• Join our community!

    Do you have questions about celiac disease or the gluten-free diet?

  • Ads by Google:
     




    Get email alerts Subscribe to Celiac.com's FREE weekly eNewsletter

    Ads by Google:



       Get email alertsSubscribe to Celiac.com's FREE weekly eNewsletter

  • Member Statistics

    77,369
    Total Members
    3,093
    Most Online
    Tesy
    Newest Member
    Tesy
    Joined
  • 0

    Preview of The Gluten Summit - Excerpts From Two Iconic Experts


    Dr. Tom O'Bryan
    Image Caption: Dr. Thomas O'Bryan

    Celiac.com 11/07/2013 - Several of the world's most prominent scientists, researchers, healthcare practitioners, nutritionists, patients, caregivers and others interested in improving the lives of those living with gluten-related disorders will gather online, November 11-17, 2013, for the first-ever Gluten Summit: A Grain of Truth.  An excerpt from two of the iconic speakers is below.


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    Dr. Thomas O'BryanHave you ever wondered what "the Godfather of celiac disease diagnosis" thinks about the fact that celiac disease is generally only recognized and treated if a patient has total villous atrophy (all the shags are worn away)? I went to the source!

    I had the tremendous honor of traveling to Wolfson College, Oxford University in the United Kingdom to interview Dr. Michael Marsh, "the Godfather of celiac disease diagnosis", after whom the Marsh classification of intestinal damage in celiac disease was named.

    Dr. Marsh has a powerful message for the world about the critical importance of identifying and treating the early stages of celiac disease in patients before it reaches the end-stage of total villous atrophy (Marsh III). In 2006 Dr. Marsh stood up at the International Celiac Disease Symposium in New York and asked the panel the hard question "If a patient has positive blood tests and a negative biopsy, and you do not recommend a gluten-free diet, and the patient dies of lymphoma in two years, which one of you will be able to say that you practiced a good standard of care medicine?" This was a wake-up call to the world, and five years later non-celiac gluten sensitivity was recognized as a separate condition in a consensus by 16 global experts.

    In the first interview he has ever given, in the 21st birthday year of the Marsh classification system, Dr. Marsh speaks out on:

    •     Why normal villi can also be associated with a state of gluten sensitivity
    •     Why physicians must not wait for total villous atrophy to occur before treating gluten sensitive patients with a gluten-free diet
    •     Why a variety of disciplines beyond immunologists must now join together to study the early stages of celiac disease
    •     Dr. Marsh calls them out!

    Dr. Hadjivassiliou - How GLUTEN can affect your NERVOUS SYSTEM!

    Dr. O'Bryan: A suggestion that you have made in a number of your papers over the years is that "It is time to move on from gut to brain." Can you tell our listeners what you mean by this?

    Prof. Hadjivassiliou: Sure. I think it was a comment in relation to try and escape from the existing belief that sensitivity to gluten is primarily or even exclusively a disease of the gut. You can see why it's always been thought of as a gastrointestinal disease, simply because that's where gluten gets ingested and absorbed. However, we are talking about an autoimmune disease, and therefore the manifestations of an autoimmune disease can be very diverse...It's about time we thought of this as a systemic disease that can affect different parts of the body rather than concentrating solely on the bowel. My main interest was whether patients can manifest exclusively with neurological (nervous system) problems.

    Prof. Hadjivassiliou goes on to explain:

    •     The ratio of patients with nervous system issues vs. intestinal issues
    •     Why an early diagnosis is CRITICALLY IMPORTANT
    •     Why neurological patients may take longer to see results when they start a gluten-free diet
    •     The true impact of an accidental gluten exposure on a person whose nervous system is affected by gluten

    Visit theglutensummit.com for a link to the world's first ever online Gluten Summit, which will take place from Nov.11-17, 2013, to listen to the entire interview with Prof.Hadjivassiliou and many, many more interviews with the experts on gluten-related disorders and diet, and their impact you and your children's health. The Gluten Summit is a unique and FREE event which aims to move the question, "Is gluten the cause?" into today's conversation between patients and healthcare professionals potentially improving the lives of millions now.

    0


    User Feedback

    Recommended Comments

    Hello ~

    Just wanted to send you a HUGE thanks for helping Dr Tom O'Bryan stage this fantastic event. He is an awesome man and a wonderful human being. The speakers he organized were tops in their fields and gave us so much important information, some of it cutting edge, some that has been 'out there' for years but widely unacknowledged. It has been a rare and extremely important summit which will help - and has already - many, many people to at last enjoy good, if not transformed, health.

     

    I now recognise that gluten is a major problem for all humans, in one way or another (systemic). In some of us it just doesn't become obvious until years down the track. Thankfully, we read Dr Davis' book "Wheat Belly" nearly two years ago and have been grain & sugar-free (teeny bits of sugar very occasionally) since then. Have also read Dr Perlmutter's "Grain Brain". We weren't overweight, didn't seem to have any problems but I bet it was affecting our bodies (insulin, brain) so we're extremely grateful to have this knowledge.

     

    Thanks again for being part of this and for supporting Dr Tom.

     

    Kind regards

    ~ Robin

    Share this comment


    Link to comment
    Share on other sites
    Guest Elizabeth

    Posted

    All Information change my life and well-being.

    Share this comment


    Link to comment
    Share on other sites


    Your content will need to be approved by a moderator

    Guest
    You are commenting as a guest. If you have an account, please sign in.
    Add a comment...

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoji are allowed.

    ×   Your link has been automatically embedded.   Display as a link instead

    ×   Your previous content has been restored.   Clear editor

    ×   You cannot paste images directly. Upload or insert images from URL.


  • Popular Contributors

  • Ads by Google:

  • Who's Online   7 Members, 0 Anonymous, 1,003 Guests (See full list)

  • Related Articles

    Scott Adams
    Dr. Kelly, who is a refractory sprue specialist, had interesting insights into Celiac Disease. He first described once having a patient say to him that eating at a restaurant or food take out is the gastronomic equivalent of promiscuous and unprotected sex because (you) dont know where food has been, who else its been with, and what you might get from it. Dr. Kelly explained that his job when seeing a patient with possible Refractory Sprue is to first confirm that the patient really has Celiac Disease and is adhering to a gluten-free (gluten-free) diet. He explained that some patients would rather prefer an iron shot than adhere to a gluten-free diet and that sensitivities vary which removes another drive to say gluten-free; however, if symptomatic, he has found that the patient has the motivation to adhere. Hes even had to recruit and train dieticians to take an interest in Celiac Disease. He said that Celiac Disease or Gluten Sensitive Enteropathy is driven by activated lamina propria T-cells to whom gliadin is being presented through their T-cell receptors. In Refractory Sprue, he said that the cells are evident at intraepithelial lymphocytes rather than lamina propria lymphocytes and they no longer require gluten in order to be driven. So, theyre on auto-pilot. He emphasized that this is a rare disease and advised that doctors get a competent dietician to help patient adhere to diet.
    If the concern is that the patient is adhering but is not responding, Dr. Kelly advised doctors to think of other disorders masquerading as Celiac Disease, especially if patient is IgA, EmA (anti-endomysial) negative or if not HLA DQ2 or DQ8 (common Celiac genes) positive. He added that not every flat mucosa consistent with Celiac Sprue is Gluten Sensitive Enteropathy but that there can be a differential diagnosis such as cow protein intolerance. He said that there are unusual immunologic disorders that can be mistaken for sprue or refractory sprue. He said that doctors should consider these if the patient was not IgA endomysial or human tTg (transglutaminase) antibody positive at diagnosis. He explained that the positive predictive value of those tests are so strong that really its in some ways has a higher positive predictive value than even biopsy that you dont get very, very if any false positives at least by the immunofluorescence assay. So, if theyre negative at diagnosis considering other possibilities and this is one instance where HLA typing actually may be clinically useful if you have a patient you think has Celiac Sprue but isnt behaving or responding as you would expect with a gluten free diet and you ask do they really have Sprue. If they are HLA DQ2/DQ8 negative, then the likelihood of them having gluten sensitive disease is much, much lower. He said that serology (blood tests) were helpful but not be relied upon. He said that IG antibody levels against gliadin, or tissue transglutaminase tend to drop fairly quickly usually within 2 to 3 months provided they (patient) were positive to begin with. ...The IgG takes much longer so it tends to be less useful and of course, if they are IgA deficient, they wont be IgA positive to begin with and you cant use then. Even if their antibody levels are high to begin with, and remain high, that to me means that theyre still exposed to the antigen and they still have T-cells. Their lamina propia T-cells are still being driven by the antigen. But if theyre negative, Im afraid that its not particularly sensitive and low levels of gluten exposure may result in symptoms and poor response would not necessarily be identifiable by antibody.... Dr. Kelly said that patients with subtle manifestations of Celiac Sprue who have been previously diagnosed with irritable bowel or host of other disorders are now being more frequently seen. He said that there has been a lot of discussion in the past year about Celiac Sprue being misdiagnosed as Irritable Bowel Syndrome.
    Dr. Kelly also described the circumstance that patients with Celiac Sprue show improvement both serologically (blood) and histologically (biopsy) but their symptoms persist. He said that doctors need to be aware that just because a patient has gluten sensitive enteropathy doesnt mean they cant get another gastrointestinal disorder. He gave examples such as microscopic colitis and what he called a classical association, hyperthyroidism, or something else which could also cause diarrhea and weight loss.
    Dr. MacDonald, a celiac specialist, discussed new insights into the pathogenesis of Celiac Disease. Dr. MacDonald discussed primarily the role that other factors besides the DQ2 (gene) molecule, control the T-cells in the gut mucosa which produce the lesion or flat mucosa. In the genesis of the lesion, he explained how the T-cell immune response in the gut wall results in a gut shape of tall villi and short crypts which results in an increase in mucosa volume with flat mucosa and an increase in mucosa thickness. My husband, a PhD immunologist, interpreted this for me; He said that imagine the villi are the hill and the crypts are the valley. The valley is where things grow. The oldest cells are at the tip of the hill and as cells mature, they get transported up the hill. As damage occurs, the hill gets chopped down, valleys get deeper making more area for cells to replicate. Dr. MacDonald assumed that because the epithelium is turning over so fast in Celiac Disease that the lamina propria, the shape of the gut itself would be turning over, but actually the data says otherwise. The flat mucosa isnt turning over at all, ... a rather stable shape, its not really dynamic, its remodeled. He said that putting Celiacs on a gluten free diet may take them a long time to get better, because it takes a long time for this to go back because this is actually stable, its remodeled....
    Dr. MacDonald explained that gliadin peptides associate with DQ2 and DQ8 molecules putting themselves into the grooves to be seen by T cells. However, he gave an instance where a particular gliadin peptide doesnt fit well into the pockets of DQ2 to be seen by T cells. Tissue Transglutaminase or Ttg deamidates (removes chemical groups on certain amino acids and allows peptide to bind to DQ2) this peptide in terms of glutamine into glutamic acid, gives a negative charge, fits very well into pocket, and binding increases 100 fold. Tightness of the binding ... controls the specificity and strength of the T-cell response.
    Dr. MacDonald also described the case of a woman with cancer who was treated with interferon. He said that she had the endomysial antibodies, was DQ2 positive, and had Celiac Disease; however, he cited that the reason why the Celiac Disease was not found earlier was that interferon alpha/gamma used to treat the cancer may have precipitated clinical Celiac Disease. He added that her son was later diagnosed with Celiac Disease as well. It was also eluded to that a viral infection like a gastrointestinal flu would stimulate or produce interferon alpha.
    Dr. Alessio Fasano from the Center for Celiac Research at the Univ. of Maryland also explained that its not just the gluten antigen and genes (i.e., HLA DQ2 or DQ8) but an added element like that alluded to by Dr. MacDonald such as a viral infection which can result in Celiac Disease. Dr. Fasano described a study performed on North African children who were thought to have symptoms resembling infectious disease with symptoms like anemia and diarrhea were found to have Celiac Disease at the rate of 1 in 18. He said because they have a high consumption of grains and seem to carry a high frequency of the genetic elements, he felt that non-profit organizations may intervene to help institute a gluten-free diet in this Celiac population. Dr. Fasano mentioned a study performed in Southern California which found Celiac Disease in 2 to 4% of people with symptoms or associated diseases and 5% in family members of Celiacs. Dr. Fasano stated that the overall prevalence is 1 in 266 which he said on a global scale, by far this is the most frequently genetic disease of human kind. Fasano said that in the 1970s, it was thought Celiac Disease was confined to the pediatric population but that since 1998 there has been a surge in adult versus child cases. He believes that the disease may have been overlooked in adults because adults have more atypical symptoms like anemia, osteoporosis, abortion that would NOT see a Gastroenterologist but would see an internist, reproductive OBGyn, endocrinologist, etc.
    Dr. Fasano said that if the iceberg idea is diarrhea, weight loss, abdominal symptoms, you will surely crash into the iceberg, but he proposed, what about the people who have joint pain, constipation, fatigue, and so on. He said that if you are willing to see the monument of the problems, you have to get down under the water because in the vast majority of cases, Celiacs will not see a Gastroenterologist and that doctors must be aware of those under the water. Dr. Fasano during the question and answer session listened to a doctor in the audience describe a patient with diarrhea and schizophrenia whose diarrhea and schizophrenia resolved when put on a gluten-free diet. The doctor didnt know what to do with the patient but explained that the patients background, being of Irish descent, gave him a red flag into the possibility of Celiac Disease. Dr. Fasano in response described how there can be a change in behavior such as attention deficit disorder, depression, and schizophrenia. He described a theory that the epitopes of gluten could cross the intestinal barrier, cut into the bloodstream, and cross the blood brain barrier. He believes that there is a clear association between Celiac Disease and change in behavior.
     

    Jefferson Adams
    Celiac.com 06/29/2011 - Serbian tennis star Novak Djokovic credits an unbeaten string of victories on the court to his special, gluten-free diet.
    Meanwhile, Sabine Lisicki recently attributed her collapse on the threshold of a major upset over third seed Vera Zvonareva in the second round of the French Open to a need for her body to adjust to her new gluten-free diet; which Lisicki adopted after discovering she is intolerant to gluten, a protein in cereal grains.
    After physically crumbling within sight of victory, a sobbing Lisicki was carried from the court on a stretcher. The 21-year-old later explained on her website (www.sabinelisicki.com) that her collapse occurred because her body simply let her down. She said that "[d]octors recently discovered that I am intolerant to gluten -- meaning I can't eat e.g. pasta, one of my biggest energy sources."
    "My body needs to adjust to the big change and needs some time. It is good that we found out and it will only make life better in the long run, she added."
    Pasta and bread are still staple foods for many top athletes, as they are important sources of energy. Athletes on gluten-free diets need to find new energy sources.
    Djokovic has enjoyed a 39-match winning streak after changing his diet in late 2010, after tests by his nutritionist showed him to be gluten intolerant.
    Like Lisicki, Djokovic's body cannot process the carbohydrates he traditionally used to fuel his body, and he was forced to find alternative foods to provide the energy and stamina needed to prevail in long matches. For Djokovic, the change has paid off handsomely.
    "I have lost some weight but it's only helped me because my movement is much sharper now and I feel great physically," said an energized Djokovic, who has beaten Rafael Nadal in four finals this year.


    Jefferson Adams
    Celiac.com 12/14/2012 - In the latest celebrity gluten-free news, actress and comedian Fran Drescher has joined stars like Lady Gaga and Miley Cyrus, and athletes like Novak Djokovic and Andy Murray, in adopting a gluten-free diet.
    Moreover, Drescher is going one step further and making her gluten-free diet a vegan one. However, it's not a desire to shed pounds that led Drescher to join the nearly 3 million people with celiac disease, and numerous others, in making her diet gluten-free. Rather, she was looking for a way to deal with exhaustion. When a doctor suggested prescription medications, Drescher decided that overhauling her diet sounded like a better place to start. So, she resolved to cut gluten, alcohol and animal products from her life. She has since lost 15 pounds, and her results have included more energy, and, she claims, better looking skin.
    Talking with host Wendy Williams on Thursday, Drescher said that changes were not easy to make.
    "I wasn’t able to knock off that kind of weight in years. I just decided that I wasn’t feeling well… and I went to a bunch of doctors, and everybody had different prescriptions for all my symptoms" said Drescher, "and I just decided, ‘No more, I’m gonna do alternative. I’m gonna to switch up my act, eat differently, clean up my act.’ And so I cut out alcohol… so that went, and I became gluten-free and vegan."
    Stay tuned to see how this and other celebrity gluten-free diets turn out…
    Read more and see the video at Examiner.com.
     

    Jefferson Adams
    Celiac.com 06/12/2013 - Pregnant women with higher levels of issue transglutaminase (anti-tTG), an antibody common in people with celiac disease, at risk for low fetal and birth weight in their babies, according to a new study in Gastroenterology.
    A number of studies before this one have confirmed an association between celiac disease and poor growth fetus growth, but very little study had been done as to how the level of celiac disease might affect fetal growth, birth weight or birth outcome.
    In an effort to better understand how the level of celiac disease affects fetal growth, birth weight, and birth outcome, a team of researchers set out to assess the associations between levels of antibodies against tissue transglutaminase (anti-tTG, a celiac disease marker) and fetal growth and birth outcomes for pregnant women.
    The research team included J.C. Kiefte-de Jong, V.W. Jaddoe, A.G. Uitterlinden, E. A. Steegers, S.P. Willemsen, A. Hofman, H.Hooijkaas, and H.A. Moll of the Generation R Study Group at Erasmus University Medical Center in Rotterdam, The Netherlands.
    They conducted a population-based prospective birth cohort study of 7046 pregnant women. Serum samples were collected during the second trimester of pregnancy and analyzed for levels of anti-tTG.
    Based on these levels, they grouped each woman into groups of negative anti-tTG (≤0.79 U/mL; n = 6702), intermediate anti-tTG (0.8 to ≤6 U/mL; n = 308), or high anti-tTG individuals (over 6 U/mL; n = 36). They then collected data for fetal growth and birth outcomes from ultrasound measurements and medical records.
    The fetal growth data showed that, on average, fetuses of women in the positive anti-tTG group were 16 g lighter than those of women in the negative anti-tTG group (95% confidence interval [CI], -32 to -1 g) during the second trimester and weighed 74 g less (95% CI, -140 to -8 g) during the third trimester.
    The birth outcome data revealed that newborns of women in the intermediate and positive anti-tTG groups weighed 53 g (95% CI, -106 to -1 g) and 159 g (95% CI, -316 to -1 g) less at birth, respectively, than those of women in the negative anti-tTG group. Of mothers in the intermediate anti-tTG group, those with HLA-DQ2 or -DQ8 had reduced birth weights that were double those of mothers without HLA-DQ2 or -DQ8.
    This study led the researchers to conclude that levels of anti-tTG in pregnant women are inversely associated with fetal growth. The higher the anti-tTG in women, the lower the birth weights of their babies. So, women with the highest levels of anti-tTG (over 6 U/mL) saw the greatest reduction in birth weight of their babies.
    Also, women with intermediate levels of anti-tTG (0.8 to ≤6 U/mL) saw lower birth weights that were even further reduced if they carried the HLA-DQ2 and -DQ8 gene markers.
    Source:
    Gastroenterology. 2013 Apr;144(4):726-735.e2. doi: 10.1053/j.gastro.2013.01.003.

  • 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