Food intolerance induces inflammation and the excessive generation of toxic free radicals and immune chemical, increasing the occurrence of metabolic, chronic and degenerative diseases.
In contrast with “True” allergy, whereby a few molecules of peanut may, for example, induce anaphylaxis, the sheer magnitude of exposures to intoleragenic foods, despite its less dramatic flare (pun intended), causes greater morbidity and mortality.
Allergy vs. Intolerance
The etiology of true allergy became known in 1967. It was soon determined that allergens (allergy generators) were taken up by antigen presenting cells and presented to T lymphocytes in a similar fashion as peptide products of pathogenic micro-organisms.
T cell signaling induces B cell transformation and production of allergen specific IgE antibodies, which play a crucial role in the pervasive mast cell production of histamine, causing excessive mucus production, smooth muscle contraction, nerve irritation, and general inflammation. The effect is quite dramatic, and intentionally so, as this pathway represents our natural defense against large parasites. Unlike other pathogens (i.e., viruses, bacterium), parasites are significantly larger than the cells that protect against them. Hence, allergy can be triggered by modest amounts of allergen, produces dramatic symptoms, and has a clearly defined pathway.
In contrast, intolerances to foods follow a different pathway, are primarily mediated by the innate branch of the immune system, and symptoms are dose related, chronic and delayed.
Offending food may be tolerable until such time as a chemical naturally occurring within the food, or that has been added, exceeds a certain threshold. Additionally, the abundance of corn and soy in the diet creates fatty acid imbalances. Excessive N-6 stimulates T cells, and higher levels of arachidonic acid provide a rich substrate for chronic, pro-inflammatory mediator production. The immune triggering novel food-like substances draw abundantly from this inflammation, producing substrates to perpetuate a chronic inflammatory state we call food intolerance.
Another consequence of the modern diet is that nutritional cofactors required for hepatic biotransformation are lower in commercially grown produce. When chemicals in foods (naturally occurring or otherwise) cannot be adequately detoxified by the liver, the immune system is called to action.
This “total load” is further impacted by the integrity of the gut membrane which, under normal circumstances, forms a natural barrier. Infection, dysbiosis, antibiotics, cortisone (exogenous or endogenously produced) and hormones used in birth control compromise the gut barrier.
Classical, or IgE allergy to food, has been recognized for centuries. The first recorded anaphylactic reaction to egg occurred in the sixteenth century1 and fish induced allergy was reported in the seventeenth century.2 However, the more recent development of other non-allergic adverse reactions to foods, including food intolerance, only began receiving recognition following the work of Chicago-based allergist Theron Randolf, in the 1950’s.3
Modern Agriculture Causes Modern Diseases, Inflammation
The link between food intolerance, chemical sensitivity and the dramatic increase in degenerative diseases is clear, coinciding, as it does, with consumption of junk food. When avoided, inflammation resolves, weight normalizes, and a number of other inflammatory based health problems subside.
As seen from this necessarily simplified analysis, adverse food reactions may be toxic or nontoxic reactions. Toxic reactions occur in anyone, given sufficient exposure. Nontoxic reactions occur in susceptible individuals and may result from chemicals occurring in aged cheese, chocolate, and may involve either immune mechanisms (allergy or hypersensitivity) or non-immune mechanisms. The former are referred to as, “hypersensitivities;” the latter, “intolerances.”
Food intolerances are the most common. They are most likely caused by the pharmacologic activities of chemicals that naturally occur in the food or, that are added to the food.
However, some intolerances result from inherited enzyme deficiencies and, thus, remain fixed. Some reactions are exacerbated by poor digestion related to intestinal dysbioses, or the overwhelming of specific detoxification pathways that are rate limited.4 Hence, addressing these underlying issues can result in tolerance of moderate quantities of the food.
Because numerous and varied mechanisms play a role in the pathogenesis of adverse reactions to foods, definitive identification of offending foods relies upon provocation of symptoms following oral challenge under double blind conditions—not always a convenient option for doctor or patient. Various serum tests exist, but are of questionable value. Whereas testing serum levels of allergen specific IgE is useful for classical allergy, it is of limited value for identification of foods and chemicals associated with intolerance that are not IgE mediated.
IgG antibodies against foods are protective, associated with exposure and, despite common misunderstandings, do not play a pathogenic role in either food allergy or food intolerance. Neither are allergy tests, such as skin tests or RAST, effective for identifying intolerances to foods. A useful test for intolerances would have to measure the effect of the food substance on the cells on the innate immune system in a non-mechanism dependent manner. It should show a good correlation with clinical symptoms, as confirmed by double blind oral challenges. The only test meeting these criteria is the ALCAT Test.
Manifestations
Previously, childhood diabetes was exclusively of the Type 1, auto-immune based type. The consequence: high blood sugar levels and tissue degeneration. Perhaps this is just the tip of the iceberg. Now, due to over activation of the innate immune system, due to food intolerance, so called, “adult onset” diabetes occurs even in children. Adult onset diabetes is not auto-immune per se, but occurs when insulin receptors on muscle, liver and brain, lose effectiveness. Insulin resistance is the hallmark of metabolic syndrome. Initially, insulin is produced, but it cannot sufficiently facilitate the uptake of glucose because of the insensitivity of the insulin receptors. The pancreas then produces increasing quantities of insulin, but of lower quality. Blood sugar levels increase.
The most probable link between food intolerance and metabolic syndrome is that Interleukin 6 and tumor necrosis factor alpha block insulin receptors. Glucose is stored in adipocytes which, in turn, produce these very same mediators and perpetuating obesity, inflammation, and degeneration.
@
Solutions
The frontline treatment for Type 2 diabetes and overweight in children and adults should be dietary, rather than pharmacological, emphasizing healthy natural, nutritious food along with exercise, stress management, intestinal health and adequate nutrtition.
Foods that act as triggers require proper identification and avoidance. Testing of white blood cell reactions, particularly the neutrophils, following in vitro challenge of whole blood, is independent of any single or limited number of mechanisms. It, thus, reflects pathological responses to foods that are mediated by immunologic, non-immunologic, pharmacologic, as well as toxic pathways. Whole blood analysis offers the additional advantage of reflecting in vivo response more accurately. The ALCAT Test exhibits the highest degree of correlation with blinded challenges and is the most accurate.5 Symptom resolution, normalization of weight, and broad clinical correlation affirm this as a useful tool to be added to the arsenal of integrative health practitioners.6
Roger Davis Deutsch founded Science Systems Corp (CSS), located in Deerfield Beach,
FL. CSS developed The ALCAT Test to determine intolerances to foods, additives, environmental chemicals, molds, drugs and other substances. He began his involvement of development in food intolerance and other Alcat technology-based tests in 1986. He may be reached at Cell Science Systems, Corp., 852 S. Military Trail, Deerfield Beach, FL 33442 or [email protected].