I was diagnosed at the age of 3 or 4 years with asthma, which is an allergic reaction to
certain, normally harmless chemicals found in Nature (in my case several different pollens and mold
spores), and is listed as one of the COPDs (Chronic Obstructive Pulmonary Disorders). Contrary to the
opinion of my physician of record (once I was old enough to know what he was saying), allergic people
do not “out-grow” their allergies; some patients “grow into” coping with,
or self-management of the disorder, weaning themselves off the prescribed medications. Food
allergies, however, do not seem to respond to self-management (except completely avoiding the
substances to which the patient is allergic).
True food allergies must be taken very seriously because the allergic reaction can, by positive feed-back mechanisms, escalate in intensity, sometimes resulting in the death of the patient. Self-diagnosed food allergies require confirmation and diagnosis because of the risks associated with true food allergies, and because “food allergy” has become fashionable among hypochondriacs. I sometimes find hypochondria-type allergies to be amusing; frequently the reported symptoms do not match allergy symptoms, and often the reported trigger of the incorrect reactions is a chemical species to which an allergic reaction is not possible. One colleague of mine (about 40 years ago) claimed to be allergic to tobacco smoke. I had gone to a business meeting early, and had filled my pipe and had just lighted a butane lighter and brought it up to my pipe, when I saw him enter the room. I extinguished the lighter, and “smoked” my un-lit pipe during the meeting. My colleague became progressively more agitated (due to discomfort) as his allergic reaction to the smoke from my un-lit pipe (he had previously been exposed to my filled but un-lit pipe resting in an ashtray on my desk without evidence of discomfort). Not only was he not “allergic” to tobacco smoke, but also there are no ingredients in tobacco smoke (of which I am aware) that can trigger the allergic reaction, although several ingredients can aggravate a respiratory allergic reaction (either in progress, or in the presence of an actual trigger).
The allergic reaction is a response of the immune system to a perceived threat. The only mechanism
known to elicit any reaction by a living organism is to present the organism with some stimulus to
which the organism can react. For the immune system, the required stimulus is an antigen, which is a protein that can be recognized by the T or B lymphocytes
as “self” or “non-self” proteins (or polypeptide fragments). Typically, an
allergic reaction occurs when an mostly harmless antigen (called an
mistaken by the lymphocytes as a massive invasion of a pathogenic organism rather than the reasonably
harmless organism (such as a pollen grain [male gametophyte of an angiosperm]) which it really is.
Since (a) the immune system responds to antigens, (b) antigens are non-self proteins, and
(c)allergens are the antigens involved in allergic reactions, therefore allergens must be non-self
proteins (or polypeptide fragments). In other words, the allergen triggers are not “almost
always a protein” (text pg 17-2), the only allergen triggers are proteins. The classic
allergic reaction is an over-reaction to a minor [non-threatening] invasion of non-self proteins.
Antibodies are produced by the T or B lymphocytes as their initial reaction to the allergen. The first time the lymphocytes encounter the allergen (the “sensitization” phase), the lymphocytes only produce the antibodies and do not continue to react. The patient exhibits no symptoms of the allergy, but they are now “sensitized” to the allergen. The simplest explanation of sensitization is that the patient has now acquired an “immunity” to the “disease” caused by the “pathogenic organism” that produced the allergen. This process is most obvious in the population of patients allergic to bee stings. The first bee sting produces edema (swelling) accompanied by an itching sensation typical of a sensitive patient's response to the sting. The second (and subsequent) stings may produce anaphylactic shock. [The toxin in bee venom is chemically identical to spider venom and some snake venom, so a spider bite may sensitize the patient to bee stings and the patient will exhibit the allergic reaction to their first bee sting.] After sensitization (or developing acquired immunity to the “disease” caused by the “pathogenic organism” that produced the allergen), the patient's immune system shifts to the “reactive” phase, and any subsequent exposure to the allergen will trigger an allergic reaction. This involves the antibodies attaching to the allergen, and the allergen-antibody complex signaling the body to secrete histamine [mediated by Immunoglobulin E] responsible for the physical signs and symptoms of the allergy [which may change over time, for example from respiratory symptoms (runny nose, watery eyes) to skin symptoms (rash). The role of histamine is a hormone-like stimulus to the entire body to prepare to react, or even to react immediately as systematic symptoms (remote from the “invasion”).
Anaphylactic shock is the most serious of allergic reactions. It is a massive, systemic reaction invloving vaso-dilation, dropping blood pressure and effectively shutting down the blood supply to the “invading organism”, as well as shutting down blood circulation to the host [patient]. Death may occur if treatment (IV epinephrine) is not administered quickly.
The common symptoms of food allergies are as follows (adapted from Table 17.1, text pg 17-3):
|Body system||symptom||% of allergic
Patients may exhibit any of the symptoms described above, or any combination of symptoms. Symptoms
may appear within seconds of ingesting the food, but may have delayed onset of symptoms for several
hours. The exhibited symptoms may change from one episode to another, or may show a long term, slow
change from one set of symptoms to a different combination. Unfortunately, you, as a Nurse, are
likely to encounter a lot of self-diagnosed “food allergies;” one of my favorites is a
acquaintance of mine who has Lactose allergies, although I was never aware, before her
self-diagnosis, that Lactose was a protein. She has enough College education (Allied Health) to know
better, but assures me that it is clearly possible to be allergic to things other than protein since
she is allergic to lactose, a sugar. It is currently fashionable to have miscellaneous allergies to
explain behavioral and attitude problems, so the number of self-diagnosed allergies is on the rise,
as clinical studies have failed to support similar claims for food additives (which are “so
yesterday” as the explanation of all of society's ills). The popularity of the food allergy
disorders coupled with the difficulty of diagnosing them makes it hard to determine the incidence
rates. Our “best guess” is that an estimated 5% of young children and infants, and an
estimated 2% of adults in the U.S. population have true food allergies. The difference is still
being attributed, in part, to the mythology of “out-growing” allergies. Knowing allergies
from the point of view of a trained Biologist with allergies, I would strongly caution against
telling parents of children diagnosed with any allergies (including food allergies) to expect the
child(ren) to out-grow their allergies. The symptoms may become less severe (such as becoming
limited to “unexplained” skin rashes [rather than hives] and/or mild upset stomach [rather
than nausea]), but the underlying allergic condition will still be there. Children probably do not
out-grow cow's milk, eggs, and wheat (gluten) allergies later in childhood as claimed in your text
(pg. 17-5). Another explanation for reduced symptoms as the child ages could be nothing more than a
dose rate per body weight issue; it may take a higher dose for the older (and larger) child to react,
but at a higher dose rate the reaction may “re-appear.”
The list of foods commonly involved is rather lengthy (and definitely not exhaustive): [tree] nuts, eggs, wheat, milk, peanuts (a legume), soy [and soy products], shellfish, fish, and other foods. The most reliable method to confirm food allergies, and to identify the foods involved, is the double-blind, placebo-controlled food challenge. After a sufficiently long period without exposure to the suspect food, the patient is presented with either the food (in pill or liquid form) or a similar placebo to verify that the food and not the placebo causes the reaction. If some mixture of foods triggered the possible allergic reaction, the double blind placebo-controlled test must test each food separately. However, once the foods that trigger the allergic reaction have been identified, this does not mean that other foods will not cause alleric reactions. If you have never eaten shellfish until you are 23 years old (and have known or unknown food allergies), the second meal with shellfish (even months or years later) could still trigger an allergic reaction.
Food intolerances do not involve the immune system, and therefore are not limited to proteins. The
symptoms may be highly similar to food allergy symptoms, but normally can not become as severe as
true food allergies. For those food intolerances that have been studied sufficiently, the cause
appears to be either the lack of an enzyme involved in digestion of the specific food ingredient
that is not “tolerated,” or to underproduction of the enzyme. Lactose intolerance is due
to insufficient to no lactase, and causes flatulence (rarely seen in allergies), bloating,
abdominal pain (as opposed to cramping), diarrhea, and/or “stomach growling.”
Sulfites are an natural ingredient found at low concentration in some foods. Sulfites have been found to preserve color in dried fruit (naturally dried friuts all have the color of raisins), and to retard spoiling of wine due to conversion of the Ethanol to Acetic acid (also known as vinegar). As a result, sulfites are added to such foods as a preservative. Among the population with true allergies, sulfites have been shown to aggravate the allergies and to dramatically increase the risk that the allergic reaction will escalate to anaphylactic shock. This was discovered in the 1970s, as an increase in the death rate among young adults (college and recent college graduate aged) due to what was reported as “alcohol poisoning” brought on by binge drinking of beer, but later recognized to be proximally caused by respiratory arrest secondary to anaphylactic shock (attributed to rather high concentrations of sulfites added to beers to retard spoilage). All patients with respiratory allergies should be advised to monitor carefully for sulfite-induced signs and symptoms; even those allergic patients who are “not sensitive” to sulfites will exhibit low grade signs of reaction (such as runny nose or itchy eyes).
Red wine and aged cheese are claimed in your text (pg. 17-9) to contain histamine and related compounds which may cause migraine headaches in sensitive patients. I was able to confirm the existance of the hypothesis that some foods trigger migraines at the Mayo Clinic website, but I infer from the wording that the writer is unsure that these claims can be borne out in clinical testing. There appear to be two problems with the hypothesis: headaches are not among the common signs or symptoms of food intolerances, and true migraine headaches have not been shown to be allergic reactions to protein triggers. I am inclined to believe that these headaches are actually sinus-headaches resulting from mucus accumulation in the ethmoid, sphenoid, frontal, and maxillary sinuses, rather than migraine headaches. The mucus production is suggestive of an allergic reaction, and may indicate that the patient is [genetically] predisposed to develop [more accurately, to become sensitized for] respiratory allergies. Some of the ingredients commonly cited are capable of aggravating respiratory allergies, so the headache could result from the aggravating influence of the active ingredients in the foods, even in the absence of the allergen trigger.
To discriminate positively between food allergies and food intolerances would involve a difficult, lengthy, and prohibitively expensive, investigation. If one could isolate each of the proteins from all food substances, and test each for allergic sensitivity, one could with high certainty detect the presence of a food allergy. If one could complete a thorough assay of all digestive enzymes in a patient, and look for clinical deficiencies among them (requiring a database of ‘normal’ ranges for all digestive enzymes in Humans), one could with high certainty detect the presence of a food intolerance. It should not take more than several decades to develop these diagnostic tests after we start working on the problem, and it is not a high priority item on the list of ‘things to do’ even after we finish the more popular research on the Human genome and stem cells as potential “cures” for miscellaneous diseases and disorders.
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