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Food intolerance causes obesity and premature aging.

Food intolerance is an increasing problem in societies exposed to commercialized agricultural products. Food intolerance differs from food "allergy" in that symptoms are usually chronic and delayed, often by several hours or even days; whereas symptoms of allergy are immediate, acute, and sometimes so dramatic as to cause death. Hence the former have received relatively little attention compared with the latter, despite the fact that their prevalence is increasing and may be responsible for the dramatic rise in rates of morbidity and mortality due to metabolic syndrome, or "syndrome X."

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Introduction

Food intolerance, rather than food allergy, may be a significant factor in the increasing occurrence of obesity and degenerative diseases worldwide. Food intolerance, rather than chronic infection, may well be the most significant underlying cause of the excessive generation of toxic free radicals that eat away at cell membranes, protein structures, and DNA. It is also likely the major as well as causative factor in the excessive production of immune chemicals that interfere with normal metabolism, and in many degenerative diseases.

Both food intolerance and food allergy are increasing in prevalence. However, despite the longstanding recognition of allergy, not to mention its potential lethality, food intolerance may be by far the more significant problem.

True allergy is such that a teaspoon full of grass, weed, or tree pollen, is enough to cause agonizing misery for an entire season. Similarly, a few molecules of peanut may be sufficient to send the victim to the emergency room, possibly even the morgue. However, the sheer magnitude of exposures to intolerogenic foods, despite its less dramatic flair (pun intended) causes greater morbidity and mortality in the long run.

Allergy vs. Intolerance

The etiology of true allergy was unknown until the nearly simultaneous discovery of IgE by the Ishizakas from Colorado State University and by a team working at the Karolinska Institute (Stockholm) in 1967. It was soon determined that allergens were taken up by antigen-presenting cells (dendritic cells, macrophages, and sometimes B lymphocytes), processed, and complexed with a major histocompatibility molecule (II), then translocated to the surface membrane, where it could be presented to interact with specialized receptors on corresponding T lymphocytes.

Given the right chemical milieu, T cell signaling induces B cell transformation and production of allergen-specific IgE antibodies. IgE antibodies play a crucial role in the pervasive mast cell production of histamine and other toxic mediators, thus giving rise to allergy symptoms, the hallmarks of which are excessive mucus production, smooth muscle contraction, nerve irritation, and general inflammation. The initial cellular degranulation and release of these mediators interact via substance P with the central nervous system and trigger the almost immediate reactions of mast cells systemically. The effect is quite dramatic, and intentionally so, as this pathway represents our natural defense against parasites that are, unlike other pathogens (e.g., viruses, bacteria), significantly larger than the cells that must defend against them.

Whereas an allergic reaction can be triggered by exceedingly modest amounts of the relevant allergen, intolerances to foods appear to be dose related--a significant factor, considering that the average Westerner now consumes more than 1000 kilos of food each year.

Economic pressure of the 1970s impelled greater commercialization of agriculture, which fostered production of less expensive foods, particularly soy and corn. Greater emphasis on tempting new processing techniques to enhance shelf life, storage, and transportation ensued. Increased use of numerous artificial ingredients, such as colorings, flavor enhancers, emulsifiers, stabilizers, and preservatives, followed. These trends triggered an increase in generalized inflammation, as the immune response to novel xenobiotic and distorted foodlike molecules became more prolific.

A confounding aspect of such intolerances is their insidious nature: smaller quantities of an offending food may be tolerable until such time as the food, a chemical naturally occurring within it, or an additive exceeds a certain threshold.

It appears likely that the increase of reports of food intolerance is directly related to these trends as they now introduce foreign substances into the diet that may be perceived by the innate immune system as smaller pathogens and toxins. In fact, many of them are toxins, or may disrupt normal physiologic function, as do azo dyes, which inhibit phenol sulfotransferase P, required to break down the gut toxin p-cresol. When p-cresol is not adequately degraded, it may become neurotoxic. Little wonder, then, that along with the increased consumption of food colorings, we also see increased cases of hyperactive and even autistic children (and adults).

Similarly, the preponderance of corn and soy products in the diet imbalances an otherwise healthy fatty acid ratio that would occur if grains were not stripped of their natural germ component; fruits and vegetables were consumed more frequently; fish, poultry, and other animals were not farm bred on these products; and cows still grazed on natural N-3 rich grass. Excessive N-6 acts as a stimulant to T cells and, along with higher levels of arachidonic acid, provide a rich substrate for proinflammatory mediator production, while, contrarily, N-3 fats balance immune function and metabolize into anti-inflammatory eicosanoids.

This "total load" phenomenon is further affected by the integrity of the gut membrane, which, under normal circumstances, forms a natural barrier to allergens entering the circulation. Infection, dysbiosis, secondary to antibiotics, cortisone (exogenous or endogenous, caused by stress), and hormones used in birth control are many of the factors that may contribute to degradation of the tight junctures of the intestine, leading to a "leaky gut."

The nutritional cofactors required for hepatic biotransformation are lower in commercially grown produce than in organic produce. Together these represent the two dynamic factors that contribute to the cyclic nature of food intolerance versus the more fixed nature of food allergy.

Classical, also known as type 1 or IgE, allergy to food has been recognized for centuries. The first recorded anaphylactic reaction to egg occurred in the 16th century, and fish-induced allergy was reported in the 17th century. (1), (2) However, the more recent development of other nonallergic adverse reactions to foods, including food intolerance, attained a modicum of recognition following the work of Chicago-based allergist Theron Randolf in the 1950s. (3)

Modern Agriculture Causes Modern Diseases, Inflammation

The link between food intolerance, chemical sensitivity, and increase in degenerative diseases associated with aging is clear. The increased incidence in metabolic syndrome, both in adults and children, coincides with the increased consumption of "junk food." Lower nutritional content of food, increased use of artificial ingredients, and synthetic chemical use constitute the major contributory factors. When dietary activators of the innate immune system are avoided, inflammation resolves, weight normalizes, and a number of other inflammatory-based health problems subside. (7)

The pathways underlying non-IgE-mediated reactions to foods, which may occur hours or even days after ingestion, making identification of offending foods complicated, still remain unclear. (3)

Adverse food reactions may be toxic or nontoxic reactions. Toxic reactions occur in anyone, given sufficient exposures, such as histamine in scombroid fish poisoning. Nontoxic reactions occur in susceptible individuals and may result from chemicals occurring in aged cheese or chocolate, and may involve either immune mechanisms {allergy or hypersensitivity) or nonimmune 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. Examples include tyramine-induced headache and untoward CNS activation following ingestion of caffeine and other stimulants.

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 if consumed on a rotational basis.

Numerous mechanisms may play a role in the pathogenesis of adverse reactions to foods. Therefore, definitive identification of offending foods relies upon provocation of symptoms following oral challenge carried out under double-blind conditions. Various serum tests exist but are of questionable value. While testing serum levels of allergen-specific IgE antibodies is useful for classical allergy, it is of limited value for identifying foods and chemicals associated with intolerance (delayed-type reactions) that are not IgE mediated. Hopes for IgG assays have not succeeded, as this appears to be a protective antibody that is associated with exposure but does not play a pathogenic role. Food allergy symptoms include anaphylaxis and urticaria. The range of manifestations of intolerance is broader, including not only GI symptoms, but also the skin, respiratory, metabolic, musculoskeletal, renal, CNS, and virtually all other organ systems. Hence, its importance in clinical practice is significant, yet it does not fall under the purview of any particular specialty and therefore has never been as well understood as allergy, nor as well managed.

Testing

Allergy tests, such as skin tests or RAST (radioallergosorbent test), are not effective for identifying intolerances to food. A good 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-blinded oral challenges, and should be repeatable. The only test that meets these criteria is the ALCAT (antigen leukocyte cellular antibody test).

Manifestations

Until recently, childhood diabetes was exclusively type 1, with autoimmune-based destruction of insulin-producing islet cells. The consequence: high blood-sugar levels and tissue degeneration. Perhaps this is just the tip of the iceberg.

Adult onset diabetes is not autoimmune per se, but occurs when insulin receptors on muscle, liver, and brain lose effectiveness. Insulin resistance is a hallmark of metabolic syndrome, or "syndrome X," characterized by obesity, diabetes, and cardiovascular disease. 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 as though there were a paucity of the sugar-transporting hormone.

The innate immune system mediates this phenomenon. Interleukin 6 and tumor necrosis factor alpha block insulin receptors. After the glucose is stored as fat in adipocytes, these cells themselves continue to produce these very same mediators and perpetuate a state of obesity-inflammation--and degeneration. Adult onset diabetes now occurs at younger ages. Along with this, we see an increase in childhood obesity and associated health risk, social, and quality-of-life factors. These occurrences coincide with a general increase of overweight in the general population.

Studies have shown that inflammatory mediators block insulin receptors. This is the likely cause of insulin insensitivity. Epidemiological studies reveal an association between chronic activation of the innate immune system and metabolic syndrome, as well as other degenerative conditions. These can target any bodily system, such as the CNS (as in Alzheimer's disease), joints, rheumatoid arthritis, and many in between.

Conclusion

The front-line treatment for type 1 diabetes and overweight in children and adults should be dietary, rather than pharmacological; emphasizing healthy natural, nutritious food along with exercise and stress management.

The above trends have, for a number of reasons, given rise to unprecedented levels of obesity and incidence of metabolic and inflammatory disorders, such that even "adult onset" diabetes is now occurring frequently in children.

Testing of white blood cell reactions, particularly the neutrophils, following in vitro challenge of whole blood, does not represent dependence on a single or limited array of mechanisms, and thus can reflect pathological responses to foods that are mediated by all on immunologic, nonimmunologic, pharmacologic, as well as toxic pathways. Whole blood analysis offers the additional advantage of reflecting in vivo response more accurately. Tests such as the ALCAT exhibit the highest degree of correlation with blinded challenges and are the most accurate. Correlation with double-blinded oral challenges with foods has been carried out under rigorous conditions, whereby only one new food is added back to the diet every seven days, and the symptom score is evaluated only on the last three days of each challenge, to avoid carryover effects from previous challenges. Overall efficiency has been demonstrated at 83.4%, with specificity at 87.9%. (5) This renders the ALCAT unique in that not only do symptoms resolve and normalization of weight occurs, but the effects are based on the elimination of a far greater preponderance of (truly) positive foods, rather than just the foods consumed in greatest quantity, as is the case with immunological assays that indicate higher IgG (exposure)-related antibodies. (6) In this way, through the ALCAT, the patient is not overly burdened with unnecessary food elimination and achieves a superior clinical outcome.

Notes

(1.) Cohen SG, Saavedra-Delgado AM. Through the centuries with food and drink, for better or worse. 11. Allergy Proc. 1989;10:363-373.

(2.) Harper DS. Egg?--ugh! In: Avenberg KM, ed. Footnotes on Allergy. Uppsala: Upplands Grafiska AB; 1980:52.

(3.) Bruijnzeel-Koomen C, Ortolani C, Aas K, et al. Adverse reactions to food. Allergy. 1995;50:623-635.

(4.) Deutsch R. The right stuff: use of ALCAT testing for determining dietary factors effecting immune balance, health and longevity. In: Klatz R, Goldman R, eds. Anti-Aging Therapeutics. Vol. 10. 2007.

(5.) Hoj L. Diagnostic value of ALCAT test in intolerance to food additives compared with double blind placebo controlled (DBPC) oral challenges. Part 3. J Alleg Clin Immunol. 1996(1).

(6.) Brostoff J et. al. 45th Annual Congress of the American College of Allergy & Immunology, Los Angeles, CA: November 12-16, 1988.

(7.) Kaats G, Pullin D, Parker L. The short term efficacy of the ALCAT test of food sensitivities to facilitate changes in body composition and self-reported disease symptoms: a randomized controlled study. Bariatrician. Spring 1996.

Roger D. Deutsch

Cell Science Systems Corp.

852 S. Military Trail

Deerfield Beach, Florida 33442

RD@ALCAT.com

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Roger Davis Deutsch founded Science Systems Corp (CSS), located in Deerfield Beach, Florida, in 2004. CSS developed the ALCAT to determine intolerances to foods, additives, environmental chemicals, molds, drugs, and other substances. Previous work experience includes having served as VP of corporate development for Williams Worldwide Television Inc. where responsibilities including establishment of a European base for distribution of American infomercials and products worldwide, and negotiation of contracts with cable and satellite services. Williams was the largest infomercial agency at that time. Mr. Deutsch was also the cofounder and chairman of Amerex Oil Associates from 1979 to 1983, during which time he implemented strategies that enabled the company to rapidly become the largest oil brokerage company in the world. Mr. Deutsch is coauthor of the book Your Hidden Food Allergies Are Making you Fat: The ALCAT Test Weight Loss Breakthrough (PRIMA CSS LTD.TH 1998) and a newly revised edition (released in July 2002). He has studied acupuncture at the International College of Oriental Medicine in the UK and frequently lectures worldwide on the subject of food allergy and intolerance and chemical sensitivity. Mr. Deutsch received an Associates of Arts degree in psychology from Nassau Community College, Long Island, New York. He also attended C. W. Post College, the State University of New York at Purchase, and the International College of Oriental Medicine in the UK.
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Author:Deutsch, Roger
Publication:Townsend Letter
Article Type:Report
Geographic Code:4EUUK
Date:Jan 1, 2010
Words:2515
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