Glutens and Lectins Alive Alive Oh!!

img_1347Wheat does have healthful properties, but the engineered gluten and lectin “anti-nutrients” likely override 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 physician visits.  One patient who stopped eating wheat six years ago, stopped multiple sclerosis progression in her brain. We expect that wheat glutens and lectins will be implicated in Alzheimers “disease”. Powerful lectins could definitely contribute to the destruction of brain tissue.   Do your own experiment.  Your nostrils and ears have a direct connection to the brain.  Compare the amount of material that collects in your nostrils and ears hours after a wheat gluten meal versus a salad?  Does brain push harmful anti-nutrients into the nose and ears?  The extent of wheat disease inflicted upon us, may be astounding.


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.





Isn’t It Time to Cure Parkinson’s Tremor and the Underlying Adrenal Insufficiency?


This is a Case Study of a 13 y/o boy who was raised on a wheat free diet (WFD) since age 4.  As an infant,  he  experienced monthly ear infections and was placed on prophylactic antibiotic therapy.  His pre-school years were mired with monthly strep throat infections. Occasionally, he had concurrent small red blotches, indicative of rheumatic fever, on his  torso.  A tonsillectomy was recommended by his pediatrician.

He began a WFD at age 4, the strep throat infections ceased …. unless he ingested wheat without antihistamine prophylaxis. Occasionally, he ate a piece of wheat pizza at school without a immediate anti-histamine.  Subsequent strep throat infections would ensue resulting in swollen cervical lymph nodes, a flushed face, swollen, red and pussy tonsils, but no fever.  All infections presented similarly, however not all tested positive for strep.   This strep-like condition was typically treated with antibiotics and resolved in a few days.  (Please see the post on “Keep the Tonsils, Pull the Strep Throat”).

As a pre-schooler,  the boy had wound healing difficulties.  During his middle school years, he experienced anxiety, fatigue, a lack of physical maturation, restless legs, painful joints, middle belly weight, athlete’s foot, and a slightly curved back.

At age 13, he ate two pieces of wheat pizza without antihistamine prophylaxis.  In the days following, his face flushed intensely, cervical lymph nodes swelled, but no fever was present.  His back was painful at the level of his adrenals. He experienced extreme fatigue, his eyes were sensitive to light, and he had a tremor.  The tremor traveled down his spine into his fingers.  He began his standard Azithromycin antibiotic therapy. However, this time, the condition did not resolve.

Within a couple days he “crashed“.  He had sufficient energy to be active for a couple of hours in the morning and then he lived on the couch for the remainder of the day.  He headed for bed shortly after dinner. Any form of stress intensified the tremor including homework or attending school.  He was started on a second antibiotic.

Differentials for these signs/symptoms included infection, PANDAS, serotonin syndrome, and depression.  Medical personnel questioned whether he was avoiding school.  Blood panels were negative.  EEG was negative.  He was prescribed Zoloft to control the tremor.  This drug made him sick and was discontinued.

One month later, a naturopathic physician identified the boy’s flushed face as being caused by adrenal problems.  Through intracellular saliva testing, he was found to be adrenal insufficient.  The flashlight adrenal insufficiency test was positive.  To support his adrenals he began began a supplemental therapy of vitamin C (1000mg/day), B complex (200mg/day), adrenal cortical extract, minerals, vitamin A, CoQ10, vitamin E, spirulina, quercetin, a probiotic, 1g/day of omega-3 fish oil (DHA+EPA) and 1000mg/day of calcium citrate.  His energy levels gradually improved but the tremor continued.

Sugar, high fructose corn syrup, caffeinated drinks, and deep fried, greasy foods harmful to his adrenals were removed from his diet.  The high levels of fruit juice previously consumed were replaced with low, no sugar, or sugar substitute juices.

It was determined that wheat contains methionine, lysine and threonine.  Methionine controls the hypophyseal-pituitary-adrenal (HPA) axis and is involved with cardiac rhythm.   Lysine is found in collagen thus supports wound heading and dental pulp formation. Threonine supports tooth enamel formation. Hypothesizing that the patient was deficient in these amino acids due to his WFD,  he was started on 1500mg/day of methionine and 1000mg/day of lysine. The boy craved red meat and eggs.  His diet was modified to include methionine containing foods such as brown rice, oranges, additional red meat, eggs, nuts, spinach, onions, peas, yogurt, and popcorn.  Within a week, the boy had regained sufficient energy to work on small hobbies.

Within a month, he began to experience some quick, sharp chest pain.  Methionine is stored in the heart.  The methionine dosage was reduced to 1,000mg/day.  Although he had more energy and felt better, the facial flushing, swollen lymph glands, fatigue, back adrenal pain, and tremor continued.

A urine amino acid profile showed the boy’s methionine level (with supplementation) in low normal range.  Also in low normal range were phosphoserine, taurine, phosphoethanolamine, aspartic acid, hydroxyproline, serine, asparagine, alanine, tryptophan, carnosine, and anserine.   Some success has been found with taurine in relieving tremor.  He was given a trial of 1000mg/day of taurine.  His energy levels increased, however evening doses made it difficult to sleep and there was no improvement in the tremor.

Repeat urine and blood amino acid profiles showed phosphoserine as the only amino acid below normal range.  The patient was supplemented with 1,000mg/day of serine.  One week post therapy, he developed a skin rash on his arms and legs.  Serine therapy was discontinued then reduced to 500mg/twice each week.  The tremor persisted.

Next, the physiological function of each of these amino acids was addressed in relation to the patient’s signs/symptoms.  Proline was found to be a critical component of cartilage and important to joint structure.  Proline works with vitamin C in this capacity and can be synthesized by glutamic acid.  Arginine was important in wound healing, the production and release of growth hormone, insulin, and glucagon release, collagen synthesis, and GABA production. Arginine can be produced from glutamic acid or proline.  Glycine is critical to GABA neurotransmitter and energy production. GABA was important to inhibitory nerve function. Tyrosine is important to the production of neurotransmitters dopamine, norepinephrine, epinephrine, and melanin.  This patient’s grandfather had Parkinson’s Disease which involves low neurotransmitter levels in the Tyrosine – Dopamine Pathway.

Hypothesizing that the boy’s current amino acid levels may not be sufficient for the age dependent physical growth, adrenal stress due to methionine deficiency, and adrenal stress due to the wheat hypersensitivity reaction, this patient was additionally supplemented with 1500mg/day glutamine,  1500mg/day glycine, and 1000 mg/day tyrosine.  After one week of therapy,  the tremor was alleviated and would resume only  under stressful conditions.

After several months, the individual dosages of amino acids were replaced with a 750mg amino acid complex capsule, three times each day. The patient continued to improve.  This complex differed from ingesting protein rich foods in that all 20 amino acids were given concurrently through the complex.  All 20 amino acids must be present concurrently for  protein synthesis to occur.  Supplementation of the 20 amino acid complex relieved the tremor whereas his protein rich diet did not.

The patient returned to school six months post amino acid therapy initiation with improved physical activity levels, reduced anxiety, and alleviation of restless legs.  The daily tremor was absent except under stressful conditions.  His night time activities were kept to a minimum to ensure sufficient rest.

In subsequent years, he remained on 1500 mg/day amino acid complex, 1 gram of DHA+EPA omega-3 fish oil, B complex 100mg/day, vitamin C 1000mg/day, bovine adrenal cortex 340 mg/day, calcium 1000mg/day,  lysine 500mg/day, choline 500mg/day, 5-HTP 100mg/day, probiotic, and minerals. He feels choline ingestion is most important to control tremor.  It appeared that minimal amounts of these supplements are required to maintain good health.

Six years post presentation, this patient continues with occasional stress and fatigue. This is typically visible as facial flushing on the outer periphery of his cheeks.  The tremor has been alleviated under normal and stress conditions.  This patient continues on a WFD and ingests no wheat.  He ingests minimal sugar and deep fried foods, and no caffeine.  Accidental wheat ingestion receives immediate antihistamine and aspirin prophylaxis. The patient is careful to obtain sufficient rest, take supplements, and eat healthy food.  His back continues to be hunched causing him back, neck, and knee pain, but is otherwise he is healthy.

Copyright © 2013.  All rights reserved.

Photograph: 8 week old dobie pup

Disclaimer:  The ERB is a literature research team presenting the findings of other researchers. The ERB is not licensed medical nor dietary clinicians and will not give medical nor dietary advice.   Any information presented on this website should not be substituted for the advice of a licensed physician or nutritionist.  Users of this website accept the sole responsibility to conduct their own due diligence on topics presented and to consult licensed medical professionals to review their material.  We make no warranties or representations on the information presented and should users utilize this research without consulting a professional, they assume all responsibility for their actions and the consequences.

An Autism Hypothesis: Vaccine + Egg + B-blood type Antigen ??


We have several case studies and informational sources that have lead us to ask the question: Is there link between the egg proteins in vaccines and an antigenic response specifically in B or AB blood types which may cause Autism?

Case Study: A 40 y/o female B-blood type has severe acne problems. When other B-blood type family members ingest chicken they have gastrointestinal problems. This female discontinues consumption of chicken and her acne resolves.

Case Study: A 45 y/o female B-blood type has severe acne problems. She finds that egg triggers the outbreaks. She avoids eggs and her acne resolves.

Case Study: An Autism support group recommends that their members place their children on a wheat gluten free diet. The children are noticeably healthier when avoiding the wheat gluten lectin. Further, their problems worsen with minimal wheat ingestion.

Case Study: A 10 y/o female has autism. Her parents first notice problems following her set of childhood vaccines. The problems became more pronounced as she aged. Extensive biochemical analysis determined that she has a biotin deficiency. Her parents, who are microbiologists, question whether the egg proteins in the vaccine have triggered the autism. She is a B-Blood type.

Contemporary Nutrition, 9th Edition ( McGraw Hill, 2013) by Gordon M. Wardlaw PhD and Anne M. Smith PhD state that the avidin protein in raw egg whites has been known to contribute to biotin deficiencies.


The E.R.B. makes this scientific hypothesis:

“Is their a Protein Component of Eggs that could be found in Vaccines that could Generate a Sufficient Immune Response with B-blood type Antigens found in either AB or B Blood Type Individuals to Trigger Autism?”

To explore this hypothesis we will review Dr. Adamo’s findings, query the public on blood type, and start the literature review process. Perhaps there are other researchers asking this same question.

This hypothesis will significantly benefit from reader input.

Autistic Child Poll:

Dr. Peter D-Adamo in his book “Eat Right 4 Your Type” (J.P. Putnam & Sons, 1996) discusses Dr. Karl Landsteiner’s discovery that the different blood types carry antibodies.  For example, A type blood carries antibodies against the B blood type antigen.  Until Dr. Landsteiner’s work, “blood transfusions were hit or miss” Dr. D’Adamo says. “Hit” meaning they were successful, “miss” meaning the patient died.

There are two important points in Dr. D’Adamo’s writing, first that the blood type agglutination reaction is so powerful that death results, and second, that every health care provider on the planet is aware of these deadly agglutination reactions of the blood types.  The patient can die if the wrong blood type is used because of the powerful agglutination reaction between donor blood carrying antigens (markers on the exterior of blood cells) and the recipient’s antibodies that recognized these markers and attack the foreign blood as they would an intruder, agglutinating the cells and clotting the blood.

Dr. D’Adamo continues discussing lectins. Health care providers are not as aware of lectins and their powerful agglutination reactions. Lectins are proteins found in plants and animals. Most lectins pass through our bodies unnoticed, he says. In the case of the B Blood type, dangerous lectins found in the muscle of chicken can agglutinate the B blood possibly causing strokes and immune disorders. How does he know this agglutination occurs? Dr. D’Adamo has purchased pure lectins from laboratories and watched them agglutinate specifically typed blood on a glass slide under his microscope. At the writing of his book in 1996, Dr. D’Adamo had recognized the agglutination of chicken with B type blood, but had not recognized agglutination of egg lectins with B type blood. We need to review his later books and website.

Medical Researchers are aware of lectins and their powerful agglutination roles, as they use lectins as tissue markers in the laboratory. Lectins are the defense genes found in plants. They have been designed by God to defend the plant and keep the plant healthy by attacking viruses and bacteria that might cause harm. Some examples are the wheat plant’s lectin,  wheat germ agglutinin, a lectin widely used in laboratories as a tissue marker. Ricin is a deadly lectin found in castor bean oil. Corn, and presumably high fructose corn syrup, contains a lectin. These lectins are not easily digestible. When consumed by humans, hey tend to remain intact in the human body through the digestion process.

When human consume these plant lectins, the lectins pass by our tonsils, enter our GI tracts and blood streams, and carry out their defense role inside the body, attacking human tissue.  As they would agglutinate plant bacteria and viruses, inside humans they agglutinate human tissues and organs.  These agglutinants bind like super glue, Dr. D’Adamo says and cause disease.

Industry in their attempt to feed the world and make plants more disease resistant, in an effort to reduce pesticide use, have created super attack lectins.  Perhaps, God made lectins strong enough to defend plants, but weak enough for man to consume.  With man’s intervention, lectins may not longer be weak enough to consume.

Copyright © 2013.  All rights reserved.

Photograph: Painted cement action balls at the sports park in Canyon Hills, California.

Dr. Malinda Schaefer, an HIV Researcher at Emory University, said that “Experiments don’t usually fail; they may not give the desired or expected results, but that’s not considered failure.  Even if you decide to end the experiment early, that’s still a result – you are learning something about yourself in the process”.  Source is “More or Less, Choosing a Lifestyle of Excessive Generosity” by Jeff Shinabarger, 2013.

Disclaimer:  The ERB is a literature research team presenting the findings of other researchers. The ERB is not licensed medical nor dietary clinicians and will not give medical nor dietary advice.   Any information presented on this website should not be substituted for the advice of a licensed physician or nutritionist.  Users of this website accept the sole responsibility to conduct their own due diligence on topics presented and to consult licensed medical professionals to review their material.  We make no warranties or representations on the information presented and should users utilize this research without consulting a professional, they assume all responsibility for their actions and the consequences.


Celiac? Irritable Bowel? Esophagitis? GERD? No Matter, Probiotics, Gluten Free Diet and Enzymes Solve This Caper.

Irritable Bowel Disease or Celiac Disease with a Gluten Free Diet Resolution Case Study:  A female college athlete had a history of loose bowels and intense stomach aches immediately following food ingestion and prior to athletic events.  She discontinued use of dairy products without resolution.  She was diagnosed by a physician with irritable bowel syndrome (IBS) and prescribed hyoscamine and ranitidine to calm her stomach and reduce inflammation.  A three month trial of these prescriptions appeared to help.

After one year, more severe stomach aches returned. She was sick after each meal on a regular basis.  She visited a gastroenterologist who ordered stool and blood samples, and an ultrasound.  She was found to be gluten intolerant.   The physician prescribed ranitidine and hysocamine and referred the athlete to another gastroenterologist for a endoscopy and colonoscopy to rule out celiac disease or a more serious condition.  The results were negative with the exception of a developing stomach ulcer.  The physician explained that the athlete’s stomach experienced difficulties digesting food, particularly gluten.  A gluten free diet was prescribed to reduce stomach irritation and unexpected bowel movements. Enzymes and probiotics were prescribed to aid with digestion.  In two weeks, her condition was much improved.

Five months post wheat gluten free diet initiation, she had few stomach aches and her condition was much improved.  Upon ingestion of gluten or excessive quantities of heavy foods, the stomach aches return and immediate bowel movements result.  She continues on a wheat gluten free diet.


Wheat Gluten and the Wheat Germ Agglutinun Lectin

An eloquent analysis written by nutritionist Sayer Ji on the website helps to clarify that  wheat has two harmful elements: the gluten protein and the wheat germ agglutinun lectin. The  gluten protein provides fuel for grass family plants and when used in baking, makes bread chewy, elastic-like, and gives it a longer shelf life.  In manufacturing, wheat gluten is used to make plastics (Cho, 2011). The process of wheat gluten plastic manufacturing can be seen at  When consumed by humans, gluten binds collagen fibers in the body forming strong gliadin-antigen-collagen complexes in joints, tissues and organs. Collagen is a basic type of tissue that is found in blood, bone, tendons, cartilage, lung and organs.   Under a microscope, collagen looks much like a cotton ball that has been pulled apart with the fibers stretched like clouds in the sky.  This meshwork is designed to move fluidly.  Clumping the collagen fibers with gliadin-antibody complexes causes functional impairment.  

These plastic like collagen complexes contribute to the long list of gluten related disease: celiac disease, dermatitis, autoimmune disease, diabetes type 1, thyroid problems, biliary cirrhosis, colitis, cerebellar ataxia, autism, peripheral neuropathy, and schizophrenia. Scientists and clinicians have identified individuals who carry the HLA-DQ2 and HLA-DQ8 alleles on the short arm of chromosome 6 as most susceptible. Curiously, it is estimated that in terms of genetics less than 1% of the population should be affected by gluten.  Why do so many individuals report benefits from wheat avoidance?

This returns us to The E.R.B’s original source for wheat avoidance, “Eat Right 4 Your Type”, written by Dr. Peter J. D’Adamo (Putnams & Sons, 1996).  In his book, Dr. D’Adamo speaks of wheat plant lectins as being the primary agent causing harm to humans.  Lectins are the plant’s defense proteins that protect grass plants against insects, fungus and bacteria.  Upon human ingestion of wheat plant material, these defense genes bind human red blood cells, tissues and immune cells by recognizing carbohydrate signaling structures on human cell surfaces (Sharon N et al, 2004).  D’Adamo and Sharon discuss the toxic lectin, ricin which is a powerful agglutinator of red blood cells and a lethal weapon.   Wheat germ has a lectin called wheat germ agglutinin (WGA) which is an insecticidal that inhibits the sporulation and growth of fungi in plants (Sharon N et al, 2004).  Consumers introduce WGA to tissues when they ingest wheat.

Consumers hear conflicting statements about wheat and wheat germ. Whole grains are thought to be healthy.  They are known for their antioxidant and anti-carcinogenic properties (Fardet A, 2010).  These beneficial properties may be due to the ability of WGA lectins to bind harmful pathogens, thereby “protecting” the human body.  Perhaps,  the WGA lectin was originally created to function in a delicate balance with nature,  lethal enough to fend off harmful plant insects and pathogens but immune compatible enough to be digested by humans and provide disease protection qualities.

Man has become involved with crop genetics.  Today’s wheat looks nothing like the ancient wheat grain. In our quest to grow high yield crops and provide food for the world, plant defense lectins have been strengthened making plants more disease resistant (Wheat Belly, Davis). When these plant lectins enter the human body they perform their defensive role by gluing themselves to human cells and tissues.  Research scientists know of the strong binding abilities of WGA because the antigen is utilized in laboratories as a tissue identifying marker (Sharon N et al 2004).

Dr. Karl Landsteiner of the University of Vienna first described agglutination complexes in 1900 when he brilliantly identified the ABO blood types.  All health care providers and scientists now recognize that blood types must be carefully matched before transfusion to avoid lethal red blood cell agglutination reactionsUnfortunately, food lectin agglutination reactions are generally unknown.  This may be because in Immunology food is generally not recognized as an antigen, even though most emergency room anaphylactic attack presentations are food related.

In his book, Dr. Peter J. D’Adamo gave detailed guidance as to which foods are beneficial, neutral or avoids for each blood type based upon these harmful plant lectins.  In 2012, almost 20 years later, his book remains a best seller at health food stores. Consumers and clinicians are only now becoming familiar with the inflammatory health conditions caused by gluten and wheat germ agglutinun.  However, in placing all of the blame on gluten, they have identified only one culprit.  Per Dr. Adamo, the WGA lectin is a second and more problematic culprit, particularly for O blood types which represent 40-45% of the population.  This level of affliction better reflects the widespread benefits that consumers are recognizing from a wheat free diet.

Tissue Damage

Much work has been done to understand the effect of wheat as it passes the tonsils and descends the esophagus, stomach and intestines.  Many celiac patients present with esophageal motility problems including gastroesophageal reflux disease, stomach and small bowel, regurgitation and  heartburn, chest or epigastric pain delayed gastric emptying time, and abnormally long colonic transit time (cite). Gluten is not digested well and the stomach may be producing additional acid in an attempt to digest gluten.  This causes the erosive damage to the stomach and esophagus.

Gluten causes inflammation by immune system antigen presenting cells offering the digested gliadin peptide to T helper immune cells.  This leads to inflammatory cytokines and harmful immune chemicals being produced in an effort to rid the body of gluten and the wheat germ agglutinun lectin.  The chemicals produced increase the permeability of the intestinal epithelium (Festen EA, 2009) at the tight junctions.  Helping to move food along and aid in digestion are finger-like projections called villi. These villi resemble the finger-like rock projections in the Sedona picture above.  The additional acid production and inflammation generated by wheat presumably causes intestinal villi atrophy (death). Damaged villi causes malabsorption of nutrients (Nova E, 2010).  IgA and IgG antibodies have been identified in serum against the tissue transaminase enzyme and the endomysium. The intestinal tissue is remodeled and flattened. There’s no doubt that these symptoms are eliminated with a wheat gluten free diet (Lucendo AJ, 2011).

Individuals can potentially eliminate the cause of wheat related inflammation and the progression of related illnesses by eating ancient grains, and in doing so, put a stop to the increase in tissue damage.  The next challenge is to correct bacterial imbalances and provide nutrients that will aid the body in repairing the damaged gastrointestinal tissue.

Good Bacteria, Probiotics and Tissue/Organ Repair

Probiotics being “good bacteria” may promote healthy intestinal tissue and a healthy liver.  There are more than 500 species of microorganisms in the human intestine.  Most importantly, this gut flora exists in a delicate equilibrium (Li YT, et al, 2010).  Antibiotics, drugs, poor diets, stress, and disease destroy the balance between good and bad bacteria. The appendix stores this beneficial bacteria.  “The delicate balance can be seriously altered in acute pancreatitis, hemorrhagic shock, burns, surgical trauma, or multiple organ failure because these events can alter the makeup of bacteria populations” (MacFie J, et al, 1999, Shimizu K, et al., 2006). Under these serious conditions the gut can play an important role in the clinical outcome (Clark, JA, et al., 2007).  It has been shown that orally administered probiotics can improve gut ecology and prevent liver damage (Xing HC, et al., 2006). Oral administration of Lactobacillus and Bifidobacterium were found to inhibit the growth of Enterobacter bacterium, decrease concentrations of Enterococcus and significantly improve liver health (Li YT, et al., 2010). Health food stores can help with beneficial tips on probiotics and healing the GI tract.

Yogurt contains the Lactobacillus bulgaricus and Streptococcus thermophilus bacteria (Meydani SN, et al, 2000).  Many studies have shown the beneficial effects of yogurt against enteric and respiratory infections (Villena J, et al, 2006), anticarcinogenic properties, and against damaging anti-inflammatory cytokine release (Perdigon G, et al, 2002, de Moreno de LeBlanc A, et al, 2004, Meyer AL, et al, 2007 4-16).  Researchers have demonstrated that oral probiotics help prevent the breakdown of intestinal barrier function, reduced bacterial translocation, and attenuate liver injury in mice induced by d-galactosamine (Cachi A, et al, 2005, Lazarte S, et al, 2001).  Hepatotoxicity is a common side effect from many therapeutic drugs. These researchers showed that “cow or goat yogurts were effective at protecting against experimental acute liver injury.  In addition, researchers showed that Spirulina maxima prevented lead acetate-induced changes on plasma and liver lipid levels and on the antioxidant status of the liver and kidney.  Spirulina maxima succeeded to improve the biochemical parameters of the liver and kidney towards the normal values of the control group, showing protective effects (Ponce-Canchihuaman JC, 2010).

Improving Wellness

An added benefit of not consuming wheat products is that bad bacteria flourish in wheat.  They depend upon the presence of wheat.  In eliminating this bacterial food source, common bacteria can still exist, but tend not to thrive. While more research needs to be conducted on this hypothesis, those wishing to avoid colds and flus, and hospitals wishing to reduce infection rates may find it beneficial to evaluate a wheat free diet.

Individually, we can take action to make ourselves healthier by avoiding the gluten and lectins in wheat and by taking probiotics.  This helps our families improve wellness, reduce our health care costs, and reduces our downtime.  As health care providers and society increasingly recognize wheat avoidance benefits and institute more appropriate diets, true disease prevention will take hold.

As a country, our health care costs are skyrocketing due to many of these wheat caused preventable diseases.   Our country may benefit financially with improved wellness by consuming ancient grains and rices or by modifying the wheat grain to be void of the immune stimulants (Hall EH, 2011). Researchers have found that the production of better strains of wheat that will preserve wheat’s  technological baking properties (chewiness, elasticity) but eliminate  the T-cell immune stimulating epitopes can be produced (van den Broeck HC, 2009).

In addition, let’s evaluate the super lectins.  Seed manufacturers currently have many plants that are considered to be “Roundup Ready” and they are working to have wheat ‘Roundup Ready’. Can we re-engineer  these harmful lectins to reduce their attack on the human body?

In doing so, we may find an unimaginable reduction in disease: celiac disease, dermatitis, autoimmune disease, diabetes type 1, thyroid problems, biliary cirrhosis, colitis, cerebellar ataxia, autism, peripheral neuropathy, and schizophrenia.  A wheat diet may also help prevent cancer.  A research study with  Resus Maquaes found that a gluten free diet upregulated cancer protecting cells.  Surprise!  Apparently, if the human immune system is not preoccupied protecting the body from wheat plant defense lectins, cancer protection mechanisms are restored!  Blessings!


Cho SW, Gallstedt M, Johansson E, Hedenqvist MS, “Injection-molded Nanocomposites and Materials based on Wheat Gluten”, Intl J BiolMacrommol 2011 Jan 1; 48(1):146-52. Epub 2010 Oct 28

Cachi A, Lazarte S, Alvarez S, Nunuz de Kairuz M, Salva S, Aguero G, “Effect of goat yogurt administration on bacterial translocation in a model of acute liver injury”, Biocell 2005;29-72.

Clark, Jessica A., Coopersmith, Craig M., “Intestinal crosstalk: a new paradigm for understanding the gut as the “motor” of critical illness.  Shock. 2007;28:384-393.

Davis, William, “Wheat Belly”, Rodale Books, 2011

de Moreno de LeBlanc A, Perdigon G, “Yogurt feeding inhibits promotion and progression of colorectal cancer”, Med Sci Monit 2004;10:BR96-BR104.

Fardet A, “New hypotheses for the health-protective mechanisms of whole-grain cereals: what is beyond fibre?”, Nutr Res Rev. 2010 Jun;23(1):65-134. Epub 2010 Jun 22.

Festen EA, Szperl AM, Weersma RK, Wijmenga C, Wapenaar MC, “Inflammatory bowel disease and celiac disease: overlaps in the pathology and genetics, and their potential drug targets.”, Endocr Metab Immune Disord Drug Targets. 2009 Jun;9(2):199-218.

Hall EH, Crowe SE, “Environmental and lifestyle influences on disorders of the large and small intestine: implications for treatment”, Dig Dis. 2011;29(2):249-54. Epub 2011 Jul 5. PMID: 21734392

Lazarte S, Alvarez S, Olivia I, Aguero G, “Murine model of acute liver injury”. Biocell 2001;25:108.

Lucendo AJ, “Esophageal manifestations of Celiac Disease”, Dis Esophagus 2011 Mar 25 doi:10.1111/j.1442-2050.2011.01190.x

MacFie J, O’Boyle C, Mitchell C, Buckley PM, Johnstone D, Sudworth P, “Gut origin of sepsis: a prospective study investigating associations between bacterial translocation, gastric microflora, and septic morbidity”, Gut. 1999;45:223-228.

Meydani SN, Ha WK: Inmunologic effects of yogurt. Am J Clin Nutr 2000;71:861-872

Meyer AL, Elmadfa I, Herbacek I, Micksche M, “Probiotic, as a well as conventional yogurt, can enhance the stimulated production of proinflammatory cytokines”, J Hum Nutr Diet 2007;20:590-598.

Nutritional Analysis:

Nova E, Pozo T, Sanz Y, Marcos A., “Dietary strategies of immunomodulation in infants at risk for celiac disease”, Proc Nutr Soc. 2010 Aug;69(3):347-53. Epub 2010 Jun 28.

Perdigon G, de Moreno de LeBlanc A, Valdez J, Rachid M, “Role of yoghurt in the prevention of colon cancer”, Eur J Clin Nutr 2002;56:S65-S68.

Ponce-Canchihuamán JC, Pérez-Méndez O, Hernández-Muñoz R, Torres-Durán PV, Juárez-Oropeza MA, “Protective effects of Spirulina maxima on hyperlipidemia and oxidative-stress induced by lead acetate in the liver and kidney”, Lipids Health Dis. 2010 Mar 31;9:35

Sharon N, Lis H., “History of lectins: from hemagglutinins to biological recognition molecules.”, Glycobiology. 2004 Nov;14(11):53R-62R. Epub 2004 Jun 30.

Shimizu K, Ogura H, Goto M, et al., “Altered gut flora and environment in patients with severe SIRS”, J. Trauma. 2006;60:126-133.

van den Broeck HC, van Herpen TW, Schuit C, Salentijn EM, Dekking L, Bosch D, Hamer RJ, Smulders MJ, Gilissen LJ, van der Meer IM, “Removing celiac disease-related gluten proteins from bread wheat while retaining technological properties: a study with Chinese Spring deletion lines”, BMC Plant Biol. 2009 Apr 7;9:41, PMID: 19351412

Villena J, Racedo S, Aguero G, Alvarez S, “Yogurt accelerates the recovery of defense mechanisms against Streptococcus pneumoniae in protein-malnourised mice”.  Br J Nutr 2006;95:591-602

Xing HC, Li LJ, XU KJ, et al., “Protective role of supplement with foreign Bifidobacterium and Lactobacillus in experimental hepatic ischemiareperfusion injury”. J Gastroenterol Hepatol. 2006;21:647-656.

Copyright © 2012.  All rights reserved.

Photograph: Avid riders at Cathedral Rock, Sedona, Arizona

Disclaimer:  The ERB is a literature research team presenting the findings of other researchers. The ERB is not licensed medical nor dietary clinicians and will not give medical nor dietary advice.   Any information presented on this website should not be substituted for the advice of a licensed physician or nutritionist.  Users of this website accept the sole responsibility to conduct their own due diligence on topics presented and to consult licensed medical professionals to review their material.  We make no warranties or representations on the information presented and should users utilize this research without consulting a professional, they assume all responsibility for their actions and the consequences.

Concussion (mild TBI) Brain Food: A Review of Fish Oil, B-Complex and Protein (Amino Acid) Treatments


Please see the new for this and other brain food related posts.

Concussion (mild Traumatic Brain Injury) Brain Food Treatment Research Summary:  Research shows that fish oil supplements if supplied before or after brain trauma aid in protecting cell membrane from damage and death. The Institute of Medicine research report shows that by immediately providing sufficient protein to brain damaged victims, mortality rates and Second Injury (damage surrounding the initial injury) can be significantly reduced.  Protein builds DNA, cell structures, and neurotransmitters. Researchers have found that Bcomplex vitamins are critical to maintaining reactions involved in the production of red blood cells, cell membrane, the myelin coating surrounding nerves fibers, and neurotransmitter production, making B-complex vitamins vital for nerve communication and brain function.   This report reviews these findings to encourage further evaluation and testing.  Home laboratory testing to monitor these nutrient levels should be evaluated.

High School Soccer Player Concussion Case Study:

As he jumped into the air, the soccer player was struck on the back of the head (posterior parietal, right side). He fell to the ground and lost consciousness for 10 – 15 seconds.  Afterwards, he felt normal and returned to play for 40 minutes. The next morning, the back of his head was swollen.  He described the pain as a “bad migraine”. The subject was lethargic and bright lights made him nauseous.  He experienced no balance nor vision problems.  Quick movements intensified his headache. He did not attend school, as it was difficult to concentrate, read, write, or spell.  He had memory difficulties. Bright light caused dizziness and irritated his headache.  He experienced no improvement of his condition during the first two weeks.

The third week post concussion, the subject began taking Fish Oil (600mg DHA+EPA, twice daily), B-complex (100mg/twice daily) , and Amino Acids (750mg/twice daily).  Feeling better, he attempted to attend school, but found himself “fading out”. At his physician’s office, he was unable to memorize colors or spell simple words.  Swelling was identified on the right side of his parietal lobe and left side of his frontal lobe.  He returned to school several days later for a few hours. He was unable to complete homework.  The third week he attended school part-time and on the fourth week, he attended full time. He felt “fairly normal”, however, continued to have difficulties with bright lights and could not recall elementary school memories.  He discontinued the vitamins at the end of the fourth week.

One year later, the subject suffered a minor concussion as the front of his head (right frontal lobe) struck a goal post.  His pupils were dilated.  He could remember colors and spell however, he was dizzy in bright light.  He discontinued play, but did not consider this event as serious as the previous. He took the vitamins for a few days and felt better.  The following year, he again hit his head during soccer season and took the vitamins for a couple days.

Since most concussions improve about the third to fourth week, it is difficult to determine whether fish oil, b-complex, and amino acids shortened recovery time. The subject believes that the improvements began with the vitamins.  He states that upon taking the vitamins, he felt like returning to school. Additional research would be more valuable should baseline, post concussion, and post treatment neurocognitive testing be completed with control and test groups.

Concussion – mild Traumatic Brain Injury Discussion:

The human brain is about the size of a cauliflower head with the density of medium soft cheese and can be easily sectioned with a spatula. The brain stem protrudes from the posterior-inferior surface sending commands up and down pathways and through relay centers to the pinky-sized spinal cord. The brain and spinal cord are surrounded by clear cerebral spinal fluid (CSF) and membranes which provide a shock absorber-like environment internal to the bony cranium and vertebrae.

When the cushion environment is disrupted by an “external mechanical force such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile” (Maas AI, et al., 2008), a traumatic brain injury (TBI) results.  A mild TBI is referred to as a concussion.

TBIs are the leading cause of death/disability worldwide  (Alves OL, et al., 2001) and the number one cause of coma (Farag E, et al., 2011).   One third of TBI fatalities are firearm accidents (75% suicide) and another third are motor vehicle accidents (Leon-Carrion J,, 2005). A total of 1.5 million people experience head trauma each year in the U.S. resulting in an annual cost exceeding $5.6 billion.  While most head injuries are mild (Cassidy JD, et al., 2004), the death rate to TBI is estimated at 21% by 30 days post injury (Greenwood, et al, 2003). The greatest number of TBIs occur in the male 15-24 age group (Hardman JM, et al., 2002) (Mass AI, et al., 2008). Sport and recreational activities in the U.S. alone may cause between 1.6 – 3.8 million TBIs each year (CDCP, 2007).  In addition, the military has seen a significant increase in TBIs. Approximately, 10-20% of veterans returning from the Middle East have experienced a TBI. The Department of Defense is conducting research to reduce the serious problems associated with these injuries and has requested a report from the Institute of Medicine (2011).

Clinically, a mild TBI or concussion is defined as post-traumatic amnesia of less than one day and a loss of consciousness between 0 -30 minutes (DOD TBI Task Force).  Symptoms include “headache, vomiting, nausea, lack of motor coordination, dizziness, and difficulty balancing” (Kushner D, 1998) along with “lightheadedness, blurred vision or tired eyes, ringing in the ear, bad taste in the mouth, fatigue or lethargy, and changes in sleep patterns.  Cognitive and emotional symptoms include behavioral or mood changes, confusion, and trouble with memory, concentration, attention, or thinking” (NINDS, 2008). Social behavior or emotional problems may also occur. Damage to the left side of the brain may involve speech, reading and writing difficulties.  Damage to the back of the brain may involve vision, balance, and coordination problems.

Current diagnostic techniques include neurological exam and neuro-imaging studies such as CT (CAT scan) or MRI (Magnetic Resonance Imaging).  CT scans are quickly completed in an emergency department. They are less expensive and better at showing bleeds than MRI  however, brain CT delivers a 1-2 millisievert dose of radiation.   MRI, which utilizes a magnetic field,  (no radiation exposure), delivers more detail of the brain and brain stem, but it is more time consuming and costly.  A CT of a more serious TBI may show hemorrhage, skull fracture, contusions (bruising), fracture, and/or edema (swelling).  An MRI of a more serious TBI, might show a shifting of brain structures, contusion, and hematoma. When blood exerts pressure upon the brain surface it can impair brain function. Interestingly, when brain tissue is seriously injured,  it appears to be cracked open on MRI, much like the appearance of a sponge that is torn open every 1-2 inches. The tears create fluid inlets, perhaps designed to bring nutrient rich CSF to the damaged areas.

A mild TBI or concussion will often show little damage on CT or MRI neuro-imaging studies, thus the increasing use of imPACT or CNS Vital Signs neurocognitive testing.  These computerized tests  have been more effective at assessing mild concussive damage by evaluating general mental functioning. To date, many athletic programs have been using them to compare pre and post injury results to determine ‘return to play’. Since they measure brain function in terms of verbal and visual memory, processing speed, reaction time, attention span, and non-verbal problem solving capabilities, neurocognitive testing has been successfully utilized to identify emotional and cognitive deficits related to mild TBIs.

When the brain is damaged, it immediately begins self repair. Raw materials are sought from nutrients in the blood supply and from CSF to rebuild the initial injury site.  When nutrient supply is insufficient, surrounding brain tissue may be broken down to supply substrate for reconstruction.

Damage apparent in adjacent tissue, has been defined as Second Injury and may result in more serious injury than the initial TBI (Park E, et al., 2008). When death results weeks later, it is typically caused by secondary damage (Ghajar J, 2000). In the past, this Second Injury has been commonplace and no therapy has been available to stop progression (Park E, et al., 2008). However, recent military studies found that by immediately supplying sufficient amounts of protein to the injured patient, Secondary Injury is significantly reduced (Institute of Medicine, 2011).  Providing omega-3 essential fatty acids (DHA/EPA) before injury or immediately after injury also reduces TBI damage (Mills JD, et al., 2011) (Wu A, et al., 2007).

Brain injury brings immune cells and fluids to the injury site, resulting in inflammation, but with the brain enclosed in the cranium there is minimal space to accommodate swelling.  The resultant increase in intracranial pressure may occlude blood vessels responsible for bringing oxygen and nutrients to brain cells and lymph vessels responsible for removing waste products (Scalea TM, 2005). Increased pressure can force the brain to herniate into spaces where it does not belong.  This renders the tissue non-functional and eventually will cause death.  A variety of anti-inflammatory medications are often utilized to diminish swelling.

Mild TBIs physically appear to resolve in 3 weeks and patients tend to return to normal activities.  Some patients have “physical, cognitive, emotional and behavioral problems such as headaches, dizziness, difficulty concentrating, and depression” (Parik S et al., 2007). Movement disorders, seizures, and substance abuse may also develop (Arlinghaus KA, et al., 2005). Depending upon the severity of the injury, the number of repeat injuries and the presence of adequate nutrients before and after the injury, the prognosis ranges from complete recovery to permanent disability, neurological disease or death. “Permanent disability is thought to occur in 10% of mild TBIs, 66% of moderate injuries, and 100% of severe injuries” (Frey LC, 2003). In many situations, particularly athletics, a second concussion may occur before the first concussion has healed.  This is of particular concern as multiple TBIs may have a cumulative effect (Kwasnica C, et al., 2008).

Brain Biochemistry:

As discussed in ‘The ERB Vision for Wellness‘ tab on this website, Dr. James Watson of Watson and Crick, the scientists who discovered the DNA double helix, tells us that to eliminate disease we must return to Biochemistry.  We expect that the many dedicated researchers referenced below would agree.  They have found that in Traumatic Brain Injury, nutrition matters.  Adequate supplies of the major tissue nutrients are critical.

In looking at a section of brain tissue, the lighter tan colored structures are called “white matter.” White matter consists of nerve fiber tracts or pathways traveling in both directions to and from the brain through the brainstem down the spinal cord and extending out to organs, arms, and legs.  A nerve can be up to four feet long. White matter nerve tissue is composed of essential fatty acids called omega-3s such as DHA (docosahexanoic acid) and EPA (eicosapentanoic acid).  Most nerve tissue contains a myelin coating.  The resistance created by this coating allows for impulse transmission at approximately 100m/sec ( 245 mph)! Nerve and myelin formation require B-complex vitamins.  The darker structures on a brain section are called  “gray matter.”  These are decision-making nuclei made from proteins composed of amino acid building blocks.  Proteins and amino acids formulate all structures, most noticeable of which are neurotransmitters.  Neurotransmitters are critical to brain function and communication throughout the body.

Essential Fatty Acids (DHA and EPA):

40% of brain tissue is essential fatty acids (DHA and EPA).   While EPA provides important anti-inflammatory actions (Sears B, 2011) and is included in supplements, 97% of the brain’s essential fatty acids are the 22 carbon chain,  Docosahexanoic Acid (DHA).  DHA is found in foods such as walnuts (ALA), microalgae, microplants, cod, salmon, mackerel, sardines, hake, caviar, herring, oysters, organ meats (liver), grass fed and finished beef, and fish oil or algae supplements.  Fish receive DHA from ocean phytoplankton (microalgae or microplants).  Cattle receive DHA from grass.  However, as we increasingly draw our food from farm-raised fish and grain-raised cattle, our dietary intake of DHA is being depleted, (Abel R, 2002).

Most humans consume an overabundance of vegetable oil and butters which contain no double bonds in their carbon chains.  DHA has six double bonds (22:6), one at every third carbon (omega-3 or n-3). In cell membrane, these double bonds allow the fatty acid to neutralize damaging free radicals.  In addition, the double bonds increase the fluidity properties of cell membrane which helps to protect the cell from trauma and cell death (apoptosis) (Eckert GP, et al., 2011). Proper cell communication and signaling is critical for brain function. Fifty percent of nerve cell plasma membrane is DHA (Collins C, et al., 2002) which is important in cell communication, neuronal survival, and growth.  DHA is found in three cell membrane phospholipids:  phosphytidylethnolamine, ethnolamine plasmalogens, and phosphatidylserine. Upon injury, these phospholipid pools are important reservoirs to reconstruct cell membrane (Chang CY, et al., 2009).  In the absence of dietary DHA, the brain will improvise and construct brain tissue from vegetable oil.  However, under traumatic conditions  vegetable oil fed rat brain falls apart, (Eckert  GP, et al., 2011) (Abel R, 2002).

Researchers found that in rats subject to TBI which then received 40mg/kg/day pharmaceutical grade fish oil rich in DHA and EPA for 30 days post TBI had more healthy nerve cells.  Essential fatty  acids  were shown  to be neuroprotective by reducing  the  number of  injured nerve axons, decreasing the level of inflammation,  and reducing oxidative stress and cell death (Mills JD et al., 2011). DHA fed to rats immediately post TBI was found to counteract cognitive decay, maintain membrane signaling function, and support the potential of DHA supplementation to reduce the effects of TBI. (Wu A, 2011).  In addition, essential fatty acids DHA and EPA given to rats 4 weeks prior to TBI was found to help maintain brain homeostasis and reduce oxidative damage due to TBI (Wu A, et al., 2007). 

DHA and EPA have been found to improve the outcome of stroke studies of both rat and human models (Kong W, (Hagiwara H,  Few human studies have been conducted using DHA as prophylaxis for TBI.  In 2006, 20 grams per day of omega-3 fish oil (CNN, 2012)  and hyperbaric oxygen treatment were used by Dr. Julian Bailes to treat the sole survivor of the West Virginia mining disaster, Randal McCloy, who suffered carbon monoxide poisoning. This patient now claims that his brain function is near normal.  Dr. Bailes and his colleagues have since published many research papers demonstrating the benefits of essential fatty acids and fish oil supplements.  In addition, “individual case reports using fish oil doses of 2-4 grams per day have been described, however sufficient human research is unavailable to recommend dosages”  (Maroon, JC and Bost J, 2011).

One new human case study was published in October 2012, when Peter Ghassemi convinced physicians to give his son Bobby, who was in a coma following a motor vehicle accident, omega-3 fish oil ( a similar dose to Randal McCloy).  Bobby  had a Glasgow Coma Score of 3 (scale 3 – 15), which Dr. Michael Lewis says that “a brick or piece of wood has a Glasgow Coma Score of 3. It’s dead.”  Peter Ghassemi, Bobby’s father, indicates that it was difficult to convince physicians to give their son fish oil.  They wanted to see 1000 case studies first, to prove its efficacy.  Eventually, physicians agreed.  Thanks to his father’s perserverance, Bobby has recovered today.  U.S. Army Colonel Lewis who recommended the therapy to Peter Ghassemi describes the therapy like this.  “If you have a brick wall and it gets damaged, wouldn’t you want to use bricks to repair the wall?  Omega-3 fatty acids are literally the bricks of the cell wall of the brain.”  (CNN,2012)

The textbook “Contemporary Nutrition” written by  Gordon M. Wardlaw and Anne M. Smith in 2013 tells us that EPA and DHA are very slowly synthesized (perhaps only 1% conversion) in the brain from alpha linoleic acid and can be found in “fatty fish such as salmon, tuna, sardines, anchovies, striped bass, catfish, herring, mackerel, trout or halibut “(listed highest to lowest omega-3 content) and in foods such as “canola and soybean oils, walnuts, flax seeds, mussels, crab and shrimp”.  The authors warn about high mercury levels in swordfish, shark, king mackerel, and albacore, and indicate that fish with low mercury levels include salmon, sardines, bluefish, herring and shrimp.  Eating fish twice each week is recommended.  Omega-3 fatty acids tend to act to reduce blood clotting and inflammation, while omega-6 foods tend to increase clotting and inflammation.  Vitamin K and calcium carbonate are also involved in the clotting process. “Fish oil capsules should be limited for individuals who have bleeding disorders, take anticoagulant medications, or anticipate surgery, because they may increase risk of uncontrollable bleeding and hemorrhagic stroke”.

Wardlaw and Smith recommend 1.6 grams per day of omega-3 fatty acids for men and 1.1 grams per day for women.  Elevated blood triglycerides are treated with 2 to 4 grams per day.  Omega 3 fatty acids have been found to reduce the inflammation of rheumatoid arthritis and help with behavioral disorders and cases of mild depression.  Freezing fish oil capsules helps to reduces the fishy after taste.  “2 tablespoons of flax seed per day is typically recommended as an omega-3 fatty acid source”.  Approximately 3 walnuts (6 halves) supposedly yield approximatley 1 gram of DHA, but the conversion to DHA is not good.  Care should be taken to keep DHA sources refrigerated as they turn rancid easily.  For TBI patients on IV feeding it is important to investigate the quantity of DHA and EPA present in total parenteral nutrition.  One researcher takes approximately 1 gram of DHA/EPA through fish oil daily and regulates intake by the dryness/moistness of the skin.  In drier climates, she finds this daily intake amount must be doubled.  Mercury consumption in fish oil is a serious risk and mercury free alternatives should be explored.

More human studies are needed to establish the benefits/risks of DHA and EPA with TBI. Eventually these will come however, the bureaucracy is heavy, and the cost estimates of bringing a new drug to market varies from $500 million to $2 billion (Adams C, et al., 2006) (JHE, 2010). A bottle of fish oil, with a small profit margin, may not provide sufficient return on investment to entice investigation.  One subject with a fish oil allergy could mire the researching organization in million dollar legal proceedings for years to come. That said,  research studies are important for physicians to have as legal and medical support for their recommendations.  Given this climate, many individuals and their health care providers have taken on the responsibility to evaluate whether  fish oil supplements are a safe and worthwhile benefit or a risk addition to their diet.  By 2020, we expect clinicians and individual to measure and maintain their optimum DHA/EPA levels.

B Complex Vitamins:

Vitamin B is a vitamin complex  of B-1-thiamine, B-2 riboflavin, B-3 niacin, B-5 pantothenic acid, B-6 pyridoxine, B-9 folate, B12-cobalamin.  B complex vitamins are important for nerve, DNA and neurotransmitter synthesis,  and for cell energy production and metabolism.  The majority of the information cited below regarding the effects of B complex vitamins on brain function has been obtained from animal studies.

Thiamine (B1):

  • Required for red blood cells to carry oxygen (Combs GF Jr, et al., 2008)
  • Acetylcholine neurotransmitter production(Butterworth RF, et al., 2006)
  • Myelin synthesis in nerve cells (Butterworth RF, et al., 2006)
  • High school female RDA 1.0 mg/day, male 1.2 mg/day.
  • Adult RDA is 1.1 – 1.2 mg/day, Daily Value 1.5 mg/day, no upper limit set because water soluble and rapidly lost in urine, alcohol consumption reduces thiamin levels (Wardlaw,, 2013)
Riboflavin (B2):
  • A component in all flavoproteins and  red blood cells (erythrocytes)
  • Reduced TBI lesions, edema, and improved outcome (Hoane MR, et al., 2005)
  • High school female RDA 1.0 mg/day, male 1.3 mg/day.
  • Adult RDA is 1.1 – 1.3 mg/day, Daily Value 1.7 mg/day, no upper limit set.  Alcohol consumption reduces riboflavin levels (Wardlaw,, 2013)

Niacin (B3):

  • Involved in DNA repair, cholesterol, and energy production
  • Helps produce neurotransmitters in the adrenal gland
  • Reduces TBI lesion size and improves sensory, motor, cognitive, and behavioral recovery (Voner Haar C, 2011)
  • High school female RDA 14 mg/day, male 16 mg/day.
  • Adult RDA is 14 – 16 mg/day, Daily Value is 20 mg/day, upper limit is 35mg/day of nicotinic acid form. Alcohol consumption reduces niacin levels (Wardlaw,, 2013)

Pantothenic Acid (B5)

  • Neurotransmitter acetylcholine production
  • Involved in signal transduction, and enzyme control
  • High school female and male 5 mg/day.
  • Adult Adequate Intake is 5 mg/day, Daily Value is 10 mg, no upper limit set (Wardlaw, et. al, 2013).

Pyridoxal Phosphate (B6):

  • Controls all amino acid metabolism  (Sahley BJ, 2002)
  • Red blood  cell and  antibody formation (Sahley BJ, 2002)
  • Dopamine and GABA neurotransmitter production
  • Nerve myelin sheath phospholipid production
  • High school RDA female 1.2 mg/day, male 1.3 mg/day.
  • Adult RDA is 1.3 – 1.7 mg/day, Daily Value is 2 mg, Upper Level is 100 mg/day based upon nerve damage.  Studies have shown that 2 – 6 grams/day of B-6 for 2 or more months can lead to irreversible nerve damage.  Symptoms of toxicity include walking difficulties and hand and foot numbness (Wardlaw, et. al, 2013)

Folate  (B9):

  • Required to synthesize, repair, and methylate DNA.
  • Provides neuroprotection in TBI (Naim MY, et al., 2010)
  • Important in rapid cell division and growth.
  • Production of healthy red blood cells and anemia prevention
  • Forms cell membrane phospholipids and receptors (Karakula H, et al.,2009) (Surtees R, 1998)
  • Prevents nerve damage and neural tube defects during development
  • Required for myelin regeneration (van Rensburg SJ, et al., 2006) (Guettat L, et al., 1997)
  • High school RDA female and male 400 mcg/day.
  • Adult RDA and Daily Value is 400 mcg/day,  pregnant women 600mcg/day  (important to prevent neural tube defects), Upper Level is 1 mg/day alcoholism and poor absorption reduces folate levels (Wardlaw,, 2013)

Cobalamin (B12):

  •  Involved in blood formation.
  • Critical to DNA synthesis through folate regeneration
  • Formation of cell membrane phospholipids and receptors (Karakula H, et al., 2009) (Surtees R, 1998)
  • B12 supplementation partially resolved cognitive deficits and myelin imaging abnormalities (Chatterjee A,, 1996) (Jongen JC, et al., 2001)
  • Improves cerebral and cognitive functions.  (Bourre JM, 2006)
  • Required for myelin synthesis (Hall CA, 1990) (van Rensburg SJ, et al, 2006) (Guettat L, et al., 1997)
  • Promotes nerve regeneration (Okada K, et al., 2010)
  • High school RDA female and male 2.4 mcg/day.
  • RDA is 2.4 mcg/day, Daily Value is 6 mcg/day, no Upper Limit set, stored in liver, 50% of dietary intake may be absorbed.  Nerve damage and anemia may result from insufficient intake.

There are 150mg time release (9-10 hours) capsules available for B complex.  All  B vitamins are water soluble and need to be replenished daily.  Vitamin B complex has an important  role  in  alleviating anxiety and lactic acid buildup.  Dietary supply may be inadequate under stress (Sahley BJ, 2002).

Protein (Amino Acids):

Linear chains of amino acids form proteins. Proteins produce nuclei in the brain, DNA,  cell membrane, enzymes, and neurotransmitters. Twenty amino acids are commonly identified.  All 20 amino acids need to present concurrently for protein synthesis to occur.  A problem may be that most foods do not provide all 20 amino acids concurrently as is provided by a 20 amino acid complex supplement.  More research needs to be completed on this topic.

Alanine – Precursor of neurotransmitter dopamine (Coxon KM, et al., 2005)

Arginine – Through agmantine, it is neuroprotective in trauma and ischemia models by significantly reducing  brain swelling volume and blood-brain barrier protection (Kim JH, et al., 2009)

Cysteine – Forms DNA double helix disulfide bonds

Glutamate – Important for calcium ion binding; may reduce blood glucose levels in the injured spinal cord reducing neurological impairment (Zhang TL, et al., 2010)

Glutathione – Critical to relieve oxidative stress in cells

Glycine – Important in red blood cell formation (Shemin D, et al., 1946); gives amino acid structures flexibility

Histidine – Used throughout the brain;  improves TBI outcome (Faden AI, et al., 1993) (Krusong K, et al., 2011)

Lysine – Important for connective tissue maintenance, and affects protein binding to phospholipid membranes (Blenis J, et al., 1993)

Methionine – The sole methyl donor in the central nervous system; increases S-adenylmethionine (SAMe) in CSF aiding in neurological disorder treatment (Chishty M, et al., 2002); forms Glutathione, important in reducing free radical-mediated traumatic injury  (Gidday JM, et al., 1999).  The first amino acid on each new strand of DNA.

Phenylalanine – Produces chlorophenylalanine (CPA) which slowed the breakdown of the blood-brain barrier permeability, brain edema and blood flow; reduced the number of damaged and distorted nerve cells (Sharma HS, et al., 2000).

Proline – Maintains connective tissue (Bhattacharjee A, et al., 2005)

Serine – Acts as a neurotransmitter in the brain (Wolosker H, et al., 2008)

Taurine – Major component of brain tissue and muscle (Brosnan JT, 2006)

Threonine – A component of the serine/threonine kinase; neuroprotective following traumatic brain injury (Erlich S, et al.,2007)

Tryptophan – Precursor to neurotransmitter serotonin (Savelieva KV, et al., 2008); a modulator of serotonin which alters plasticity-related signaling pathways and matrix degradation (Penedo LA, et al., 2009)

Tyrosine – Precursor of the neurotransmitter dopamine, norepinephrine, epinephrine

Under prolonged stress or illness the body is unable to produce sufficient non-essential amino acids (Sahley BJ, 2002).  Trauma has been found to damage DNA and RNA, and to deplete neurotransmitters.  Neurological dysfunction is caused by traumatic brain injury (Cole J, et al., 2010

As amino acids are utilized for energy and substrate, they are oxidized to urea and carbon dioxide producing high levels of glutamate.  These high levels seen in the TBI patient can include oxidation of branched chained amino acids. Dietary consumption of Branched Chain Amino Acids (BCAAs) restored BCAA concentrations to normal, improved nerve cell communication, and reinstated cognitive performance after concussive brain injury (Cole J, et al., 2010). BCAAs and amino acid complex (protein) are available at nutrition stores.

The Institute of Medicine committee report of April 20, 2011 on Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel   found that supplying high levels of protein to the TBI patient within the first 24 hours severely reduced mortality.  This report calls for standardized protocols to require  a level of nutrition that represents more than 50 percent of the injured person’s total energy expenditure and provide 1 to 1.5 grams of protein per kilogram of body weight for two weeks. They expect this nutritional intervention limits the inflammatory response, thereby improving outcome.  Most importantly, in following this protein therapy, the detrimental secondary injury process was not apparent.

Protein needs of a sedentary adult are estimated at .8 grams/kilogram  or 56 grams/day for a 70-kilogram, 154lb man.  (Pounds/2.2 kilograms per pound * .8 grams/kilogram).   Protein needs of a football, power sport playing athlete are approximately 1.4 – 1.7 grams/kilogram for males and 1.1 – 1.5 grams/kilogram for females or 98-119 grams/day. Athletes in a strength training program can be recommended up to 2.0 grams of protein per kilogram per day, almost twice the RDA (Wardlaw, et. al., 2013).

The objective of this discussion has been to bring current research advancements to light given the realization that concussive TBIs cause damage and disease, such that this information may be further evaluated by the public, health care providers, and the medical research community.

Traumatic Brain Injury References:

Alves OL, Bullock R (2001). “Excitotoxic damage in traumatic brain injury”. In Clark RSB, Kochanek P. Brain injury. Boston: Kluwer Academic Publishers. p. 1. ISBN 0-7923-7532-7. Retrieved 2008-11-28.

Arlinghaus KA, Shoaib AM, Price TRP (2005). “Neuropsychiatric assessment”. In Silver JM, McAllister TW, Yudofsky SC. Textbook Of Traumatic Brain Injury. Washington, DC: American Psychiatric Association. pp. 63–65. ISBN 1-58562-105-6.

Center for Disease Control and Prevention, National Center for Injury Prevention and Control. “Traumatic brain injury” ( 2007.

Cassidy JD, Carroll LJ, Peloso PM, Borg J, von Holst H, Holm L et al. (2004). “Incidence, risk factors and prevention of mild traumatic brain injury: Results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury”. Journal of Rehabilitation Medicine 36 (Supplement 43): 28–60. DOI:10.1080/16501960410023732. PMID 15083870.

Carlson K, Kehle S, Meis L, Greer N, MacDonald R, Rutks I, Wilt TJ, “The Assessment and Treatment of Individuals with History of Traumatic Brain Injury and Post-Traumatic Stress Disorder: A Systematic Review of the Evidence [Internet].” Washington (DC), Department of Veterans Affairs (US); 2009 Aug, VA Evidence-based Synthesis Program Reports

Department of Defense and Department of Veterans Affairs (2008). “Traumatic Brain Injury Task Force”.

Farag E, Manno EM, Kurz A. (2011) “Use of hypothermia for traumatic brain injury: point of view” Minerva Anesthesiol. 2011 Mar;77(3):366-70. Epub 2011 Feb 1. PMID: 21283076

Frey LC (2003). “Epidemiology of posttraumatic epilepsy: A critical review”. Epilepsia 44 (Supplement 10): 11–17. DOI:10.1046/j.1528-1157.44.s10.4.x. PMID 14511389.

Furlow, B (2010 May-Jun). “Radiation dose in computed tomography.”. Radiologic Technology 81 (5): 437-50. PMID 20445138.

Ghajar J (September 2000). “Traumatic brain injury”. Lancet 356 (9233): 923–29. DOI:10.1016/S0140-6736(00)02689-1. PMID 11036909.

Greenwald BD, Burnett DM, Miller MA (March 2003). “Congenital and acquired brain injury. 1. Brain injury: epidemiology and pathophysiology”. Archives of Physical Medicine and Rehabilitation 84 (3 Suppl 1): S3–7. DOI:10.1053/apmr.2003.50052. PMID 12708551.

Hardman JM, Manoukian A (2002). “Pathology of head trauma”. Neuroimaging Clinics of North America 12 (2): 175–87, vii. DOI:10.1016/S1052-5149(02)00009-6. PMID 12391630. “TBI is highest in young adults aged 15 to 24 years and higher in men than women in all age groups.”

Kushner D (1998). “Mild traumatic brain injury: Toward understanding manifestations and treatment”. Archives of Internal Medicine 158 (15): 1617–24. DOI:10.1001/archinte.158.15.1617. PMID 9701095.

Kwasnica C, Brown AW, Elovic EP, Kothari S, Flanagan SR (March 2008). “Congenital and acquired brain injury. 3. Spectrum of the acquired brain injury population”. Archives of Physical Medicine and Rehabilitation 89 (3 Suppl 1): S15–20. DOI:10.1016/j.apmr.2007.12.006. PMID 18295644.

León-Carrión J, Domínguez-Morales Mdel R, Barroso y Martín JM, Murillo-Cabezas F (2005). “Epidemiology of traumatic brain injury and subarachnoid hemorrhage”. Pituitary 8 (3–4): 197–202. DOI:10.1007/s11102-006-6041-5. PMID 16508717.

Maas AI, Stocchetti N, Bullock R (August 2008). “Moderate and severe traumatic brain injury in adults”. Lancet Neurology 7 (8): 728–41. DOI:10.1016/S1474-4422(08)70164-9. PMID 18635021.

“NINDS Traumatic Brain Injury Information Page”. National Institute of Neurological Disorders and Stroke. 2008-09-15. Retrieved 2008-10-27.

Parikh S, Koch M, Narayan RK (2007). “Traumatic brain injury”. International Anesthesiology Clinics 45 (3): 119–35. DOI:10.1097/AIA.0b013e318078cfe7. PMID 17622833.

Park E, Bell JD, Baker AJ (April 2008). “Traumatic brain injury: Can the consequences be stopped?”. Canadian Medical Association Journal 178 (9): 1163–70. DOI:10.1503/cmaj.080282. PMC 2292762. PMID 18427091.

Salomone JP, Frame SB (2004). “Prehospital care”. In Moore EJ, Feliciano DV, Mattox KL. Trauma. New York: McGraw-Hill, Medical Pub. Division. pp. 117–8. ISBN 0-07-137069-2. Retrieved 2008-08-15.

Scalea TM (2005). “Does it matter how head injured patients are resuscitated?”. In Valadka AB, Andrews BT. Neurotrauma: Evidence-based Answers to Common Questions. Thieme. pp. 3–4. ISBN 3-13-130781-1.

Essential Fatty Acids References:

Abel R,  “The DHA Story, How Nature’s Super Nutrient Can Save Your Life”.  2002, ISBN 1-59120-001-6, (2002).

Adams C, Brantner V (2006). “Estimating the cost of new drug development: is it really 802 million dollars?”. Health Aff (Millwood) 25 (2): 420–8. DOI:10.1377/hlthaff.25.2.420. PMID 16522582.

CNN 2012

Eckert GP, Chang S, Eckmann J, Copanaki E, Hagl S, Hener U, Müller WE, Kögel D, “Liposome-incorporated DHA increases neuronal survival by enhancing non-amyloidogenic APP processing”.  Biochim Biophys Acta. 2011 Jan;1808(1):236-43. Epub 2010 Oct 29. PMID 21036142

Mills JD,  Hadley K, Bailes JE, “Dietary Supplementation with the Omega-3 fatty acid Docosahexaenoic Acid in Traumatic Brain Injury”. Neurosurgery, 2011 Feb;68(2):474-81

Journal of Health Economics 2010 Study,

Sears, B (2011). “The fallacy of using DHA alone for brain trauma.”

University of Maryland Medical System and University of Maryland Medical School:  Omega-3 fatty acids:

Wardlaw, Gordon M. and Smith, Anne M., “Contemporary Nutrition”, 2013, ISBN 978-0-07-340254-3, McGraw-Hill.

Vitamin B Complex References:

Bourre JM.  “Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients”.  Nutr Health Aging. 2006 Sep-Oct;10(5):377-85. PMID: 17066209

Butterworth RF, Thiamin. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, editors. Modern Nutrition in Health and Disease, 10th ed. Baltimore: Lippincott Williams & Wilkins; 2006.

Chatterjee A, Yapundich R, Palmer CA, Marson DC, Mitchell GW. Neurology. “Leukoencephalopathy associated with cobalamin deficiency”, 1996 Mar;46(3):832-4. PMID: 8618695Acta Neurol Taiwan. 2009 Dec;18(4):231-41.

Chang CY, Ke DS, Chen JY, “Essential fatty acids and human brain”, Acta Neurol Taiwan. 2009 Dec;18(4):231-41.

Combs GF Jr., “The vitamins: Fundamental Aspects in Nutrition and Health. 3rd edition. Ithaca, NY: Elsevier Academic Press; 2000

Coxon KM, Chakauya E, Ottenhof HH et al. (August 2005). “Pantothenate biosynthesis in higher plants”. Biochemical Society Transactions 33 (Pt 4): 743–6. DOI:10.1042/BST0330743. PMID 16042590.

Guettat L, Gille M, Delbecq J, Depré A, “Folic acid deficiency with leukoencephalopathy and chronic axonal neuropathy of sensory predominance”.  Rev Neurol (Paris). 1997 Jun;153(5):351-3. PMID: 9296172

Hall CA, “Function of Vitamin B12 in the central nervous system as revealed by congential defects”, Am J Hematol. 1990 Jun;34(2):121-7

Hoane MR, Wolyniak JG, Akstulewicz SL, “Administration of riboflavin improves behavioral outcome and reduces edema formation an glial fibrillary protein expression after traumatic brain injury”, J Neurotrauma, 2005 Oct 22;(10):1112-22

Jongen JC, Koehler PJ, Franke CL, “Subacute combined degeneration of the spinal cord: easy diagnosis, effective treatment”, Ned Tijdschr Geneeskd. 2001 Jun 30;145(26):1229-33. PMID: 11455686

Karakuła H, Opolska A, Kowal A, Domański M, Płotka A, Perzyński J, “Does diet affect our mood? The significance of folic acid and homocysteine”  Pol Merkur Lekarski. 2009 Feb;26(152):136-41.

Naim MY, Friess S, Smith C, Ralston J, Ryall K, Helfaer MA, Marguiles SS, “Folic acid enhances early functional recovery in a piglet model of pediatric head injury”, Dev Neurosci. 2010;32(5-6):466-79. Epub 2011 Jan 5. PMID: 21212637

Okada K, Tanaka H, Temporin K, Okamoto M, Kuroda Y, Moritomo H, Murase T, Yoshikawa H. “Methylcobalamin increases Erk1/2 and Akt activities through the methylation cycle and promotes nerve regeneration in a rat sciatic nerve injury model.”, Exp Neurol. 2010 Apr;222(2):191-203. Epub 2010 Jan 4.

Surtees R, “Demyelination and inborn errors of the single carbon transfer pathway” Pediatr. 1998 Apr;157 Suppl 2:S118-21. PMID: 9587038

van Rensburg SJ, Kotze MJ, Hon D, Haug P, Kuyler J, Hendricks M, Botha J, Potocnik FC, Matsha T, Erasmus RT, “Iron and the folate-vitamin B12-methylation pathway in multiple sclerosis”, Metab Brain Dis. 2006 Sep;21(2-3):121-37. Epub 2006 May 26. PMID: 16729250

Vonder Haar C, Anderson G, Hoane MR, “Continuous nicotinamide administration improves behavioral recovery and reduces lesion size following bilateral frontal controlled cortical impact injury.”, Behav Brain Res, 2011 Oct 31;224(2):311-7.  Epub 2011 Jun 17.

Wardlaw, Gordon M. and Smith, Anne M., “Contemporary Nutrition”, 2013, ISBN 978-0-07-340254-3, McGraw-Hill.

Protein (Amino Acids) References:

Bhattacharjee A, Bansal M (March 2005). “Collagen structure: the Madras triple helix and the current scenario”. IUBMB Life 57 (3): 161–72. DOI:10.1080/15216540500090710. PMID 16036578.

Blenis J, Resh MD (December 1993). “Subcellular localization specified by protein acylation and phosphorylation”. Current Opinion in Cell Biology 5 (6): 984–9. DOI:10.1016/0955-0674(93)90081-Z. PMID 8129952.

Brosnan JT, Brosnan ME (June 2006). “The sulfur-containing amino acids: an overview”. The Journal of Nutrition 136 (6 Suppl): 1636S–1640S. PMID 16702333.

Chishty M, Reichel A, Abbott NJ, Begley DJ. “S-adenosylmethionine is substrate for carrier mediated transport at the blood-brain barrier in vitro.” Brain Res. 2002 Jun 28;942(1-2):46-50. PMID: 12031851

Jeffrey T. Cole, Christina M. Mitala, Suhali Kundu, Ajay Verma, Jaclynn A. Elkind, Itzhak Nissim,and Akiva S. Cohena, “Dietary branched chain amino acids ameliorate injury-induced cognitive impairment”,.Proc Natl Acad Sci U S A. 2010 January 5; 107(1): 366–371. Published online 2009 December 29. doi: 10.1073/pnas.0910280107 PMCID: PMC2806733

Erlich S, Alexandrovich A, Shohami E, Pinkas-Kramarski R. “Rapamycin is a neuroprotective treatment for traumatic brain injury.” Neurobiol Dis. 2007 Apr;26(1):86-93. Epub 2007 Jan 31.  PMID: 17270455

Faden AI, Labroo VM, Cohen LA. “Imidazole-substituted analogues of TRH limit behavioral deficits after experimental brain trauma.” J Neurotrauma. 1993 Summer;10(2):101-8.  PMID: 8411214

Gidday JM, Beetsch JW, Park TS. “Endogenous glutathione protects cerebral endothelial cells from traumatic injury.”  J Neurotrauma. 1999 Jan;16(1):27-36. PMID: 9989464

Instituteof Medicine committee report, Nutrition and Traumatic Brain Injury; Improving Acute and Subacute Health Outcomes in Military Personnel.  April 20, 2011.

Kim JH, Lee YW, Park KA, Lee WT, Lee JE. “Agmatine attenuates brain edema through reducing the expression of aquaporin-1 after cerebral ischemia”, J Cereb Blood Flow Metab. 2010 May;30(5):943-9. Epub 2009 Dec 23. PMID: 20029450

Krusong K, Ercan-Sencicek AG, Xu M, Ohtsu H, Anderson GM, State MW, Pittenger C. “High levels of histidine decarboxylase in the striatum of mice and rats.” Neurosci Lett. 2011 May 16;495(2):110-4. Epub 2011 Apr 1. PMID: 21440039

Penedo LA, Oliveira-Silva P, Gonzalez EM, Maciel R, Jurgilas PB, Melibeu Ada C, Campello-Costa P, Serfaty CA. “Nutritional tryptophan restriction impairs plasticity of retinotectal axons during the critical period.”Exp Neurol. 2009 May;217(1):108-15. Epub 2009 Feb 10. PMID: 19416666

Sahley BJ (2002), “The Anxiety Epidemic”, ISBN: 1-889391-23-9

Savelieva KV, Zhao S, Pogorelov VM et al. (2008). Bartolomucci, Alessandro. ed. “Genetic disruption of both tryptophan hydroxylase genes dramatically reduces serotonin and affects behavior in models sensitive to antidepressants”. PloS ONE 3 (10): e3301. Bibcode 2008PLoSO…3.3301S. DOI:10.1371/journal.pone.0003301. PMC 2565062. PMID 18923670.

Sharma HS, Winkler T, Stålberg E, Mohanty S, Westman J. “p-Chlorophenylalanine, an inhibitor of serotonin synthesis reduces blood-brain barrier permeability, cerebral blood flow, edema formation and cell injury following trauma to the rat brain.” Acta Neurochir Suppl. 2000;76:91-5.  PMID: 11450100

Shemin D, Rittenberg D (1 December 1946). “The biological utilization of glycine for the synthesis of the protoporphyrin of hemoglobin”. Journal of Biological Chemistry 166 (2): 621–5. PMID 20276176.

Wardlaw, Gordon M. and Smith, Anne M., “Contemporary Nutrition”, 2013, ISBN 978-0-07-340254-3, McGraw-Hill.

Wolosker H, Dumin E, Balan L, Foltyn VN (July 2008). “D-amino acids in the brain: D-serine in neurotransmission and neurodegeneration”. The FEBS Journal 275 (14): 3514–26. DOI:10.1111/j.1742-4658.2008.06515.x. PMID 18564180.

Zhang TL, Zhao YW, Liu XY, Ding SJ. “Effects of L-lysine monohydrochloride on insulin and blood glucose levels in spinal cord injured rats”. Chin Med J (Engl). 2010 Mar 20;123(6):722-5.  PMI

Copyright © 2013.  All rights reserved.
Disclaimer:  The ERB is a literature research team presenting the findings of other researchers. The ERB is not licensed medical nor dietary clinicians and will not give medical nor dietary advice.   Any information presented on this website should not be substituted for the advice of a licensed physician or nutritionist.  Users of this website accept the sole responsibility to conduct their own due diligence on topics presented and to consult licensed medical professionals to review their material.  We make no warranties or representations on the information presented and should users utilize this research without consulting a professional, they assume all responsibility for their actions and the consequences.

A Potential Therapy for Accidental Wheat Gluten Ingestion

Wheat Gluten Allergy:  Treatment with Anti-Histamines and Aspirin Case Study:

A female in her late forties on a gluten free diet for the past decade, enjoyed wheat pizza, and ingested one piece every 1-2 weeks.  To prevent inflammation of her tonsils, she followed each ingestion with  25mg Benadryl (diphenyhydramine hydrochloride) antihistamine immediately and every 4-6 hours for the next 48 hours.  During the past year,  the subject ingested wheat on Day One with antihistamine therapy immediately following and every 4-6 hours for the next 48 hours.  On Day Three she again ingested wheat and continued with antihistamines.  On Day Five, she presented with an infection in her ears, sinuses, throat, and chest.  One week later, the infection had not resolved.   The subject was placed on amoxicillin antibiotic for 10 days.  The infection cleared, however, a bronchial cough with fatigue continued for the next few weeks.  She was then placed on a 10 day azithromycin prescription.  The cough and fatigue persisted.

It was suspected that gliadin peptide-antibody-collagen complexes formed in her bronchi.  The subject was taking no other medications including no anti-coagulant medication that would thin her blood. The subject was placed on aspirin (salicylic acid) therapy.  Aspirin (975mg) was given the first evening, followed by  aspirin (650mg) every 6 hours on the first full day, and aspirin(650mg) every 8 hours on subsequent days.   By the second day, most of the cough symptoms had resolved.  Therapy continued for a total of seven days during which time the cough resolved completely.  The subject now avoids all wheat, oats, and rye.  Should accidental ingestion occur, she uses antihistamines and aspirin as needed to block inflammation and gliadin peptide-antibody-collagen complex formation.

Antihistamines Discussion

On a wheat gluten free diet, subjects will unexpectedly or intentionally encounter the ubiquitous wheat.  The immune response to the gliadin peptide,after abstention,can be significantly more pronounced. “Y” shaped IgE antibodies that have been secreted in response to previous exposures are now attached by their Fc base to the Fc receptor of mast cells and basophils.

In the oral cavity, wheat may irritate the tonsils or sinuses.  As wheat enters the gastrointestinal tract, it is digested into gliadin peptide fragments which enter the blood stream.  As the finger like tips of the antibodies (attached to the Fc receptors of mast cells and basophils) recognize and attach the gliadin peptide, the mast cells and basophils release histamine.  Histamine binds H1 receptors on blood vessel walls causing migration of immune cells into tissue (Reiner PB, 1994). This immune response consisting of B cells, T cells, macrophages, basophils initiates inflammation. Inflammation is generally cleared by the lymph system. While it may be difficult to visualize internal inflammation, external signs/symptoms such as coughing, sneezing, runny nose, swollen tonsils, watery eyes, and clogged sinuses may be noticeable.

An immune response happens rapidly.  The more time the body is given to generate inflammation, typically the greater the response.  An antihistamine such as Benadryl (diphenhydramine hydrochloride) blocks the histamine H1 receptor and the migration of immune cells into tissue, diminishing the response (Yamashiro K, 2001).

Aspirin Discussion:

While an antihistamine may suppress inflammation,  a second problem with wheat ingestion is the gliadin peptide circulating in blood vessels available for  attachment to collagen fibers.

The gliadin peptide is a component of the wheat plant’s defense system.  The wheat plant has two coded regions called wheat germ agglutinin lectins. These lectins, which are more prevalent in the stem and spike of wheat, enable the plant to fend off disease (Xiang Y, 2011). Once inside the body, wheat defense lectins can attack human tissues.  Wheat germ agglutinin is commonly used in research to identify penetrance because it attaches to many human cell types. Potatoes have two defense lectins (Allen AK, 1996) while rice and sweet potatoes each have one (Xiang Y, 2011).  Thus, a diet of rice or sweet potatoes is more compatible to the human immune system.

Wheat plant lectins have a complex three dimensional structure which is stabilized by disulfide bonds (Nizheradze KA, 2000).  These bonds attach carbohydrate surface structures on collagen fibers which are found in joints, cartilage, organs, tissues, and ducts. The strength and flexibility of collagen, for example, provides for fluid movement in a joint, the lattice support structure in pulmonary tissue, and the passage of nutrients in a liver duct.  The binding of lectins on collagen changes the alignment, density, and uniformity of the fiber network (Nizheradze KA, 2000).

Imagine thin collagen fibers, like a cotton ball, stretched out as a wispy cloud. Collagen function is altered when small amounts of lectin are glued throughout. Collagen plus lectin “glue” causes rheumatoid arthritis in a joint, asthma in lung tissue, and primary biliary cirrhosis in the liver.  Perhaps, instead of these conditions being “disease”, they are analogous to grease in the plumbing.

To eliminate this wheat lectin from the body, we look to the manufacturing industry, where wheat gluten is used to produce biodegradable plastics.  To lengthen the temperature window for the hardening of these plastic products, aspirin (salicyclic acid) can be utilized. Salicylic acid reduces the viscosity of wheat gluten by delaying the formation of the disulfide bonds such that the aggregation and cross-linking rate of the hardening plastic is slower (Ullstein H, 2011).  It has also been found that on collagen fibers in human cell culture, the binding of wheat germ agglutinin is significantly decreased by chemicals such as salicylic acid (Nizheraze KA, 2000).

The scientific investigate community is cognizant of aspirin’s anti-platelet aggregation properties, however, these scientists may not have realized that it also weakens wheat gluten-antigen-collagen bondsGiven aspirins widespread use, this recent finding has been inadvertently discovered. Dr. James Watson (Watson and Crick, Nobel Prize 1964, DNA double helix) on Reach MD,  tells us to return to biochemistry to thwart disease.  Indeed, the discovery of this interconnection provides a practical basis to confirm the accuracy of man’s research.


Allen AK, Bolwell GP, Brown DS, Sidebottom C, Slabas AR, “Potato lectin: a three-domain glycoprotein with novel hydroxyproline-containing sequences and sequence similarities to wheat-germ agglutinin”.  Int J Biochem Cell Biol. 1996 Nov;28(11):1285-91

Di Domenico F, Owen JB, Sultana R, Sowell RA, Perluigi M, Cini C, Cai J, Pierce WM, Butterfield DA,  “The wheat germ agglutinin-fractionated proteome of subjects with Alzheimer’s disease and mild cognitive impairment hippocampus and inferior parietal lobule: Implications for disease pathogenesis and progression”.  J Neurosci Res. 2010 Dec;88(16):3566-77. doi: 10.1002/jnr.22528. Epub 2010 Oct 8.

Nizheradze KA, “Binding of wheat germ agglutinin to extracellular network produced by cultured human fibroblasts”. Folia Histochem Cytobiol. 2000;38(4):167-73  PMID 11185721

Reiner PB, Kamondi A, “Mechanisms of antihistamine-induced sedation in the human brain: H1 receptor activation reduces a background leakage potassium current”. Neuroscience 59 (3): 579–88. DOI:10.1016/0306-4522(94)90178-3. PMID 8008209, April 2004

Ullsten HN, Sung-Woo C, Spencer G, Gallstedt M, Johansson E, Hedenqvist M, “Properties of Extruded Vital Wheat Gluten Sheets with Sodium Hydroxide and Salicyclic Acid”.  Biomacromolecules 2009, 10, 479-488

Xiang Y, Song M, Wei Z, Tong J, Zhang L, Xiao L, Ma Z, Wang Y, “A jacalin-related lectin-like gene in wheat is a component of the plant defense system”. J Exp Bot. 2011 Nov;62(15):5471-83. Epub 2011 Aug 23

Yamashiro, K; Kiryu, J; Tsujikawa, A; Nonaka, A; Honjo, M; Tanihara, H; Nishiwaki, H; Honda, Y et al. (2001). “Suppressive effects of histamine H1 receptor antagonist diphenhydramine on the leukocyte infiltration during endotoxin-induced uveitis”. Experimental eye research 73 (1): 69–80. DOI:10.1006/exer.2001.1008. PMID 11428864.

Copyright © 2012.  All Rights Reserved.

July 10, 2012

Disclaimer:  The ERB is a literature research team presenting the findings of other researchers. The ERB is not licensed medical nor dietary clinicians and will not give medical nor dietary advice.   Any information presented on this website should not be substituted for the advice of a licensed physician or nutritionist.  Users of this website accept the sole responsibility to conduct their own due diligence on topics presented and to consult licensed medical professionals to review their material.  We make no warranties or representations on the information presented and should users utilize this research without consulting a professional, they assume all responsibility for their actions and the consequences.

Keep the Tonsils, Pull the Strep Throat!

Tonsillitis Gluten Allergy Case Study  of a three year-old boy:  As an infant this subject had experienced recurrent ear infections and was prophylactically placed on low dose amoxicillin.  As a two and three year old, this subject would present with tonsillitis bi-monthly.  His submandibular lymph nodes were swollen bilaterally, palantine tonsils were bright red with a whitish exudate, there was difficulty swallowing, malaise, and no fever.  All tonsil infections presented with similar signs/symptoms,  some tested positive for Group A Streptococcus. Amoxicillin was no longer effective. To alleviate recurrent infections, subject was treated with various antibiotics.   Tonsillectomy was discussed.  This patient began a wheat gluten free diet (WGFD). After initiating a wheat gluten free diet, this subject was tonsillitis free …unless he ingested wheat.  Most ingestion was immediately treated with antihistamines every 4-6 hours for the next 24 hours or until sore throat resolved.  Untreated ingestion resulted in tonsillitis and required a 5 day course of azithromax to resolve symptoms. This patient continued on a wheat gluten free diet.  

Tonsillitis Discussion: We often hear about the circulatory system with the heart at its center supplying blood with nutrients to cells.  As the cells burn this food and oxygen, they create waste products which they either dissolve or excrete through their cell walls. It’s the function of the lymphatic system to provide small vessels to remove these waste products and filter them through lymph nodes ultimately returning this fluid to the heart.  This is why when a surgeon checks for cancer, he checks the affected tissue but also the lymph nodes draining that tissue.

Lymph vessels and tissue are present throughout the body.  Because food is ingested through the gastrointestinal (GI) tract and can be a major source of foreign bacteria, etc. the GI tract contains a major portion of the lymphatic tissue.  As food is brought into the mouth, the lymph tissue of the tonsils and adenoids are immediately present to defend the body against pathogens.  These tonsilar lymph tissues filter the harmful bacteria and viruses to keep them from entering the body and carry away the waste filtrate that is produced. Thus, the high level of importance for fluid in our bodies. Within the lymph system are immune system cells called lymphocytes.  These cells travel in the lymph filtrate and are present in tonsil tissue. When pathogens present in food or from the fingers, these lymphocytes respond.  They call other immune cells to the location, burn fuel and secrete waste products, which generates dead cells and inflammation within the tonsil tissue.  The tonsil becomes inflamed, red, swollen, and painful.  Fluids bring relief to the tonsil tissue as they aid in washing away some of the congested filtrate.

When wheat gluten presents to the tonsil tissue it is recognized by the immune system as a pathogen and is attacked by lymphocytes which generate an immune response, inflaming the tonsil tissue. For years, now we have “solved” the tonsillitis symptom by surgically removing the tonsils.  Unfortunately, we have also removed important tissues that are an important line of defense to kill pathogens before they enter the GI tract.  Removing the tonsilar policemen at the gate is merely passing the immune system defense job of the tonsils further down the GI tract,  placing additional stress on the esophagus, stomach, and small/large intestine, and colon lymph tissue.

An important microbiology concept that is helpful to understand is that good and bad bacteria are most always present on our bodies,  as good and bad people are always present within a population.  The balance of good to bad is critical. Our police and parole departments keep crime in check under normal circumstances, but when 50,000 prisoners are released, they are overwhelmed.  The same is true for probiotics and good bacteria keeping disease under control. Streptococcus pneumoniae bacteria are most always present as normal flora on the body, but they are under control.  When wheat gluten causes an overwhelming immune response with immune complex formation and inflammation,  S. pneumoniae may be more likely to cause disease.

Copyright © 2012.  All rights reserved.

Photograph: Beautiful horses, Caymus, Utah

Disclaimer:  The ERB is a literature research team presenting the findings of other researchers. The ERB is not licensed medical nor dietary clinicians and will not give medical nor dietary advice.   Any information presented on this website should not be substituted for the advice of a licensed physician or nutritionist.  Users of this website accept the sole responsibility to conduct their own due diligence on topics presented and to consult licensed medical professionals to review their material.  We make no warranties or representations on the information presented and should users utilize this research without consulting a professional, they assume all responsibility for their actions and the consequences.

Gluten Free USTA Tennis Player Aces Sinus Infections!

Sinusitis Case Study:   A female USTA Tennis Player in her thirties, who enjoys playing doubles,  presented with a history of recurrent sinus and tonsil infections.  The subject’s  sinusitis frequently required multiple antibiotic doses to clear and some infections appeared unresponsive to therapy.   This subject experienced annual colds requiring antibiotic therapy.  She also experienced heartburn (gastro esophageal reflux disease (GERD)) which was treated with over the counter medications.  This tennis player began a wheat gluten free diet.

Fourteen years post wheat free diet initiation, this subject has experienced no sinus infections nor incidents of heartburn.   She  has experienced an occasional cold requiring the use of amoxicillin.  Upon exposure to wheat, rye, oats, or vegetation she has used over the counter anti-histamine therapy to prevent inflammation of her tonsils.  She avoids potatoes as they cause sinus congestion.  With continued avoidance of wheat products, her immune response to ingested wheat has become more pronounced.  During the past decade, wheat ingestion every two weeks would require antihistamines prior to and post ingestion to avoid inflammation of her tonsils and sinuses.  She continues on a wheat free diet with no sinus or tonsil  infections.

Sinusitis Discussion:

Normal respiratory epithelium contains cells resembling columns.  Many of these cells have brush-like hairs on their borders which are called cilia.  Goblet cells which secrete mucous are also present but they are rare.    Both the cilia and mucous help to move particles through respiratory structures.

In a pathologic disease process,  the structure of this respiratory epithelium changes.   When exposed to wheat germ agglutinin (WGA),  respiratory epithelial cells with sparce quantities of goblet cells are found to change into epithelium with heavy quantities of goblet cells secreting acid mucin.  These are the front line immune response defenders. It is theorized that the increase in mucous secretions could be a host defense mechanism meant to make bacterial adherence to tissue more difficult. Additional sialic and fucose residues are produced to immunologically conceal the mannose sugar and carbohydrate moieties from the  wheat germ, presumably disallowing attachment to the tissue.   The number of ciliated cells is reduced and the quantity of normal good bacterial flora present in the sinuses is decreasedThe resultant disease etiology is sinusitis and allergic rhinitis. 

Rhinitis and nasal allergies are frequently associated with Celiac Disease(CD). In a wheat challenge test of 23 bakers with a history of wheat flour induced ocular hypersensitivities, 17 subjects had symptoms of rhinitis within 10-30 minutes of wheat flour exposure (Wittczak, et al., Otori, et al. 1998).

Kaneko, et al. (2000) demonstrated that the use of wheat germ agglutinin showed that this lectin “strongly reacts with cilia and goblet cells”.  In a study of 258 baker’s apprentices, 54 developed IgE antibodies against wheat, rye and/or barley. The IgE antibodies developed in response to typical grass and pollen type allergies were found to correlate well with flour sensitization.  Radiographs were performed from these subjects and showed “mucosal thickening, opacity, air/fluid levels, and/or polypous shadowing” of the paranasal sinuses (Popp, et al. 1994).

Sinusitis References:

Wittczak,  “Challenge testing in diagonsis of occupational allergic conjunctivitis”  Occp Med 2007:57:532-534  DOI: 10.1093/occmed/kqm049

Otori N., Carlsoo  B., Stierna P.,  “Changes in Glycoconjugate Expression of the Sinus Mucosa during Experimental Sinusitis: A Lectin Histochemical Study of the Epithelium and Goblet Cell Development”, Acta Otolaryngol (Stockh) 1998; 118: 248-256

Popp W., Wagner C, Kiss D, Zwick, H, Sertl K, “Prediction of sensitization to flour allergens”, Allergy 1994; May; 49(5):376-9

Copyright © 2012.  All rights reserved.

Photograph: Pacific Coast Highway 1  Cambria, California 

Disclaimer:  The ERB is a literature research team presenting the findings of other researchers. The ERB is not licensed medical nor dietary clinicians and will not give medical nor dietary advice.   Any information presented on this website should not be substituted for the advice of a licensed physician or nutritionist.  Users of this website accept the sole responsibility to conduct their own due diligence on topics presented and to consult licensed medical professionals to review their material.  We make no warranties or representations on the information presented and should users utilize this research without consulting a professional, they assume all responsibility for their actions and the consequences.


Kick Wheat and Asthma Rides Off the Back

Mountain Bicyclist Asthma Case:  A male in his forties, a former NORBA sectionals downhill mountain biking champion,  experienced a 40 year history of asthma upon exposure to grass, yard trimmings, or pets. Childhood allergy patch testing showed allergies to most all allergens.  His typical medical routine prior to and following allergen exposure included use of antihistamines, corticosteroids,  and the use of a nebulizer.  This patient experienced a 10 year history of gastro-esophageal reflux disease (GERD).  Treatment included use of  proton pump inhibitors and histamine H2 receptor antagonists.  The acid had inflammed the esophageal stricture, the opening between his esophagus and stomach.  To allow for the passage of food, his gastroenterologist had balloon dilated his esophagus and recommended dilation every six months.   This athlete frequently experienced gastrointestinal (GI) upsets with diarrhea and vomiting. In 1998, his physician diagnosed him with pneumonia and treated him with antibiotics.  To alleviate the long-term asthma, esophagitis and GERD the patient began a wheat gluten free diet (WGFD).

Thirteen years post  WGFD initiation this cyclist no longer has asthma nor requires asthma therapy.  Anti-histamines are occasionally required upon exposure to wheat, grass or pets. He utilizes Citrus sinesis (orange peel extract containing 98.5% d_limonene, 1000mg) or fresh kumquat to reduce stomach acid. He sleeps on a wedge pillow elevating his chest and head to protect his esophagus from stomach acid.  Esophageal balloon dilation was not required at six month intervals for the next ten years.  Then the procedure was repeated.  Patient has contracted no further cases of pneumonia.  He experiences typical cold/flu illnesses less than once each year.  Antibiotics are rarely required and amoxicillin is effective.  Patient maintains GI bacterial balance with acidophilis and lactobacilli probiotics (more discussion on the Gastrointestinal Post on  He continues on a WGFD with no ingestion of wheat gluten.

Asthma Discussion:

In the food industry, cross pollinations are utilized to produce high quality wheat (Kuchel et al. 2006).  Gluten protein forms a proteinaceous matrix and a viscous elastic network. Three loci (Glu-A1, Glu-B1, Glu-D1)  present on the long arm of group 1 wheat chromosomes code for wheat gluten (WG), which determines the functional properties of wheat flour including elasticity and shelf life.  (Mondal et al. 2008)  Genetic engineering can be utilized to manipulate these subunits to produce a hearty wheat gluten with strong elastic properties which help bread rise and make it soft and chewy.

In manufacturing, the elastic and tensile properties of wheat gluten are utilized as a matrix material for plastic injection molding.  The resultant glue-like product is a strong oxygen barrier and produces films which are cytotoxic and  restrictive to cell growth (Cho et al. 2011) (Reddy et al. 2010).

Given this genetic modification of wheat, the gastrointestional (GI) system does not digest WG well.  Decomposition occurs by an enzyme called a tissue transaminase which produces a gliadin peptide product.  This peptide has a lectin, a powerful agglutinin, which causes inflammatory complexes to be formed within the body. Gliadin is a potent stimulator of the immune system, stimulating T lymphocytes which activate both B lymphocytes and secrete harmful chemicals known as cytokines.   The B lymphocytes produce the allergy Ig E antibodies which bind gliadin, form gliadin-antibody complexes, and are found crosslinked on collagen sites.   The T lymphocyte activated cytokines destroy collagen and activate phagocytes.  Thus, the effect of wheat gluten is in initiating a comprehensive immune cascade which damages collagen both physically through immune complex formation and chemically through cytokine secretion and phagocytic actions.

As gliadin-antibody complexes travel through the circulatory system they attach to various tissues containing collagen.  Collagen is found in the walls or septum of lung tissue where it supports the oxygen-carbon monoxide exchange sacs called alveoli (Ross & Romrell, 1989).   As immune complexes attach septal collagen and damaging chemicals are secreted, the ability of lung tissue to function properly is impaired.  Breathing difficulties and a decreased oxygen tissue saturation results.

Gliadin specific IgE  antibodies may cause both Baker’s asthma and wheat dependent exercise induced anaphylaxis  (Ueno et al. 2010).  While the most prevalent upper respiratory allergen is recognized as grass and tree pollens,  the cross reactivity of IgE antibodies to wheat flour and grass pollens has been demonstrated (Merget et al. 2011). Given this high cross reactivity and the inhalation of flour dust, there is an increased risk that allergic asthma reactions will occur.   Of 25 subjects with mild asthmas and hay fever, given no previous occupational exposure to flour products, each one of these subjects showed sensitization to flour (Merget et al. 2010).  Beyond occupational exposure, bronchial activity leading to asthma, can be associated with food allergy to wheat (Salvatori et al. 2008)

Sinus mucosa undergoes modification when exposed to wheat gluten antigen (WGA).  Respiratory epithelial cells with low quantities of goblet cells are found to change into epithelium with heavy quantities of acid mucin secreting goblet cells.  These are the front line immune response defenders (Otori et al. 1998)   Sialic and fucose residues are produced to immunologically conceal the mannose sugar and carbohydrate moieties from the  WGA.  The resultant disease etiology is sinusitis and allergic rhinitis.  In a wheat challenge test of 23 bakers with a history of wheat flour induced ocular hypersensitivities, 17 subjects had symptoms of rhinitis within 10-30 minutes of wheat flour exposure. (Wittczak, et al. 2007)

While conjunctivitis and urticaria are more prevalent wheat manifestations, respiratory problems are more disabling.  30% of workers in a flour mill were found to have chronic bronchitis or chronic productive cough.  Chest tightness was an affliction of 22% of the workers, while bronchial asthma developed in 18%.  At the end of a work shift three fifths of the workers had a significant drop in Forced Expiratory Volume(FEV) and Forced Vital Capacity(FVC).  Flour disease etiologies were found to match those of cotton, hemp and flax milling. (Awad el Karim, et al. 1986)

In addition to asthma, our male bicyclist experienced esophageal and GI problems.  Our subject was not tested for Celiac Disease (CD), however, rhinitis and nasal allergies are frequently associated with CD.  Gluten peptide inflammation is shown to induce zonulin release in the GI tract opening tight junctions between intestinal cells.  The activity is inserted in to the lamina propria of the gut.  The immune system responds with CD4+  T helper lymphocytes which are sensitive to gluten and  cause damage in the gut and esophagus. (Lucendo, 2011) The  release of T cell mediated cytokine interferon remodel the gut tissue , flattening the mucosa and causing malabsorption.  This is a cytotoxic attack on the epithelium.  (Nova et al. 2010)  Motility disorders in celiac subjects have been reported to affect the gastric mucosa, small bowel, gallbladder and colon.  GERD can develop in untreated CD which is often associated with esophageal maladies. (Lucendo, 2011)

The cure for this plethora of disease is generally considered to be a  gluten free diet (GFD).  A GFD is associated with the resolution and improvement of intestinal and esophageal symptoms in celiac subjects.  Reflux symptoms are relieved and heartburn, chest or epigastric pain, and regurgitation significantly reduced.   With elimination of gluten, the clinical symptoms are reversed.  (Lucendo, 2011)  With a GFD the CD8+ cytotoxic T lymphocyte counts, TCR antibodies  return to normal and the villi recover.  (Nova et al. 2010)


Awad el Karim MA, Gad el Rab MO, Omer AA,  El Haimi YAA, “Respiratory and Allergic Disorders in Workers Exposed to Grain and Flour Dusts”, Archives of Environmental Health, September-October 1986, Vol. 41 No. 5

Cho SW, Gallstedt M, Johansson E, Hedenqvist MS, “Injection –Molded Nanocomposites and Material based on Wheat Gluten”, Int J Biol Macromol 2011 Jan 1;48(1):146-52. Epub 2010 Oct 28

Kuchel H, Langridge P, Mosionek L, Williams K, Jefferies SP, “The Genetic Control of Milling Yield, Dough Rheology and Baking Quality of Wheat”, Theor Appl Genet, 2006 May;112(8);1487-95. Epub 2006 Mar 21

Lucendo AJ,  “Esophageal Manifestations of Celiac Disease”,  Dis Esophagus 2011 Mar 25. Doi: 10.1111/j.1442-2050.2011.01190.x. [Epub ahead of print]

Merget R, Sander I, van Kampen V, Bechmannn U, Heinze E, Raulf-Heimsoth M, Bruening T, “Allergic Asthma after Flour Inhalation in Subjects without Occupational Exposure to Flours: an Experimental Pilot Study”, Int Arch Occup Environ Health; 2011 Jan 30 [Epub ahead of print]

Mondal S, Tilley M, Alviola JN, Waniska RD, Bean SR, Glover KD, Hays DB, “Use of Near-isogenic Wheat Lines to Determine the Glutenin Composition and Functionality Requirements for Flour Tortillas”, J Agric Food Chem 2008 Jan 9;56(1);179-84. Epub 2007 Dec 12.

Nova E, Pozo T, Sanz, Marcos A, 3rd International Immunonutrition Workshop.  Session 4: Dietary Strategies to Prevent and Mitigate Inflammatory Disease.  Dietary Strategies of Immunomodulation in Infants at Risk for Celiac Disease, Proceedings of the Nutrition Society (2010), 69, 347-353

Otori N, Carlsoo B, Stierna P, “Changes in Glycoconjugate Expression of the Sinus Mucosa during Experimental Sinusitis: A Lectin Histochemical Study of the Epithelium and Goblet Cell Development”, Acta Otolaryngol (Stockh) 1998; 118: 248-256

Reddy N, Jiang Q, Yang Y, “Novel Wheat Protein Film as Substrates for Tissue Engineering”,  J Biomater Sci Polym Ed 2010 Occt 27. [Epub ahead of print]

Ross, Michael H., Romrell, Lynn J., “Histology, A Text and Atlas”, Second Edition, 1989

Salvatori N, Reccardini F, Convento M, Purinan A, Colle R, De Carli S, Garzoni M, Lafiandra D, De Carli M, “Asthma Induced by Inhalation of Flour in Adults with Food Allergy to Wheat”, Clin Exp Allergy, 2008 Aug;38(8):1349-56. Epub 2008 May 28

Ueno M, Adachi A, Fukumoto T, Nishitani N, Fujiwara N, Matsuo H, Kohno K, Morita E, “[Analysis of Causative Allergen of the Patient with Baker’s Asthma and Wheat-Dependent Exercise-Induced Anaphylaxis (WDEIA)]”, Arerugi, 2010 May;59(5):552-7.

Wittczak T, Krakowiak A, Walusiak J, Pas-Wyroslak A, Kowalczyk M, Palczynski C, “Challenge Testing in the Diagnosis of Occupational Allergic Conjunctivitis”, Occupational Medicine 2007;57:532-534

Copyright © 2012.  All rights reserved.

Updated January 20, 2013

Photograph: Traveling on the Pacific Coast Highway 1 south of Hearst Castle.

Disclaimer:  The ERB is a literature research team presenting the findings of other researchers. The ERB is not licensed medical nor dietary clinicians and will not give medical nor dietary advice.   Any information presented on this website should not be substituted for the advice of a licensed physician or nutritionist.  Users of this website accept the sole responsibility to conduct their own due diligence on topics presented and to consult licensed medical professionals to review their material.  We make no warranties or representations on the information presented and should users utilize this research without consulting a professional, they assume all responsibility for their actions and the consequences.