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Food Allergies

 


 

 

 

 

Introduction
Food allergies (FA) cause the immune system to release cytokines, lymphokines, and interferon’s influencing all tissue physiology; toxins initiate similar reactions; food allergy and toxicity are intimately connected; FA is the culprit behind ‘mysterious’ undiagnosable symptoms; allergy testing uncovers causes of illness, reveals unsuspected food sensitivities in asymptomatic patients; bronchial hypersensitivities doubled in the last decade; atopic dermatitis in 10-15% of population, provoked by food antigens; adverse food reactions in 25% of younger children; the leading cause of most undiagnosed symptoms.

 

Causes and development


• Increased incidence: regular consumption of a limited number of foods; hidden ingredients in processed foods; food additives; medicinal drugs (e.g. penicillin) added to foods; environmental pollution; early weaning and solid foods given to infants; genetic manipulation of food components which cross-react with normal tissues; impaired digestion; less dietary diversity.


• FA is an expression of genetic predisposition; allergic histories in both parents and siblings; if both parents are allergic, 67% of children are allergic; if one parent allergic, 33% of children are allergic.


• Maldigestion; hypochlorhydria (low stomach acidity) and/or pancreatic enzyme deficiency; undigested proteins retain antigenicity, are exposed to immune system or absorbed through a ‘leaky gut’, and create chronic hypersensitivity.

 

Signs and symptoms
__________________________________________________________________________________

System                                Symptoms and diseases

__________________________________________________________________________________


Gastrointestinal                Canker sores, celiac disease, chronic diarrhoea, duodenal ulcer, gastritis,

                                     irritable colon, malabsorption, ulcerative colitis.


Genitourinary                   Bed-wetting, chronic bladder infections, nephrosis


Immune                          Chronic infections, frequent ear infections


Mental/Emotional              Anxiety, depression, hyperactivity, inability to concentrate,

                                     insomnia, irritability,   mental confusion, personality change, seizures


Musculosketal                   Bursitis, joint pain, low back pain


Respiratory                      Asthma, chronic bronchitis, wheezing


Skin                               Acne, eczema, hives, itching, skin rash


Miscellaneous                  Arrhythmia, oedema, fainting, fatigue, headache, hypoglycaemia,

                                    itchy nose or throat, migraines, sinusitis

 

Types of immune reactions


• Type I – immediate hypersensitivity: < 2 h after contact; antigens bind to pre-formed IgE mast cells and basophils, release histamine and eosinophilic chemotactic factor; symptoms vary with tissue location of mast cells.


• Type II – cytotoxic reactions: binding of IgG or IgM to cell-bound antigen; antigen-antibody binding activates complement and destruction of cell bound to antigen.


• Type III – immune complex-mediated reactions: antigens bound to antibodies; usually cleared via phagocytosis; deposition in tissues/vascular endothelium causes tissue injury; vasoactive amines increase vascular permeability and deposition of more complexes; delayed hours or days after exposure; involve both IgG and IgM.


• Type IV – T-cell-dependent: delayed reaction by T-lymphocytes after allergen makes contact with mucosal surface; sensitised T-cells may induce inflammation within 36-72h; does not involve antibodies.

 

The allergic reaction: antigens are proteins or large polysaccharides > 8,000 Da; food is the largest antigenic challenge to immune system; food hypersensitivity is a result of interactions among food antigens, GI tract, tissue mast cells and circulating basophils, and food antigen-specific immunoglobulins.

 

Role of IgE and IgG4


• Repeated antigen exposure produces hypersensitivities: IgE antibodies cross-link on GI mast cells, stimulate the release of histamine, proteoglycans, and leukotrines, instigating mucosal permeabilitiy and allowing food antigens into blood; other organs may be involved, causing perpetual autoimmune response.


• Most severe, immediate allergy symptoms are IgE-mediated; but IgG and IgG complex involved in 80% of all food allergies; 60% of patients exhibit delayed reactions to provoking foods; primarily mediated by IgG.


• Specific IgE has half-life in circulation="1-2" days, and on the mast cell="14" days; IgG circulating half-life=21 days, and on mast cells="2-3" months; IgG assay is essential for ‘hidden’ allergies undetected by IgE RAST or skin testing.


• IgG4 subclasses: associated with high antigen levels, particularly food antigens; increases with increasing antigens; higher levels than other IgG subclasses; IgG4 is the only IgG subclass inducing basophil degranulation, triggering histamine release.


• IgG increases GI permeability, due to selective transport mediated by Fc receptors on mucosa; this increases exposure to antigens.


• Production of IgG4 and IgE is controlled by interleukin-4 (IL-4) and interferon-? (IFN-?); there is increased synthesis of IgG4 and IgE from decreased inhibitory effect of IFN-? postulate: defective immunoregulation involving IL-4 and IFN-? support synthesis of IgG4 and IgE.

 

Food Allergy and Related Testing

 

• Oral challenge test: most accurate for immediate hypersensitivities, but costly, time-consuming, and potentially dangerous; not easily applicable to delayed sensitivities.


• Food-specific IgE and IgG4: correspond more closely with patient history than challenge test.


• RAST and skin testing: only measure IgE reactions, not delayed non-IgE reactions; skin testing is sometimes unfeasible and may trigger life-threatening reactions.


• Follow-up testing necessary: monitors changing sensitivities from changing in eating habits; helps modify therapy, as needed.


• Intestinal permeability: evaluates GI effectiveness as macromolecules barrier, and determines causes of systemic problems linked to GI function.


• Comprehensive digestive stool analysis (CDSA): maldigestion is a significant cause of food allergy; examines digestion and absorption status of GI tract.


• Fecal secretory IgA: sIgA is the predominant immunoglobulin in intestinal secretions and saliva; first-line defender against microbes and toxins; forms immune complexes with pathogens preventing binding to mucosa; fecal sIgA evaluates status of mucosal immunity.


• Adrenocortex and melatonin profiles: many sensitised individuals have endocrine dysfunctions; severity of symptoms often follows chronobiotic pattern influenced by circadian hormone rhythms.

 

Therapeutic considerations

 

Five essential components that the Irish Centre of Integrated Medicine applies to treatment are to: avoid identified allergens; rotate diet until sensitivity decreases; re-establish proper microbial milieu; heal damaged intestinal mucosa; correct causative factors, such as maldigestion.

 

• Evaluate each case carefully using variety of criteria: antibody tests, detailed medical history, thorough physical exam, challenge tests once certain antigens have been ruled out by preliminary tests.


• Oligoantigenic diet: highly effective in treating food allergies; ADD children show improved hyperactivity; 93% of children with migraine recover, even when migraines are provoked by other factors (blows to head, exercise, flashing lights); reduces colic in infants and chronic urticaria with arthralgia in adults.


• Rotation diet: prevents new allergies, gives immune system rest, and intestines a chance to heal; infrequent consumption of tolerated foods not likely to induce new sensitivities or worsen old ones.


• Re-establish healthy bowel microflora: suppresses toxic microbes; probiotics are normal bacteria in healthy intestines (Lactobacillus and Bifidobacteria); probiotics are enzymatically indigestible substrates selective for healthful bacteria; increase intestinal SigA with oligosaccharides, especially fructo-oligosaccharides (onions, asparagus, bananas, maple syrup).


• Healing damaged gut: eliminate all factors injuring mucosa; re-establish microflora, remove intestinal toxins; improve digestion; decrease inflammation; promote metabolism, repair of mucosa.


• Decrease inflammatory gut reaction: quercetin is a natural flavonoid which inhibits mast cell histamine release, scavenges free radicals, inhibits intestinal smooth muscle irritability; also reduces damage by food allergens with vitamin C; fish oils: polyunsaturated N-3 fatty acids, EPA, DHE; they reduce inflammation. PAF, neutrophil chemotaxis, and cell adherence to endothelium.


• Stimulating regeneration of gut mucosa: glutamine is the most abundant amino acid in blood, and a substrate for mucosa cells (35% of their energy production); supplementation stimulates regeneration, prevents mucosal damage, decreases bacterial leakage across mucosa after damage.


• Re-establishing normal digestion: oral betaine HCL if achlorhydria or hypochlorhydria present; pancreatic insufficiency; treat with beef or pork pancreatin or microbial-derived digestive enzymes.

 

This article is to be used for information and guide line purpose. Any advice and/or suggestions from this article should be supervised by your health professional. ICIM can offer a medical professional at the centre to guide you through your health complaints. Contact ICIM for more information.

 

 

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ICIM Medics, St. Johns Grove, Johnstown, Naas, Co. Kildare, Ireland.

          Tel: 00353 (0)45 844 819  -  www.icim.ie  -  info@icim.ie 

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