Food Sensitivity & Leaky Gut Syndrome

The Gluten File


Many people with Celiac Disease or Non-Celiac Gluten Sensitivity find they have problems with additional food intolerances. In Celiac Disease, this might be temporary and once the intestinal villi have healed, sometimes the secondary problem foods can be successfully added back. In those with multiple food sensitivies, one has to question overall gut health and other factors that may be involved.

The difference between IgE (classic food allergy) and IgG (delayed) food allergy is still somewhat controversial, but...it seems IgG food allergy is gaining recognition as a real player in ill health.

I'm not pretending to have all the answers when it comes to food allergy, but I do know it can be a subject of great interest as we struggle to be well. Hope some of the information I leave here can speed your journey to better health!

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Discussing Leaky Gut Syndrome

Leaky Gut by Dr. Scot Lewey

Leaky Gut by Direct-MS   

Leaky Gut by Dr. Kaslow

Leaky Gut Syndrome by Jake Paul Fratkin, OMD

LEAKY GUT SYNDROMES: BREAKING THE VICIOUS CYCLE

LGS by Life Extension Foundation

Mechanisms Behind the Leaky Gut  by Susan Costen Owens, Autism Research Institute

More on Zonulin



Other Articles:

Clinical Aspects of Gastrointestinal Food Allergy in Childhood

eMedicine - Protein Intolerance 

A critcal review of IgG immunoglobulins and food allergy- implications in systemic health

The clinical relevance of IgG food allergy testing through ELISA - Enzyme-Linked Immunosorbent Assay


PubMed on Intestinal Permeability (aka "Leaky Gut")

Autoimmune diseases are characterized by tissue damage and loss of function due to an immune response that is directed against specific organs. This review is focused on the role of impaired intestinal barrier function on autoimmune pathogenesis. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to non-self antigens. Zonulin is the only physiologic modulator of intercellular tight junctions described so far that is involved in trafficking of macromolecules and, therefore, in tolerance/immune response balance. When the zonulin pathway is deregulated in genetically susceptible individuals, autoimmune disorders can occur. This new paradigm subverts traditional theories underlying the development of these diseases and suggests that these processes can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing the zonulin-dependent intestinal barrier function. Both animal models and recent clinical evidence support this new paradigm and provide the rationale for innovative approaches to prevent and treat autoimmune diseases.
Leaky gut and autoimmune diseases.
PMID 22109896  Feb 2012

Recent studies investigating the underlying mechanisms involved in disease development in diabetes point to the role of the dys-regulation of the intestinal barrier. Via alterations in the intestinal permeability, intestinal barrier function becomes compromised whereby access of infectious agents and dietary antigens to mucosal immune elements is facilitated, which may eventually lead to immune reactions with damage to pancreatic beta cells and can lead to increased cytokine production with consequent insulin resistance. Understanding the factors regulating the intestinal barrier function will provide important insight into the interactions between luminal antigens and immune response elements. This review analyses recent advances in the mechanistic understanding of the role of the intestinal epithelial barrier function in the development of type 1 and type 2 diabetes. Given our current knowledge, we may assume that reinforcing the intestinal barrier can offer and open new therapeutic horizons in the treatment of type 1 and type 2 diabetes.
Leaky gut and diabetes mellitus: what is the link?
PMID:21382153  June 2011

Effect of probiotics on intestinal barrier function.
PMID: 19538305   May 2009

B. lactis inhibited the gliadin-induced increase dose-dependently in epithelial permeability, higher concentrations completely abolishing the gliadin-induced decrease in transepithelial resistance. The same bacterial strain also inhibited the formation of membrane ruffles in Caco-2 cells induced by gliadin administration. Furthermore, it also protected the tight junctions of Caco-2 cells against the effects of gliadin, as evinced by the pattern of ZO-1 expression. We conclude thus that live B. lactis bacteria can counteract directly the harmful effects exerted by coeliac-toxic gliadin and would clearly warrant further studies of its potential as a novel dietary supplement in the treatment of coeliac disease.
Live probiotic Bifidobacterium lactis bacteria inhibit the toxic effects induced by wheat gliadin in epithelial cell culture.
PMID: 18422736   June 2008

PubMed on Food Sensitivity:  


BACKGROUND: Elevation of the gastric pH increases the risk for sensitization against food allergens by hindering protein breakdown. This can be caused by acid-suppressing medication like sucralphate, H2-receptor blockers and proton pump inhibitors, as shown in recent murine experimental and human observational studies.  CONCLUSIONS: Antacids and dietary supplements influencing the gastric pH increase the risk for sensitization against allergenic food proteins. As these substances are commonly used in the general population without consulting a physician, our data may have a major practical and clinical impact.
Antacids and dietary supplements with an influence on the gastric pH increase the risk for food sensitization.

PMID: 20214670  July 2010


CONCLUSION: This is the first randomised, cross-over study in migraineurs, showing that diet restriction based on IgG antibodies is an effective strategy in reducing the frequency of migraine attacks. [Free full text available on PubMed]
Diet restriction in migraine, based on IgG against foods: a clinical double-blind, randomised, cross-over trial.
 
PMID: 20647174  July 2010

Anti-Saccaromyces Cerevisiae antibodies (ASCA) are elevated in autoimmune thyroid disease ASCA in autoimmune thyroid disease. 
PMID: 21046480
  July 2010

Milk protein IgG and IgA: the association with milk-induced gastrointestinal symptoms in adults.
PMID: 19842221  Oct 2009

We demonstrated a high IgG response in a very large subject group to milk and milk derivatives, and egg albumin antigens, and we conclude that the validated ELISA test may be applied for the serum/plasma IgG antibody level determination as a useful indicator of adverse reactions to food and food hypersensitivity.
Serum IgG responses to food antigens in the italian population evaluated by highly sensitive and specific ELISA test.
PMID: 19117202 2009

Purpose: To establish the interdependence between the intensity of the clinical symptoms and the acid reflux index in children with primary GER and GER secondary to cow's milk protein allergy (CMA) and/or other food allergies (FA).
Acid gastroesophageal reflux and intensity of symptoms in children with gastroesophageal reflux disease. Comparison of primary gastroesophageal reflux and gastroesophageal reflux secondary to food allergy.
PMID: 19095581 2008

CONCLUSION: Serum IgG4 assay may play a role in rul-ing out food intolerance, because of its satisfactory negative predictive value (0.99).
Time to reconsider the clinical value of immunoglobulin G4 to foods?
PMID: 18839470  2008

PMID: 18397414  May 2008

Testing for IgG4 against foods is not recommended as a diagnostic tool: EAACI Task Force Report*
PMID: 18489614 May 2008
There are studies supporting IgG testing, as well as many anecdotal success stories based upon IgG testing. jcc


CONCLUSIONS: Food allergy is one of major causes of chronic childhood diarrhea. Food specific IgG antibody detection may assist in the dietary management of this disorder.
PMID: 18289464  Feb 2008

CONCLUSION: According to the results obtained, serum IgG antibodies to common food should be investigated in patients with migraine.
Food allergy mediated by IgG antibodies associated with migraine in adults.
PMID: 18693538  Sept 2007

CONCLUSIONS: Abnormal immune reactions mediated by IgG antibodies coexisted in patients with IBS. It is of great significance in treating IBS by eliminating the allergic foods according to the serum level of food-specific IgG antibodies.
[The therapeutic effects of eliminating allergic foods according to food-specific IgG antibodies in irritable bowel syndrome]
PMID: 17967233  Aug 2007

[Focal villous atrophy of the duodenum in children who have outgrown cow's milk allergy. Chromoendoscopy and magnification endoscopy evaluation]
PMID: 17625280  June 2007

Treating irritable bowel syndrome with a food elimination diet followed by food challenge and probiotics.
PMID: 17229899 Dec 2006

A mucosal inflammatory response similar to that elicited by gluten was produced by CM protein in about 50% of the patients with coeliac disease. Casein, in particular, seems to be involved in this reaction.
Mucosal reactivity to cow's milk protein in coeliac disease.
PMID: 17302893 March 2007

Review article: chronic constipation and food hypersensitivity - an intriguing relationship.
PMID: 17059511 Nov 2006

Changes in humoral responses to beta-lactoglobulin in tolerant patients suggest a particular role for IgG4 in delayed, non-IgE-mediated cow's milk allergy.
PMID: 16925689 Sept 2006

The mechanism by which food activates mucosal immune system is uncertain, but food specific IgE and IgG4 appeared to mediate the hypersensitivity reaction in a subgroup of IBS patients. Exclusion diets based on skin prick test, RAST for IgE or IgG4, hypoallergic diet and clinical trials with oral disodium cromoglycate have been conducted, and some success has been reported in a subset of IBS patients.
Is there a role of food allergy in irritable bowel syndrome and functional dyspepsia? A systematic review.

PMID: 16918724 Aug 2006

In some cases, nausea and vomiting are directly triggered by food, e.g. in patients suffering from food allergy or food intolerances. In other cases, food is not the primary cause but dietetic manipulations may still contribute to the management of the nausea and vomiting. Therefore, food plays an important pathophysiological and therapeutic role in nausea and vomiting. In the present article, we describe the most relevant nutrient triggers for nausea and vomiting, discuss food allergy and intolerance as cause of nausea and vomiting, propose a clinical classification of nausea and vomiting, and present in detail dietetic and other therapeutic strategies of relevance for the management of nausea and vomiting.
Nausea and nutrition.  
PMID: 16935033 Aug 2006

 RESULTS: Significant improvement has been noted in infants receiving Lactobacillus GG in their extensively hydrolyzed formula. CONCLUSIONS: It is likely more studies will be forthcoming with different probiotic organisms in the prevention and treatment of allergic disorders in children and adults.
Role of probiotics in the management of patients with food allergy.

PMID: 12839122 June 2003

Probiotics may be unsafe in infants allergic to cow's milk.
PMID: 16512815  April 2006 

 These results indicate that food avoidance may help in asthma control in children.
Avoidance of food allergens in childhood asthma.
PMID: 15876598 April 2005

Food allergies are increasing in incidence, and the variety of triggering antigens is widening. There is also an increased recognition of the breadth of immunologically mediated responses to dietary antigens; the area of non-IgE-mediated food allergy is belatedly acquiring scientific respectability, aided by improved clinical recognition and basic scientific studies.
Clinical manifestations of food allergy: the old and the new.
PMID: 16292079 Dec 2005

It seems that the physician's opinion is influenced by "general knowledge" more than by his own experience. We suggest emphasizing through education that there are two distinct entities of cow's milk intolerance: IgE-mediated allergy and non-IgE-mediated.
[Food allergy--effect of physician attitude on the diagnosis and reported prevalence]
PMID: 16281757 Oct 2005


Non-IgE-mediated or T-cell-mediated allergic GI disorders include dietary protein enteropathy, protein-induced enterocolitis, and proctitis. All these conditions share a common denominator: the response of the immune system to a specific protein leading to pathologic inflammatory changes in the GI tract. This immunological response can elicit symptoms such as diarrhea, vomiting, dysphagia, constipation, or GI blood loss, symptoms consistent with a GI disorder.
Gastrointestinal manifestations of food allergies in pediatric patients.
PMID: 16207693  Oct 2005

Gut mucosal granulocyte activation precedes nitric oxide production: studies in coeliac patients challenged with gluten and corn.
Kristjánsson G, Högman M, Venge P, Hällgren R.
Gut. 2005 Jun;54(6):769-74.
P
MID: 15888782

Food elimination based on IgG antibodies in irritable bowel syndrome: a randomised controlled trial.
PMID: 15361495   Oct 2004

The overall results demonstrated a 71% success rate for all symptoms achieving at least a 75% improvement level. Of particular interest was the group of patients with chronic, disabling symptoms, unresponsive to other intensive treatments. Whereas 70% obtained 75% or more improvement, 20% of these patients obtained 100% relief.
Treatment of delayed food allergy based on specific immunoglobulin G RAST testing.
PMID: 10889481  July 2000

Gastrointestinal immunopathology and food allergy.
PMID: 15562871


Although immunoglobulin (Ig)E-mediated allergies are readily identifiable, non-IgE-mediated allergies present more diagnostic difficulty. Gastroesophageal reflux, esophagitis, subtle enteropathy, and constipation were frequent in both groups.
A consistent pattern of minor immunodeficiency and subtle enteropathy in children with multiple food allergy.
PMID: 12915822


Abnormalities of Th1 function in non-IgE food allergy, celiac disease, and ileal lymphonodular hyperplasia: a new relationship?
PMID: 12839120

Although previously thought to be triggered primarily by an IgE-mediated mechanism of injury, considerable evidence now suggests that non-IgE mechanisms may also be involved in the pathogenesis of FA.
IgE and non-IgE food allergy.
PMID: 12839117

Clinical aspects of gastrointestinal food allergy in childhood.
PMID: 12777600

Gastrointestinal food allergies: do they exist?
PMID: 11470005


Clinical symptoms are unspecific and include nausea, vomiting, abdominal pain, cramping and diarrhea. Intestinal mast cells, as well as intestinal eosinophils, have been shown to be involved in the pathogenesis of food-allergy-related enteropathy. Elimination diet still presents the main basis of therapy.
Allergy and the gut.
PMID: 10828717

 Labs for Food Allergy Testing

  
ALCAT Worldwide

Enterolab

Genova Diagnostics (GSDL)

The Great Plains Laboratory

Immuno Laboratories

Meridian Valley Laboratory

Metametrix  

Optimum Health Resource
Laboratories


Sage Medical Laboratory

US BioTek
 

More on Food Allergy:

Dr. Scot Lewey

Dr. Braly Allergy Relief

Food Allergy Solutions articles 
 

Oxidative Stress 

"Oxidative stress plays an important role in inflammatory process of celiac disease.....

Lycopene, quercetin and tyrosol inhibited all these effects. The results here reported suggest that these compounds may represent non toxic agents for the control of pro-inflammatory genes involved in celiac disease."
Lycopene, quercetin and tyrosol prevent macrophage activation induced by gliadin and IFN-gamma.
PMID: 17477920  April 2006

  

"Autoimmune states can be induced by food sensitivities that cause intestinal gut permeability and complicate leaky gut syndrome (Kitts et al. 1997)." Oxidative stress and autoimmune problems by LEF  LEF 

 

"We've had many patients who were extremely sensitive to dairy and wheat.... and did marvelously after the CF/GF diet. Many of these same patients completely lost their sensitivity to casein and gluten after the antioxidant supplementation..... and now can eat a normal diet without a problem. (Aug 21, 2003) "  [NOT Celiac Disease...jcc.. please read in entirety.]

Oxidative Stress by William Walsh