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    Dr. Joseph Murray's Lecture at the September 5-7, 1996 Conference in Tampere, Finland


    Scott Adams

    From an oral report by Dr. Murray; transcribed for the list by Ann Whelan, editor of the bi-monthly newsletter Gluten-Free Living. To subscribe, write to P.O. Box 105, Hastings-on-Hudson, NY 10706. Dr. Joseph Murray, one of the leading USA physicians in the diagnosis of celiac disease (celiac disease) and dermatitis herpetiformis (DH). Dr. Murray (murray.joseph@mayo.edu) of the Mayo Clinic Rochester, MN, is a gastroenterologist who specializes in treating Celiac disease:


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    THE DAILY REPORT: The big story today from Finland is oats. There were two talks and several posters presented about the topic.

    In the first talk, Dr. Risto Julkunen spoke about the Finnish five-year follow-up study in which oats were given to a population of well-controlled celiacs. They ingested an average of 34 grams, which is slightly over one ounce, daily for up to five years. The oats used in the study were specially grown and tested to be free of wheat, barley and rye. The researchers claim there was no difference in those allowed the oats and those who were not.

    There was a second study presented from Dublin, and reported by Dr. Conleth Feighery. This 12-week study looked at a small group of patients with healed celiac disease to start with, who were given 50 grams of oats a day. Again, the oats were carefully screened and tested to make sure there was no contamination.

    After 12 weeks, no effect was seen on biopsy or through antibody tests. The researchers also took 2 of the 12 participants and did what they called a micro challenge of 500 milligrams of gluten a day. Both patients got reactions, so the researchers felt that at least two of the participants were sensitive celiacs -- and they still did not respond to the oats.

    A poster from Italy showed biopsies taken from celiacs that had been studied in the culture plate in the presence of oats, which did show some effect on the biopsies. In other words, tissue from biopsies from patients with treated celiac disease were put in a plate and grown in the presence of oat protein, and the oat protein had an effect on the biopsies.

    This sounded odd, so I made sure Id really understood what Joe reported and paraphrased: In other words, theyre seeing no reaction from oats within the body in some studies but this one showed a reaction outside the body? Yes, Joe said, this of course is puzzling. Continuing on the oats issue, a series of short studies from several places also showed what the Finns had shown in the body, i.e., no problem in the short term.

    This is Joes summary on Oats:

    Over the short term, in well-controlled, healed celiacs who are compliant in every other way, it may be safe for them to take oats that have been tested to be free of contamination of other grains. He also mentioned that there were a few studies showing that contamination of commercial oats may be common in several European countries.

    (NOTE: I went to Digestive Disease Week in May, where I met several Irish doctors who have studied oats. I would describe their strong beliefs about oats as very adamant. They are adamant in believing that uncontaminated oats are safe for people with Celiac Disease. If all of this oats talk pans out as being acceptably correct to gluten-sensitive individuals in this country, that would seem to be pretty good news. Then, the next big challenge would be to figure out how gluten-sensitive people are going to get access to contamination-free oats. I, for one, will be all ears.).

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  • Related Articles

    Scott Adams
    I am always amused by the argument that one grain or another is more likely to be contaminated than another, as I believe the real source of danger for contamination is found at mills and processing plants, and is more or less spread out equally for most gluten-free grains. Oats are often cited as having a higher chance of cross-contamination with wheat than other grains because it is often a rotational crop with wheat or barley, and kernels of these gluten-containing grains occasionally get mixed with the non-gluten grains. I do not understand why the same people who make this claim do no also include soy in this category, as it is one of the crops that is most commonly rotated with wheat.
    In any case, from the knowledge that I have gathered over the years about farming and processing grains, I must say that with most grains there is little likelihood of contamination due to the mixing of two different whole grains (i.e., the rotational crop hypothesis). This is due to the different sizes and shapes of different grains, and the machines which sort them after a harvest. If any grains do get mixed together the amount of actual contamination would likely be extremely low.
    In Trevor Pizzeys (Vice President of Operations for Can-Oat Milling) October 30, 1998 letter he expresses his belief that celiacs should avoid oats because he finds between 2.1 and 4.1 kernels of barley or wheat in every 4,000 (0.0525% and 0.1025% respectively). He says that this level can legally go up to a maximum level of 10 kernels per 4,000 (0.25%). In either of these scenarios we are talking about very low amounts. Even at these amounts the likelihood that a celiac eating these grains would eat 1 or 2 kernels of wheat or barley on a given day would be very, very low. Also, since most people who eat oatmeal tend to eat the whole oatmeal as a hot cereal, which means they can take very simple additional precautions to make their chances of eating any kernels of wheat or barley practically zero. The obvious way to do this is to look at the oats before you eat them or mill them and pull out any kernels that are of non-oat type.
    Now we turn to the other part of the argument to scare people away from grains that, taken by themselves, do not cause harm to people with celiac disease. This is the wheat dust in the mill (or during transport, or somewhere else) argument. There are many reasons, both health and safety, why mills take steps to keep dust levels down. Dust contamination is still possible, but I think we are also talking about even lower amounts that we were with the occasional kernel of wheat that pops up in oats, although there is no data that I know of to back this up. I think with whole oats (i.e., oatmeal) people can reduce any possible risk of wheat-dust contamination to almost zero by rinsing off their oats well with water before cooking or milling them.
    The famous oat study that was done in Finland and published in the NEJM used a source of non-contaminated oats to eliminate any possible factors that could ruin the results of their long and expensive study. It is possible that they could have used regular, uncontrolled Quaker oats for their study and gotten the same results, but again, the reasons for not doing so were to eliminate any possible factors that might affect the results of their study. This is the scientific process, and it is important with any study to eliminate any possible factors which could affect the outcome of the study.
    Last, there is a danger of contamination which comes from unclean equipment at mills, and at processing plants. This danger is present with any gluten-free grain, bean, etc., that is milled using the same equipment as is used to mill a gluten-containing grain. In other words we cannot speak of only oats with regard to this issue, as rice flour, soy flour, etc., could be contaminated equally in this way. Aside from legislation to require cleaning between milling runs, those who are worried about this need to buy flours from mills which they have researched and found to be gluten-free, or ones that adequately clean their equipment between runs.
    I think contamination issues are real, but need to be put in perspective with regard to other, perhaps more important issues, like labeling laws and getting agreement between the major celiac organizations in this country with regard to which grains are safe.
    See Also:
    Journal of the American Dietetic Association, Dec. 1997 v97n12p1413(4). Do oats belong in a gluten-free diet? by Tricia Thompson.

    Jefferson Adams
    Celiac.com 01/08/2008 - Our recent article on oats brought a number of comments calling our attention to another recent study in which certain types of oats were found to be more beneficial, while others were more likely to be problematical.  There still isn’t any official definitive evidence one-way or the other as to just how safe oats are for folks on a gluten-free diet, though there are more studies of this nature being undertaken, and data collection and genetic mapping and testing help us to build a better picture.
    A team of Italian and Australian doctors conduced in vitro tests on three different kinds of oats. They wanted to see if certain kinds of oats showed any kind of toxicity in people with celiac disease. These tests showed that the Avenins of the Italian variety Astra and the Australian variety Mortlook showed a much higher activity than those of the Australian Lampton variety, while Rice of the Roma variety showed no activity. Gliadin which is found in wheat and rye showed the expectedly high levels of activity.
    Of the oat types tested in this study, the Lampton variety seems to be safer than either the Astra or the Mortlock. However, even oats that are “safer” must still be processed in a dedicated facility that is free of contamination and routinely tested to make sure they meet the minimum levels to be gluten-free. For oat products to be considered gluten-free, they must show less than 20ppm of gliadin.
    A study published in the New England Journal of Medicine by Trisha Thompson, M.S., R.D.,* showed that no commercial brand of oats were reliably gluten-free. In fact, nine of the twelve samples from three major brands of oats showed gluten levels ranging from 1,807 to 23 ppm.
    There are several companies who now sell "certified gluten-free oats," which are oats that are farmed, harvested, processed and packed using special methods to avoid cross-contamination with gluten during every step of the way. Gluten-free oats currently sell for around $4 to $5 a pound. These type of oats are typically tested for gliadin to less than 3ppm, and are thus considered safe for celiacs who are not sensitive to Avenins.
    As far as certain types of oats being better than others, it’s worth some checking, but I’m unsure of the availability of, say, the Lampton strain in America. Also, given the results of commercially available oat brands, the question of the conditions under which the oats were processed becomes very important. Previous studies have shown children with celiac produce significantly greater numbers on antibodies to oat protein than non-celiac children (Scand J Gastroenterol. 2003 Jul; 38(7):742-6).
    Many folks with celiac disease are looking to avoid contamination, as no one wants to suffer the unpleasant symptoms of a gluten reaction. Basically, people just want to know what’s safe and to be able to enjoy those items without worrying about getting sick. Since cross-contamination is such a problem of particular importance to celiacs, and since oats grown and processed commercially are likely not gluten-free, it would seem wise to start with gluten-free oats just to be on the safe side.
    But anyone looking for a definitive answer will just have to wait. And remember, as with so much with the gluten-free diet, you are the best judge of your own body.
    *Thompson T. Gluten Contamination of Commercial Oat Products in the United States. N Engl J Med 2004; 351:2021-2022
    Main article:
    Journal of Gastroenterology and Hepatology 22 (4), 528–531, 2007.
    Marco Silano, Mariarita Dessì, Massimo De Vincenzi, Hugh Cornell (2007).


    Dr. Ron Hoggan, Ed.D.
    This article originally appeared in the Winter 2004 edition of Celiac.com's Journal of Gluten-Sensitivity.
    Celiac.com 09/19/2014 - Experts have decreed that pure oats are safe for people with celiac disease(1,2,3).  The definition of this disease is based on a very specific type of injury to the intestinal wall that heals following the removal of gluten from the diet.  This intestinal damage, called villous atrophy, is caused by the interaction between the immune system and certain proteins found in wheat, rye, and barley.  Identical proteins are not found in oats (although there is also some variation between the protein groups found in wheat, rye, and barley).  Further, many newly diagnosed celiac patients have been shown to recover from their celiac symptoms while eating significant quantities of oats and their intestinal biopsies do not show signs of villous atrophy1 (Admittedly, the quantity of oats consumed by these study subjects does not rival the grain protein consumption in a regular, gluten-laden diet, but the quantity is significant).  Therefore, this food is considered safe for celiac consumption.
    Given these facts, it is not surprising that many gastroenterologists are now recommending that their patients eat oats.  Some claim that patients are more likely to follow a gluten-free diet if that diet allows oats.  Others point to the definition of celiac disease, which clearly requires gluten-induced villous atrophy.  Still others insist that since we now know which proteins cause the villous atrophy, oats must be safe for celiac patients to consume.
    There are several problems with these perspectives, beginning with the assumption that patients will be more compliant with the diet if it includes oats.  I have explored the medical literature and have been unable to find a single study that investigates dietary compliance as a function of including oats in the gluten-free diet.  I’d be happy to hear about such a study.  But until the question is investigated, the assumption is just one more opinion afloat in a sea of unfounded beliefs about grains and diet.
    Many celiac patients experience an addictive element in gluten.  I have long suspected that is the result of morphine-like, opioid peptides found in the digests of gluten(4-8).  Are some peptides from oats capable of producing these opioids?  Has anyone investigated that issue?  Again, I can find no evidence that this issue has been studied.
    Reliance on the biopsy to reveal problems with oat consumption is another relevant problem.  As many of us can attest, and the medical literature reports, gluten challenges that intentionally involve ingestion of relatively large quantities of gluten often fail to reveal villous atrophy for weeks, months, and sometimes, years(9).  Many celiac patients will also agree that despite our best efforts at compliance, gluten sometimes manages to sneak into our diets, particularly in the early months of following the diet.  Yet a second biopsy usually shows dramatic healing of the intestinal wall, despite these dietary errors.  Clearly, the intestinal biopsy is a fairly crude tool for measuring intestinal health.  Its use in exonerating oats thus becomes suspect.  An even more troubling element of this issue is that there are gastroenterologists who are recommending that their patients consume breakfast cereals that contain malt flavoring, because patients consuming such small quantities of malt do not show villous atrophy(10).
    Also troubling is the fact that many of the studies that support the safety of oats have not employed the Marsh system for identifying intestinal injury, a refinement that significantly increases the sensitivity of the intestinal biopsy.
    The greatest weakness of the pro-oats position is the underlying assumption that we fully understand celiac disease and gluten sensitivity.  This is simply not the case.  The research shows that some celiacs do develop symptoms when consuming oats.  While most newly diagnosed celiacs experience reduced symptoms and improved health, this may simply be the result of consuming less grain-derived protein.  Researchers have long known that even partial compliance with the gluten-free diet produces health improvements in celiac patients(11).
    The definition of celiac disease that requires villous atrophy followed the discovery of the beneficial impact of the gluten-free diet by more than 20 years (If in doubt about this point, please refer to the English translation of Dr. Dicke’s Ph.D. thesis at http://www.dangerousgrains.com).  Our current understanding of the disease began with the observed benefits of the gluten-free diet.  Intestinal biopsies were a much later development.
    A similar debate arose regarding the inclusion of wheat starch.  It was long held to be a safe nutrient in the gluten-free diet in many European countries.  In fact, the studies that showed a reduced risk of cancer and a variety of celiac-associated conditions were often conducted among patient groups living where wheat starch was deemed acceptable(12, 13).  Yet when wheat starch consumption was studied in Canada, against a back-drop of zero tolerance, most of the subjects developed signs and symptoms of celiac disease(14).
    Many celiacs and gluten-sensitive individuals know that their symptoms do not fit with the conventional view of celiac disease.  Some of us believe that there is a continuum of severity.  Others believe that there are many sub-types of celiac disease.  Still others believe, me included, that it really doesn’t matter whether a person has intestinal damage.  The important, defining characteristic should be whether a person is mounting an immune response against the proteins in the most common substance in our food supply.  
    Whatever our beliefs we turn to the experts when faced with health concerns and crises.  However, those answers often rely on the medical definition of celiac disease, where villous atrophy heals in response to a gluten-free diet.  In cases where the biopsy was improperly taken, or too few samples were taken, or patchy intestinal lesions were missed, or other forms of gluten-induced ailments are causing symptoms, we may not get answers that aid our health.  Many individuals who are gluten sensitive will be, under such circumstances, dismissed with a diagnosis of IBS.
    Given the facts, we have several hurdles to overcome before we can, in my opinion, render an informed judgment about the safety of oats.  We need a much better understanding of gluten-induced disease in all of its manifestations.  We also need a definition of celiac disease that is more useful to the patient who is experiencing symptoms of gluten sensitivity/celiac disease.  As part of this, we also need a test that is more accurate, and can identify celiac disease after beginning the diet––a challenge that many of us face.  Until we have overcome these hurdles, any pronouncement regarding the safety of oats is premature.
    Further research is, in my opinion, the greatest need of the celiac community.  We need to know more, not just about celiac disease, but about the whole range of nutritional and pathological impacts of eating grains. In my own quest, I have learned from the experiences of other celiac patients.  Each new facet of my own experience has been illuminated by someone else’s story.  I have come to understand ADHD as a frequent companion of celiac disease.  Learning disabilities are also common among celiacs.  Behavioral disturbances are the norm, and speech problems are common.  My understanding continues to grow as I hear from others who struggle with gluten sensitivity.
    Despite its usefulness, this patient-to-patient network of information sharing is not enough.  We need well designed, well executed research.  We need a better understanding of our disease and how to protect future generations from the current, inaccurate assumptions about grains.  The oats question is only one facet of a much larger need for more information and better testing methods.
    Sources:
    Storsrud S, Olsson M, Arvidsson Lenner R, Nilsson LA, Nilsson O, Kilander A.    Adult coeliac patients do tolerate large amounts of oats. Eur J Clin Nutr. 2003 Jan;57(1):163-9. Kilmartin C, Lynch S, Abuzakouk M, Wieser H, Feighery C.  Avenin fails to induce a Th1 response in coeliac tissue following in vitro culture. Gut. 2003 Jan;52(1):47-52. Janatuinen EK, Kemppainen TA, Julkunen RJ, Kosma VM, Maki M, Heikkinen M, Uusitupa MI.  No harm from five year ingestion of oats in coeliac disease. Gut. 2002 Mar;50(3):332-5. Teschemacher H.  Opioid receptor ligands derived from food proteins. Curr Pharm Des. 2003;9(16):1331-44. Review. Yoshikawa M, Takahashi M, Yang S. Delta opioid peptides derived from plant proteins. Curr Pharm Des. 2003;9(16):1325-30. Review. Horvath K, Graf L, Walcz E, Bodanszky H, Schuler D. Naloxone antagonises effect of alpha-gliadin on leucocyte migration in patients with coeliac disease. Lancet. 1985 Jul 27;2(8448):184-5. Zioudrou C, Streaty RA, Klee WA. Opioid peptides derived from food proteins. The exorphins. J Biol Chem. 1979 Apr 10;254(7):2446-9. Hoggan R.  Considering wheat, rye, and barley proteins as aids to carcinogens. Med Hypotheses. 1997 Sep;49(3):285-8. Fukudome S, Yoshikawa M.   Opioid peptides derived from wheat gluten: their isolation and characterization. FEBS Lett. 1992 Jan 13;296(1):107-11. Kuitunen P, Savilahti E, Verkasalo M.  Late mucosal relapse in a boy with coeliac disease and cow's milk allergy. Acta Paediatr Scand. 1986 Mar;75(2):340-2. Holmes, et. al. "Malignancy in coeliac disease - effect of a gluten free diet" Gut 1989; 30: 333-338 Holmes GK.  Coeliac disease and malignancy.Dig Liver Dis. 2002 Mar;34(3):229-37 Collin P, Pukkala E, Reunala T.  Malignancy and survival in dermatitis herpetiformis: a comparison with coeliac disease. Gut. 1996 Apr;38(4):528-30. Chartrand LJ, Russo PA, Duhaime AG, Seidman EG.  Wheat starch intolerance in patients with celiac disease. J Am Diet Assoc. 1997 Jun;97(6):612-8.

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
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    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
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    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics