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Found 9 results

  1. The following are links to sites have of dermatitis herpetiformis. Some of the photos are biopsies as seen through a microscope, and some are regular photographs of people with dermatitis herpetiformis, some of which are quite graphic. Pictures and an excellent article on dermatitis herpetiformis by Harold T. Pruessner, M.D., University of Texas Medical School at Houston: http://www.aafp.org/afp/980301ap/pruessn.html The University of Iowa: http://hardinmd.lib.uiowa.edu/dermnet/dermatitisherpetiformis.html Dermis.New Web Page: http://www.dermis.net/dermisroot/en/29366/diagnose.htm Medline: https://www.nlm.nih.gov/medlineplus/ency/article/001480.htm The Dermatitis Herpetiformis Online Community: http://www.dermatitisherpetiformis.org.uk/
  2. 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.
  3. Celiac.com 01/05/2012 - I was disappointed to read this opinion article in The Atlantic (titled: A Gluten-Free Diet Reality Check) when there are three U.S. studies demonstrating that about half of overweight and obese children and/or adults with newly diagnosed celiac disease lose weight following institution of a gluten free diet (GFD) (2,3,4). Some of these researchers make statements such as “The GFD has a beneficial effect upon the BMI [body mass index] of overweight children with celiac disease” after following 27 children who, at diagnosis, were overweight or obese (2). Similarly, Cheng et al reported that “A GFD had a beneficial impact on BMI, underweight patients gained weight and overweight/obese patients lost weight” (3). Murray et al report that only 30% of their obese patients with celiac lost weight after six months of following a gluten free diet (4). There isn’t much ambiguity in any of these three studies conducted by three separate groups of reputable medical scientists and published in the peer reviewed medical and scientific literature. Clearly, the gluten free diet is an effective weight loss tool for some of the individuals investigated. Yet Fontenot asserts that “there is no evidence that gluten-free foods promote weight loss….” (1). Exactly what evidence does she want? She goes on to say that “The only condition that necessitates a gluten free diet is celiac disease” (1). Yet she previously states, when discussing several other conditions that have been connected with gluten that “the research shows mixed results” (1). Surely the “mixed results” suggests that there is evidence that at least some cases benefit from a gluten free diet. Neither does the notion of ‘necessity’ apply to celiac disease. A person with celiac disase can consume gluten. They may place their health at risk by so doing, but that applies equally to those individuals with other conditions that have been shown to benefit from a gluten free diet. So the distinction she makes is, at best, one of degree. For decades many highly regarded investigators have published test results clearly showing that a gluten free diet is beneficial in the conditions listed by Ms. Fontenot, as well as many other ailments. These range from autism (5,6,7) to schizophrenia (8,9,10,11) to a variety of neurological (12,13,14) conditions to attention deficit disorder (15,16), to many other forms of autoimmunity (17,18,19), learning disabilities (20) and even to AIDS patients (21). Ms. Fontenot even asserts that “A person with celiac disease has increased levels of certain autoantibodies circulating in their blood due to their intake of gluten”(1). Again, she overlooks seronegative celiac disease which is frequently seen in the context of IgA deficiency (22, 23, 24) and may be present in many other contexts. Opinion pieces are probably easier to write when ignoring relevant facts. In this case, the overwhelming body of personal bias that drives Ms. Fontenot’s article is offered in the absence of a single supporting research finding and only one other professional opinion which is offered by one of Ms. Fontenot’s colleagues. She certainly hasn’t let the facts get in the way of her story, but it is deeply disturbing to discover that The Atlantic has chosen to republish this unsupported rant. Sources: http://www.theatlantic.com/health/print/2012/01/a-gluten-free-diet-reality-check/250750/ Reilly NR, Aguilar K, Hassid BG, Cheng J, Defelice AR, Kazlow P, Bhagat G, Green PH. Celiac disease in normal-weight and overweight children: clinical features and growth outcomes following a gluten-free diet. J Pediatr Gastroenterol Nutr. 2011 Nov;53(5):528-31. Cheng J, Brar PS, Lee AR, Green PH. Body mass index in celiac disease: beneficial effect of a gluten-free diet. J Clin Gastroenterol. 2010 Apr;44(4):267-71. Murray JA, Watson T, Clearman B, Mitros F. Effect of a gluten-free diet on gastrointestinal symptoms in celiac disease. Am J Clin Nutr. 2004 Apr;79(4):669-73. Whiteley P, Haracopos D, Knivsberg AM, Reichelt KL, Parlar S, Jacobsen J, Seim A, Pedersen L, Schondel M, Shattock P. The ScanBrit randomised, controlled, single-blind study of a gluten- and casein-free dietary intervention for children with autism spectrum disorders. Nutr Neurosci. 2010 Apr;13(2):87-100. Reichelt KL, Knivsberg AM. The possibility and probability of a gut-to-brain connection in autism. Ann Clin Psychiatry. 2009 Oct-Dec;21(4):205-11. Knivsberg AM, Reichelt KL, Høien T, Nødland M. A randomised, controlled study of dietary intervention in autistic syndromes. Nutr Neurosci. 2002 Sep;5(4):251-61. Cascella NG, Kryszak D, Bhatti B, Gregory P, Kelly DL, Mc Evoy JP, Fasano A, Eaton WW. Prevalence of celiac disease and gluten sensitivity in the United States clinical antipsychotic trials of intervention effectiveness study population. Schizophr Bull. 2011 Jan;37(1):94-100. De Santis A, Addolorato G, Romito A, Caputo S, Giordano A, Gambassi G, Taranto C, Manna R, Gasbarrini G. Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3. Dohan FC, Grasberger JC, Lowell FM, Johnston HT Jr, Arbegast AW. Relapsed schizophrenics: more rapid improvement on a milk- and cereal-free diet. Br J Psychiatry. 1969 May;115(522):595-6.. Singh MM, Kay SR. Wheat gluten as a pathogenic factor in schizophrenia. Science. 1976 Jan 30;191(4225):401-2. Hadjivassiliou M, Kandler RH, Chattopadhyay AK, Davies-Jones AG, Jarratt JA, Sanders DS, Sharrack B, Grünewald RA. Dietary treatment of gluten neuropathy. Muscle Nerve. 2006 Dec;34(6):762-6. Hadjivassiliou M, Rao DG, Wharton SB, Sanders DS, Grünewald RA, Davies-Jones AG.Sensory ganglionopathy due to gluten sensitivity. Neurology. 2010 Sep 14;75(11):1003-8. Turner MR, Chohan G, Quaghebeur G, Greenhall RC, Hadjivassiliou M, Talbot K. A case of celiac disease mimicking amyotrophic lateral sclerosis. Nat Clin Pract Neurol. 2007 Oct;3(10):581-4. Niederhofer H, Pittschieler K. A preliminary investigation of ADHD symptoms in persons with celiac disease. J Atten Disord. 2006 Nov;10(2):200-4. Zelnik N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2004 Jun;113(6):1672-6. Rodrigo L, Hernández-Lahoz C, Fuentes D, Alvarez N, López-Vázquez A, González S. Prevalence of celiac disease in multiple sclerosis. BMC Neurol. 2011 Mar 7;11:31. Malalasekera V, Cameron F, Grixti E, Thomas MC. Potential reno-protective effects of a gluten-free diet in type 1 diabetes. Diabetologia. 2009 May;52(5):798-800. Epub 2009 Feb 14. Iuorio R, Mercuri V, Barbarulo F, D'Amico T, Mecca N, Bassotti G, Pietrobono D, Gargiulo P, Picarelli A. Prevalence of celiac disease in patients with autoimmune thyroiditis. Minerva Endocrinol. 2007 Dec;32(4):239-43. http://www.timesonline.co.uk/tol/news/uk/article444290.ece Quiñones-Galvan A, Lifshitz-Guinzberg A, Ruíz-Arguelles GJ. Gluten-free diet for AIDS-associated enteropathy. Ann Intern Med. 1990 Nov 15;113(10):806-7 Evans KE, Leeds JS, Sanders DS. Be vigilant for patients with coeliac disease. Practitioner. 2009 Oct;253(1722):19-22, 2. Mozo L, Gómez J, Escanlar E, Bousoño C, Gutiérrez C. Diagnostic Value of Anti-Deamidated Gliadin Peptide Igg Antibodies for Celiac Disease in Children and Iga Deficient Patients. J Pediatr Gastroenterol Nutr. 2011 Dec 23. Wang N, Shen N, Vyse TJ, Anand V, Gunnarson I, Sturfelt G, Rantapää-Dahlqvist S, Elvin K, Truedsson L, Andersson BA, Dahle C, Ortqvist E, Gregersen PK, Behrens TW, Hammarström L. Selective IgA deficiency in autoimmune diseases. Mol Med. 2011 Aug 4.
  4. Recently I have noticed a trend in articles that demonize the gluten-free diet, and imply that there is something unhealthy or even dangerous about it. Here is an example of one that I forwarded to Dr. Ron Hoggan: http://www.post-gazette.com/pg/11017/1118230-114.stm and below is his response to its author: Dear China Millman, Thank you for your interesting article on gluten-free dieting. I was very pleased to read that you include patients with non-celiac gluten sensitivity among those who should follow a gluten free diet. I assume that you have arrived at your estimate of 20 million who are afflicted with wheat allergy, non-celiac and celiac gluten sensitivity using Dr. Fasano’s estimate that 6 to 7 percent of Americans have what you refer to as this “milder form of gluten intolerance”. There are other estimates. For instance, Dr. Kenneth Fine did random blood draws at a shopping center in Dallas, Texas and found an 11% rate of gluten sensitivity. Congruently, Dr. Marios Hadjivassiliou has reported rates as high as 12% in the United Kingdom and Dr. Rodney Ford reports a prevalence estimate of 10% in New Zealand. Each investigator used different methods to arrive at their estimate, and each method is likely to underestimate the true prevalence of non-celiac gluten sensitivity. For instance, they all rely on a single class of antibody reaction against a single sub-group of proteins found in gluten grains. Thus, Dr. Fasano’s estimate may be unduly conservative as it is substantially lower than others have found in similar populations and the testing used to arrive at Dr. Fasano's estimate also carries all of the other limitations mentioned above. As for the notion that non-celiac gluten sensitivity is milder than celiac disease, Anderson et al, in their study titled “Malignancy and mortality in a population-based cohort of patients with coeliac disease or ‘gluten sensitivity’ World J Gastroenterol 2007 January 7; 13(1): 146-151, report a higher rate of malignancy and early mortality among those with non-celiac gluten sensitivity than among those with celiac disease. This finding may be the result of the common recommendation that patients ignore test results that show non-celiac gluten sensitivity, as many physicians believe that such results are “non-specific” and do not warrant a gluten free diet. However, it may also reflect that non-celiac gluten sensitivity is a more serious illness than celiac disease. It may also reflect something entirely different than these two interpretations, but it does make a very good case for the need for more research in this very neglected area. As for the comments by Heather Mangieri and the American Dietetics Association, they might benefit from reading studies such as the one by Dr. Cheng et al titled “Body Mass Index in Celiac Disease Beneficial Effect of a Gluten-free Diet” in the 2009 Journal of Clinical Gastroenterology. They found that, after diagnosis with celiac disease, about half of the overweight and obese patients lost weight. Given the conservative data you report, suggesting that at least 90% of American cases of celiac disease go undiagnosed, there can be little doubt that a large portion of those with undiagnosed celiac disease who are overweight or obese would be likely to lose weight. The number who would lose weight should be greater among those who chose to follow a gluten free diet to lose weight, as some of those who are diagnosed with celiac disease do not comply with the diet. If one accepts the proposition that those with non-celiac gluten sensitivity, IBS, and IBD often have similarly problematic reactions to gluten, the number of Americans who could lose weight and live healthier, and therefore happier, lives (eating a gluten free diet) rises exponentially. On a personal level, my mother lost 66 pounds during her first years on a gluten free diet. Now, some 15 years later, she has lost almost 100 pounds. I doubt that she would still be alive had she not undertaken the gluten free diet purely on the basis of test results suggestive of non-celiac gluten sensitivity. In the current context of excessive under-diagnosis of celiac disease and limited understandings of the dynamics by which a gluten free diet causes weight loss among celiac patients, and an enormously greater number of Americans who have non-celiac gluten sensitivity, it is difficult to understand why anyone would be cautioned against following a gluten free diet with weight loss as their objective. Whether these individuals are undiagnosed celiac patients, have undiagnosed non-celiac gluten sensitivity, or they find that a gluten free diet is helping them to achieve their body mass objectives, there is little legitimate cause to "warn" people away from a gluten free diet. Overall, your article does raise awareness of gluten as a potential health threat, so its overall impact is positive despite the misinformation that a gluten free diet does not help with weight loss. Sincerely, Ron Hoggan, Ed. D. Royal Roads University, Continuing Studies
  5. The following report comes to us from The Sprue-Nik Press, which is published by the Tri-County Celiac Sprue Support Group, a chapter of CSA/USA, Inc. serving southeastern Michigan (Volume 7, Number 6, September 1998). The degree of mucosal damage varies from one celiac patient to another. Also, the amount of the small intestine that is affected also varies, with the damage usually progressing from the beginning of the small intestine and then moving downward toward the end of the small intestine. This may explain the variable symptoms in different patients. For example, when a significant portion of the small intestine is involved, diarrhea, malabsorption, and weight loss result. When damage is isolated to only the top portion of the small intestine, the only affect may be iron deficiency. (Incidentally, when iron deficiency is not corrected by iron supplements, it is highly likely that celiac disease is the cause of the deficiency.) Gluten in a celiacs diet causes the immune system to produce gliadin antibodies in the intestine. Some of these leak into the bloodstream where they can be detected in blood tests. These blood tests are useful for screening for celiac disease, though a small intestinal biopsy remains the gold standard for diagnosing celiac disease (celiac disease). There are few diseases for which diet and nutritional issues are more important than for celiac disease. At this time, the only known treatment of celiac disease is the removal of wheat, barley, rye, and oats from the celiacs diet. On the surface this sounds simple, but complete removal of dietary gluten can be very difficult. Gluten-containing grains are ubiquitous in the Western diet. Also, grain-derived food additives such as partially hydrolyzed vegetable protein [and modified food starch] are widely used in processed foods and oral medications. Content labels are often vague or incomplete regarding these additives. What further complicates matters is a lack of significant experience on the part of physicians and dietitians in the dietary treatment of celiac disease. This is mainly because there are so few celiac patients for anyone practitioner. Therefore the best sources of dietary information for a new patient are other knowledgeable, more experienced celiacs. It is very important that the diet be followed with full and strict compliance. Celiacs, especially if theyve had active celiac disease for a longtime, are at higher than normal risk for GI malignancies.(Fortunately, compliance to a good gluten-free diet returns the risk of malignancy and life expectancy to that of the general population.)Another complication of long-term untreated celiac disease is bone loss, which maybe irreversible in older patients. When a large portion of the small intestine is affected by active celiac disease, the result can be a generalized malabsorption problem, resulting in deficiencies of water- and fat-soluble vitamins and minerals. Folic acid deficiency is particularly common in celiac disease because, like iron, it is absorbed in the upper small intestine [where the highest concentration of celiac-related damage generally occurs]. Folic acid is necessary for DNA replication, which occurs in cell turnover. So a deficiency of folic acid can impair the regenerative ability of the small intestine. Vitamin B12, also essential to DNA synthesis, is not malabsorbed as commonly as folic acid. Magnesium and calcium deficiency are also common in active celiac disease, because of decreased intestinal absorption AND because these minerals tend to bind with malabsorbed fat which passes through the system. It is particularly important for doctors to assess the magnesium status of celiacs, because without correction of a magnesium deficiency, low levels of calcium and potassium in the blood cannot usually be corrected with supplements. In severe cases, magnesium supplementation should be done intravenously because of the tendency of oral magnesium to cause diarrhea. Supplemental calcium generally should be provided to celiacs, possibly with vitamin D, to help restore tissue and bone calcium levels to normal. The exact dose of calcium is not known. Dr. Fine usually recommends 1500-2000 mg of elemental calcium per day, divided into two doses, for several years and sometimes indefinitely. [4], [5], [6] Zinc is another mineral that often becomes depleted in patients with chronic malabsorption. Zinc supplementation (usually the RDA via multi-vitamin and mineral supplements) helps avoid skin rashes and restores normal taste. Up to 20% of celiacs will continue to experience loose or watery stools even after going on a gluten-free diet. Sometimes this is due to inadvertent gluten in the diet, but a recent study at Dr. Fines medical center showed that in these cases other diseases epidemiologically associated with celiac disease are present.[7] These include microscopic colitis, exocrine pancreatic insufficiency, lactose intolerance, selective IgA deficiency, hypo- or hyperthyroidism, and Type I diabetes mellitus. When diarrhea continues after beginning a gluten-free diet, a search for these associated diseases or others should be undertaken and treated if found. The use of cortico steroids has been advocated in celiacs when the response to the gluten-free diet is sluggish or absent. This is necessary more often in older than in younger patients. However, pancreatic enzyme supplements (prescribed by a doctor) may be needed to help digestion and resolve ongoing malabsorption in some patients. The endomysial antibody blood test is highly accurate and specific for detecting celiac disease. However, the current method of detecting these antibodies involves an operator looking through a microscope and observing the antibody binding on monkey esophagus or human umbilical cord tissue substrates. The correct interpretation of results is highly dependent on the skill and experience of the technician interpreting the fluorescence pattern through the microscope. Moreover, determination of the amount of antibody present relies upon repeat examinations following dilutions of the blood serum, with the last positive test being reported as a titer. A new discovery was reported by a research group in Germany.[8] The antigen substrate of the endomysial antibodies has been identified. This allows the development of a new test that can detect and measure serum endomysial antibodies in one, chemically-based test run [thus greatly reducing the potential for human error and significantly reducing the time needed for each test--ed.] These new tests should be available for clinical use shortly. In a recent study, Dr. Fine found that the frequency of positive stool blood tests was greater in patients with total villous atrophy relative to partial villous atrophy, and all tests were negative in treated patients without villous atrophy.[9] This suggests that fecal occult blood may be a non-invasive and inexpensive method of following the response of the damaged intestine to treatment. Also, it should be noted that the high frequency of positive tests due to villous atrophy will decrease the accuracy of the tests when used for cancer screening in this same patient population (which is how these tests are normally used by health care providers). There have been two recent reports touting the lack of deleterious effects when 50 grams of oats per day are added to the diet of celiac patients. Although this finding is exciting for celiacs, both studies possess certain limitations. In the first study, published by a Finnish group, the exclusion criteria for symptoms and histopathology were somewhat strict, so that patients with more mild forms of celiac disease seemingly were selected for study. And though no damage to duodenal histology occurred after one year of oats consumption, no physiologic or immunologic parameters of disease activity were measured. Furthermore, several patients in the treatment group dropped out of the study for reasons not mentioned in the article.[10] The second and more recent study involved only 10 patients, studied for twelve weeks. The favorable results of this study must be interpreted with caution because of the small sample size and short study period.[11] Even the one-year treatment period in the Finnish study may be too short to observe a harmful effect, as it is known that small intestinal damage sometimes will not occur for several years following there introduction of gluten to a treated celiac. At the worst, an increase in the incidence of malignancy may result from chronic ingestion of oats, an effect that could take decades to manifest. Therefore, this issue will require further study before oats can be recommended for the celiac diet. 3. From the September 1998 newsletter of the Houston Celiac-Sprue Support Group, a chapter of CSA/USA, Inc. 4. Ciacci C, Maurelli L, et el, Effects of dietary treatment on bone mineral density in adults with celiac disease; factors predicting response, Am J Gastroenterol, 1997; 92 (6): 992-996. 5. Mautalen C, Gonzalez D, et al, Effect of treatment on bone mass, mineral metabolism, and body composition in untreated celiac patients, Am J Gastroenterol, 1997; 2 (2):313-318. 6. Corazza gluten-free, Di Sario A, et al, Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult coeliac disease, Bone, 1996; 18 (6):525-530. 7. Fine, KD, Meyer RL, Lee EL, The prevalence and causes of chronic diarrhea in patients with celiac sprue treated with a gluten-free diet, Gastroenterol, 1997; 112 (6):1830-1838. 8. Dieterich W, Ehnis T, et al, Identification of tissue transglutaminase as the autoantigen of celiac disease, Nat Med, 1997; 3 (7):797-801. 9. Fine KD, The prevalence of occult gastrointestinal bleeding in celiac sprue, N Engl J Med, 1996; 334 (18):1163-1167. 10. Janatuinen EK, Pikkarainen PH, et al, A comparison of diets with and without oats in adults with celiac disease, N Engl J Med, 1995; 333 (16):1033-1037. 11. Srinivasan U, Leonard N, et al, Absence of oats toxicity in adult coeliac disease, BMJ, 1996; 313 (7068):1300-1301.
  6. I wrote this response below to address a recent New York Times article: Confirming a Diagnosis of Celiac Disease. Celiac.com 01/13/2010 - The problem with current diagnosis criteria for celiac disease is that it takes a certain degree of damage to intestinal villi in order to get a formal diagnosis. Since celiac disease with villi damage are just one manifestation of a much broader and more widespread problem--gluten sensitivity--many people who could still develop serious health problems if they continue to eat gluten, will go undiagnosed under the current definition of celiac disease. The reality of gluten sensitivity is that around 7 to 12% of the US population test positive for antibodies which are an indicator that their immune system is mounting a response to gliadin, the part of gluten that causes the reaction in those who are sensitive. Many of these people may never get flattened villi, however, many may end up with other conditions that are triggered by gluten exposure in sensitive individuals, for example nerve damage (ataxia), liver problems, diabetes, thyroid issues, etc.. In the past 10 years the diagnostic criteria for celiac disease have been changed significantly to include various degrees of villi damage (Marsh Criteria), and as a result, more people are now being properly diagnosed. In the next 10 years I predict that blood tests alone will replace the use of all biopsy results to diagnose celiac disease, as they are a far more sensitive indicator of gluten sensitivity. Once this happens we will finally reach a point where those affected can be properly treated and avoid the risk of the many disorders that have been associated with sensitive individuals who eat gluten, some of which are described here.
  7. Celiac.com 07/30/2009 - Here is Dr. Ron Hoggan's response to Slate's unfortunate article "Throwing Out the Wheat" which was written by Daniel Engber: Dear Mr. Engber, You represented Dr. Fasano as saying: “For every patient whose intestinal biopsy turns up positive, he says, nine or 10 more test clean but commit to going gluten-free all the same.” This ratio is well established in the medical and scientific literature. The rate of gluten sensitivity, as measured by IgA and IgG antibodies against gliadin, (a protein family that is a sub-group of gluten) constitutes about 10% to 12% of the general population. That is about ten times the rate of celiac disease found in the general population. These anti-gliadin antibodies (AGA) clearly demonstrate that gliadin proteins or derivative peptides are reaching the bloodstream and sensitizing the immune system to this foreign (non-self) protein. Many of these gluten sensitive individuals experience all of the same signs and symptoms as celiac patients. Similarly, you state: “Since there's no way to "prove" a case of gluten-intolerance in the lab...” This is grossly inaccurate. Although many practitioners will state that AGA are non-specific, I doubt that any of them would argue against the statement that the presence of AGA clearly indicates that gliadin or its fractions have managed to get into the bloodstream. When they say AGA are non-specific, they simply mean that these antibodies are not associated with any specific disease. They seem to be found in a wide range of autoimmune diseases, cancers, and behavioral/psychiatric disorders. You also say: “If you're paying more attention to what you eat, there's a good chance your symptoms will lessen. That's not because gluten or red meat or another food is damaging your small intestine; it's because eating less makes it easier for your gut to recover.” This assertion is based on a flawed assumption. Gluten-free foods are much more calorie-dense than those made with gluten. Thus, a common mistake made by those beginning a gluten-free diet is to eat about the same quantities they are used to eating. For instance, if one is in the habit of taking two sandwiches in their lunch, they are likely to pack two gluten free sandwiches. Since the gluten-free bread is much more nutrient dense. Increased nutrient densities apply to pasta, baked goods, and almost all gluten-free substitutes. Thus, the switch to eating a gluten-free diet usually leads to eating less, not more, as you claim in the above statement. Later you state: “Chances are you'll have reduced your total intake of carbs, and thus the amount of α-amylase in your gut.” For the reasons stated above, this is also inaccurate. You go on to say: “In other words, the mere fact of being on a gluten-free diet could make you more sensitive to grains and cereals—which would only reinforce your conviction that you're gluten-intolerant.” I am not aware of any data indicating a reduction of alpha almylase in the context of a gluten free diet. I would be amazed if you can find any such data. It reflects an assumption about the production and function of amylase that appears indefensible to me. The low carb craze has followed a very different path to the media, and began with a fellow named Banting in the 1800s whose doctors suggested a low carb diet to him as a means of losing weight. It worked, and he published a pamphlet about it. It saw a resurgence in the form of a ketogenic diet in the 1920s, at Johns Hopkins, as a treatment for epilepsy. Subsequent development of anti-seizure medications during the 1930s left the treatment without any patients, so it was abandoned until 1997 with the airing of First Do No Harm, a movie about one child’s plight and his parents’ struggle to find a treatment for his life threatening seizures. Meanwhile, research suggested that the growth of insulin sensitive tumors might be stalled by a ketogenic diet, and various case reports and subsequent clinical trials both support that perspective and indicate that most folks won’t maintain such a boring diet. The gluten-free diet was suggested by a concerned mom in 1932 and it was fully 18 years before Dr. Willem Karel Dickie’s doctoral thesis would be accepted and the world would begin to treat celiac disease with a gluten free diet. I won’t bore you with the details of this evolution but there are many twists and turns to the story of gaining acceptance of a gluten-free diet for the effective treatment of celiac disease. Both of these developments occurred quite separately. The two things they have in common are: 1. They both gained popular notice and support through the Internet, and; 2. They both defied conventional medical wisdom when they were first considered. Your graph simply identifies the impact that the Internet has had on democratizing health care. Your ill-informed attack on a gluten free diet is regrettable because it suggests it is a fad diet rather than a therapeutic one. At best, that will make it more difficult for people to get cooperation when trying to look after their own health by avoiding gluten. At worst, it will dissuade people from sticking to their diets if they believe your false assertion that gluten sensitivity cannot be identified in a lab. It can be, and is, on a very regular basis. Your information on celiac disease was mostly well researched and solid, but you clearly did not put any thought or effort into finding out about gluten sensitivity (often called gluten intolerance). I wish you would correct some of this misinformation, as it is really misleading and potentially harmful. Daniel Engber responded to the above email insisting that “it's impossible to prove gluten intolerance in the lab.” And that “Many of the strongest advocates for those with this condition describe it as one that can only be diagnosed by process of elimination. Or, to be more specific, by an elimination/reintroduction test.” He also challenged me asking if “All those who have AGA are gluten-intolerant?” Then he said that he just doesn’t believe it. Here is my reply: July 31, 2009 Hi Daniel, Thanks for your response. I don't know who these "strongest advocates" are, but your information about elimination/reintroduction testing being the only way gluten sensitivity is absolutely inaccurate. Check with any reputable blood testing lab that does IgA and/or IgG anti-gliadin antibody testing. They will set you right on this score. The presence of AGA in the bloodstream is clear, incontrovertible evidence that the body is mounting an immune response against gluten. This antibody reflects a delayed-type food sensitivity that is sometimes erroneously called an allergy. This is gluten sensitivity. It may be transient, chronic, or permanent, but there can be no doubt that it reflects the condition that is referred to as gluten intolerance. Not everyone who is gluten sensitive will show these antibodies but, yes, everyone who shows these antibodies is gluten sensitive. It is a basic principle of immunology that elevated selective antibodies reflect prior or current exposure of these antigens to the bloodstream. You must have spoken with Alessio Fasano to get that quote. Just ask him about AGA testing. He will tell you the same thing I'm telling you. I have discussed these and related matters with him at some length. I think you are mistaken in your claim that you linked to anything that Joe Murray said. I'll be very surprised if he has said anywhere that a gluten-free diet leads to eating less (although he has repeatedly said it can cause weight loss in the context of celiac disease). Could you tell me where this link appears? Nonetheless, even if the volume of food consumed is less (more on that in a moment) the increased caloric density would very likely be offset by the significant increase in caloric density of gluten-free foods. While Dr. Murray has treated and spoken with many more celiac than I have, I'd be willing to wager that I have observed many more of them while eating. :-) Apparently I misunderstood your thesis. I took you to say that public awareness of low-carb/Atkin's dieting and gluten sensitivity followed a largely parallel path because they are both pop culture trends that reflect a kind of hysteria about nutrition that is not based on science. Thus, I offered some data showing that the rise in public awareness of these two nutritional perspectives are based on scientific insights and the rapid increase of public awareness of these issues in 2004 and 2006-2008 was probably the result of improved access to information on the Internet in combination with scientific discoveries during those periods. I should have detailed the discovery and development of serological tests for celiac disease and gluten sensitivity as well as the research that began to reverse the vilification of saturated fats at about the same time. (snip) The vast majority of those eating a gluten-free are eating a very high carb diet. On this issue your article is quite misled and misleading. Please take the time to respond again, as I am most interested in that link to Joe Murray's comments. I also urge you to look at the significance and nature of AGA serum antibodies. Gluten sensitivity is readily demonstrated by these simple blood tests. Best Wishes, Ron Monday, August 03, 2009 4:50 PM Dan replied admitting that he had not, after all, linked to an article by Joe Murray. The link he apparently intended to put in was the following: http://www.montanaceliacsociety.com/physiciansmanual.htm I responded with the following message: Mon 8/3/2009 9:02 PM Hi Dan, I gave you the wrong url. Please try this one: https://www.celiac.com/gluten-free/index.php?showtopic=60511 I'm wondering how you can continue to assert "it's impossible to prove gluten intolerance in the lab" when I have given you ample information to the contrary as well as directing you to blood testing labs (Great Smokies, Immuo, Imco Diagnostics, etc. etc.) that will verify my assertion. There is also a wealth of information in the peer reviewed medical literature supporting what I'm saying. I'd be happy to provide a list of relevant research reports if you are interested. You don't mean to suggest that this quote from Joe Murray somehow justifies your above assertion do you? Just pick up a telephone and give him a call. I'm very confident that he will not support your notion that gluten sensitivity cannot be identified in the lab. Do remember that Dr. Murray is a sub-specialist in celiac disease. He may not be a big fan of assertions of non-celiac gluten sensitivity, but he won't deny that the AGA blood tests establish immune sensitization and hence, gluten sensitivity. Rodney Ford and Marios Hadjivassiliou are a couple of other world renowned researchers who are reporting AGA as a significant marker of serious disease in the absence of celiac disease. Your assertion that "it's impossible to prove gluten intolerance in the lab" was the lynchpin of your entire article. Without it, you may have to acknowledge that you have just discredited a group of people who, on the basis of solid science, are trying to improve their health. Yet you have set back their relationships with skeptical family members and friends based on your inadequate research. I really do think that you owe these people a retraction or at least a statement that mitigates some of the damage your article is doing. Sincerely, Ron Tuesday, August 04, 2009 3:14 AM Dan responded saying that he thought we were having a semantic argument. It became clear to me that he was confusing gluten sensitivity with gluten sensitive enteropathy – which is another name for celiac disease. He thought I was talking about latent celiac disease. He insisted again that gluten intolerance is not defined by any standard such as celiac disease is. He went on to say: “If you want to define "gluten intolerance" and/or "gluten sensitivity" so it applies to some subgroup of those who suffer from symptoms related to gluten, that's fine with me. I'm using the phrase "gluten intolerance" to describe all those who experience relief from the gluten-free diet without having been diagnosed with celiac.” I responded with the following: From: Ron Hoggan, Ed. D. Tue 8/4/2009 11:01 AM To: Daniel Engber Subject: RE: Throwing Out the Wheat Hi Dan, It sounds like you may be confusing gluten sensitive enteropathy with gluten sensitivity. The former is a descriptive name for celiac disease, while the latter indicates an immune system sensitized to gliadin. Selective antibodies are produced in response to foreign proteins or peptides that have breached a barrier (skin or mucosal) and are now present in the bloodstream or imbedded in self tissues. The immune system reacts as if these foreign proteins were bacterial invaders. (In fact, they are cytotoxic and neurotoxic but that is not at issue here (1, 2). If there was only one event during which gliadin proteins or peptides reached the circulation, as might be the case during a bout of flu, for instance, AGA levels usually diminish quite quickly. Thus, when a person shows elevated levels of AGA, the condition is usually chronic. It indicates that they are leaking gliadin proteins and/or peptides into the bloodstream. Celiac disease only afflicts between 10% and 15% of these people with elevated AGA. Serological tests for celiac disease identify endomysium antibodies (EMA) and tissue transglutaminase (tTG). There is no debate about the foregoing. It is common knowledge and is accepted by the vast majority of researchers and practitioners working in this area. The controversy comes in when we ask what elevated AGAs mean. Many claim that it is a non-specific finding. That is, AGAs are not diagnostic for celiac disease or any other currently recognized disease. They are much more common among those with autoimmune diseases, AIDS, and several other groups, but they do not provide any clues that will help diagnose a particular illness. AGAs are also found in some apparently healthy individuals. The only condition for which they fairly specific is what is often called a "leaky gut". However, most practitioners do not recognize increased intestinal permeability as a disease entity. There is no debate regarding the connection between elevated AGAs and leakage of gliadin into the body. In the past, the debate has been about whether AGAs are diagnostic for any disease and whether a leaky gut is an issue of any real concern. However, in the late 90s, researchers at U. Maryland, working to develop a cholera vaccine, found a protein messenger called zonulin. As its presence increases in the intestinal lumen, it relaxes the tight junctions between gut epithelial cells (3). Zonulin is overproduced by some individuals in response to gluten ingestion. It turns out that those with celiac disease, type 1 diabetes, and a variety of autoimmune diseases are particularly inclined to produce excessive quantities of zonulin in response to gluten ingestion (4). Similarly, Marios Hadjivassiliou and his neurological research group at the Royal Hallamshire Hospital in Sheffield have found that AGA are elevated in more than half of all patients with neurological disease of unknown origin and only about a third of those have celiac disease. The remaining two thirds are simply gluten sensitive, as identified by AGA (5). Variation in zonulin production, from one individual to another, is likely the factor that determines gluten sensitivity. Gluten sensitivity does not identify celiac disease, latent celiac disease, or any other enteropathy that I'm familiar with. It identifies an immune system sensitized to gluten. Avoidance of gluten in such cases can help to avoid developing additional autoimmunity, just as it sometimes does in celiac disease, but current evidence suggests that it will usually not reverse it once that autoimmunity has begun. The use of Rodney Ford's term "gluten syndrome"(2) might well have saved us considerable cyber ink, as we might have been able to begin by disagreeing about the value of a gluten free diet across the gluten syndrom spectrum, rather than taking several emails to determine that you were equating gluten sensitivity with celiac disease. Best Wishes, Ron Sources: Paganuzzi AS, Zucco F, Cardelli M, de Angelis I, Mattei R, Pino A, Rocca E, Zampaglioni F.Cytotoxic effects of wheat gliadin-derived peptides.Toxicology. 1985 Dec;37(3-4):225-32. Ford RP.The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29. Drago S, El Asmar R, Di Pierro M, Grazia Clemente M, Tripathi A, Sapone A, Thakar M, Iacono G, Carroccio A, D'Agate C, Not T, Zampini L, Catassi C, Fasano A. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines.Scand J Gastroenterol. 2006 Apr;41(4):408-19. Visser J, Rozing J, Sapone A, Lammers K, Fasano A. Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Ann N Y Acad Sci. 2009 May;1165:195-205. 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. Clemente MG, De Virgiliis S, Kang JS, Macatagney R, Musu MP, Di Pierro MR, Drago S, Congia M, Fasano A. Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function.Gut. 2003 Feb;52(2):218-23. Note: I should have added that since Dan was using the phrase gluten intolerance “to describe all those who experience relief from the gluten-free diet without having been diagnosed with celiac,” he has defeated his own argument. If a person has symptoms and they get relief from a gluten free diet, they would have to be pretty self destructive, foolish, or self-indulgent to go back to eating gluten. In a private email I received from another person, he said: “After reading his original article I had the distinct feeling that a girlfriend of his (or friend/relative) had gone on a gluten-free diet and had recently dumped him--maybe because he wasn't so supportive of this change...but I don't have any proof... ” I am most inclined to agree with this poster’s suspicions. Finally, I forwarded a copy of the letter titled: “Is gliadin really safe for non-coeliac individuals? Production of interleukin 15 in biopsy culture from non-coeliac individuals challenged with gliadin peptides” by D Bernardo1, J A Garrote2, L Fernández-Salazar3, S Riestra4, E Arranz5 from Gut 2007;56:889-890; doi:10.1136/gut.2006 These investigators report that “gluten elicits its harmful effect” on all the individuals they studied, not just those with celiac disease. I believe that Jefferson Adams has written a detailed account of this research that appears elsewhere on celiac.com. Although Mr. Engber declined to give me permission to publicly post his emails, and hence, his side of this discussion, I have invited Dan to respond to the above on celiac.com, as I would like to give him every opportunity to either provide some evidence to support his unfortunate claims about non-celiac gluten sensitivity, or to retract his damaging comments in the original article he penned. Although I have been a little rough on him, I do hope he will present his side of this debate, as it is of great importance to many individuals who must negotiate with friends and relatives to safeguard their health. These people would not dream of casually scattering rat poison on food to be served to a loved one. However, they seem to feel imposed upon by those who are gluten sensitive, because they do not want gluten scattered on their food. This attitude is just as inappropriate and sometimes, just as dangerous as scattering rat poison on food. Sincerely, Ron Hoggan
  8. Those patients for whom there is a high suspicion for celiac disease should have a small bowel biopsy which can be obtained by an experienced endoscopist in the distal duodendum. The best noninvasive tests available for screening for asymptomatic celiac disease are the specific serological tests. These are of several varieties: the anti-gliadin, anti-endomysial, or anti-reticulin antibodies. Our experience and the literature support the use as of endomysial antibody test as the single most specific and probably most sensitive for celiac disease. This test has now become available in specialty laboratories as well as in a small number of academic institutions. All of the tests should be done with the subjects on a normal gluten containing diet. A combination of endomysial and gliadin testing would seem to be the most sensitive as a screening method. A positive test is not, however, considered to be diagnostic and would usually require a small bowel biopsy for confirmation. A trial of dietary exclusion of gluten is *not* recommended as a diagnostic test without a prior abnormal biopsy. Because the body will recover when one goes gluten-free, the tests will then come up negative. Without a definitive test one may then stray from the diet, as one will feel well and was never sure that they had it in the first place. As for the two tests: The biopsy will look for flattened villi on the intestinal wall. After one goes gluten-free they will grow back. The blood antibodies are formed as a bodys reaction to the presence of the gluten. If no gluten, then no antibodies are present.
  9. In volume 334, number 13 of the New England Journal of Medicine was published a follow-up article concerning additional research which seems to contradict their October 19, 1995 (Vol. 333, No. 16) article which stated that pure oats are safe for celiacs. David Branski, M.D., Margot Shine, M.D., and Shaare Zedek Medical Center, Jerusalem 91031, Israel report their belief that allowing oats in the diet is premature. They sited the short duration of the study and the increased risk of cancer related through small intake of gluten (Holmes et al). It does appear that the initial study is being continued for an additional five years.
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