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
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 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
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
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.
Listen to an Introduction to Food Allergy Diagnosis and Tests
The Food Allergy Center is devoted to explaining a complicated
subject. We offer rich resources online and encourage our readers to further
pursue their interest by reading our books. This is an educational
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Managing Food Allergy
Stephen Gislason MD explains how
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