• 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

    77,514
    Total Members
    3,093
    Most Online
    DeanaV
    Newest Member
    DeanaV
    Joined
  • 0

    Can Autoimmune Disease Symptoms Vary Depending on the Time of Day?


    Jefferson Adams


    • Loss of the molecular clock in myeloid cells exacerbates T cell-mediated CNS autoimmune disease. Does this tell us something about new about autoimmune diseases?


    Image Caption: Photo: CC--David Dennis

    Celiac.com 01/03/2018 - A recent study indicates that symptoms for some autoimmune disease can vary depending on the time of day.


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    A substance called transcription factor BMAL1 plays a crucial role in the human molecular clock, regulating biological pathways that drive 24 hour circadian rhythms in behavior and physiology. The molecular clock has a major influence on innate immune function, and disturbances in circadian rhythms are associated with increases in multiple sclerosis (MS), for example.

    But, researchers just don't have much good information on the factors that influence this association. A team of researchers recently set out to better understand the factors that influence this association. The research team included Caroline E. Sutton, Conor M. Finlay, Mathilde Raverdeau, James O. Early, Joseph DeCourcey, Zbigniew Zaslona, Luke A. J. O'Neill, Kingston H. G. Mills, and Annie M. Curtis.

    They are variously affiliated with the Immune Regulation Research Group, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; the Inflammatory Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; and with the Department of Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland (RCSI), Dublin, Ireland.

    In a recent study, the research team found that BMAL1 and time-of-day regulate the accumulation and activation of various immune cells in a CNS autoimmune disease model, experimental autoimmune encephalomyelitis (EAE).

    In myeloid cells, BMAL1 maintains anti-inflammatory responses and reduces T cell polarization. Loss of myeloid BMAL1 or midday immunizations to induce EAE create an inflammatory environment in the CNS through expansion and infiltration of IL-1β-secreting CD11b+Ly6Chi monocytes, resulting in increased pathogenic IL-17+/IFN-γ+ T cells.

    These findings show the important role played by the molecular clock in processing innate and adaptive immune crosstalk under autoimmune conditions.

    Understanding the exact ways in which the human molecular clock influences innate immune function, and by extension, autoimmune diseases, will help doctors to better understand these disease, and to develop better approaches to treatment, among other things.

    Source:

    0


    User Feedback

    Recommended Comments

    There are no comments to display.



    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.


  • Ads by Google:

  • About Me

    Jefferson Adams is a freelance writer living in San Francisco. He has covered Health News for Examiner.com, and provided health and medical content for Sharecare.com. His work has appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate, among others.

  • Popular Contributors

  • Ads by Google:

  • Who's Online   13 Members, 1 Anonymous, 538 Guests (See full list)

  • Related Articles

    Jefferson Adams
    Celiac.com 02/20/2013 - Scientific evidence indicates that the risk of developing celiac disease cannot be explained solely by genetic factors. There is some evidence to support the idea that the season in which a child is born can influence the risk for developing celiac disease. It is known that babies born in summer months are likely to be weaned and introduced to gluten during winter, when viral infections are more frequent.
    A number of studies indicate that early viral infections can increase risk levels for celiac disease, however, earlier studies on birth season and celiac disease have been small, and their results have been contradictory.
    To better answer the question, a research team recently set out to conduct a more thorough study of the relationship between birth month and celiac disease.
    The research team included B. Lebwohl, P.H. Green, J.A. Murray, and J.F. Ludvigsson. The study was conducted through the Department of Paediatrics at Örebro University Hospital in Örebro, Sweden.
    To conduct the study, the team used biopsy reports from all 28 Swedish pathology departments to identify individuals with celiac disease, which they defined as small intestinal villous atrophy (n=29 096).
    Using the government agency Statistics Sweden the team identified 144,522 control subjects, who they matched for gender, age, calendar year and county.
    The team then used conditional logistic regression to examined the association between summer birth (March-August) and later celiac disease diagnosis (outcome measure).
    They found that 54.10% of people with celiac disease were born in the summer months compared with 52.75% of control subjects.
    So, being born in the summer is associated with a slightly higher risk of later celiac disease (OR 1.06; 95% CI 1.03 to 1.08; p).
    While summer birth was not associated with a higher rates of celiac diagnosis in later childhood (age 2-18 years: OR 1.02; 95% CI 0.97 to 1.08), it did show a slightly higher risk of developing celiac disease in adulthood (age ≥18 years: OR 1.04; 95% CI 1.01 to 1.07).
    In this study, the data show that people born during the summer months had a slightly higher risk of developing celiac disease, but that excess risk was small, and general infectious disease exposure early in life were not likely to increase that risk.
    Source:
    Arch Dis Child. 2013 Jan;98(1):48-51. doi: 10.1136/archdischild-2012-302360.

    Jefferson Adams
    Celiac.com 07/28/2016 - Celiac disease is an immune-mediated enteropathy triggered by gluten in genetically susceptible individuals. Researchers know that innate immunity plays a role in triggering celiac disease, but they don't understand the connection very well at all.
    Although previous in vitro work suggests that gliadin peptide p31-43 acts as an innate immune trigger, the underlying pathways are unclear and have not been explored in vivo.
    The research team included RE Araya, MF Gomez Castro, P Carasi, JL McCarville, J Jury, AM Mowat, EF Verdu, and FG Chirdo. They are variously affiliated with the Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP)(CONICET-UNLP), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina; the Catedra de Microbiología, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina; the Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada; the Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, Scotland, United Kingdom; and with the Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP)(CONICET-UNLP), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina.
    Their team observed that introduction of p31-43 into the gut of normal mice causes structural changes in the small intestinal mucosa consistent with those seen in celiac disease, including increased cell death and expression of inflammatory mediators. The effects of p31-43 were dependent on MyD88 and type I IFNs, but not Toll-like receptor 4 (TLR4), and were enhanced by co-administration of the TLR3 agonist polyinosinic:polycytidylic acid.
    Together, these results indicate that gliadin peptide p31-43 activates celiac-related innate immune pathways in vivo, such as IFN-dependent inflammation.
    These findings also suggest a common mechanism for the potential interaction between dietary gluten and viral infections in the pathogenesis of celiac disease, meaning that certain viral infections may pave the way for celiac disease to develop.
    Source:
    Am J Physiol Gastrointest Liver Physiol. 2016 Jul 1;311(1):G40-9. doi: 10.1152/ajpgi.00435.2015. Epub 2016 May 5.

    Jefferson Adams
    Celiac.com 04/11/2017 - A new study shows that people living in the southern United States have less celiac disease than their Northern counterparts, regardless of race or ethnicity, socioeconomic status, or body mass index.
    Rates of celiac disease vary by region, with a sharp variation between Americans living in the northern United States and Americans living in the southern part of the country. A team of researchers recently examined geographic, demographic, and clinical factors associated with prevalence of celiac disease and gluten-free diet in the United States.
    The research team included Aynur Unalp-Arida, M.D., Ph.D, of the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Constance E. Ruhl, M.D., Ph.D., of Social & Scientific Systems, Inc., Silver Spring, MD, and Rok Seon Choung, M.D., Ph.D., Tricia L. Brantner, and Joseph A. Murray, M.D., of the Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN.
    For their population-based study, their team analyzed data on gluten-related conditions from the US National Health and Nutrition Examination Survey, from 2009 through 2014, on 22,277 participants 6 years and older. The team found celiac patients using results of serum tests for immunoglobulin A against tissue transglutaminase and endomysium, or of both, a health clinical diagnosis, and adherence to a gluten-free diet.
    The team also accounted for patients who follow a gluten-free diet without a diagnosis of celiac disease. Using the patients' status of gluten-related conditions, the team then compared average serum levels of biochemical and nutritional markers.
    Their results showed that 0.7% of participants had celiac disease, while 1.1% of participants avoid gluten without celiac disease. People who lived at latitudes of 35–39º North or at latitudes of 40º North were more likely to have celiac disease than individuals who lived at latitudes below 35º North, regardless of race or ethnicity, socioeconomic status, or body mass index. People who lived at 40º North or higher were more likely to avoid gluten without a celiac diagnosis, regardless of demographic factors and BMI.
    People with undiagnosed celiac disease, as determined by positive blood tests, had lower average levels of B12 and folate than persons without celiac disease. People with a clinical celiac diagnosis diagnosis had a lower average level of hemoglobin than those without celiac disease.
    Both those with gluten-related conditions and those without showed comparable average levels of albumin, calcium, iron, ferritin, cholesterol, vitamin B6, and vitamin D.
    American living at latitudes of 35º North or greater have higher rates of celiac disease and/or avoid gluten than persons living south of this latitude, independent of race or ethnicity, socioeconomic status, or body mass index.
    Average levels of B12 and folate are lower in individuals with undiagnosed celiac disease, and levels of hemoglobin are lower in participants with a diagnosis of celiac disease, compared to individuals without celiac disease.
    Source:
    Gastroenterology

    Jefferson Adams
    Celiac.com 01/01/2018 - A team of researchers recently set out to conduct a genome-wide association study (GWAS) of general cognitive ability ("g"), further enhanced by combining results with a large-scale GWAS of educational attainment.
    The research team included Max Lam, Joey W. Trampush, Jin Yu, Emma Knowles, Gail Davies, David C. Liewald, John M. Starr, Srdjan Djurovic, Ingrid Melle, Kjetil Sundet, Andrea Christoforou, Ivar Reinvang, Pamela DeRosse, Astri J. Lundervold, Vidar M. Steen, Thomas Espeseth, Katri Räikkönen, Elisabeth Widen, Aarno Palotie, Johan G. Eriksson, Ina Giegling, Bettina Konte, Panos Roussos, Stella Giakoumaki, Katherine E. Burdick, Antony Payton, William Ollier, Ornit Chiba-Falek, Deborah K. Attix, Anna C. Need, Elizabeth T. Cirulli, Aristotle N. Voineskos, Nikos C. Stefanis, Dimitrios Avramopoulos, Alex Hatzimanolis, Dan E. Arking, Nikolaos Smyrnis, Robert M. Bilder, Nelson A. Freimer, Tyrone D. Cannon, Edythe London, Russell A. Poldrack, Fred W. Sabb, Eliza Congdon, Emily Drabant Conley, Matthew A. Scult, Dwight Dickinson, Richard E. Straub, Gary Donohoe, Derek Morris, Aiden Corvin, Michael Gill, Ahmad R. Hariri, Daniel R. Weinberger, Neil Pendleton, Panos Bitsios, Dan Rujescu, Jari Lahti, Stephanie Le Hellard, Matthew C. Keller, Ole A. Andreassen, Ian J. Deary, David C. Glahn, Anil K. Malhotra, and Todd Lencz. They are variously associated with the dozens of research facilities listed below.
    Their study provided a large-scale GWAS of cognitive performance, combined with GWAS of educational attainment; 70 independent genomic loci associated with individual differences in cognition. The study found that implicated genes suggest potential treatment targets for cognitive enhancement. The team also observed genetic overlap between cognitive ability and multiple health-related phenotypes.
    For their genome-wide association study (GWAS) of general cognitive ability ("g"), the team evaluated 107,207 subjects. They further enhanced their data pool by combining results with a large-scale GWAS of educational attainment. They also identified 70 independent genomic loci associated with general cognitive ability.
    Observing the outcomes, the team saw substantial enrichment for genes triggering Mendelian disorders with an intellectual disability phenotype. Analysis of competitive pathways pointed to neurogenesis and synaptic regulation, as well as the gene targets of two pharmacologic agents: cinnarizine, a T-type calcium channel blocker, and LY97241, a potassium channel inhibitor.
    According to the researchers: "we observed modest, yet nominally significant, inverse correlations between cognition and autoimmune diseases such as eczema and Crohn's disease, attaining Bonferroni significance for rheumatoid arthritis (rg for MTAG results = −0.2086; p = 1.60E−08). There was also a Bonferroni-significant positive genetic correlation with celiac disease (rg for MTAG results = 0.1922; p = 0.0001)."
    Full analysis of both the transcriptome and epigenome showed that the implicated loci were enriched for genes expressed across all brain regions; mostly in the cerebellum.
    Interestingly, only genes expressed in neurons were enriched, not those expressed in oligodendrocytes or astrocytes.
    Lastly, the team observed genetic correlations between cognitive ability and various phenotypes, including psychiatric disorders, autoimmune disorders, longevity, and maternal age at first birth.
    Source:
    Cell.com. DOI: http://dx.doi.org/10.1016/j.celrep.2017.11.028 
    The research team members are variously associated with the following:
    Campbell Family Mental Health Institute, Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada Institute of Mental Health, Singapore, Singapore BrainWorkup, LLC, Los Angeles, CA, USA Institute for Behavioral Genetics, University of Colorado, Boulder, CO, USA Division of Psychiatry Research, Zucker Hillside Hospital, Glen Oaks, NY, USA Department of Psychiatry, Hofstra Northwell School of Medicine, Hempstead, NY, USA Center for Psychiatric Neuroscience, Feinstein Institute for Medical Research, Manhasset, NY, USA Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA Department of Genetics and Genomic Science and Institute for Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, USA Mental Illness Research, Education, and Clinical Center (VISN 2), James J. Peters VA Medical Center, Bronx, NY, USA Department of Neurology, Bryan Alzheimer's Disease Research Center and Center for Genomic and Computational Biology, Duke University Medical Center, Durham, NC, USA Department of Psychiatry and Behavioral Sciences, Division of Medical Psychology, Duke University Medical Center, Durham, NC, USA Laboratory of NeuroGenetics, Department of Psychology & Neuroscience, Duke University, Durham, NC, USA Human Longevity Inc., Durham, NC, USA Department of Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA Department of Psychology, Yale University, New Haven, CT, USA Department of Psychology, Stanford University, Palo Alto, CA, USA Clinical and Translational Neuroscience Branch, Intramural Research Program, National Institute of Mental Health, National Institute of Health, Bethesda, MD, USA Lieber Institute for Brain Development, Johns Hopkins University Medical Campus, Baltimore, MD, USA Neuroimaging, Cognition & Genomics (NICOG) Centre, School of Psychology and Discipline of Biochemistry, National University of Ireland, Galway, Ireland Neuropsychiatric Genetics Research Group, Department of Psychiatry and Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin, Ireland Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK Department of Psychology, University of Edinburgh, Edinburgh, UK Alzheimer Scotland Dementia Research Centre, University of Edinburgh, Edinburgh, UK Division of Brain Sciences, Department of Medicine, Imperial College, London, UK Centre for Epidemiology, Division of Population Health, Health Services Research & Primary Care, The University of Manchester, Manchester, UK Centre for Integrated Genomic Medical Research, Institute of Population Health, University of Manchester, Manchester, UK Division of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Salford Royal NHS Foundation Trust, Manchester, UK Department of Biological and Medical Psychology, University of Bergen, Bergen, Norway Department of Medical Genetics, Oslo University Hospital, University of Bergen, Oslo, Norway NORMENT, K.G. Jebsen Centre for Psychosis Research, University of Bergen, Bergen, Norway Dr. Einar Martens Research Group for Biological Psychiatry, Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway Department of Psychology, University of Oslo, Oslo, Norway Department of Psychology, University of Edinburgh, Edinburgh, UK Dr. Einar Martens Research Group for Biological Psychiatry, Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge, UK Department of Medical Genetics, University of Helsinki and University Central Hospital, Helsinki, Finland Department of General Practice, University of Helsinki and Helsinki University Hospital, Helsinki, Finland National Institute for Health and Welfare, Helsinki, Finland Folkhälsan Research Center, Helsinki, Finland Helsinki Collegium for Advanced Studies, University of Helsinki, Helsinki, Finland Department of Psychiatry, Martin Luther University of Halle-Wittenberg, Halle, Germany Department of Psychology, University of Crete, Crete, Greece Department of Psychiatry, National and Kapodistrian University of Athens Medical School, Eginition Hospital, Athens, Greece University Mental Health Research Institute, Athens, Greece Neurobiology Research Institute, Theodor-Theohari Cozzika Foundation, Athens, Greece Department of Psychiatry and Behavioral Sciences, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD, USA McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA 23andMe, Inc., Mountain View, CA, USA

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/20/2018 - Currently, the only way to manage celiac disease is to eliminate gluten from the diet. That could be set to change as clinical trials begin in Australia for a new vaccine that aims to switch off the immune response to gluten. 
    The trials are set to begin at Australia’s University of the Sunshine Coast Clinical Trials Centre. The vaccine is designed to allow people with celiac disease to consume gluten with no adverse effects. A successful vaccine could be the beginning of the end for the gluten-free diet as the only currently viable treatment for celiac disease. That could be a massive breakthrough for people with celiac disease.
    USC’s Clinical Trials Centre Director Lucas Litewka said trial participants would receive an injection of the vaccine twice a week for seven weeks. The trials will be conducted alongside gastroenterologist Dr. James Daveson, who called the vaccine “a very exciting potential new therapy that has been undergoing clinical trials for several years now.”
    Dr. Daveson said the investigational vaccine might potentially restore gluten tolerance to people with celiac disease.The trial is open to adults between the ages of 18 and 70 who have clinically diagnosed celiac disease, and have followed a strict gluten-free diet for at least 12 months. Anyone interested in participating can go to www.joinourtrials.com.
    Read more at the website for Australia’s University of the Sunshine Coast Clinical Trials Centre.

    Source:
    FoodProcessing.com.au

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

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

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

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    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.