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    Will Other Foods Affect the Villi? - by Kemp Randolph


    Scott Adams


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    The following is a March 11, 1998 post by Kemp Randolph krand@PIPELINE.COM.

    According to Dr. Hugh Sampson, Mt. Sinai Medical Center, at an AMA sponsored press briefing on Nutrition, in a list of Facts vs. Fictions, Fiction: Skin tests or blood tests can be used to diagnose food sensitivities. Fact: ...A positive test does not mean a person will react to a food...furthermore these tests do not tell whether a person has a non-IgE mediated sensitivity to food.

    He describes these tests only as useful guides and points out that diet testing is the only reliable way to identify a food allergy, preferably where the person does not know whether they have eaten the suspect food.

    Q: If I am sensitive to milk and eggs...could they damage my villi in the same way as gluten?

    A: Theres a specific note in Michael Marshs book about food allergies causing villi damage. Thats the book On Coeliac Disease, page 155. Table there shows that the Type 3 stage of intestinal response, flat destructive does occur with milk, egg, soy and chicken or fish allergies. It differs from the celiac response in that only 1 or 3 of the 5 stages of lesion connected with celiac disease occur with an allergy.

    Whats unclear from this reference and from Medline searches Ive made is whether food allergies in adults cause villi damage. All the references I found were for children. Villi destruction does occur in children with milk allergy, but this like other pediatric allergies, apparently is usually outgrown.

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    Guest Patricia Benites Wright

    Posted

    My son had a serious case of celiac disease as a child, now he's over 40. They discovered that he is now allergic to sugar cane products.The article doesn't mention anything about such changes.

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    Guest Catherine Lasota

    Posted

    Thanks for the info... hope to see more good data...my family is in denial... as they are Italian. I know that Italians are predisposed to have celiac disease.

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    Guest elizabeth kelly

    Posted

    Appreciate the information. Thank you very much.

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    Interesting as I have been diagnosed with many food allergies and have been off wheat for years and felt great, had genetic testing for celiac which was negative, and just eliminated sugar cane from diet and I feel like a newer person than when I went off wheat!!

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    I was diagnosed 9 years ago and this was never something that I would have considered a problem. Thanks for this interesting information.

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    Guest Shirley

    Posted

    I had the blood test for celiac disease, which was negative but after having a capsule endoscopy it showed the villi were worn down in patches. I have had bowel problems for years, also anaemia and doctors have been unable to tell me what the problem is.

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    Scott Adams
    Introduction
    Through his writings, we know that Hippocrates, the father of medicine, had already recognized the presence of allergic reactions in people as early as ancient times. However, the term allergy is a relatively new one, as compared to many other commonly used medical terms. In 1906, Viennese pediatrician Baron Clemens von Pirquet used the term for the first time to describe an altered response of his patients bodies. Von Pirquet believed that this altered reaction manifested itself in changes of the immune system, effected by external influences on the body, such as: food intake, the air breathed or direct skin contact. The term allergen (the substance responsible for the altered reaction) was born. At that point in time, however, von Pirquet had no means of scientifically proving that these immunological changes actually occurred in the body. It was not until the mid-1920s, that a second significant event occurred.
    Researchers found that, by injecting a minute quantity of purified allergen under the skin, certain individuals would develop a clear skin response; a welt, with or without itching and redness, could be provoked. This positive skin test for allergies would show itself most prominently in patients with hay fever, asthma, chronic rhinitis, hives and eczema. The prick test became a method of demonstrating the involvement of the immune system in allergic reactions. However, the precise biological reason for the reaction continued to remain a mystery.
    It was not until the Sixties, when an important discovery occurred which provided long-awaited scientific support for the classical allergy theory and removed any doubts about the relationship of the immune system with allergies. This breakthrough came about with the scientific discovery of immunoglobulin E (IgE) by a Japanese couple named Ishizaka.
    Classical Allergic Reaction
    The following are the chain of events which happen in allergic reactions:
    An allergen must be present in the body. This allergen is the substance which causes us to have an abnormal immunological response. Allergens tend to be protein molecules. Interestingly enough, the immune system only detects particles of a certain size as potential troublemakers and protein molecules are just the right size. In a small number of cases, the body actually responds to molecules other than proteins. These molecules, which are generally much smaller, are called haptens. By combining with protein molecules, haptens form larger complexes which can then be detected by the immune system. The allergen is detected by the B cells. These are specialized immune cells, capable of producing antibodies. Just like allergens, antibodies are protein molecules, which have the capacity to neutralize allergens. Every B cell produces its own, specific antibody, depending on the type of intruder it needs to respond to. It is easy to understand why the body must have a ready pool of millions of antibodies, in order to combat these numerous offenders. There are five main categories of antibodies (IgG, IgA, IgM, IgD and IgE) which the body releases under different circumstances (for instance to fight off various infections, etc.). In the case of allergies, the body produces the antibody immunoglobulin E (IgE), first discovered by the Ishizakas. Usually, antibodies will bind directly to the appropriate damaging substance and neutralize it. However, IgE deviates from this common path. It first attaches one of its legs to one of the bodys numerous mast cells. The other leg is used to hold on to the offending allergen. This action signals the mast cells to begin disintegrating, thereby releasing histamine. Histamine is a chemical substance responsible for a great number of complaints which may arise during allergic reactions. It causes muscle cramps and an inflammation-like process with redness and swelling of mucous membranes.
    Allergic reactions can occur under a variety of circumstances. For instance, inhaling certain substances, such as grass pollen, house dust, etc., may cause an allergic response. However, the consumption of certain foods may do the same. Allergies typically bring on complaints very rapidly upon contact with the allergen. Complaints may vary from a runny nose, sinusitis, earache or runny eyes to itching of the skin, eczema and shortness of breath.

    Intolerance
    Conventional medicine can easily diagnose and treat allergies for foods or inhalants. Here, the so-called RAST test plays a very important role, because this test can demonstrate the presence of IgE.
    However, demonstrating the presence of intolerance is more difficult. In this situation, similar to the case of classical allergies, the body responds abnormally and, in addition, the immune system does not produce IgE. It quite often takes much longer for complaints to come on, thereby masking the possible link between the offensive substance and the complaints themselves.
    These are only a few of the reasons why food intolerance is considered a fairly controversial concept in conventional medicine. Intolerance can be responsible for a wide variety of complaints which, at first glance, seem to lack a plausible explanation. Intolerance can manifest themselves as the following:
    Gastrointestinal complaints: stomach ache, irritable bowel, Crohns disease, ulcerative colitis Skin complaints: itching, eczema, hives, acne (in adults) Joint and muscle complaints: ranging from atypical pains to rheumatoid arthritis Headache and migraine Chronic fatigue Asthma, chronic rhinitis or sinusitis Pre-menstrual syndrome Hypoglycemia Depression, anxiety Sleeping disorders
    Diagnosing Intolerance
    It is impossible to accurately demonstrate intolerance through conventional testing methods.
    The Amsterdam Clinic currently uses the following test, which is very reliable.
    Another useful test is the IgG(4) antibody test. Here, the presence of IgG(4) antibodies is determined. These antibodies are the slowly occurring variety, which do not appear in the blood until 24 to 48 hours after exposure to an offending food or substance. The reliability of this test varies between 80 and 90%.
    Treatment
    Diet
    In the treatment of inhalant allergies (such as asthma, hay fever) and food allergies and intolerance, avoidance (elimination) of allergens plays an extremely important role. In the case of food sensitivities, either the cytotoxic test or IgG(4) test can help determine reactions to specific foods. Based on the test results, an elimination/rotation diet can be specifically tailored.
    Foods causing strong reactions in these tests, should (temporarily) be excluded from the diet. More moderate reactions allow for rotation of certain food items in the diet. These may be eaten once every four days. Especially during the first week(s) of the diet, withdrawal symptoms, similar to complaints stemming from the cessation of coffee, tobacco or alcohol consumption, may occur. The body seems to crave offending food items. Generally, these withdrawal symptoms disappear after a couple of weeks. Concurrently, those complaints relating to food sensitivity also diminish.
    Using this dietary approach, the reaction to food allergens may decrease in the course of time. After a three month moratorium, reintroduction of forbidden food items can be attempted, one at a time. In this way, food items still causing reactions can be isolated more easily. Often, at least part of existing intolerance completely disappear after an elimination/rotation diet.
    With the treatment for inhalant allergies, elimination is also the first step. It is obvious that patients having an allergy for cats or dogs, should avoid any contact with these pets. The situation becomes more difficult when dealing with allergies to grass or tree pollen, since total elimination is basically impossible. The same goes for house dust mite allergy. The house dust mite lives in mattresses, pillows, carpeting, drapes, upholstery, etc. Through mite-killing pesticides, special mattress and pillow covers, non-carpeted floors, etc. reasonable results can be obtained.
    Medication
    Medicines for inhalant allergies, such as antihistamines (Triludan), corticosteroids (Prednisone, Pulmicort, Becotide), cromoglycates (Lomudal, Lomusol), and airway dilating medication (Ventolin, Berotec, Atrovent) do suppress symptoms, however, they do not cure the allergy! In the realm of conventional medicine, effective medications for food allergy and intolerance do not exist at all.
    Desensitisation
    Enzyme-potentiated desensitisation (EPD) and the provocation/neutralization method are very effective treatments for food allergy/intolerance and inhalant allergy problems. These methods tackle allergy problems at the root.
    During EPD treatment, a small quantity of a food or inhalant allergen mixture is injected intradermally into the skin, in conjunction with the enzyme beta-glucuronidase. This combination causes the body to gradually adjust its exaggerated responses to food and inhalant allergens. In this way, the immune system is readjusted and reset. Initially, the injections have to be given once every two months. Gradually, however, the intervals between injections become longer and the injections can often be discontinued after a time. According to conservative estimates, at least 80% of those patients treated with EPD show considerable improvement in the course of time. Provocation/neutralization can be used both diagnostically and therapeutically. Here, separate extracts of food or inhalants, suspected as possibly offending, are injected intradermally. This causes a welt to appear in the skin. After 10 minutes, the size and nature (firmness, color, etc.) of the welt are evaluated. A positive welt will generally bring on symptoms (provocation). Depending on the size and nature of the welt, as well as, the presence of symptoms, varying concentrations are injected, until a dose is found which does not cause any welt changes or symptoms. This is the neutralizing dose. Injections with the proper neutralizing dose will bring on immediate protection against the symptoms caused by the offending food and/or inhalant. Copyright © 1996 the Amsterdam Klikiek
    For further information please contact:
    Also in THE NETHERLANDS:
    Amsterdam Kliniek
    Reigersbos 100
    1107 ES Amsterdam Z.O.
    Telephone 31 (0)20 697 53 61
    Telefax 31 (0)20 697 53 67
    Lydia S. Boeken M.D. London/Amsterdam

    Dr. Vikki Petersen D.C, C.C.N
    This article originally appeared in the Autumn 2010 edition of Celiac.com's Journal of Gluten-Sensitivity.
    Celiac.com 12/06/2010 - The hazards to health created by celiac disease and gluten sensitivity are well understood.  From nutritional deficiencies to osteoporosis, from depression to autoimmune disease, and from psoriasis to thyroid disease, there are few areas of the human body that gluten doesn’t touch in a negative way. 
    There is so much emphasis on our inadequate abilities to diagnose gluten intolerance, that when we do finally make the diagnosis I believe we are guilty of another problem—lack of adequate education to those affected patients.
    Just last month a research study was released by the American Journal of Gastroenterology, 2010 Jun; 105(6):1412-20.  The article was entitled “Mucosal recovery and mortality in adults with celiac disease after treatment with a gluten-free diet”.  The research team hailed from the Division of Gastroenterology and Hepatology at Mayo Clinic College of Medicine.
    They stated that while a positive clinical response is typically observed in most adults with celiac disease after treatment with a gluten-free diet, the rate of small intestine recovery is less certain.  Their aims were to estimate the rate of intestinal recovery after a gluten free diet in a cohort [a group of people with statistical similarities] of adults with celiac disease, and to assess the clinical implications of persistent intestinal damage after a gluten-free diet. 
    Of 381 adults with biopsy-proven celiac disease, 241 had both a diagnostic and follow-up biopsy.  Among these 241, the confirmed mucosal recovery at 2 years following diagnosis was 34% and at 5 years was 66%.  Most patients (82%) had some positive clinical response to the gluten-free diet, but it did not prove a reliable marker of intestinal recovery. 
     Poor compliance to the gluten-free diet, severe celiac disease as defined by diarrhea and weight loss, and total villous atrophy at diagnosis were strongly associated with persistent intestinal damage. 
    There was a trend toward an association between mucosal recovery and a reduced rate of all-causes of death, adjusted for gender and age. 
    The conclusions were that intestinal recovery was absent in a substantial portion of adults with celiac disease despite treatment with a gluten-free diet, and that there was an association between confirmed intestinal recovery (vs. persistent damage) and reduced mortality independent of age and gender. 
    So what can we learn from this?

    Eating gluten-free when you are sensitive will cause you to feel better.  Going on a gluten-free diet is not enough to ensure that your intestines will heal. Failing to heal your intestines puts you at increased risk for disease and death. Successfully healing your intestines reduces your incidence of death from disease.
    While you likely knew the first point, 2, 3, and 4 are perhaps less well known.  Where I see that we are failing the gluten intolerant population is in the narrow focus of eliminating gluten as the only needed treatment.  What the above research proves is that, unfortunately, for over 30% of those diagnosed simply eliminating gluten is insufficient to ensure intestinal healing. 
    If patients were educated that healing their intestine would make the difference between contracting disease or not and extending their life expectancy or not, I think they’d be more interested in ensuring that it occurs.
    I am not a researcher but my clinic sees hundreds of patients who align with the results of this study completely.  Patients come to see us who have been told that they shouldn’t consume gluten and for the most part they follow that recommendation.  They know that they feel better when they are gluten-free so that is an impetus to not cheat.  When they do cheat they know that they’ll “pay” for it but they still do so fairly regularly. 
    Why do they cheat?  Because they believe that the diarrhea, headache, bloating, etc is temporary and that when it goes away they are “fine” again.  Their thought process is not unreasonable, it’s just wrong!
    If each patient was educated that cheating created intestinal destruction that in turn put them on a fast track towards disease and early death, I believe that cheating would take on a whole new perspective.
    Patients need this education and they need it often.  Our book “The Gluten Effect” was written with this intention—our patients actually requested it.   They asked for a written reminder of why they should maintain their gluten-free lifestyle.  Later I began taping Youtube videos because other patients preferred a reminder in a video form. 
    I’m trying to say this in a few different ways because it is terribly upsetting to meet patients, as I so often do, who have been diagnosed celiac or gluten sensitive and do not follow their diet solely due to ignorance.
    After almost 25 years of clinical experience I also know that some people “hear what they want to hear” and doctors with the best of intentions cannot get through to everyone.  But I strongly believe that we could be doing a much better job at enlightenment.
    Further, we also need to educate patients about the secondary effects associated with gluten.  When the immune system of the intestine is suppressed, as is the case in the presence of gluten pathology, inhospitable and pathogenic organisms can gain entry into the intestine and remain there.  These organisms may be in the form of bacteria, parasites, amoebas or worms and if they are not identified and eradicated, complete healing of the intestines is all but impossible. 
    The good bacteria that are housed in the gut, known as the microbiome or probiotics, make up much of the intestinal immune system.  In gluten intolerant patients this important population of organisms is often insufficient due to the onslaught from gluten and pathogenic organisms.  If the population of these probiotics is not restored to a healthy, robust balance, any attempt to achieve a healthy intestine will be unsuccessful.
    Lastly, it is an interesting catch-22 that in order to digest our food we need enzymes and enzymes are made from the nutrients we digest.  This circular pattern is dramatically interrupted in the gluten intolerant patient.  Celiacs in particular suffer from very poor absorption.  It shouldn’t then come as a surprise that augmenting with proper enzymes may be critical for “priming the pump” until proper digestion of nutrients is restored.
    Unfortunately I find that few, if any, of these points are made clear to patients who are gluten intolerant.  Most believe they are doing all they need to do simply by maintaining a mostly gluten-free diet.  Nothing could be further from the truth.
    To review we need to do the following:

    Maintain a “perfect” avoidance  of gluten Test for the presence of pathogenic organisms Test for any imbalance of the probiotic organisms Evaluate the need for enzymes Evaluate for the presence of any other food sensitivities, e.g.  dairy Educate the patient until they have a full understanding of the above Test to ensure that the intestine is healed

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    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 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
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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