Food Allergy


I provide testing for food sensitivities (allergies). We use tests that include antibodies of various types that may be present to numerous foods. This may be a potential cause of many diverse health issues. Research shows that in many cases, immune reactions caused by otherwise innocent foods,are a significant hidden cause of  many chronic conditions relating to many organ systems, including digestive complaints, autoimmune issues, inflammation and weight gain.The remainder of this article describes why I recommend testing.

Reactions to food affect nearly everyone at some point. When people have an unpleasant reaction to something they ate, they often think that they have an allergy to the food. There are actually three different reactions that one may have to a particular food: an allergic reaction, food “sensitivity” or food intolerance. The first two are reactions that are due to interaction of a food with the immune system.

Food intolerance is not an allergy nor sensitivity, as it does not involve an immune response. The classic food intolerance involves milk. People who experience digestive distress after consuming dairy products often think they have an allergy, when in fact they have lactose intolerance. This is due to a genetic lack of the digestive enzyme lactase, which digests the major sugar, found in milk, lactose. Bacteria then ferment the sugar, leading to gas and discomfort. Other reactions to foods that are not allergies include food poisoning and toxic reactions due to certain chemicals the body cannot process (such as poisoning from certain mushrooms).

A true food allergy is much less common than food sensitivity. It is an abnormal response to food that is triggered by a specific immune reaction, caused by a class of antibody called IgE (Immunoglobulin E). Allergens in food (also called antigens) are those components that cause an allergic reaction. They may be proteins or partially digested proteins that may resist being broken down by cooking or complete digestion by stomach acid, and intestinal digestive enzymes. As a result, the antigens survive to cross the gastrointestinal lining, where they enter the bloodstream, and go to target organs, causing allergic reactions throughout the body. A true allergic reaction involves IgE and a type of white blood cell, called a mast cell, a specialized cell that stores histamine that is found in all tissues, especially the nose, throat, lungs, skin, and gastrointestinal tract. When IgE recognizes an antigen, they bind to the surface of the mast cell, causing release of histamine. This is called an immediate hypersensitivity reaction, because it occurs within minutes of exposure to the antigen. This can cause typical allergy symptoms or can be severe; causing an anaphylactic reaction that can lead to death. Usually the connection between the food eaten and the reaction are obvious, so people know to which foods they are allergic.

Unlike the very apparent immediate hypersensitivity reaction caused by the combination of antigen with IgE; three other classes of antibodies; IgA, IgG and IgM cause the most common and yet least appreciated reactions. To distinguish these immune reactions from IgE food allergy, these reactions are technically called “food sensitivities”, although most people use the terms interchangeably. In contrast to the obvious, rapid and usually severe onset of symptoms caused by the immediate hypersensitivity reaction; these sensitivities cause a delayed hypersensitivity reactions. These symptoms are usually less severe and may take up to 72 hours to appear. Therefore the connection between the food consumed and generalized, vague and multiple symptoms; is not apparent. Unidentified food sensitivities may cause or contribute to many chronic health conditions, including: Irritable Bowel Syndrome, Autoimmune diseases, chronic infections, ADD and ADHD, headaches and many others. Celiac disease is an example of the worst form of food sensitivity.

The common denominator in food sensitivity reactions is inflammation. This is the hallmark of immune system reactions. The binding of IgA or IgG to an antigen coats or opsonifies the antigen. White blood cells, such as macrophages, are attracted to the immune complex and engulf and break down the antigen. In the process, these cells release chemical signals to other cells, called cytokines and interleukins (with some bizarre names like: Interleukin 1 (IL-1), IL-6, IL-12, tumor necrosis factor and nuclear factor kappa beta). These chemicals are the direct cause of inflammation, working by causing the body to generate free radicals and enzymes that digest the antigen.

The purpose of acute inflammation is to assist in the process of killing invading organisms. With repetitive ingestion of foods to which one is sensitive, a chronic low-grade state of inflammation exists. Virtually all chronic diseases have as their root cause, chronic inflammation, including: diabetes, heart disease, cancer and arthritis, to name a few. The classic expression of inflammation is redness, swelling, increased temperature and pain. Everyone has experienced this with a sprained joint. Imagine a condition when your cells constantly were experiencing an inflammatory response!

Unfortunately, sometimes the body cannot distinguish between antigens from food and those of foreign invader microbes (bacteria and virus). This leads to the above-described immune response to the detriment of the affected individual. Food antigens are essentially innocent and, absent an immune response, would do little damage. It is the unnecessary and unwanted immune response that causes the damage.

A significant difference does exist between microbial infection and food sensitivities. In the case of invading microbes, one is only exposed occasionally. Surviving the first attack by a specific microbe (Called a primary response) causes the body to produce certain white blood cells (called memory B Cells). With a second exposure to the same type of foreign invader (called a secondary or anamnestic response), the white blood cells that produce antibodies directed against that invader, mount a more intense and aggressive response. This causes the invader to be killed more rapidly, so that the disease caused by the invader does not recur. The person is then immune to the disease caused by the invader. This is the principle by which vaccination works.

In contrast to the occasional contact with an invading microbe, the scenario with foods that cause an immune response is usually different. In this case, if the food is frequently consumed, the body is repeatedly exposed to the antigen, so antibodies are constantly being produced. This triggers an ongoing immune response. With long-term exposure to a specific antigen, the immune system undergoes two major changes, called class switching and affinity maturation.

Immunoglobulin class switching changes a B cell’s production of antibody from one class to another, During this process, the part of the antibody that recognizes the antigen stays the same and the region that attaches to the surface of a white blood cell changes. Since the variable region does not change, class switching does not affect antigen specificity. Instead, the antibody retains affinity for the same antigens, but can interact with different effector molecules. Initially, most antibodies are of the IgM or IgD type. If these activated B cells encounter specific signaling molecules called cytokines and interleukins, they undergo antibody class switching to produce IgG, IgA or IgE antibodies. This allows cells produced from replication of the initial B cells that produced the first antibodies to now produce antibodies of a different type. The presence of IgG4 antibodies in serum may serve as an indicator of repeated exposure to a specific antigen (food), as it seems that IgG4 antibodies develop after other classes. Repeated exposure to food antigens causes IgG1 to switch to IgG4. It also appears that there may be a correlation between IgE and IgG4 antigens as those antigens that can cause production of IgE antibodies also cause IgG4 antibodies to be produced, however the reverse is not true. Antigens that stimulate IgG4 production do not necessarily cause IgE to be produced.

MetaMetrix Labs, in their “White Paper” called “Understanding IgG4 Food Sensitivities”, explains the effects of repeated exposure to a food antigen as follows:
“Upon continued exposure to the antigen, it is proposed that IgG1 antibody production will “class switch” to IgG4. Interestingly, IgG4 antigen complexes do not activate the complement cascade. IgG4 acts as a blocking agent against the actions of IgE and can form small complexes as antigen exposure increases. These IgG4 food immune complexes have a relatively long half-life and are subject to alterations that would affect the structure enough to present as a “new” antigen. It is thought that IgG1 is then produced to attack this complex. Thus begins a whole new cycle: IgG1→IgG4 →complex→modification→IgG1→IgG4. Consequently, 
the complexes can get larger and larger. These larger complexes can activate the complement cascade, initiating inflammatory responses in the body. It is this inflammatory response to a food that is thought to be the root cause
 of symptoms in this type of adverse food reaction. The symptoms resulting from food sensitivities, therefore, can come from the activation of complement via IgG1/IgG4 food immune complex. Deposition of these complexes
can also occurs in tissue or organs, leading to damage. This sequence of events is thought to be the most common way individuals develop adverse reactions to foods they eat on a regular basis.”

MetaMetrix Labs, describes their test for IgG4 antibodies as follows:
“Food IgG4 levels increase in response to the presence of the food antigens that penetrate a weakened intestinal barrier and enter the bloodstream, particularly with commonly eaten foods (e.g., corn, wheat, dairy, and egg). IgG4 antibodies combine with specific food antigens to form food immune complexes, which cause the problems associated with delayed allergic responses. The complexes can cause inflammatory reactions at various sites in the body, including the small and large intestines, skin, kidneys, ears, sinuses, head, lungs, and joints.
Your test results show the total amounts of IgG4 antibodies that react to each food measured in the profile. The relative degrees of IgG4 present for each food are reported as mild, moderate or severe, in addition to the quantitative levels. The results are ranked in classes of negative (blank “response” column) or +1 to +5 according to cutoff points shown. Foods sensitivity reactions may have one of several mediators, so it’s possible for you to react to certain foods even with low or negative levels of IgG4. The test results are still valuable since they may guide your clinician to look for non-immunological causes.

If your report has only a few +1 reactions, the data indicates a lack of IgG4-reactive food sensitivity or intestinal issues. Very strong reactions to only a few foods may simply be an indication that those foods are used excessively. In that case, the food elimination guides can be useful for choosing alternatives. A report with many foods showing moderate or severe total IgG4 elevations may reflect a chronic intestinal permeability problem. Progressive loosening of the junctions between intestinal cells can produce a “leaky gut” situation where undigested particles of food enter the blood in higher amounts. The solution for such problems is to eliminate highly reactive foods while rotating all other classes of food so that new food reactions do not appear, and the tight junctions of the intestinal cells can be restored.

The “leaky gut” phenomenon causes food antigens to permeate into the bloodstream where the immune system generates IgG4 antibodies to protect against more dangerous types of reactions. The process of antibody production and removal causes a metabolic stress. Complete elimination of all highly reactive foods for one month, and rotation of ones with low levels, can relieve symptoms related to this type of food reaction. Avoiding reactive foods in this way will prevent IgG4-food antigen reactions that cause symptoms. If symptoms return after one month when normal eating habits are resumed, the elimination/rotation diet and nutritional support should be continued.

Avoiding reactive foods may not completely heal the leaky gut because antibodies to whatever foods are consumed are formed at such high rates. Sometimes additional nutritional therapy is needed to improve the integrity of the intestine.

When numerous foods are taken out of the diet because they show significantly elevated total IgG levels, there is potential for protein deficiency, which is known to have a negative impact on the immune system and may, in turn, make symptoms worse. Protein deficiency may be avoided by using non-antigenic medical food substitutes or crystalline, pure free-form amino acid blends.”

With affinity maturation, repeated or continued exposure to an antigen, selects for B-cells that produce antibodies that have a higher affinity to be preferentially produced. This means that the antibodies bind tighter to the antigen, creating bigger, more stable immune complexes to which other white blood cells can recognize and respond.

Current research shows significant connections between a number of common conditions and food sensitivity, including: autism; rheumatoid arthritis; cystic fibrosis; atopy (Atopy is a syndrome characterized by a tendency to be “hyperallergic”. A person with atopy typically presents with one or more of the following: eczema, hay fever, conjunctivitis, or asthma. Patients with atopy also have a tendency to have food allergies); irritable bowel syndrome; epilepsy; and migraine headaches. A brief summary of a few recent research articles follows.

1) The results of a study on autistic children suggest that autism is characterized by increased total serum protein, a unique pattern of the various classes of proteins found in serum, including IgG subclass IgG2 and IgG4. The increased serum concentrations of IgG’s in autism may indicate an underlying autoimmune disorder or may reflect different cytokine-dependent influences on autoimmune B cells and their products.

2) Patients with Rheumatoid Arthritis (RA), an autoimmune disorder, were evaluated for dietary antigens to IgA, IgG and IgM antibodies in the GI tract and were compared to healthy subjects. The results showed a significant increase in intestinal antibodies to multiple foods tested in the RA patients. The authors concluded, “The production of cross-reactive antibodies is strikingly increased in the gut of many RA patients. Their food-related problems might reflect an adverse effect of multiple, modest hypersensitivity reactions mediated by immune complexes promoting autoimmune reactions in the joints.

3) Food allergy was investigated in children with Cystic Fibrosis (CF) who suffered from diarrhea and failure to thrive despite diet and digestive enzyme treatment. IgE mediated food allergy and food sensitivities to IgA, IgG and IgM were elevated in this group compared to controls. Symptoms improved in 90% of the patients when the offending foods were removed from the diet.

4) 48 children between 6-36 months old with food allergy symptoms were compared to age-matched children without symptoms. 22.9% had IgE reactions to food and 62.5% had IgG reactions, while children in the control group had no reactions.

5) A landmark study on allergen-induced cytokine production in allergic children compared antigen-specific cytokine regulation of IgG antibodies. This same group had previously shown that atopic symptoms were associated with elevations of IgG4 antibodies. They found several cytokines to be elevated by the antigens they used in their test, indicating that these food-derived immune complexes were capable of inducing inflammatory reactions.

6) Patients with Irritable Bowel Syndrome (IBS) who had failed with “standard medical therapies” were tested for IgE and IgG antibodies and were also given a Comprehensive Stool Analysis (CDA). 100% of the patients had IgG antibodies directed against the foods tested. Treatment consisted of food avoidance, a rotation diet and probiotics. Significant improvement was seen in stool frequency, pain and questionnaire scores and improvement in beneficial bacteria with decreases in dysbiotic bacteria.

7) Children with epilepsy with migraines and hyperkinetic behavior and GI symptoms were studied for the effect of avoidance to allergenic foods. A significant number improved with diet therapy. When offending foods were reintroduced in a double blind, placebo controlled study, symptoms recurred in 15 of 16 children, including seizures, whereas the placebo caused no recurrence of symptoms.

In summary, if you have a variety of chronic complaints to which you have received no satisfactory explanation or treatment, consideration of testing for food allergies and sensitivities should be given. I offer several choices for testing including serum testing for IgA, IgE and IgG4 antibodies to 96 foods. Serum testing for IgG4 antibodies can also be performed in conjunction with other tests at a discount. For people who have a fear of needles, a simple finger-stick test for IgG4 antibodies to 96 foods can be performed.