecologists have claimed to "neutralize" the reaction by injecting further doses of antigen at different concentrations, and often test many substances in one session, lasting several hours. We do not believe any meaningful conclusions can be drawn from these testing marathons. The subject tends to have fluctuating, confusing sensations, and is extremely vulnerable to suggestion from the testing person. The ID provocation test is not reliable in predicting responses to foods, actually eaten, and should not be used as the basis for recommending diet revision.
Cytotoxic tests were offered in the early 80's for definitive "food sensitivity" determination, and were condemned by the American College of Allergists as ineffective. Cytotoxic tests expose blood cells to food extracts in a chamber, viewed through a microscope; cell counts before and after reveal cell damage.. Automation can be applied to cell counting and evaluation with computer print-outs of test results. While the earlier cytotoxic tests have little to offer, more sophisticated analysis of food antigen and blood-cell interactions is always relevant to understanding pathogenic mechanisms. A recent automated test has been offered as the ALCAT diagnostic system. The ALCAT brochure repeats the understanding that multiple mechanisms are involved in food allergy and that responses to food antigens by various blood components should be measured in food allergic individuals. The predictive significance of these measurements remains to be discovered.
The IgE model of allergy inspired development of antibody-measuring laboratory tests. The idea was to show the affinity of circulating antibodies to different food antigens. RAST has been used instead of, or in addition to, skin prick and scratch tests to assess food allergy. Whenever IgE mechanisms dominate the food allergy problem, RAST may be a useful test. Variations of the RAST bear the acronyms ELIZA, FAST, and MAST - all tests for antibodies directed at selected antigens.
Negative RAST results have been used to deny food allergy and seem authoritative, looking official and "scientific" on a computer printout from the lab. This RAST-test denial only demonstrates ignorance of the many mechanisms of food allergy, not related to IgE or not involving the small number of test antigens, selected from a much larger number of possible antigens in the food supply.
The principles of RAST testing for IgE are now applied to the measurement of other antibody types. The measurement of IgG is of interest. Current studies suggest frequent IgG responses to food antigens. Tests measuring food-antigen specific IgG have been offered with an impressive computer-report of "food sensitivities". The levels of food-specific IgG are listed, and avoidance of foods with increased antibody levels is advised. Helpful food lists and food rotation instructions accompany some of the lab reports. It would appear the problem of food allergy diagnosis is solved. Again, this simplistic approach to food allergy diagnosis is bound to mislead. While it is possible that avoidance of IgG-positive foods will be helpful, we do not know if that avoidance will really resolve the illness problem. In my experience with the IgG RAST, the predictive value for real-life food reactions is limited.
The measurement of total blood levels of four antibody species (immunoglobulin electrophoresis) is of some interest in the complex food allergy patterns. Shifts in the distribution of IgG, IgM, IgA, and IgE may manifest immune activity in response to antigen loading through GIT. The most common pattern is an elevation of the IgM with a low IgE level. Depressed levels of IgM, IgG are seen in patients who have severe or prolonged food allergy; often white cell counts are also depressed. When IgE levels are low, skin testing and IgE RAST are of little value. Low IgA predisposes to food allergy, and always suggests the diagnosis. Occasionally, elevations in IgA and IgG are seen in the food allergy complex. High IgG is associated with the more serious immune-mediated diseases, and reflects increased antibody production, often against unknown antigens. Normal levels of these antibodies do not rule out the diagnosis of food allergy.
Immune Complex Assays
The detection of circulating immune complexes is an important test of the antigen-entry mechanisms. Usually this procedure is reserved for research, and is not routinely employed in patient evaluation. Improvement in techniques and automation is currently making CIC measurement more practical. The most interesting test procedures not only detect CICs, but also determine what food antigens have complexed with antibody. This demonstration of food-antigen-containing CICs is gratifying, since the phenomenon of antigen-entry is demonstrated.
The conclusions regarding immunological tests for food allergy can be summarized; no single antibody measurement will predict the immune response to food; and no single type of lab measurement should be used as the only diagnostic test for food allergy. One reason for not pursuing immunological tests as a basis for practical problem-solving in the Doctor's office is that they are too expensive for the uncertain results they provide.
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