Glutens and Lectins Alive Alive Oh!!

img_1347Wheat does have healthful properties, but the engineered gluten and lectin “anti-nutrients” are likely overriding these healthful properties. Modified wheat is affecting all of us to varying degrees. In the article “The Dietary Intake of Wheat and other Cereal Grains and Their Role in Inflammation by Karin de Punder and Leo Pruimboom in Nutrients 2013, the researchers discuss the harmful gluten and lectin “anti-nutrients” in wheat.  Wheat gluten now has increased plasticity, likely to enhance bread shelf-life. Car parts and credit cards are made from the same wheat gluten.  Gluten crosslinks collagen fibers found in our joints, tissues and organs causing disease.   Additionally, two harmful wheat lectins exist.  These lectins are super defense genes designed to help the wheat plant resist bacteria and viruses.  Humans consume anti-nutrient glutens and lectins resulting in a plethora of disease including: asthma, GERD, GI disorders, rhinitis, urticaria, ankylosing spondylitis, schizophrenia, dermatitis, arthritis, IBD, PCOS, primary biliary cirrhosis, hemochromatosis, diabetes, ataxia, MS, Alzheimers and celiac disease(CD).

Gluten proteins are called gliadins.  The tissue transglutaminases in the gut carry consumed wheat gliadins across the intestinal wall.  The body makes antibodies to the gliadins and the attached transglutaminases.  This results in cytokine and immune chemical release.  Antibodies attack the gluten and the attached “self” transaminase.  Thus, the term autoimmune disease, because it appears that the body is attacking “self”.  Zonulin, the regulator of gut permeability, is released.  Junctional complexes and actin filaments are reorganized in the gut wall.  Leaky gut results.  Per de Punder, “zonulin was activated by gliadin in intestinal biopsies from both CD and non-CD patients (Drago S et al., 2006)(Lammers KM et al, 2008).”  “Serum antibodies…. against tissue transglutaminases, are … found in CD.  The HLA-DQ2 of HLA-DQ8 is expressed in 99.4% of the patients suffering from CD, (Troncone and Jabari, 2011), however, … there is a group of HLA-DQ2/DQ8-negative patients suffering from gastrointestinal symptoms that respond well to a gluten-free diet.  This group of “gluten-sensitive” patients does not have the CD serology and histopathology, but does present the same symptoms and shows improvements when following a gluten-free diet (Biesiekierski, et al.,2011) (Sapone et al., 2011).”

“There are at least 50 gliadin epitopes that exert immunomodulatory, cytotoxic and gut-permeating activities that can be partially traced back to different domains of alpha-gliadin.  Where some immunomodulatory gliadin peptides activate specific T-cells, others are able to include a pro-inflammatory innate immune response (Troncone and Jabari, 2011).  Stimulation of immune cells by gliadin is not only restricted to CD patient; the incubation of peripheral blood mononuclear cells (PBMC) from healthy HLA-DQ2 positive controls and CD patients with gliadin peptides stimulated the production of IL-23, IL-1B and TNF-alpha in all donors tested.  Nevertheless, the production of cytokines was significantly higher in PBMC derived from CD patients (Harris KM et al, 2008).  Similar results were obtained by Lammers et al., who demonstrated that gliadin induced an inflammatory immune response in both CD patients and healthy controls, through IL-6, IL-13, and IFN-gamma were expressed at significantly higher levels in CD patients.”

 

“Besides gliadin from wheat gluten, the wheat plant’s defense lectin wheat germ agglutinin (WGA) has also been shown to stimulate cells of the immune system and increase intestinal permeability.”  “Lectin activity has been demonstrated in wheat, rye, barley, oats, corn and rice.”  Wheat, rye, and corn each have two lectins.  The more immune friendly rice and sweet potatoes have only one lectin.  These lectins hemagglutinate and clot the blood, much like mixing the wrong blood types in patients will hemagglutinate the blood.  “WGA induces inflammatory responses by immune cells.  For example, WGA has been shown to trigger histamine secretion and granule extrusion from non-stimulated rat peritoneal mast cells (Lansman and Cochrane, 2008), induce NADP-oxidase activity in human neutrophils (Karlsson A, 1999) and stimulate the release of the cytokines IL-4 and IL-13 from human basophils (Haas H, et al., 1999).  In human PBMC, WGA induced the production of IL-2, while simultaneously inhibiting the proliferation of activated lymphocytes (Reed JC et al, 1985).  WGA stimulated the secretion of IL-12, in a T and B cell independent manner in murine spleen cells.  IL-12, in turn activated the secretion of IFN-gamma by T or natural killer cells (Muraille E, et al.,1999).  In murine peritoneal macrophages WGA induced the production of the pro-inflammatory cytokines TNF-alpha, IL-1B, IL-12 and IFN-gamma (Sodhi and Kesherwani, 2007).  Similar results have been observed in isolated human PBMC, given that nanomolar concentrations of WGA stimulated the release of several pro-inflammatory cytokines… including IL-1B.”  “WGA is capable of directly stimulating monocytes and macrophages, cells that have the ability to initiate and maintain inflammatory responses.”  “Human data showing the influence of WGA intake on inflammatory markers are lacking, however antibodies to WGA have been detected in the serum of healthy individuals (Tchnernychev & Wilcheck, 1996). Significantly higher antibody levels to WGA were measured in patients with CD compared to patients with other intestinal disorders.”  Laboratory researchers use WGA to mark human tissue given its strong adherence to cells.  Human studies may be lacking with WGA, given it’s potentially lethal hemagluttination properties.

Rodents fed a wheat cereal diet showed a higher incidence of diabetes, whereas gluten free animals “showed a decrease incidence and delayed onset of this disease.”  “Rats fed a cereal [wheat] based diet showed increased intestinal permeability and a significant increase in the percentage of IFN-gamma-producing TH1 lymphocytes… and higher mRNA levels of the pro-inflammatory cytokines IFN-gamma and TNF-alpha and inflammatory marker inducible NO synthase in the small intestine.”  A “WGA depleted diet was associated with reduced responsiveness of lymphocytes.”  In humans, “intake of whole grain products is associated with reduced risks for developing type 2 diabetes, cardiovascular diseases, obesity and some types of cancer (Jonnalagadda SS et al., 2011).”  “Some studies have shown that associations between the intake of whole grain and decreased inflammatory markers (CRP, IL6) are found (Lefevre and Jonnalagadda, 2012).”  Other studies have not shown a clear affect on inflammatory, it could be that the phytochemicals in wheat, exert anti-inflammatory effects against the pro-inflammatory glutens and lectins (Fardet A,  2010).  Diabetic patients on a paleolithic diet for three months “resulted in a lower BMI, weight and waist circumference, higher mean HDL, lower mean levels of hemoglobin A1c, triacylglycerol and diastolic blood pressure, though levels of CRP were not significantly different (Jonsson et al, 2009).”

One research family are 18 year veterans of a wheat free diet eliminating asthma, sinusitis, GERD, GI disorders, tonsillitis, viruses and 75% of our physician visits.  We met a patient last week who stopped eating wheat six years ago and stopped the multiple sclerosis  in her brain. We expect that wheat glutens and lectins will be implicated in Alzheimers “disease”. Once attached inside the cranium there are few ways out.  What else besides a lectin could be powerful enough to devour the brain?  The brain does not shrink by itself.  Do your own experiment.  Your nostrils and ears have a direct connection to the brain.  How much material collects in your nostrils and ears hours after a wheat gluten meal versus a salad?  The brain is looking for a way to push out these harmful anti-nutrients. They cause harm.  No one wants you to know.  Once fully recognized, the extent of wheat disease inflicted upon all of us, will be astounding.

References:

Biesiekierski, J.R.; Newnham, E.D.; Irving, P.M.; Barrett, J.S.; Haines, M.; Doecke, J.D.;

Shepherd, S.J.; Muir, J.G.; Gibson, P.R. Gluten causes gastrointestinal symptoms in subjects without celiac disease: A double-blind randomized placebo-controlled trial. Am. J. Gastroenterol. 2011, 106, 508–514.

Drago, S.; El Asmar, R.; Di Pierro, M.; Grazia Clemente, M.; Tripathi, A.; Sapone, A.; Thakar, M.; Iacono, G.; Carroccio, A.; D’Agate, C.; et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand. J. Gastroenterol. 2006, 41, 408–419.

Fardet, A. New hypotheses for the health-protective mechanisms of whole-grain cereals: What is beyond fibre? Nutr. Res. Rev. 2010, 23, 65–134.

Farmer, A.  New hypotheses for the health-protective mechanisms of whole-grain cereals: What is beyond fiber? Nutr. Res. Rev. 2010, 23, 65-134.

Haas, H.; Falcone, F.H.; Schramm, G.; Haisch, K.; Gibbs, B.F.; Klaucke, J.; Poppelmann, M.; Becker, W.M.; Gabius, H.J.; Schlaak, M. Dietary lectins can induce in vitro release of IL-4 and IL-13 from human basophils. Eur. J. Immunol. 1999, 29, 918–927.

Harris,K.M.;Fasano,A.;Mann,D.L.Cuttingedge:IL-1controlstheIL-23responseinducedby gliadin, the etiologic agent in celiac disease. J. Immunol. 2008, 181, 4457–4460.

Jonsson, T.; Granfeldt, Y.; Ahren, B.; Branell, U.C.; Palsson, G.; Hansson, A.; Soderstrom, M.; Lindeberg, S. Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: A randomized cross-over pilot study. Cardiovasc. Diabetol. 2009, 8, doi: 10.1186/ 1475-2840-8-35.

Jonnalagadda S.S., Harnack L, Li RH, McKeown N, Seal C, Liu S, Fahey GC. Putting the whole grain puzzle together:  Health benefits associated with whole grains-summary of American Society for Nutrition 2010 Satellite Symposium.  J. Nutr. 2011, 141, 1011S-1022S

Karlsson, A. Wheat germ agglutinin induces NADPH-oxidase activity in human neutrophils by interaction with mobilizable receptors. Infect. Immun. 1999, 67, 3461–3468.

Lammers, K.M.; Lu, R.; Brownley, J.; Lu, B.; Gerard, C.; Thomas, K.; Rallabhandi, P.; Shea-Donohue, T.; Tamiz, A.; Alkan, S.; et al. Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3. Gastroenterology 2008, 135, 194–204.

Lammers, K.M.; Khandelwal, S.; Chaudhry, F.; Kryszak, D.; Puppa, E.L.; Casolaro, V.; Fasano, A. Identification of a novel immunomodulatory gliadin peptide that causes interleukin-8 release in a chemokine receptor CXCR3-dependent manner only in patients with coeliac disease. Immunology 2011, 132, 432–440.

Lansman, J.B.; Cochrane, D.E. Wheat germ agglutinin stimulates exocytotic histamine secretion from rat mast cells in the absence of extracellular calcium. Biochem. Pharmacol. 1980, 29, 455–458.

Lefevre M.  Jonnalagadda S.  Effect of whole grains on markers of subclinical inflammation.  Nutr. Rev. 2012, 70, 387-396.

Muraille, E.; Pajak, B.; Urbain, J.; Leo, O. Carbohydrate-bearing cell surface receptors involved in innate immunity: interleukin-12 induction by mitogenic and nonmitogenic lectins. Cell Immunol. 1999, 191, 1–9.

Reed, J.C.; Robb, R.J.; Greene, W.C.; Nowell, P.C. Effect of wheat germ agglutinin on the interleukin pathway of human T lymphocyte activation. J. Immunol. 1985, 134, 314–323.

Sapone, A.; Lammers, K.M.; Casolaro, V.; Cammarota, M.; Giuliano, M.T.; de Rosa, M.; Stefanile, R.; Mazzarella, G.; Tolone, C.; Russo, M.I.; et al. Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: Celiac disease and gluten sensitivity. BMC Med. 2011, 9, doi:10.1186/1741-7015-9-23.

Sodhi, A.; Kesherwani, V. Production of TNF-alpha, IL-1beta, IL-12 and IFN-gamma in murine peritoneal macrophages on treatment with wheat germ agglutinin in vitro: involvement of tyrosine kinase pathways. Glycoconj. J. 2007, 24, 573–582.

Tchernychev,B.;Wilchek,M. Natural human antibodies to dietary lectins.FEBSLett.1996,397, 139–142.

Troncone, R.; Jabri, B. Coeliac disease and gluten sensitivity. J. Intern. Med. 2011, 269, 582–590.

 

 

 

 

Advertisements