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Avoid Gluten with Elevated Antibodies but No Celiac Disease?
Dr. Tom O'Bryan posted an article in Winter 2008 Issue
Celiac.com 01/09/2021 - Ever stand on a school playground when a very loud siren would go off and feel like it was rattling your brain because it was so loud? If not from the local school ground, perhaps that siren was at the fire station, or other public building in your neighborhood? For the last 40 to 50 years, many of us remember hearing an ‘air raid siren' go off. In our area, it was on the first Tuesday of the month at 1:00PM. Air raid drills were a ‘warning system' to let us know that we had to take cover. From the days of the attack on Pearl Harbor through the dawning of the Nuclear Age, the air raid siren was designed to give us all a chance to ‘take cover' to get ourselves and our families to safety. Well as it turns out, our bodies have a similar early warning system. The National Institutes of Health tells us that Auto-Immune Diseases (the immune system attacking our own body tissue) collectively affect more than 24 million people per year in the U.S.(1) To put this in perspective, Cancer affects nearly 9 million people per year and Cardiovascular Disease affects close to 22 million people. And we know that only about 1/3rd of the people with an Auto-immune Disease are diagnosed.(2) That means about 72 million people are suffering with a self-destruction process (the immune system attacking its own body tissue). That puts Auto-Immune Diseases at the top of the list of the most common diseases in America today. But it's not screened for. To most of us, autoimmune diseases are unknown. Our medical system waits until the signs and symptoms are severe enough with organ failure and irreversible damage before we identify it. It's not screened for, it's looked at as a ‘last-resort' type of diagnosis. In general, autoimmune disorders can be classified as either organ specific or non-organ specific. In organ-specific autoimmune diseases, antibodies are specifically directed against targets localized in a particular organ and are often detected in the blood. Examples of organ-specific autoimmunity include Hashimoto's Thyroiditis (thyroid tissue), Type I Diabetes (pancreas tissue), Multiple Sclerosis (brain and nerve tissue), and Myasthenia Gravis (muscle tissue). In contrast, the non-organ-specific autoimmune disorders are characterized by the presence of antibodies directed against multiple targets (not specific to a particular organ). This results in the involvement of several organs or endocrine glands and is often characterized by the presence of specific circulating antibodies. Non-organ-specific autoimmunity includes diseases such as Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis (RA), and Scleroderma.(9) A growing number of studies have identified that the body makes these antibodies directed against itself—otherwise known as auto-antibodies—years, and sometimes for a decade before a diagnosis is made. The antibodies damage tissue slowly and steadily until finally people begin showing symptoms, and eventually receive a diagnosis. In Systemic Lupus, for example, research shows that the progression of auto-antibodies for Systemic Lupus Erythematosous (S.L.E.) begin to present five years before a diagnosis is typically made. The immune system began an ‘early-warning system' (by producing auto-antibodies), and was starting to say "there's a problem here". At this initial point, the patients did not have symptoms severe enough that warranted seeing their doctor. Unfortunately, in the vast majority of cases, no one is monitoring this early warning system. And so the body has to speak a little louder (more and different antibodies begin being produced)—no one is listening. And then a little louder—no one is listening. This continues for years until the body has to begin screaming. And how does the body scream? Pain. Have you ever stood under the telephone pole on the school playground when that Tuesday 1:00 PM siren went off? It rattles your brain. That's what is happening in the body when there eventually is enough damage that a diagnosis of an autoimmune disease becomes obvious-it can't be ignored. Researchers are telling us that autoimmunity appears to be a warning system that has gone beyond ‘early warning' to ‘take cover'. It takes years from the first identification of antibody presence to the point of ‘clinical onset'—when the symptoms are obvious that something is wrong, and a diagnosis is made. The levels of up to seven different antibodies may continue to rise for five years or more before the diagnosis. If patients were armed with such information, they could start fighting the ailment years before the threshold of damage has been passed and a diagnosis is evident, thereby preventing or delaying symptoms. One just has to look for the evidence. Arguably, the most common auto-immune disease is also the only one where the ‘cure' is known and uncontested. For some, gluten causes an ‘alarm reaction' in the immune system with a ‘call out the troops' type of attack response. (upregulating macrophage pro-inflammatory gene expression and cytokine production).(5,6) When this allergy to gluten (found in wheat, rye, barley and spelt) stimulates the production of auto-antibodies to the intestinal tissue (anti-transglutaminase or anti-endomysium antibodies), Celiac Disease is the diagnosis. And this auto-immune disease is readily put into remission and disappears with a life-long avoidance of gluten in any form.(4) Are there early warning signs of Celiac Disease? Yes, there are. We know that Celiac Disease-associated antibodies can be identified up to 5.2 years before a diagnosis of Celiac Disease can be made. (17) Numerous pain syndromes and auto-immune diseases have been associated with an ‘alarm response' to gluten. From peripheral neuropathies (numbness and tingling in the arms and legs) to crippling migraines and ataxia, from acute myocarditis (inflamed heart) to chronic pancreatitis, from vitiligo (loss of pigment-white spots-in the skin) to Primary Biliary Cirrhosis (Gall Bladder problems), from Multiple Sclerosis to Rheumatoid Arthritis, from Attention Deficit Hyperactivity Disorder (ADHD) to Epilepsy, in sensitive individuals, gluten may initiate this auto-immune response.(5,14) So which organ is vulnerable to this auto-immune attack, this calling out of the troops? The target tissue seems to be determined by one's genetics (the blueprint you were born with) and all of the mitigating factors (accumulated exposures we've had in our lives such as toxic chemical accumulation, repeated use of antibiotics or other drugs contributing to intestinal permeability, heavy metal toxicity, excess stress hormone production, poor food choices…).(7) This response may affect tissue throughout the body and has been identified with brain and peripheral tissue(8), liver epithelial cells, pancreatic beta-cells(8), thyroid tissue (9), bone cells(10), skin tissue(11), skeletal muscle(12), myocardium(13), and the brain and nervous system. And it does not require the production of auto-antibodies to the intestines-that is, gluten intolerance can occur and be associated with other autoimmune diseases without the diagnosis of Celiac Disease (14). As an example, 57% of patients with neurological dysfunction of unknown cause have elevated antibodies to gliadin (a protein in wheat). Only 35% of this group also have evidence of intestinal damage (Celiac Disease). The remaining 65% have gluten sensitivity and elevated antibodies to the brain (cerebellum) or the nerves in the arms and legs, a situation analogous to that of the skin in Dermatitis Herpetiformis.(14) It appears that wheat can directly stimulate an auto-immune attack on the brain and nervous system in sensitive individuals without the diagnosis of Celiac Disease. Elevated antibodies to gliadin and gluten (the protein in wheat) are the immune systems way of saying "this food is not good for me". Many researchers take the position that if there are elevated antibodies to wheat, but there is no evidence of Celiac Disease, there is no evidence of value to avoiding wheat. This position is historic and is in the process of changing. The idea that until the sirens are screaming, it's ok to eat wheat, even if the immune system is saying "this is not good for me", is a position that more and more doctors are realizing is causing unnecessary suffering. Many doctors and health care practitioners believe that even in the absence of indicators of outright Celiac Disease-that is with normal transglutaminase or endomysial antibodies, or a normal biopsy, we are best served by heeding the message our body is giving us, and avoiding these foods. The concern is that if we ignore the actions of our immune system (elevated antibodies to wheat), the auto-immune process of the body (attacking its own tissue), may years down the road leave us standing under that telephone pole with the siren going off rattling our brains, or thyroid, or pancreas, or heart… Dr. Thomas O'Bryan is a graduate of the University of Michigan and the National College of Chiropractic. He is a Diplomate of the National Board of Chiropractic Examiners, a Diplomate of the Clinical Nutrition Board of the American Chiropractic Association, and a Certified Clinical Nutritionist with the International and American Association of Clinical Nutritionists. He is a Certified Applied Kinesiologist. He is a Certified Practitioner in Functional Biomechanics from the Motion Palpation Institute. He is a member of the Institute of Functional Medicine, the International and American Association of Clinical Nutritionists, the American Chiropractic Association, the International Academy of Preventive Medicine and numerous other professional organizations. References: 1. National Institutes of Health. Autoimmune Diseases Coordinating Committee. Autoimmune Diseases Research Plan. Accessed 1/18/07. 2. Bland, J, Understanding The Origins and Applying Advanced Nutritional Strategies For Autoimmune Diseases. March 2006. 3. Notkins, A, Predictors of Disease, Scientific American, March 2007, 72-78. 4. Murray, J, The Widening Spectrum of Celiac Disease. Am J Clin Nutr 1999;69:354–65. 5. Betterle C., Update on autoimmune polyendocrine syndromes (APS), ACTA BIOMEDICA 2003; 74;9-33. 6. Zanoni,G, In Celiac Disease, a Subset of Antibodies against Transglutaminase Binds Toll-Like Receptor 4 and induces Activation of Monocytes, PLoS Med. 2006 Sep;3(9):e358. 7. Kumar,V,Celiac Disease-Associated Autoimmune Endocrinopathies, Clinical and Diagnostic Labortory Immunology,July 2001, p. 678–685. 8. Alaedini,A, Immune Cross-Reactivity in Celiac Disease: Anti-Gliadin Antibodies bind to Neuronal Synapsin 1,J Immunology,2007,178:6590-6595. 9. Freeman HJ. Hepatobiliary and pancreatic disorders in celiac disease. World J Gastroenterol 2006; 12(10): 1503-1508. 10. Moreno, M,The IL-1 gene family and bone involvement in celiac disease, Immunogenetics (2005) 57: 618–620 . 11. Abenavoli L, Cutaneous manifestations in celiac disease. World J Gastroenterol 2006;12(6): 843-852. 12. Kozanoglu, E, Proximal myopathy as an unusual presenting feature of celiac disease, Clin Rheumatol (2005) 24: 76–78. 13. Frustaci,A, Celiac Disease Associated with Autoimmune myocarditis, Circulation, 2002;105:2611-2618. 14. Hadjivassiliou, M, Gluten Sensitivity as a Neurological Illness. J Neurol Neurosurg Psychiatry, 2002;72:560-563. 15. Sategna-Guidetti C., Prevalence of Thyroid Disorders in Untreated Adult Celiac Disease Patients and Effect of Gluten Withdrawal: An Italian Multicenter Study, AJG—Vol. 96, No. 3, 2001. 16. Oderta G., Thyroid Autoimmunity in Childhood Coeliac Disease, . J Paediatr Gastroenterol Nutr, 2002 Nov;35(5):704-5. 17. Salmi,T., Immunoglobulin A autoantibodies against transglutaminase 2 in the small intestinal mucosa predict forthcoming coeliac disease Aliment Pharmacol Ther 24, 541–552- 3 comments
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Celiac.com 06/08/2010 - Paul Seelig of Durham, owner of Great Specialty Products; a bread company that claimed to manufacture gluten-free bread which actually contained gluten and made many people sick, is now facing additional indictments for false murder implications. Selling, 48, is facing nine felony fraud charges for selling gluten contaminated bread which he claimed was gluten-free. People began complaining about Seelig's bread products after getting sick from them, which led state state officials to close Seelig's business in January, and arrest Seelig on criminal charges in February. In March, State School Board member Kathy Taft was raped and left for dead. She later died, and almost two months after that Jason K. Williford was charged with Kathy Taft's rape and murder. Prosecutors said that Seelig volunteered information about Taft's killer to barter for reducing or dismissing his felony charges. Seelig implicated a former co-worker who was entirely innocent, and had no connection to Taft's murder. On Monday, Seelig was expected to plead guilty to his felony charges and accept a plea deal, but he refused. Instead, Wake Superior Court Judge Donald Stephens arraigned Seelig on felony charges, is seeking additional indictments against Seelig for false murder accusations, and at the prosecutors request raised Seelig's bond to 750,000. Sources: NewsObserver.com News-Record.com
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Celiac.com 08/21/2017 - Can a tiny Virginia start-up change the world with a cheap, reliable devise to test food for gluten on the fly? With their startup called Altede, Ed and Anna Champion, together with business partner Briana Petruzzi, hope to build quick, cheap tests for all sorts of food allergens. Their first target is gluten. Altede is looking to develop a test that is reliable, sensitive to FDA levels of 20ppm gluten, costs less than $5 and could be performed within a couple of minutes while sitting at a restaurant table. The Altede team doesn't expect anyone to test everything they eat. But those with severe gluten intolerance might find peace of mind in a pinch. "We really want to keep the cost low. We think that's going to be critical," says Ed Champion. "You know, $15 and you're not going to do it. It's going to be too painful. But $3 or $5…what's your afternoon worth?" Altede has developed an antibody that they grow inside of and later extract from mice, a technique also used by pregnancy test manufacturers. The antibody is specially engineered to latch onto protein molecules inside gluten. A user like Anna Champion would carry the kit, which is about the size of a pack of M&M's. When she comes across a food she wants to eat but suspects may make her sick, she puts a pea-sized sample into a liquid container that comes inside the pouch. She would shake it up and then dip the test strip. The liquid would creep along the paper, passing a stripe of the antibodies Altede designed. If gluten is present, the antibodies will latch on to the proteins, accumulate on the paper and produce a visible pink line. So far, their prototype device can detect small amounts of gluten. The prototype looks and operates just like a pregnancy test. But the test currently takes hours, instead of minutes. Ed Champion says that tweaks to the chemistry will provide quicker results, though there are still a number of technical challenges to overcome. But after two years of development, Champion says the team is getting close. To help the, prepare their portable gluten tester for a product launch, Altede recently enrolled in the first cohort of RAMP, Roanoke's business accelerator, and received a $50,000 grant from the state's Commonwealth Research Commercialization Fund. Once the company can quickly and reliably test for gluten, it will use the same technology to build tests for a number of different food allergens. Champion has invested more than $30,000 in the venture to date. He supplies the business knowledge for the company, while Anna Champion, a Virginia Tech researcher, and Petruzzi, a Ph.D. student, are the scientific brains behind the operation. Stay tuned for updates on Altede and their efforts to build a better gluten test.
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Celiac.com 08/03/2017 - Some evidence indicates that feeding in the first months of life might have an impact on the risk of later celiac disease. Numerous patients with celiac disease or type 1 diabetes show high levels of antibodies against cow milk proteins. For infants with genetic susceptibility for type 1 diabetes, avoiding of cow’s milk-based formula can lower the levels of diabetes-associated autoantibodies. Could the same be true for celiac disease? To find out if weaning to an extensively hydrolyzed formula lowered the risk of celiac disease of celiac disease autoimmunity, a research team performed a randomized controlled trial. The research team included Mila Hyytinen, Erkki Savilahti, Suvi M. Virtanen, Taina Härkönen, Jorma Ilonen, Kristiina Luopajärvi, Raivo Uibo, Outi Vaarala, Hans K. Åkerblom, and Mikael Knip for the Finnish TRIGR Pilot Study Group. For their double-blind controlled trial, they enrolled 230 infants with HLA-defined predisposition to type 1 diabetes and at least 1 family member with type 1 diabetes. The infants were randomly assigned to groups, with 113 fed a casein hydrolysate formula, and 117 receiving a conventional formula whenever breastmilk was not available during the first 6–8 months of life. The team collected serum samples over an average of 10 years, and screened for antibodies to tissue transglutaminase (anti-TG2A) using a radiobinding assay, to endomysium using an immunofluorescence assay, and antibodies to a deamidated gliadine peptide using an immunofluorometry assay. In patients with anti-TG2A levels over 20 relative units, the team conducted duodenal biopsy. They measured cow’s milk antibodies during the first 2 years of life. Their results showed that about 13% of the 189 participants they analyzed for antiTG2A 25 tested positive. Just ten of the 230 study participants were diagnosed with celiac disease. The team found no significant differences in total cases of anti-TG2A positivity (hazard ratio, 1.14; 95 % CI, 0.51–2.54) or celiac disease (hazard ratio, 4.13; 95% CI, 0.81–21.02) between the casein hydrolysate and cow's milk group. Interestingly, children who developed celiac disease did show higher levels of cow's milk antibodies before the appearance of anti-TG2A or celiac disease. This study of infants with genetic risk factors for celiac disease showed evidence that weaning to a diet of extensively hydrolyzed formula compared with cow’s milk-based formula would lower the risk for celiac disease later in life. Elevated levels of cow's milk antibody before anti-TG2A and celiac disease indicates that many people may experience increased intestinal permeability before they develop celiac disease. Source: GASTROENTEROLOGY
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Celiac.com 06/05/2015 - For anyone with celiac disease, following a lifelong gluten-free diet has been shown to relieve symptoms, and in celiac patients it has been shown to normalize serologic markers of celiac disease, and to restore damaged intestinal villi. Not following a gluten-free diet, on the other hand, can result in serious complications associated with malabsorption. When celiac disease goes untreated, when people who have celiac disease refuse to follow a gluten-free diet, chronic gluten-related inflammation and damage impairs absorption of nutrients, and likely causes malabsorption of oral medications. Malabsorption resulting from damaged mucosa can lead to: Nutritional deficiencies of the fat-soluble vitamins A, D, E, and K, as well as the B vitamins, thereby diminishing the absorption of iron, calcium, and folic acid. Nutritional deficiencies can lead to: Iron-deficiency anemia refractory to oral iron supplementation, and potentially osteoporosis and osteopenia due to bone loss due to decreased calcium and vitamin D absorption. A combination of nutritional deficiencies and the damaging effects of systemwide chronic inflammation can cause: Reproductive abnormalities, such as delayed puberty, secondary amenorrhea, infertility, or decreased fertility. Adverse immune responses to gluten ingestion can trigger other common manifestations, such as: Dermatitis herpetiformis, a papulovesicular rash. Beyond that, problems can include: Fractures secondary to low bone mineral density. In some cases, untreated celiac disease can lead to intestinal malignancies such as: Intestinal T-cell lymphomas. Small-bowel adenocarcinoma. Esophageal cancer. B- and T-cell non-Hodgkin lymphomas. Rapid, proper diagnosis and effective treatment of celiac disease are crucial to preventing a cascade of related problems that can further impair diagnosis, and cause irreparable damage to patient health. Source: US Pharmacist. 2014;39(12):44-48.
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Celiac.com 02/11/2014 - More and more people are reporting gastrointestinal symptoms that improve when wheat and/or gluten are removed from the diet. There is a diverse group of people who avoid wheat and/or gluten (PWAWGs), and who predominantly self-diagnose prior to presenting for clinical evaluation for celiac disease. A team of researchers recently set out to compare patients who avoid wheat and/or gluten against patients with celiac disease, and with healthy control subjects. The research team included A. Tavakkoli, S.K. Lewis, C.A. Tennyson, B. Lebwohl, and P.H. Green, all with the Department of Medicine of the Celiac Disease Center at Columbia University in New York, NY. The team set out to characterize PWAWGs who were receiving treatment at a tertiary care referral center and to compare them to patients with celiac disease, and with subjects from the National Health and Nutrition examination survey (NHANES). The team conducted a cross-sectional study to evaluate patients seen by four gastroenterologists at a celiac disease referral center. They compared baseline characteristics, laboratory values, and medical comorbidities for these patients against results for celiac disease patients who presented at the same center, as well as for subjects enrolled in NHANES. The team compared results for eighty-four PWAWGs against results for 585 celiac disease patients and 2,686 NHANES patients. The found that doctors made a total of thirty-two alternative diagnoses in 25 PWAWGs (30%). Diagnoses included small intestinal bacterial overgrowth and fructose/lactose intolerance. When compared to patients with celiac patients, PWAWGs had similar body mass index (BMI, 23.1 vs. 23.5, p = 0.54) and mean hemoglobin value (13.4 vs. 13.3, p = 0.6). When compared to male and female patients in NHANES, PWAWGS showed lower BMI, folate, and mean hemoglobin values, while both male and female PWAWGs had a lower prevalence of hypertension. While there are similarities between celiac disease patients and PWAWGs that could arise from shared HLA haplotypes or result from the gluten-free diet, alternative diagnoses are common in these patients. PWAWGs have a similar cardiovascular profile as celiac disease patients in terms of lower BMI and lower prevalence of hypertension. Source: Dig Dis Sci. 2013 Dec 28.
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Below is Ron Hoggan's reply the editor of the Montreal Gazette regarding the article: "Is gluten really something that most people should avoid?" Dear Health Editor: Mr. Dunning represents corn as a choice for bread-making prior to the advent of wheat, rye, and barley cultivation. However, the evidence suggests that corn was not yet available 10 to 15 thousand years ago when wheat, the earliest of these three grains, was first cultivated so it wasn’t available more than 20 thousand years ago when wild barley was first exploited ( 1 ). The evidence also indicates that corn was not available in the Near East, where wheat was first cultivated, as corn was a New World food developed by Mesoamerican indigenous peoples ( 2 ) half a world away. In short, corn was not a discarded option for bread making when and where gluten grains were first cultivated. Perhaps Mr. Dunning should be forgiven such a relatively minor mistake. After all, he is a journalist, not a cereal scientist. However, as he is identified, in the article in question, as a science writer and a critical analyst, that should set the bar a little higher. Surely we may expect him to conduct basic research in an area by at least glancing at some of the peer reviewed reports on this topic. The one time he does this, he harkens to a report on autism as a tool for arguing against the connection between ADHD and gluten*. For instance, he decries the adoption of a gluten free diet by those without celiac disease, gluten induced neuropathy, or wheat allergy. Yet more than 90% of those with celiac disease currently go undiagnosed in the USA (3) and the average delay between onset of symptoms and diagnosis is 11 years (4). Here in Canada, we have very long delays before most of us can get to see a gastroenterologist, so our delays to diagnosis may be even longer. This suggests that our rates of diagnosis are even lower than those of the USA. Perhaps Mr. Dunning’s querulous rhetoric could be more constructively directed at these long delays and the alarming rates of under-diagnosis of celiac disease. In the interim, it seems very sensible for those with undiagnosed celiac disease to follow a gluten free diet and experience the improved health and quality of life which Mr. Dunning admits are available to these individuals through a gluten free diet. This is an issue that might be revisited when our health care system is providing a timely diagnosis to at least a majority of cases of celiac disease. Recent research has also shown that those with non-celiac gluten sensitivity, which afflicts about 12% of the general population ( 5), experience even higher rates of morbidity and early mortality than those with celiac disease (6 ). Yet this group is either entirely ignored in Mr. Dunning’s article, or, more likely, it is the unstated focus of his attack. Mr. Dunning also seems to be unaware that humans lack the full compliment of enzymes necessary for full digestion of gluten proteins thus making many of the constituent amino acids beyond our ability to metabolize when he states that gluten is “a protein that your body uses.” He further asserts that there is no good reason to avoid gluten if one does not have one of the three conditions he lists. Yet my own work suggests that the morphine-like opioids derived from gluten grains may be a contributing factor in several types of malignancy ( 7). I was pleased to read that Mr. Dunning had at least glanced at data on gluten sensitive idiopathic neuropathy, but chagrined to read his speculation regarding the prevalence of this condition. I have devoted many years to the study of gluten’s impact on human health and have yet to read any work suggesting its prevalence. Perhaps Mr. Dunning could at least hint at his source when making such contentious claims. Nonetheless, there is clear evidence that a majority of those who experience gluten sensitive idiopathic neuropathy (5) do so in the presence of non-celiac gluten sensitivity, an autoimmune dynamic. Closer to home, our own Scott Frazer has demonstrated that consumption of gluten proteins is a potent force behind the development of many cases of type 1 diabetes (8). Reports of the causal connection between gluten consumption and autoimmune disease abound in the peer reviewed literature and are too numerous to warrant citing. Mr. Dunning also asserts “there is no evidence that incidence of disease increased worldwide once wheat became a staple.” The field of Archaeology differs dramatically with Mr. Dunning’s claim. In general, it is quite well established that pre-agricultural, hunter-gatherers were much taller and had stronger bones than their descendants who adopted agriculture (9). For instance, a common finding in the skeletal remains of early farmers is a condition of porotic hyperostosis (10). Mr. Dunning also seems to be unaware that fats, per gram, provide more than twice the energy available in either carbohydrates or proteins and this ignores the added weight of indigestible fibre. The increased caloric density of fats is a principle that most students learn in high school Biology classes. Yet Mr. Dunning asserts that bread was a source of high energy and light weight. While science requires scepticism and criticism to function, polemic rhetoric based on personal bias generates more heat than light. Mr. Dunning’s report is rife with errors and emotion. Publication of such dogma does little to enhance either the Gazette’s or Mr. Dunning’s credibility. Newspapers are given considerable credence as many readers, myself included, assume that journalists are exercising due diligence in checking their facts prior to publication of these reports. It is only when I read an article such as this one, that is deeply flawed and falls within my area of expertise, that my faith in journalists and the media is undermined. *note: The only report I could find that fits the meagre description provided by Mr. Dunning is one that involved 15 children who were studied over a 12 week period (11). If this is, indeed, the study Mr. Dunning referred to, it hardly provides conclusive evidence of anything beyond the obvious need for more comprehensive study in this area. His use of these data as a springboard for his absolutist claims seems highly questionable, to say the least. Sincerely, Ron Hoggan, Ed. D. Royal Roads University, Continuing Studies co-author: Dangerous Grains ISBN: 978158333-129-3 www.dangerousgrains.com editor: Journal of Gluten Sensitivity www.celiac.com editor/co-author: Cereal Killers http://tiny.cc/s7neg Sources: http://en.wikipedia.org/wiki/Wheat http://en.wikipedia.org/wiki/Maize Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago S, Elitsur Y, Green PH, Guandalini S, Hill ID, Pietzak M, Ventura A, Thorpe M, Kryszak D, Fornaroli F, Wasserman SS, Murray JA, Horvath K. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study. Arch Intern Med. 2003 Feb 10;163(3):286-92 Green PHR, Stavropoulos SN, Panagi SG, Goldstein SL, Mcmahon DJ, Absan H, Neugut AI. Am J Gastroenterol. 2001 Jan;96(1):126-31 Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71. Anderson LA, McMillan SA, Watson RG, Monaghan P, Gavin AT, Fox C, Murray LJ. Malignancy and mortality in a population-based cohort of patients with celiac disease or "gluten sensitivity". World J Gastroenterol. 2007 Jan 7;13(1):146-51. Hoggan R. Considering wheat, rye, and barley proteins as aids to carcinogens. Med Hypotheses. 1997 Sep;49(3):285-8. http://www.ohri.ca/profiles/scott.asp Lutz W. [The carbohydrate theory]. Wien Med Wochenschr. 1994;144(16):387-92. Wright L, Chew F, Porotic Hyperostosis and Paleoepidemiology: A Forensic Perspective on Anemia among the Ancient Maya. Am Anthro. 1998 Dec; 100: 924-939. Elder JH, Shankar M, Shuster J, Theriaque D, Burns S, Sherrill L. The gluten-free, casein-free diet in autism: results of a preliminary double blind clinical trial. J Autism Dev Disord. 2006 Apr;36(3):413-20.
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