Food Allergies - An Unrecognized Epidemic

I am passionate about food. I like to buy it. I love to cook it. And I really love eating it. However, what we eat is becoming more and more important. Interestingly, it is not just unhealthy foods that are problematic. Below is an article I wrote about food allergies several years ago. I would love to hear your comments or questions.


Food Allergies – An Unrecognized Epidemic

It is estimated that 95 out of every 100 people in industrialized nations suffers from some type of adverse food reaction.1 Over 50 medical conditions have now been associated with food allergies (Table 1) and many more chronic, persistent symptoms may actually be manifestations of adverse food reactions. Although there is a growing amount of medical literature implicating foodstuffs in the etiology of various medical disorders, most often food allergies are not considered as a possible underlying cause.

A food allergy is an immune system response that occurs after ingestion of a specific food. Although any food is capable of producing an immune response upon ingestion, foods that commonly cause allergy are dairy products, eggs, shellfish, soybeans, tree nuts, wheat, corn, citrus, and peanuts. Reactions can be divided into two categories: IgE mediated (immediate) and nonIgE mediated (delayed). IgE mediated, type I immediate hypersensitivity reactions have been well studied, and their involvement in food allergies has been firmly established. Symptoms of IgE reactions occur within minutes after exposure to the offending agent and can vary in intensity from mild localized erythema and edema, to rhinitis, urticaria, asthma, tongue itching and in severe cases throat swelling and anaphylaxis. Most individuals with IgE allergies know that they have them, since the correlation between ingestion of the food and resulting symptoms is clear. IgE allergies are often permanent and can be easy to identify without further testing. However, IgE-radioallergosorbent (RAST) tests, IgE enzyme linked immunosorbent assay (ELISA) tests, and skin-prick tests can at times be used to aid in the diagnosis.

Only 6-8% of children and 2-3% of adults suffer from IgE mediated food allergies.2 There is increasing evidence that many if not most food sensitivities involve other mechanisms, most of which are immunological in nature.3 Therefore, limiting diagnosis of food allergies through the use of IgE mediated testing may be insufficient.

It is estimated that 80% of all food allergy reactions are nonIgE mediated, often involving the IgG immunoglobulin class and its complex mediators.4 IgG mediated immune reactions have vastly different characteristics than those associated with IgE mediated responses. Although the IgG4 subclass has been implicated as an anaphylactic antibody in some animal models of food allergy5, most often IgG reactions have a delayed response time – they occur hours to sometimes days after the offending agent has been ingested. Symptoms can vary from person to person and can virtually affect any system, organ, or tissue of the human body. They are rarely self-diagnosed, and the allergy often resolves after 3-6 months of avoidance.

There are several theories surrounding the development of food allergies. Poor digestive health may increase the chances of developing food allergies. If the digestive system is functioning optimally, food is broken down into vitamins, minerals, and amino acids through the use of hydrochloric acid, digestive enzymes, and peristalsis. These particles are small enough to be absorbed between the cells of the digestive tract, pass into the blood stream and then travel to their final destination to be used as needed. Hypochlorhydria, insufficient chewing, and rapid swallowing of foods lead to the improper digestion of food proteins. These larger food proteins can trigger histamine release and degranulation of intestinal mast cells. This degranulation may then cause increased intestinal permeability leading to more systemic symptoms of food allergy.5 A study reported in the Journal of Allergy and Clinical Immunology supports the risks associated with poor digestive function. The authors examined the role of drugs that hinder peptic digestion in the development of food allergies. They concluded that antacid medication impairs gastric digestion and inhibits digestion of dietary proteins promoting IgE synthesis toward novel dietary proteins, leading to food allergy.6

It is known that heating and cooking can change the allergenicity of foods by altering protein structure. Paul Bragg states, “The average person is poisoning himself day by day with the food he eats. Our tiny sensitive taste buds have been polluted by unnatural, artificially seasoned and stimulating foods…Foods must be fixed, hashed, mashed, smashed, boiled, broiled, stewed, baked, pickled, preserved, flavored, salted, creamed, dried, roasted, fried, greased, peppered, vinegar-laden, smoked, toasted, crushed, rolled, mealed, oiled, fermented, beaten, sweetened, spiced, soured, peeled, shredded, steamed, braised, colored, and otherwise seasoned in order to offer an appeal to the civilized man.” This alteration of foods through processing, heating, fortifying, purifying, homogenizing, pasteurizing, etc. may lead to the development of food allergens from what would otherwise have been health-promoting whole foods.

Additional factors associated with the possibility of developing food allergies include: repetitive ingestion of the same foods, excessive stress, digestive tract infections, dysbiosis, family history of food allergies, birth via Caesarian section, high maternal age, failure to breast feed, early introduction of solid foods (especially dairy, wheat, and eggs), and overexposure or increased sensitivity to environmental irritants.1,7 A thorough medical history will often provide clues as to the possibility of food allergy.

The gold standard in the diagnostic work-up of suspected food allergy is double blind placebo controlled oral food challenges.8,9 However, this process can be very tedious, time-consuming, and potentially dangerous, triggering possible life threatening reactions. If delayed sensitivities are suspected, oral food challenge may not provide timely results. In addition, larger quantities of foods are often needed to trigger an IgG reaction, and a false negative response may occur if substantial amounts are not consumed. The possibility also exists of interactions or cumulative effects amongst allergenic foods. In this case, any one food alone may not trigger symptoms, but ingestion of a combination of reactive foods is required to produce symptoms.

Various diagnostic methods exist to determine adverse reactions to foods. These include the atopy patch test, serum tests for specific IgG to foods, provocation/neutralization testing, kinesiology, cytotoxic tests, and electrodermal testing.9 Many of these tests are considered investigational, however, as there is limited research substantiation, few clinical studies, and in some cases no scientific basis. An accurate diagnosis is important to avoid unnecessary diets and to establish a proper treatment plan.

Regardless of which form of testing is used, treatment of food allergies is the same. Initial steps include elimination of the offending foods and incorporation of an oligoantigenic diet. A rotation diet may also be used to prevent the development of new allergies.10 Probiotics, such as Lactobacillus acidophilus, may be added to help recolonize the digestive tract and increase production of secretory IgA. Reducing digestive inflammation through the removal of artificial colors/sugars/sweeteners/flavors from the diet, eliminating concentrated sugars and refined carbohydrates, decreasing stress, avoiding unnecessary medications, and chewing food thoroughly will aid in repair of the intestines. Glutamine, bioflavonoids, and essential fatty acids, namely fish oil, have been shown to support the regeneration of the mucosal lining. Incorporating digestive enzymes and hydrochloric acid may help prevent new allergies from developing while supporting proper digestive function.

There are a few treatment options available if the allergens are unable to be eliminated. Clinical trials involving cromolyn sodium have shown efficacy in preventing allergic reactions by stabilizing mast cell degranulation. Hesperidin and quercetin are two bioflavonoids, which also act as mast cell stabilizers. However, their effectiveness has not been proven. A promising traditional Chinese herbal formula named FAHF-1, has been shown to protect peanut sensitized mice from anaphylactic reactions and significantly reversed already established IgE mediated peanut allergy.11 These recommendations, however, do not replace avoidance as the most effective form of treatment.

Food allergies are an often-unrecognized cause of many chronic health conditions today. Many individuals are being continuously treated for the annoying and nagging symptoms associated with food allergies. However, little or no attention is being given to the actual underlying cause. It has been my experience that the cause of these symptoms is an adverse reaction to the common everyday foods that are consumed and identification and elimination of these foods can lead to resolution of many chronic health complaints.


Table 1. Conditions Linked to Food Allergy

Aphthous Ulcers
Arthritis
Allergic Rhinitis
Anxiety
Asthma
Attention Deficit
Bedwetting
Bronchitis
Celiac Disease
Chronic Diarrhea
Chronic Fatigue Syndrome
Colic
Colitis

Ulcerative Colitis
Frequent Illness
Croup
Hay Fever
Hyperactivity
Inflammatory Bowel Disease
Insomnia
Learning Disorders
Malabsorption Syndrome
Muscle Pain
Acne Vulgaris
Allergic Sore Throat

Migraine Headaches
Ear Infections
Candidiasis
Chronic Constipation
Crohn's Disease
Transient Dyslexia
Edema
Gastric and Duodenal Ulcers
Hypochlorhydria
Juvenile Rheumatoid Arthritis
Loss of Voice
Memory Loss

Indigestion
Eczema
Premenstrual Syndrome
Overweight
Psoriasis
Rheumatoid Arthritis
Tinnitus
Vertigo
Skin Rashes
Mood Swings
Excessive Mucous Production
Sleep Disorders

References

1. Zavik, Jeffrey S. Toxic Food Syndrome. 2002
2. Papageorgiou, P. Clinical aspects of food allergy; Biochem Soc Trans.2002; 30(Pt 6):901-6.
3. Sandberg, D. Gastrointestinal complaints related to diet; Int Ped. 1990; Vol 5 (1): 23-9.
4. Hamburger, R. Proceedings of the First International Symposium on Food Allergy;Vancouver, B.C.1982.
5. Metcalfe, D., Sampson, H., Simon, R. Food Allergy: Adverse Reactions to Foods and Food Additives. Blackwell Scientific. 1997: 42.
6. Untersmayr, E., et al. Antacid medication inhibits digestion of dietary proteins and causes food allergy: a fish allergy model in BALB/c mice. J Allergy Clin Immunol. 2003; 112(3): 616-23.
7. Bjorksten, B. Genetic and environmental risk factors for the development of food allergy. Curr Opin Allergy Clin Immunol. 2005; 5(3): 249-53.
8. Sampson, HA. Food allergy–accurately identifying clinical reactivity. Allergy. 2005; 60 Suppl 79:19-24.
9. Beyer, K, Teuber, SS. Food allergy diagnostics: scientific and unproven procedures. Curr Opin Allergy Clin Immun. 2005; 5(3): 261-6
10. Pizzorno, J, Murray, M. Textbook of Natural Medicine. Churchill Livingstone. 1993:458-59.
11. Li, XM, et al. Food Allergy Herbal Formula – 1 (FAHF-1) blocks peanut induced anaphylaxis in a murine model. J Allergy Clin Immunol. 2001; 108(4): 639-46.