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    Do Vitamin Supplements Benefit Celiac Patients?


    Jefferson Adams

    Celiac.com 03/10/2009 - A recent study confirms that B-vitamin supplements are helpful in raising vitamin B6, B12 and folate levels and in reducing homocysteine levels in people with celiac disease.


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    Celiac disease is a typical malabsorption syndrome, and is associated with higher rates of numerous deficiencies, including folate and vitamin B12. People with celiac disease face higher rates of Hyperhomocysteinemia than do healthy controls.

    A team of Dutch researchers led by Dr. Muhammed Hadithi recently set out to evaluate the efficacy of daily supplements of vitamin B6, B12 and folate on homocysteine levels in patients with celiac disease.
    The study measured levels of vitamin B6, folate, vitamin B12, and fasting plasma homocysteine in 51 adults with celiac disease and 50 healthy control subjects of similar age and sex.

    The results show that the celiac disease subjects who used vitamin supplements had higher blood levels of vitamin B6 (P = 0.003), folate (P < 0.001), and vitamin B12 (P = 0.012) than celiac patients who did not use supplements, or healthy controls (P = 0.035, P < 0.001, P = 0.007, for vitamin B6, folate, and vitamin B12, respectively).

    Patients who use vitamin supplements also showed lower levels of plasma homocysteine than in patients who did not (P = 0.001) or healthy controls (P = 0.003). Vitamin B6 and folate were both associated with homocysteine levels, whereas vitamin B12 was not. Twenty-four (48%) of 50 controls and 23 (50%) of 46 of the celiac disease patients carried the MTHFR thermolabile variant T-allele (P = 0.89).

    The research team concludes that Homocysteine levels are dependent on Marsh classification and the regular use of B-vitamin supplements reduces of homocysteine levels in patients with celiac disease.The study confirms earlier studies suggesting that both the presence and severity of celiac disease determined homocysteine levels.

    The regular use of supplemental B vitamins resulted in higher levels of serum vitamin B6, folate, vitamin B12 and lower levels of plasma homocysteine in patients with celiac disease. Moreover, supplemental B vitamins seem to offer protection against the effects of villous atrophy on homocysteine levels, independent of the genetic susceptibility status as determined by carriage of the C677T polymorphism of 5,10 methylenetetrahydrofolate reductase.


    World J Gastroenterol. 2009;15:955–960

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    Recommended Comments

    Guest Barbara Feeser

    Posted

    There doesn't seem to be much information out on celiac & gluten food and side effects. I found out 2 years ago I have Celiac Disease and it has been hard to become gluten free due to the fact so much is hidden.

    I am very glad to find good information that will help me return to good health.

     

    I am looking forward to your articles and the help they will do.

     

    Thank you.

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    Guest Marie Zarankevich

    Posted

    I have read about about celiac causing extreme Thiamine (B1) deficiency, and the consequent result of congestive heart failure due to the effects of BeriBeri. Perhaps this should be added to your list of recommended supplements.

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    Guest Jo Lucas

    Posted

    Thank you for this information. It explains why very expensive B shots 'appeared' to work for over 2 years for my father. Ultimately he died of non-hodgkins lymphoma which my research indicates could have resulted from untreated celiac disease.

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    Guest Dan Lappin

    Posted

    I suggest that you change the title of this article to 'Role of B vitamins to reduce homo cysteine in celaic patients. I wish I had read this article months ago. I just started using Trimethylglcine and have had life changing benefits. I am a person with long standing gluten intolerant symptoms that only two years ago got clear on the gluten connection. This is a great article, it is not well titled. Please change the title so that others can get this info.

    Thanks, Dan

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    Guest Mary Rodgers

    Posted

    At age 80, 2 years ago, I went to IU Medical Hospital Diagnostic clinic. After testing three months, I was told I have refactory celiac. I was told I was born with celiac Thank you for this article. A gluten-free diet has stopped all pain and improved my digestion, but I am still anemic and cannot gain weight and am very weak. This

    week my doctor made tests about vitamins.

    After reading your information - at last I have hope !!!

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  • Related Articles

    Scott Adams
    This article originally appeared in the Summer 2004 edition of Celiac.coms Scott-Free Newsletter.
    Celiac.com 10/27/2004 - I recently decided to have my DNA and that of my son screened for the genetic markers, also known as HLA alleles, which make celiac disease possible. Both my mother and I have long since been diagnosed with the disease, so I naturally worry that my son Spencer may also end up with it at some point in his life. Even though he has been mostly symptom-free for his entire life—all three and a half years of it—last year I subjected him to serological screening after he had a several week bout with diarrhea. We were happy to discover that he did not have it, but I still knew that such tests could not rule the disease out of his future. Even so, it was nice to learn that he did not have the active disease, although a blood draw at two years of age was not exactly a pleasant experience for him—or for his parents! I swore then that I would try to avoid any unnecessary blood draws in the future, even though I knew that it might still be necessary from time to time—unless he somehow did not inherit the genetic markers for it—the idea of which led me to my decision to have Spencers DNA screened for celiac disease.
    After mentioning my plans for the DNA screening at a family dinner, my brother also grew interested, as he too has had unexplained symptoms and a recent negative celiac disease antibody panel and biopsy. He too felt that it would be nice to find out once and for all if this was something that he was going to have to worry about in the future. He also pointed out to me that genetic screening had the potential to save him money over the long haul, since the test is only necessary once in a lifetime. Periodic antibody screening for the disease can prove to be quite expensive, and a negative DNA test would effectively rule out the necessity of any future testing. After we finished our dinner that evening I sat down with my brother and we reviewed several offerings on the Internet by companies who provide genetic services for celiac disease, and were particularly impressed by one of them—Kimball Genetics, located in Denver, Colorado, as their DNA collection method did not require a blood draw and instead employed a simple and painless cheek cell collection using a swab.
    The next day I telephoned Kimball Genetics and was connected with a very knowledgeable genetic counselor. After a discussion with her about my familys history I decided to order three celiac disease genetic tests, one each for my son, my brother, and myself. I requested three cheek cell collection kits to be sent to my home, where the samples would be collected and sent back to Kimball Genetics for testing. For individuals the cost of a kit is 10% off of $325, or $292.50 per test, and they offer a 20% family discount for testing additional family members, which brings the per test price down to $260. Kimball Genetics also offers assistance with billing your health insurance company, which can often result in the recovery of all or part of the costs incurred for the tests. This includes detailed help with the forms, insurance CPT codes for the procedure, as well as obtaining the ICD9 codes, which are the diagnostic and symptom codes that come from your doctor. At this point I realized that to get reimbursed for the tests a person should first make an appointment with their doctor, and ideally this appointment should take place before actually ordering a test kit. This will ensure that you and your doctor are on the same page regarding the importance and necessity of the genetic tests.
    The cheek cell collection kits arrived in the mail within a couple of days, and I phoned my brother to arrange a "DNA collection party" at my house. On collection day we opened the kits to find enclosed two brushes for sample collection, a Test Request Form, a consent form, medical literature regarding Kimball Genetics DNA screening test for celiac disease, and detailed instructions that outlined how to properly collect and mail the samples. The kits also included a stamped return envelope that was pre-addressed to their laboratory. The Test Request Form included an area where one could enter their credit card information, and this form along with the consent form and a check or card information were required to be sent along with the sample in the return envelope.
    The medical literature included with the kits comprised of a three page document titled "Celiac Disease DNA Test." The following two sections, which I found to be particularly helpful, are reproduced below from this document, which is also available on their Web site www.kimballgenetics.com:
    Indications for Celiac Disease DNA Testing:
    Clinical diagnosis of celiac disease. Negative or equivocal antibody results (antiendomysial, tissue transglutaminase, or antigliadin) or intestinal biopsy results in an individual with symptoms of celiac disease. Relatives of individuals with celiac disease. Individuals with iron-deficient anemia. Individuals with dermatitis herpetiformis. Adults with diarrhea, abdominal pain and distention, recurrent aphthous stomatitis (canker sores), osteoporosis, infertility, multiple miscarriages, anxiety, and/or depression. Children with abdominal pain, diarrhea, abdominal distention, failure to thrive, short stature, delayed puberty, irritability, attention-deficit disorder and/or poor school performance. Children with Type I diabetes. Our Celiac Disease DNA Test Service Provides:
    PCR analysis for DQ2 alleles (DQA1*0501, DQA1*0505, and DQB1*0201/*0202) and DQ8 allele (DQB1*0302). Detailed reports with genetic interpretation, recommendations, and education. Free genetic counseling for physicians, patients, and families. Free shipping. The sample collection went very smoothly for each of us, and Spencer found it to be slightly more annoying than having to brush his teeth. We each rinsed our mouths out with water beforehand, and then rolled one brush at a time 20 times over the entire inside surface area of one check, and then did the same on the other cheek with the second brush. We let the samples dry for 30 minutes, and then put everything in their respective packages and envelopes along with the filled out paper work. Our final step was to put them out for the Mail Carrier to pick up. Their literature promised a 3-4 day turn around, and sure enough, both my brother and I got a call from someone at Kimball Genetics several days later who needed our doctors fax numbers, which we had forgotten to include on the paperwork. Once they had this information, a call to our doctors was all that was necessary to have our doctors forward the results directly to us by fax, and we also received the original reports by mail. Amazingly the Celiac Disease DNA Test at Kimball Genetics takes just one business day from the day the lab receives the sample (if it arrives by noon) to reporting of results.
    I have to admit that besides hoping that my son did not inherit the genetic makeup that makes celiac disease possible—as the results were printing out from my fax machine—I still held out the very slight hope that they had not found the markers in my genetic sample, and that my whole diagnosis was some sort of big mistake. This hope was quickly crushed as the report indicated that I was in fact part of an elite genetic group—one that carries both markers for celiac disease: DQ2 and DQ8—which I later discovered meant that I inherited genetic traits for celiac disease from both of my parents, rather than just from my mother, which was my original assumption. My father is no longer alive, but after discussing his results with my mother we decided that it is possible that he also had undiagnosed celiac disease, and it is interesting to note that he had diabetes.
    I couldnt help but think that my results make me something like a "Super Celiac," although the genetic counselor at Kimball Genetics reassured me that having both markers for it doesnt necessarily mean that the disease will present itself any differently. Spencer turned out to be positive for DQ2, and my brother found out that he too tested positive for both DQ2 and DQ8. On the down side their results indicate that they will need to watch out for any future signs of the disease for the rest of their lives, and probably get screened for it from time to time. On the up side there is still only a small chance that either will ever develop the disease, and at least we will know to watch for its symptoms in the future, which likely would lead to a quick diagnosis and treatment should one of them ever get it.
    Ultimately anyone who decides to undergo genetic screening must be comfortable with the results—positive or negative. I advocate testing because I believe in the saying that knowledge is power, and that it is better to know than not to know—especially when it comes to your health. Unlike other testing methods, genetic screening for celiac disease has the amazing potential to reveal whether someone has been misdiagnosed with the disease, even though the odds for such a scenario are small. It also can confirm a diagnosis, or let relatives of celiacs know that they do or dont need to worry about it in the future. My mother felt vindicated by our results, as they indicated that she wasnt the only person who passed celiac genes to her children—my father did too. Who knows, your genetic results may even have the potential to elevate your celiac status, as it did in my case, to that of—Super Celiac!

    Scott Adams
    Celiac.com 05/12/2006 - Dear Colleagues in the Celiac Community: We would like to provide you with a progress report of the Celiac Management Clinic (CMC) at Stanford Medical Center. Realizing that many physicians and gastroenterologists have a limited understanding of the frequency of Celiac Sprue in the population and the subtlety of the clinical manifestations of this disease, we instituted the CMC at Stanford Medical Center in January 2005. This clinic is staffed by Dr. Gail Pyle and myself. A large number of patients who carried the diagnosis of Celiac Sprue have chosen to be seen in consultation--the majority of these did have Celiac Sprue, as estimated from blood antibody tests and the small intestinal (duodenal) biopsy. For many of these patients, comprehensive emphasis on gluten exclusion has been very effective in eliminating symptoms and the malabsorption of nutrients. However, both in this patient group and in those healthy gluten-free Celiac volunteers who participated in the trial supported by the Celiac Sprue Research Foundation in collaboration with the Palo Alto Medical Foundation on pre-treatment of grocery store gluten with a special peptidase(1) there was a surprising discovery. Fully half (~50%) of those presumed to be in remission from the disease had malabsorption of important nutrients. This major finding was a surprise, and it gives us pause concerning Celiac Sprue therapy.
    Is gluten exclusion not optimal or is it insufficient therapy for this large proportion of Celiac Sprue patients?
    The concerns about the effectiveness of long-term dietary therapy in Celiac Sprue have prompted us to reassess our approach to this disease. For those of you who reside within reach of Stanford Medical Center, we invite you to visit us at the Celiac Management Clinic for an up-to-date assessment of the status of your Celiac condition. If you are the one out of every two healthy Celiacs with malabsorption, we will take a comprehensive approach to determine the reasons and to facilitate your return to complete remission.
    If strict gluten exclusion is insufficient to achieve this, we offer other approaches. Indeed, by the end of this year or the beginning of 2007 in collaboration with the Celiac Sprue Research Foundation, we expect to be able to determine the effect of an oral pill therapy for those who continue with malabsorption of nutrients.
    Stanford accepts most PPO insurance and MediCal and MediCare outpatient coverages. Those who suspect they have Celiac Sprue based on symptoms or blood antibody tests will be seen by Dr. Gray, and those with biopsy-verified disease will be seen by Dr. Pyle. For an appointment, call 650-723-6961, and please state that you wish to see us at the Celiac Management Clinic.
    Sincerely,
    Gary M Gray, M.D.
    Professor of Medicine, Emeritus
    (Gastroenterology)
    References:
    Pyle GG, Paaso, B Anderson, BE, Allen D, Marti T, Chaitan Khosla C, Gray, GM. Low-dose Gluten Challenge in Celiac Sprue: Malabsorptive and Antibody Responses. Clinical Gastroenterology and Hepatology, 3: 679-686, 2005. Pyle GG, Paaso, B Anderson, BE, Allen D, Marti T, Li Q, Matthew Siegel, M, Khosla C, Gray, GM. Effect of Pretreatment of Food Gluten With Prolyl Endopeptidase on Gluten-Induced Malabsorption in Celiac Sprue Clinical Gastroenterology and Hepatology, 3: 687-694, 2005.

    Jefferson Adams
    Celiac.com 10/20/2010 - U.S. doctors and patients looking for accurate early diagnosis of celiac disease now have a state of the art celiac disease assay with a high level of sensitivity and specificity. The US Food and Drug Administration (FDA) has given 510(k) clearance for the first two fully automated gliadin tests featuring deamidated peptides for celiac disease.
    Manufactured by Phadia US, the tests, EliA GliadinDP IgA and EliA GliadinDP IgG, are designed to be used in conjunct with other laboratory and clinical findings in the early diagnosis of celiac disease.
    According to Gabi Gross, autoimmune franchise leader for Phadia US, "EliA GliadinDP IgA and EliA GliadinDP IgG will offer physicians who suspect a possible case of celiac disease, antibody tests with the lowest number of false positive results." This means less "unnecessary endoscopies and biopsies," she adds.
    EliA GliadinDP IgA and EliA GliadinDP IgG will offer antibody tests with the lowest number of false positive results for doctors who suspect a patient has celiac disease.
    The assays are optional on Laboratory Systems Phadia 100Є and Phadia 250 instruments with features like quick turnaround, monthly calibration, onboard instrument dilution, and a discrete single-well, random-access, nonmicrotiter plate format.
    Phadia also manufactures other approved CLIA moderately complex assays in the EliA autoimmune product line, including anticardiolipin IgG/IgM, anti-B2-glycoprotein 1 IgG/IgM, cyclic citrullinated peptide, tissue transglutaminase IgA/ IgG, gliadin IgA/IgG, dsDNA, antinuclear antibody screen, and ENA antibodies to the following antigens: Sm, U1RNP, RNP70, Ro, La, Scl-70, CENP, and Jo-1.
    Source:

    Medscape

    Jefferson Adams
    Celiac.com 04/22/2013 - A recent study of celiac screening methods shows that testing for antireticulin antibodies (ARA) in patients with celiac disease is obsolete. The study includes a review of the medical literature, and recommendations for improved celiac blood screening.
    Researchers S. L. Nandiwada, and A. E. Tebo are affiliated with the Department of Pathology of the University of Utah, and ARUP Laboratories in Salt Lake City, Utah.
    Citing advances in celiac disease-specific serologic testing, Nandiwada and Tebo are calling for the elimination of ARA as a test for diagnosing celiac disease.
    People with celiac disease nearly always carry HLA-DQ2 and/or -DQ8 haplotypes, suffer from any of a range of diverse clinical presentations, including gluten-sensitive enteropathy.
    Celiac disease patients typically produce several autoantibodies, of which endomysial, tissue transglutaminase, and deamidated gliadin peptide antibodies are considered specific indicators of celiac disease.
    Although antireticulin antibodies (ARA) have traditionally been used to screen for celiac disease, these tests do not provide the best sensitivities and specificities for celiac screening.
    This review highlights recent advances in celiac-specific blood testing and supports the elimination of ARA from celiac disease screening and diagnosis.
    Source:
    Clin Vaccine Immunol. 2013 Apr;20(4):447-51. doi: 10.1128/CVI.00568-12. Epub 2013 Jan 30.

  • 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 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    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.
    14. 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.

    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