• 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

    Could Green Banana Pasta be on Your Plate Soon?


    Jefferson Adams

    Celiac.com 08/24/2012 - Tired of the standard choices for gluten-free pasta? If researchers at the University of Brazil have their way, you may soon be enlivening your current gluten-free choices with pasta made from the flour of green bananas.


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    Photo: CC--zenobia_joyThe researchers included Renata Puppin Zandonadi, PhD, Raquel Braz Assunção Botelho, PhD, Lenora Gandolfi, PhD, Janini Selva Ginani, MSc, Flávio Martins Montenegro, MSc, and Riccardo Pratesi, PhD.

    According to an article in the Journal of the Academy of Nutrition and Dietetics, the team found a way to make pasta out of green banana flour. The flour is completely gluten-free, and the pasta compares favorably with pasta made from whole wheat, according to taste test results.

    Currently, green bananas are regarded an undesirable product, with low commercial value, and limited industrial use. In an effort to change that reality, the researchers set out to develop and analyze a gluten-free pasta made with green banana flour.

    When they tested their finished product, they found "no significant difference between the modified pasta and standard samples in terms of appearance, aroma, flavor, and overall quality," study researcher Renata Puppin Zandonadi, PhD, of the University of Brazil, said in a statement.

    For the study, researchers had 50 people without celiac disease, and 25 with celiac disease, taste whole wheat pasta made with eggs, and compare it with pasta made from green banana flour, egg whites, gums and water.

    Both the test group with celiac disease and the group without celiac disease reported that the banana flour pasta tasted better overall than the whole wheat pasta.

    If the project pans out, it could be a win-win-win, offering banana growers and pasta product makers a way to expand their markets, and offering consumers of gluten-free pasta a new and delicious alternative.

    What do you think about the idea of gluten-free pasta made from green bananas? Share your comments below.


    Source:

    0


    User Feedback

    Recommended Comments

    Guest dappycharlie

    Posted

    I can now only eat corn pasta - the rice pasta is so mushy as to be inedible, even when cooked al dente. So if they can come up with something closer to "real" pasta - GREAT !!

    Share this comment


    Link to comment
    Share on other sites
    Guest Susan Z

    Posted

    OK, but how digestible is it? I would never eat a green banana because I feel it would be more resistant to breaking down and being absorbed by the gut, which would create more food for the bacteria way down below, causing a lot of gas.

     

    Often folks with celiac disease don't have the optimal amount or types of gut bacteria to handle this sort of unripe food.

     

    Save it for those with diabetes who need resistant start to slow food from turning to blood sugar.

    Share this comment


    Link to comment
    Share on other sites
    Guest Montie Vogt

    Posted

    Sounds great! Hope it works out.

    Share this comment


    Link to comment
    Share on other sites

    Sounds Fantastic! I am all for finding a better gluten-free pasta.

    Share this comment


    Link to comment
    Share on other sites
    Guest Regina

    Posted

    OK, but how digestible is it? I would never eat a green banana because I feel it would be more resistant to breaking down and being absorbed by the gut, which would create more food for the bacteria way down below, causing a lot of gas.

     

    Often folks with celiac disease don't have the optimal amount or types of gut bacteria to handle this sort of unripe food.

     

    Save it for those with diabetes who need resistant start to slow food from turning to blood sugar.

    Hi Susan, it will be digestible. People in the Caribbean have been eating boiled green bananas and green banana porridge for centuries. I am celiac and I eat them. I just had the most delicious green banana porridge made with coconut milk last month, very nutritious also. Google and you will see recipes and nutritional info.

    Take care.

    Share this comment


    Link to comment
    Share on other sites

    This is great. I'm pretty sure that a flour made out green plantains would be good. In Puerto Rico we make "pasteles", they are made with the masa from green plantains and green bananas.

    Share this comment


    Link to comment
    Share on other sites

    I think this sounds great and would DEFINITELY try it! And "dappycharlie" - I can't eat the rice pastas either - texture is AWFUL - and I am allergic to corn but, LOVE the texture and taste of the potato, soy and rice blend pasta. Don't know if I am allowed to say brands but, Bionaturae is our favorite!

    Share this comment


    Link to comment
    Share on other sites
    Guest Maggie

    Posted

    Sounds interesting! And hopefully better-cooking and -tasting than rice or corn pasta (which usually turns out mushy), or quinoa pasta, which cooks and cooks and still doesn't seem done! And, just as long as it doesn't TASTE like green bananas, it gives me hope!

    Share this comment


    Link to comment
    Share on other sites
    Guest Arthur

    Posted

    This is very promising. There is a company in Marin County working on introducing the flour commercially in the Bay Area. Stay tuned.

    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   8 Members, 0 Anonymous, 928 Guests (See full list)

  • Related Articles

    Scott Adams
    Celiac.com 03/19/2002 - For the past several years, Gary M. Gray, M.D. and Chaitan Khosla, Ph.D., both at Stanford University, have been studying the underlying causes of Celiac Disease, with an eye toward finding a therapeutic solution that would not require the strict adherence to a gluten-free diet. For the past two years, I have helped organize the Celiac conference at Stanford University; and we have collected blood from Celiac volunteers for their research. Based on a series of studies involving animal tissue, Drs. Gray, Khosla, and coworkers have developed a hypothesis for the cause of the disease. Their findings in animal studies need to be confirmed on human tissue, and any differences in normal and Celiac intestine must be defined. The Stanford researchers are now in need of volunteers who are scheduled for a follow-up biopsy as part of their optimal care to provide intestinal tissue samples. Volunteers must be biopsy-diagnosed Celiacs who, as part of their care, will be undergoing an upper gastrointestinal endoscopy for recovery of small biopsies from the duodenum. For this research, two small (a few milligrams) of additional tissue will be taken during the biopsy, frozen immediately, and transported to Stanford. Please note that volunteers undergoing procedures at locations other than Stanford Hospital could participate. The small amount of additional tissue does not constitute a significant additional risk over and above that you will undergo due to the endoscopy and routine biopsies for the pathologist to examine. The research has been approved by the Human Subjects Committee at Stanford University Medical Center.
    If you would like to participate in this study, please contact Kelly Rohlfs at 650-725-4771 or kellyr@bonair.stanford.edu.If you have questions concerning the risks and benefits of this study, please contact Dr. Gray at 650-725-3366 or gray@stanford.edu. Dr. Gray will coordinate the study with your gastroenterologist at the time of your endoscopy.

    Jefferson Adams
    Celiac.com 03/28/2011 - While rates of diagnosed celiac disease are less than 1 in 2,000 in the United States, screening studies in European and other populations have shown a much higher prevalence.
    A team of researchers recently set out to assess rates of celiac disease and the benefits of screening in the general adult population in certain geographically isolated areas.
    The research team included Kent D. Katz MD, Shahrooz Rashtak MD, Brian D. Lahr BS, MS, L. Joseph Melton III MD, Patricia K. Krause BS, MBA, Kristine Maggi PA-C, Nicholas J. Talley MD, PhD, and Joseph A. Murray MD.
    They are affiliated variously with the Wyoming Medical Center in Casper, Wyoming, the Department of Dermatology, the Division of Gastroenterology and Hepatology of the Department of Internal Medicine, the Division of Biostatistics, and the Division of Epidemiology in the Department of Health Sciences Research at the Mayo Clinic in Rochester, Minnesota.
    The team measured serum tissue transglutaminase antibodies (tTG-IgA) in adult volunteers at the annual Casper, Wyoming, Blue Envelope Health Fair blood draw. The team then checked endomysial IgA antibodies in those with positive tTG-IgA results.
    For those who tested positive for both screens, the team offered endoscopy with small bowel biopsy. All participants completed a short gastrointestinal (GI) symptom questionnaire.
    The team did blood tests on a total of 3,850 subjects, 34 of whom tested positive for both tTG and endomysial antibody (EMA) IgA.
    The team excluded three individuals who had been previously diagnosed with celiac disease, leaving 31 subjects, and making the total positive celiac serology in this community sample 0.8%.
    The team offered small bowel biopsy to those 31 subjects. They performed a total of 18 biopsies, with 17 patients (94%) showing at least partial villous atrophy.
    Symptoms reported by test subjects did not predict positive diagnosis. In fact, most subjects showed no symptoms, or else showed atypical symptoms.
    Serologic testing readily detects celiac disease in a general population. Screening results showed that undiagnosed celiac disease affects 1 in 126 individuals in this Wyoming community.
    Source:

    Am J Gastroenterol advance online publication 1 March 2011. doi: 10.1038/ajg.2011.21

    Tina Turbin
    Celiac.com 10/12/2011 - According to recent estimates, three million Americans suffer from celiac disease—approximately 1% of the population, and only three percent of them have to this writing been correctly diagnosed. As startling as that sounds to us all, according to a news article on Medscape Today, the incidence of celiac disease has increased markedly over the last three decades, perhaps even as fourfold, and studies are suggesting the incidence may actually be higher than 1% of the population.
    What is the reason for this? According to Dr. Jonas Ludvigsson, MD, from the Department of Medicine, Epidemiology Unit at the Karolinska Institute and Orebro University Hospital in Sweden, and a renowned celiac expert, there may be many factors explaining this, but there probably is an actual increase underlying these.
    The Medscape article went on to report that the Mayo Clinic has confirmed increase in celiac disease incidence, reported in Discovery's Edge, the Mayo Clinic's research magazine. Dr. Joseph Murray, MD, and colleagues analyzed stored blood samples from Air Force recruits in the early 1950s for gluten antibodies. It was assumed that 1% would be positive, given today's estimates, but the number of positive results was far smaller. Dr. Murray and his colleagues compared their results with two more recently collected sets with the conclusion that celiac disease is about four times more common today than it was in the 1950s.
    Additionally, Dr. Ludviggon's research team in Sweden has found that those living with celiac disease and latent celiac disease have higher mortality than those who don't have these conditions. Latent celiac disease is also known as "gluten sensitivity," a term to describe those who have "normal small intestinal mucosa but positive celiac disease serology," estimated to affect 1 in 1000 people. According to Dr. Ludvigsson's research team, in 1 year, 10 of 1000 individuals with celiac disease will die, as compared with 7 in 1000 individuals without the disease. The mortality rate is increased among those who also have latent celiac disease as well. The increased risk, however, is quite small.
    As alarming as the statistics are regarding the increasing rate of celiac disease, Dr. Ludvigsson shares some good news with Medscape—the methods of diagnosing celiac disease are actually improving. According to some other estimates, the rate of celiac diagnosis rate is increasing. For those who are testing positive for the celiac disease, the only method of treatment currently available is eliminating gluten from the diet. Yes, this is a simple treatment, although it can require some challenging lifestyle adjustments for the gluten-free community, something which I address in my work as an author, researcher, and gluten-free advocate. In the future, we may see other treatments such as gluten-digesting enzymes (which are on the rise) or even the genetic modification of the structure of gluten in wheat so that it will not cause an autoimmune reaction in celiac patients. Even with celiac diagnosis incidence on the rise, with raised awareness and effective diagnosis, we can help change the lives of millions of celiac Americans for the better. This is an important endeavor.


    Jefferson Adams
    Celiac.com 09/18/2013 - New tests and new histological criteria for diagnosing celiac disease, along with changing perspectives on the disease's natural history are causing a number of researchers to question past prevalence estimates for celiac disease.
    A team of researchers recently set out to establish a more accurate estimate of celiac disease rates by using a new serogenetic method.
    The research team included Robert P Anderson, Margaret J Henry, Roberta Taylor, Emma L Duncan, Patrick Danoy, Marylia J Costa, Kathryn Addison, Jason A Tye-Din, Mark A Kotowicz, Ross E Knight, Wendy Pollock, Geoffrey C Nicholson, Ban-Hock Toh, Matthew A Brown and Julie A Pasco.
    They are variously affiliated with the Walter and Eliza Hall Institute of Medical Research, the Department of Medical Biology at the University of Melbourne, the Department of Gastroenterology at The Royal Melbourne Hospital, Melbourne Health in Parkville, Australia, ImmusanT Inc., One Kendall Square, Building 200, LL, Suite 4, Cambridge, MA, USA, the School of Medicine at Deakin University in Geelong, Australia, Healthscope Pathology in Melbourne, Australia, the Human Genetics Group at the University of Queensland Diamantina Institute, Level 5, Translational Research Institute in Woolloongabba, Australia, Endocrinology at Royal Brisbane and Women’s Hospital, Herston, Australia, the NorthWest Academic Centre of the Department of Medicine at The University of Melbourne in St Albans, Australia, Geelong Gastroenterology, Level 1, in Geelong, Australia, the Rural Clinical School at the School of Medicine of The University of Queensland in Toowoomba, Australia, and Roche Diagnostics Australia, in Castle Hill, Australia.
    The researchers assessed human leukocyte antigen (HLA)-DQ genotype in 356 patients with biopsy-confirmed celiac disease.
    They did the same for two age-stratified, randomly selected community groups of 1,390 women and 1,158 men, who served as controls. They tested and screened all patients for celiac-specific serology.
    They found that only five patients with biopsy-confirmed celiac disease lacked the susceptibility alleles HLA-DQ2.5, DQ8, or DQ2.2, and four of these patients had been misdiagnosed. HLA-DQ2.5, DQ8, or DQ2.2 was present in 56% of all women and men in the community cohorts.
    Transglutaminase (TG)-2 IgA levels were abnormal in 4.6% of the community women, and in 6.9% of the community men. Composite TG2/deamidated gliadin peptide (DGP) IgA/IgG were abnormal in 5.6% of the community women and in 6.9% of the community men.
    But in the screen-positive group, only 71% of women and of women and 65% of men possessed HLA-DQ2.5, DQ8, while 75% of women and 63% of men possessed DQ2.2.
    Medical review was possible in 41% of seropositive women and 50% of seropositive men, and led to biopsy-confirmed celiac disease in 10 women (0.7%) and 6 men (0.5%). Based on relative risk for HLA-DQ2.5, DQ8, or DQ2.2, celiac disease affected 1.3% of men and women with positive TG2 IgA screens, and 1.9% of women and 1.2% of men with positive TG2/DGP IgA/IgG screens
    Serogenetic data from these community cohorts indicated that testing screen positives for HLA-DQ, or carrying out HLA-DQ and further serology, could have reduced unnecessary gastroscopies due to false-positive serology by at least 40% and by over 70%, respectively.
    Requiring biopsy confirmation based on TG2 IgA serology leads to substantial underestimations of the community prevalence of celiac disease.
    Testing for HLA-DQ genes and affirmative blood results could reduce the numbers of unnecessary gastroscopies.

    Source:
     BMC Medicine 2013, 11:188. doi:10.1186/1741-7015-11-188

  • 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