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Found 91 results

  1. Celiac.com 01/16/2018 - More and more, people are adopting a gluten-free diet due to perceived health and weight-loss benefits. A team of researchers recently set out to ask people with celiac disease and non-celiac gluten sensitivity about their views on the health effects of gluten, and safety of vaccines and gluten-free food products. The research team included Loren G. Rabinowitz, Haley M. Zylberberg, Alan Levinovitz, Melissa S. Stockwell, Peter H. R. Green, and Benjamin Lebwohl. They are variously affiliated with the Department of Medicine, Celiac Disease Center, Columbia University College of Physicians and Surgeons New York USA; the Department of Philosophy and Religion James Madison University Harrisonburg USA, the Department of Pediatrics Columbia University College of Physicians and Surgeons New York USA, the Department of Population and Family Health, Mailman School of Public Health, Columbia University New York USA, the Department of Epidemiology, Mailman School of Public Health, Columbia University New York USA, and the Celiac Disease Center at Columbia University New York USA. Their team conducted an online survey of celiac and non-celiac gluten sensitivity patients from a celiac disease center e-mail list. They used univariate and multivariate analysis to compare responses from the two groups. The overall response rate was 27%, with 217 non-celiac gluten sensitivity responses, and 1,291 celiac disease responses. Subjects with non-celiac gluten sensitivity were more likely than those with celiac disease to disagree with the statement that "vaccines are safe for people with celiac disease." In all, 41.3% of respondents with non-celiac gluten sensitivity said vaccines are safe for celiacs, while just 26.4% of celiac patients said so. Celiac patients were slightly more likely to decline vaccination when offered, at about 31%, compared with just over 24% of gluten-sensitive respondents. After adjusting for age and gender, non-celiac gluten sensitivity subjects were more likely than celiac disease subjects to avoid genetically modified (GMO) foods, eat only organic products, believe that the FDA is not a reliable source of information, and believe a gluten-free diet will improve energy and concentration. People with non-celiac gluten sensitivity were more likely than those with celiac disease to have doubts about vaccine safety and to believe in the value of non-GMO and organic foods. The team's findings suggest that there might not be enough easily accessible information on gluten and its inclusion in food and drugs, and that may reinforce incorrect beliefs that are contrary to good public health. Source: Springer.com.
  2. 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.
  3. 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
  4. Celiac.com 10/03/2017 - As people eat less processed foods, and more people adopt a gluten-free diet, manufacturers are selling less and less refined wheat flour, less bread, rolls, and cereals. Consumption of wheat is plummeting, and that has the people who grow wheat wondering what to do. Well, one thing wheat growers can do is hire researchers to study the problem in such a way that the logical conclusion is that foods made from refined grains, such as breads, rolls, and cereals, aren’t really that bad after all. And that seems to be what happened with a recent study funded by the Grain Foods Foundation, an industry group. Unsurprisingly, perhaps, the study, published last month in the journal Nutrients, calls things like breads, rolls, tortillas, and ready-to-eat cereals "meaningful contributors" of nutrients like thiamin, folate, iron, zinc, and niacin. The study notes that such foods are also low in added sugars and fats, which is not the case with many grain foods like baked goods. Rather than being independent, both authors of the study work for PR companies that help other companies, including major food and beverage companies, communicate the benefits of their products. While it’s true that many refined grain foods provide these nutrients, there are many other sources. For example, foods like white beans, lentils, spinach, dark chocolate, and tofu provide iron, while oysters, beef, baked beans, yogurt, and chickpeas provide zinc. Is bread bad for people? Mostly not. People with celiac disease need to eat gluten-free, and should probably make an extra effort to eat foods that are nutrient dense. For most folks bread is fine, but as with many foods, not all breads are equal. Look for whole-grain breads that are nutrient dense. Watch out for the added sugar, salt, and fat that come with many processed foods. And don’t be swayed by industry-funded studies that tell you to eat more of the product they are peddling. Read more at: Healthline.com
  5. Celiac.com 09/22/2017 - Misdiagnosed my sophomore/ junior year of High School, 3 years ago, with celiac disease, I became obsessed with the science of this ailment and how it was supposedly affecting me. I was shocked by how little is known about this autoimmune disease and the many gaps in research done on it. One such gap is that of cross-contamination in the household, where it is likely to have a daily impact on those following gluten-free diets. Because of this, I decided to help fill this gap in scientific knowledge with a manageable project based on cross-contamination in the home, asking whether one can share common kitchen cookware that is used with gluten containing foods, or if people, to help maintain a gluten-free diet, need designated ones for their food preparation. Either way that this research played out would be beneficial to the gluten-free community. For example, some families with members on gluten-free diets will spend a lot of money to buy all new ‘gluten-free' designated cookware and utensils to help minimize cross-contamination. Part of the relevancy of this project is economical, as designated cookware can be very costly. Despite the cost, other factors affect the value of this research, including the impracticality of having a double set of kitchen appliances, which would be very bulky and impractical for those with limited space. Another factor that influences the significance of this project is beyond one's home; celiac disease brings a lot of social stress. By assuring there is limited or no cross-contamination from common kitchen appliances after customary washing, these individuals would be able to have some confidence when eating at friends' or families' homes. On the other end, if this research shows that there is cross-contamination with shared supplies it will highlight the need for dedicated ones to maintain a strict gluten-free diet. Just because a gluten-free recipe is used, a given dish may not be genuinely gluten free if there is contamination from cookware. Hazards and Concerns To fully understand the hazards of gluten contamination, a few things must first be established: What is gluten? Who is it harmful to? How and to what extent must it be avoided? How does cross-contamination occur? What is Gluten? The United States Food and Drug Association (FDA) have been trying to define "gluten" for years. The current proposed definition is, "the proteins that naturally occur in a ‘prohibited grain' that may cause adverse health effects in persons with celiac disease."(1) These prohibited grains are any species belonging to triticum, hordeum and secale or more commonly called respectively: wheat, barley, and rye, though other prohibited grains exist as hybrids of any of the three.(2) That being said, not all proteins in these three types of grains are toxic to those with celiac disease as there are two parts to glutens: prolamins, the immunotoxic ones, and glutenins, the safe ones.(3) The prolamins in the three main prohibited grains, wheat, barley, and rye, are gliadin, hordein, and secalin.(4) Who Does Gluten Harm? Gluten is toxic to certain individuals with celiac disease, an autoimmune disease that also goes by the names of: coeliac disease, celiac sprue, nontropical sprue, and gluten-sensitive enteropathy.(5) A Thomson Healthcare Company study estimated that up to 1.5 Million Americans, or one in 133 people, have celiac disease, though other individuals avoid gluten as well, such as those with gluten intolerance, or other ailments where a gluten-free diet is believed to lessen their symptoms.(6) This strict abstention from gluten is because celiac disease cannot be cured, or mediated with medication as yet. The only way to help those affected is by following this strict diet. How and to What Extent Must it be Avoided? Foods that contain wheat, rye, and barley, or any hybrid of these grains contain gluten. Gluten is a very common protein in foods, whether from bread, or as an additive to provide a thicker texture, such as in soups. This versatility makes processed foods, in the eyes of those on gluten-free (gluten-free) diets, something to be wary of. Because of this caution, companies want their products to be certified gluten-free, which according to the FDA calls for Despite current unknowns regarding contamination, a strict gluten-free diet must exclude all foods that contain gluten and minimize cross-contamination. This means from eating out, to staying in, gluten must be avoided. Topical products where gluten is added, such as in some lotions or body washes, should also be avoided. Despite the widespread use of gluten there are gluten-free grains and foods, such as beans, rice, millet, corn, amaranth, and soy. How Does Cross-contamination Occur? Cross-contamination is a term usually directed toward accidental spread of bacteria due to not cooking food, washing hands or materials. However, in this article it refers to the accidental transfer or content of gluten, the protein that is toxic to those with celiac disease. In my personal experience and research on celiac forums, when a member of a family goes gluten-free the family will most likely continue eating a regular diet. In addition, as the average time it takes to be diagnosed from the first onset of symptoms is 10 years in the United States, these families have kitchen supplies that they have been using with gluten.(8) With little public knowledge about celiac disease and going gluten-free, people tend to overlook cross-contamination. Theoretically, in the simple act of making a sandwich with gluten-free bread there are many different ways for it to become contaminated. For example, from a shared jar of peanut butter or jelly with crumbs accidentally getting into it and then dipped out onto the gluten-free bread, or crumbs on the surface it's prepared on sticking to the gluten-free bread. Research Investigation The investigation of common kitchen appliances that are frequently exposed to gluten and cleaned by customary sanitation techniques calls for the conduction of an enzyme linked immunoassay (ELISA) test when using them to prepare gluten-free food. Various well used kitchen appliances, wood and plastic cutting boards, cast iron skillets, both seasoned and unseasoned, Teflon and aluminum pans, and ceramic and glass bowls were contaminated with gluten, using whole wheat flour slurry, and then washed by their standard cleaning technique, either scrubbing with hot soapy water, or wiping with a paper towel and water. Afterward a certified gluten-free substance, in this case millet flour, was added and let sit to allow adherence of any gluten remaining on the ‘cleaned' surface. Figure 1 illustrates the extraction solutions that were made from the samples and injected into the Microwell plates with the anti-body coating and the various washes of the ELISA test. Then, the gliadin, if present, bound to the walls of the wells due to its antibody coating and the wells were washed to eliminate remaining parts in the well. Next, the enzyme Horseradish Peroxidase, or HRP enzyme, adheres post-injection to any gliadin present as an amplifier and is again washed to remove extra parts. Lastly, a 3,3', 5,5'-Tetramethylbenzidine, or TMB substrate was added which turns blue in the presence of a peroxidase, in this case the adhered HRP enzyme, which can only be there if there was gliadin to attach to. This color after a acid stop solution, which turns it yellow, is added is then assessed using a Microwell plate reader for its absorbency which, when compared with a standards curve made from known samples, by the company, will be used to determine the gluten content, in parts per million, of all the samples individually. Results Intuition may lead one to think that well developed standard cleaning techniques for most appliances, and the difficulty in transferring proteins to a gluten-free medium from a surface that has been cleaned, will make gluten cross-contamination unlikely. However, due to factors such as porosity and oiliness, some surfaces may harbor gluten. Typically, far less rigorous cleaning techniques are used on the seasoned cast iron skillet and it is very porous and oily so the gluten proteins have a better chance of binding to it and then transferring to a gluten free medium. Given the test results of the ELISA test, this is mostly true. Despite the logic being the same, and it being the intuitive most likely candidate for cross-contamination a different appliance with the same sanitation technique proved to exceed the gluten parts per million limit where as the cast iron did not. The only absorbency ratings from the samples that interpolated to be greater than the 20 ppm of gluten allowance were two extractions from the Teflon pan. All other ratings, including two other Teflon pan extractions, were below the limit. Conclusion Ninety-four percent of the sample extractions showed less than the 20 parts per million of gluten which is the threshold for something to be declared gluten-free. Teflon had half of its extractions above the limit, as such Teflon should be deemed cross-contaminated. However, the Teflon's other extraction samples had well below 20ppm. This could have been due to the sample's gluten free sample being rather large and thus only part of it could have gotten contaminated (positive cross-contamination) and other parts not (negative cross-contamination). All others samples were classified as gluten-free due to being below the 20ppm allowance. In conclusion, the values of gluten cross-contamination, in ppm, were too small to hinder the integrity of the gluten-free medium in all but Teflon. Thus, to the extent of the experiment done, having tested only eight different kitchen appliances, with only two different sanitation techniques, common kitchen appliances that are frequently exposed to gluten, can be cleaned by customary methods and used to prepare gluten-free food with the exception of Teflon appliances. This research project could be extended by more trials. For example, eight types of common kitchen appliance were used, but only one appliance was used to represent each type. More trials could be done within each type, using different brands, variations in extent of wear, etc. In addition, the only type of contaminant used was whole-wheat slurry. Other forms of contaminant should be tested as well, to show the universality of the cross-contamination, or lack thereof. This should include different gluten-containing substances, as well as some dry and some wet. Unfortunately, this research question will have exceptions as the extent of washing and wear on an appliance is a more subjective issue. This means that even if it is found on a larger scale that certain appliances have been found to be safe for producing gluten-free foods, it should still be avoided when possible for those with celiac disease as if not washed properly; it could go beyond the 20ppm allowance and be immunotoxic to these individuals. Vested interest is always a concern with research, and thus it must be pointed out that no company or university holds any interest in this project and no help was given financially or academically, only that The University of Detroit Mercy allowed me to use their lab for the duration of the experiment and Microwell plate reader. In addition, both sides of the results would prove beneficial, so the data were not interpreted with a bias toward any desired result. Eleanore Dara is a "rising scientist" and is an incoming biochemistry student on a Research Track Major at the University of Scranton in Pensnsylvania. References: "Questions and Answers on the Gluten-Free Labeling Proposed Rule." U S Food and Drug Administration. N.p., 23 Jan. 2007. Web. 31 Jan. 2011. https://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/Allergens/ucm362880.htm Ibid. Amaya-González, et al. "Amperometric Quantification of Gluten in Food Samples Using an ELISA Competitive Assay and Flow Injection Analysis." Electoanaylsis 23.1 (2010): 108+. Wiley Online Library. Web. 8 Mar. 2011. "What Is Gliadin? What Is Its Role In Gluten Sensitivity?." Gluten Free Around The World, Traditional Foods Make Eating an Adventure. N.p., n.d. Web. 25 Mar. 2012. http://www.gluten-free-around-the-world.com/gliadin.html Snyder, Cara et al. "Celiac Disease Coeliac Disease, Celiac Sprue, Nontropical Sprue, Gluten-Sensitive Enteropathy." The National Center for Biotechnology Information. N.p., 3 June 2008. Web. 31 Jan. 2011. Cerrato, Paul L. "Gluten Intolerance: more common than thought. (Complementary Therapies Update)." RN 66.8 (2003): 23. General One File. Web. 28 Mar. 2011. "Questions and Answers on the Gluten-Free Labeling Proposed Rule." U S Food and Drug Administration. N.p., 23 Jan. 2007. Web. 31 Jan. 2011. https://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/Allergens/ucm362880.htm Adams, Scott. "USA - Average Time to Diagnosis = 10 Years - Celiac.com." Celiac Disease & Gluten-free Diet Information at Celiac.com. Scott Adams, 26 July 1996. Web. 16 Feb. 2012. http://www.celiac.com/articles/48/1/USA---Average-Time-to-Diagnosis--10-Years/Page1.html.
  6. Celiac.com 08/23/2017 - A team of researchers recently set out to assess how many patients with a diagnosis of non-celiac wheat sensitivity (NCWS) still experienced symptoms of wheat sensitivity after an average follow-up time of 99 months. The research team included Antonio Carroccio, Alberto D’Alcamo, Giuseppe Iacono, Maurizio Soresi, Rosario Iacobucci, Andrea Arini, Girolamo Geraci, Francesca Fayer, Francesca Cavataio, Francesco La Blasca, Ada M. Florena, and Pasquale Mansueto. Using data collected from 200 participants from a previous study of non-celiac wheat sensitivity, performed between July and December 2016 in Italy, the team found that 148 of these individuals still followed a strict wheat-free diet. In total, 175 patients (88%) said that they had fewer symptoms after a diagnosis of non-celiac wheat sensitivity and general improvement. Of the 148 patients who adhered strictly to a gluten-free diet, 145 (98%) had reduced symptoms, compared with 30 of 52 patients who did not adhere to a gluten-free diet (58%) (P < .0001). Of the 22 patients who repeated the double-blind, placebo-controlled challenge, 20 reacted to wheat. The numbers and percentages of the 148 non-celiac wheat sensitivity patients on a strict wheat-free diet who reported that the following symptoms recurred after occasional and accidental wheat consumption: Lack of well-being 135 (91%); Tiredness 102 (69%); Foggy mind 68 (46%); Menstrual alterations 54 (36%); Anemia 46 (31%); Weight increase 45 (30%); Joint/muscle pain 35 (24%); Headache 31 (21%); Weight loss 30 (20%); Anxiety 18 (12%); Skin rash 16 (11%); Recurrent cystitis 12 (8%); Depression 10 (7%). From these numbers, the team concludes that non-celiac wheat sensitivity is a persistent condition. Clinicaltrials.gov registration number: NCT02823522. Source: Gastroenterology. DOI: http://dx.doi.org/10.1053/j.gastro.2017.03.034
  7. Celiac.com 04/21/2017 - Adults who have gluten sensitivities cohabitating with non-gluten sensitive adults may have a lot of unanswered questions that need to be asked. Dramatic changes in one family member's diet can have profound effects on a household (Bacigalupe & Plocha, 2015). Numerous studies document how parents and children handle everyday living when the child has food intolerances, but very few studies focus on adults living with food sensitivities. Wouldn't you like to know how other adults with food sensitivities adapt and manage over the long haul? Questions like: Does the person with the sensitivity live in fear of cross-contamination? Does the household employ methods to ensure s/he is safe? If so, what are those methods? Do the non-sensitive members of the household feel resentment? Or have they grown weary of compliance over the long haul? How adherent is the sensitive adult? Is it worth a little risk for a little pleasure once in a while? What do these cohabitating adults do to exist gracefully? These questions will be asked in a forthcoming study (on Celiac.com), and the results will be shared with viewers/readers. Food allergies affect 15 million Americans (FARE, 2015), which means that adults with food sensitivities have gone from being rare to more commonplace as the population ages (Norling, 2012). Dietary restrictions due to disease will soon become common in many households and this can be problematic because severe dietary constraints are positively associated with diminished family social activities (Komulainen, 2010). Studies indicate that adults cohabitating, when one has food sensitivities and others do not, could potentially result in problems between members of the household creating feelings of uncertainty and potentially less adherence to the diet. Regimented dietary requirements affect the quality of life when virtually every bite of food must be scrutinized before consumption. For some households, compliance may fall on the shoulders of the person who cooks. The cook in the household, caregivers, and everyone sharing the same kitchen, must be actively involved in protecting the person with the sensitivities keeping gluten-containing crumbs off the counter, out of condiment jars, thoroughly cleaning utensils, etc. (Crowley, 2012; Bollinger, 2005; Merras-Salmino et al., 2014). Of course, those living with sensitivities know there is a lot more to staying "clean and safe." Family members who share a home with someone with pervasive food sensitivities must express empathy to ensure harmony and compliance (Komulainen, 2010). However, compliance comes with a price -- every meal must be planned and cooked using alternative ingredients to avoid accidental ingestion. This takes diligence, education and ability to accomplish meal after meal (Jackson et al., 1985) especially when allergies are to ubiquitous foods such as dairy, soy, gluten or corn. Dietary restrictions can cause misgivings on the part of the other family members, who may feel deprived of their favorite foods, compromised with recipe adaptations, or forced to unwillingly comply with the other person's diet. On the contrary, the person with food sensitivity may feel pressure not to comply with the diet in order to conform to the other adult's culinary demands. In the Jackson et al. study, forty percent of people with Celiac disease did not comply with the diet because it was too difficult (1985). The relationship between the cohabitating adults may be further complicated as trust issues develop between the sensitive adult and the cook, if the sensitive adult suspects foods that make them sick are creeping into their diet. Other food-sensitive adults report non-adherence because it is "too much trouble" and causes "social isolation" (Coulson, 2007). Non-adherence for those with sensitivities can lead to reactions, anaphylactic shock and even to death (Lee et al., 2003). Even those who do not react immediately risk long-term illness with non-compliance. In my twelve years experience working with people in this arena, I have observed that dietary adherence in the household seems to go through phases. The first phase is what I'm calling the "transition" stage when a person is newly diagnosed, and everyone in the household is learning the new rules. The second stage is the "status quo" stage where cohabitants understand, and hopefully comply. Finally, the third stage is what I'm terming as 'turbulent' when other adult household inhabitants are feeling weary of compliance, may have doubts about the other's sensitivities, or even rebel. This stage may be triggered by an event that disrupts the "status quo", such as a holiday where traditional foods are expected, and where their gluten-free substitutions may not be as satisfying to the other household members. It may be triggered when the food sensitive adult decides they may be reacting to different foods than they thought before, and want to experiment with dietary changes. Dynamics between cohabitants may become turbulent during these times. After the event, the household adjusts back to equilibrium until the next triggering event, which throws them into a different part of this phase-cycle, where they may cheerfully welcome a "transition," or react with "turbulence." This cyclical pattern seems to continue as cohabitants move in and out of phases as life-events occur. One of the goals of this survey will be to determine the validity of this cycle. I also want to test the hypothesis that a component of household compliance may also be associated with the status of the adult who has the dietary restrictions – whether the head of the home enjoys full household compliance, or if a subordinate adult must comply while others are eating the foods s/he are sensitive to. Another factor that may affect compliance is how the sensitive adult was initially diagnosed. Did a medical doctor conduct tests? Or did they read an article, and notice that they had symptoms consistent with gluten sensitivity and decide to go "gluten free?" Does the diagnostic process affect the compliance of the other adult members of the household? There are many factors that need to be assessed in order to help those of us who have food sensitivities who are living with other adults. This survey/study will focus on family interactions when dealing with dietary restrictions, with the potential to increase family member's compliance. It will seek to gain insight on the impact food restrictions for one adult has on the rest of the family. This study has social significance because family unity in the future may rely on developing constructs for compliance to address this emerging social problem. I'll collect data for this study and then share it with Celiac.com and the Journal of Gluten Sensitivity readers in order to create awareness by thoroughly examining the lifestyle of food sensitive people, shedding light on how social influences affect dietary adherence. As a PhD student at the University of Denver, and an adult with Celiac disease and a lifetime of other food allergies, living with another adult who has no food sensitivities, I know first-hand that it takes cooperation and commitment from everyone to ensure my health. I hope the study can help others improve their quality of life with the insight gained from conducting this study. I'll be launching this study on Celiac.com. Thank you to Scott Adams for allowing this study to be conducted on Celiac.com.
  8. Celiac.com 03/20/2017 - Researchers really do not have really good data on rates of celiac disease in the general population of children in the United States. A team of researchers recently set out to estimate the cumulative incidence of celiac disease in adolescents born in the Denver metropolitan area. The research team included Edwin Liu, Fran Dong, MS, Anna E. Barón, PhD, Iman Taki, BS, Jill M. Norris, MPH, PhD, Brigitte I. Frohnert, MD, PhD, Edward J. Hoffenberg, MD, and Marian Rewers, MD, PhD. Their team collected data on HLA-DR, DQ genotypes of 31,766 infants, born from 1993 through 2004 at St. Joseph’s Hospital in Denver, from the Diabetes Autoimmunity Study in the Young. For up to 20 years, the researchers followed subjects with susceptibility genotypes for celiac disease and type 1 diabetes for development of tissue transglutaminase autoantibodies (tTGA). The team was looking for patients who developed either celiac disease autoimmunity (CDA) or celiac disease, and they defined CDA as persistence of tTGA for at least 3 months or development of celiac disease. Marsh 2 or greater lesions in biopsies or persistent high levels of tTGA, indicated celiac disease. For each genotype, the team assessed cumulative incidence of CDA and celiac disease. To estimate the cumulative incidence in the Denver general population, they weighted outcomes by each genotype, based on the frequency of each of these genotypes in the general population. They found that, of 1.339 patients they studied, 66 developed CDA and met criteria for celiac disease, while 46 developed only CDA. Seropositivity for tTGA resolved spontaneously, without treatment, in 21 of the 46 patients with only CDA (46%). The team estimated the total incidence for CDA in the Denver general population at 5, 10, and 15 years of age was 2.4%, 4.3%, and 5.1% respectively; incidence values for celiac disease were 1.6%, 2.8%, and 3.1%, respectively. This 20-year prospective study of 1.339 children with genetic risk factors for celiac disease showed the total incidence of CDA and celiac disease to be high within the first 10 years. Although more than 5% of children may experience a period of CDA, that is, persistently high celiac autoantibodies, not all of them develop celiac disease or require gluten-free diets. Sources: Gastroenterology.DOI: http://dx.doi.org/10.1053/j.gastro.2017.02.002 gastrojournal.org
  9. Celiac.com 01/24/2017 - Diabetes is a condition in which blood glucose rises high enough to cause: damage to blood vessel walls, neurological injury, vision loss, and a host of other maladies. Most currently recognized cases of diabetes fall into one of two categories which are identified as type 1 and type 2 diabetes. While these two types of diabetes share many symptoms, the underlying causes are, in most cases, quite distinct, although there is also some overlap which will be explored shortly. There are also cases of gestational diabetes and some researchers are now suggesting that type 3 diabetes may be yet another entity that causes accelerating cell death in the brain, resulting dementia (1) but these latter two types of this condition are not included in the current discussion. All but one of these forms of diabetes involves cellular resistance to the action of insulin, although there is some gray area between type 1 and type 2 diabetes. Type 1 diabetes is the result of an autoimmune attack on a specific group of pancreatic cells called islets of Langerhans. These are the cells that produce insulin, a hormone that moves glucose out of the bloodstream and into various cells. About 14% of type 2 diabetics are also thought to experience a late-onset, slowly developing damage to pancreatic islet cells, which results in reduced insulin production in combination with their insulin resistance(2). This may be caused by autoimmunity, similar to type 1 diabetes, or it may be damage induced by other factors. Nonetheless, while type 2 diabetes can often be controlled either during weight loss or by reduced carbohydrate consumption alone, type 1 diabetes is not typically viewed as a condition that can be remedied by a change in eating habits. Yet there are some hints in the literature suggesting that dietary interventions may be therapeutically useful, especially if begun early enough in the disease process. Researchers Amanda MacFarlane and Fraser Scott report that there are several environmental factors, including specific foods, as well as viral, bacterial, and chemical agents that have been hypothesized to incite an autoimmune attack on the islet cells (2). They also report that about half of the animals that develop type 1 diabetes are mounting an immune response to wheat, which may also be involved in the attack on the insulin producing cells of the pancreas by either or both of two pathways they outline (2, 3). These hypothesized biological processes are identified as molecular mimicry or bystander activation and cell death. While these authors favor bystander activation, either or both of these pathways may lead to an autoimmune attack on pancreatic islet cells. Regardless of the specific biological route, type 1 diabetes can be induced in a significant portion of genetically susceptible rats and mice, simply by feeding them a diet dominated by wheat gluten. Further, the severity of their disease varies directly with the proportion of wheat gluten in the diet (2). These investigators go on to say that "These similarities between coeliac disease in humans and diabetes in BB rats, NOD mice and type 1 diabetic patients are consistent with the idea that wheat is involved in diabetes pathogenesis, possibly by inducing a subclinical, gut inflammation in many individuals that develop this form of diabetes" (2). They go on to report that: "Our data suggest that dietary modulation has effects at two (or more) levels: At the target cells before classic insulitis, changing the growth pattern of insulin-producing cells, enhancing islet mass and changing metabolism and insulin reserves . Dampening an ongoing inflammatory condition in the gut." (2) Scott's work (4, 5) along with investigations conducted by several groups of his colleagues (6-10) indicate that significant numbers of diabetes patients show immune reactions to the prolamins which are storage proteins in wheat, rye, and barley. Further, investigators have long understood that there is significant overlap between celiac disease and type 1 diabetes, with estimates ranging between 5% and 12% in each disease group (2, 11). MacFarlane and Scott point out that 33% to 40% of patients with type 1 diabetes show transglutaminase autoantibodies which are similar to those found in celiac patients but usually at lower levels (2). Low concordance rates in monozygotic (identical) twins also suggest that environmental factors play a large role in causing type 1 diabetes (2). Again, the most compelling evidence indicates that dietary consumption of wheat gluten and similar prolamins is an important factor in the autoimmune attack that destroys the pancreatic capacity to produce insulin, in genetically susceptible individuals. Indirect support for this perspective is offered by animal research published in July of 2011. It shows that gamma-Aminobutryic acid (GABA) supplements not only inhibit the autoimmune attack on islet cells, GABA also incites regeneration of insulin producing cells (12). GABA is a non-toxic substance that is produced by the beta cells of the pancreas (13). It plays an inhibitory role throughout the nervous system which may be significant when taken in conjunction with Rodney Ford's identification of gluten as the agent which, directly and indirectly, induces neurological damage in those with celiac disease and those with non-celiac gluten sensitivity. One pathway Ford identifies is gluten-induced neuronal excitation leading to cellular self-destruction. In light of Ford's hypothesis, the inhibitory role of GABA on neuronal tissues, both at and near synapses, offers an inviting new window for envisioning the process that incites, and therefore may reverse, type 1 diabetes. Clearly there is considerable cause to suspect gluten grain consumption as an important factor in the onset and perpetuation of many cases of type 1 diabetes. While genetically coded HLA markers predispose to the disease, and a number of other environmental factors may play a role in its pathogenesis, prolamins from wheat and its close relatives are clearly a frequent and important contributor to this life-long condition in which exogenous insulin (injection with hypodermic needles) is necessary for maintaining optimal health (12) while living with this malady. However, given the insights offered by the above, the following case history may offer insights that might otherwise incite only scepticism. MacFarlane and Scott suggest the following: "One approach to achieving this [prevention] is to understand and modify the environmental factors that induce disease or equip those at risk with better means of avoiding or handling these agents"(2). Case Study: On January 18, 2008, three year old K and her anxious mother were taken to a hospital emergency department in Gilbert, AZ, where the attending physician concluded that the child had experienced a febrile seizure of about 5 minutes' duration. At examination, she had a 102.5 degree temperature. In addition to fevers, K complained of abdominal pain and showed abdominal bloating. During this examination of K, she vomited. Laboratory tests showed elevated glucose (133 mg/dl) and an elevated white blood cell count (19,000). Tylenol was used to bring K's temperature down and she was discharged with instructions for the parents to administer more Tylenol as needed, and to follow up with her regular health care provider within two days. By February 29, K experienced more fevers, ranging between 101 and 104, intermittently over 24 hours. Every four hours, when the effects of the previous dose of Tylenol wore off, the fever would, again, spike to 103-104. K was taken to see her regular physician the following day and urinalysis revealed ketone bodies. K and her parents were then sent to the emergency department of Banner Children's Hospital. At the hospital, testing showed elevated urinary ketone bodies in the Large category, and blood showed elevated glucose at 193 mg/dL. Type 1 diabetes was diagnosed and K was admitted to hospital where she stayed for four days. Her condition was stabilized with ½ unit of Novalog and 4 units of Lantus. Meanwhile parents were educated about type 1 diabetes, insulin measurement and injection. They were taught to inject 1 unit of insulin for every 20 grams of carbohydrates consumed (20:1 ratio). K's parents repeatedly wondered, in the presence of the diagnosing endocrinologist, just how much insulin K was producing and how many carbohydrates a thirty pound child needed to be healthy? * K's father has a history of joint pain when consuming gluten grains. K was still experiencing abdominal bloating and because of the overlap between type 1 diabetes and celiac disease (2) serum IgA antibody tests were undertaken and both transglutaminase and gliadin antibody tests were negative. However, the parents observed that variations in the types of food K ate seemed to have a greater impact on blood glucose than a specific food's putative sugar content. In keeping with their observations that different foods, despite their equal sugar content, produced different blood glucose results, the father's history of joint pain when eating gluten, K's abdominal bloating, and the widely documented connection between gluten grains and type 1 diabetes, these foods and several others were eliminated from her diet. K's parents were quickly able to adjust the insulin therapy to a 40:1 ratio while K typically maintained a blood glucose range of between 80 and 95 mg/dl, which is well within the reference range for a healthy, non-diabetic person. In fact, this is a far narrower range than is prescribed by the American Diabetes Association which is 70-120 mg/dl for diabetic patients. K's family continued to target and achieve the 80-95 mg/dl range. After a few months of lower than normal blood sugars, still on insulin therapy, with the carbohydrate ratio now 40/1, the parents sought permission from the endocrinologist to take K off insulin completely, on the condition that her blood sugar continued within the normal range of 85-95 mg/dl. This was monitored on a daily basis. The first 24 hours were a success and another day was granted. After six months of following a strict and intense food therapy diet for K, the family started reintroducing foods. Some foods were reintroduced without a rise in blood sugar. She was also able to eat a larger amount of carbohydrate each meal with the same blood sugar control. Clearly, the pancreas was producing increasing quantities of insulin. On August 21, 2008, six months into this intensive and individualized food therapy, the patient's blood test results indicated a regeneration of the pancreas and a complete reversal of her type 1 diabetes. Her A1C was 4.8, well within the normal range for a non-diabetic person. Today, more than three years later, the patient is still insulin free and is using food therapy alone to maintain healthy and normal glucose control. Signs of pancreatic inflammation were also absent. Each of these findings echo MacFarlane and Scott on the issue of dietary intervention in animal studies. The intensive food therapy has now been replaced with a maintenance program. The variety of foods the patient can eat is vast. However, grain and casein continue to be avoided. It appears that, in this case, these foods may have contributed to K's Type 1 diabetes. It may also be that the underlying cause of the fever K experienced early in this process was a factor in the onset of her type 1diabetes, and the transient nature of this fever, and its cause, may be at the root of her recovery from this ailment. Nonetheless, given the many converging research findings indicting grains and dairy proteins, along with K's suggestive signs and symptoms, and her father's reactions to gluten, continued avoidance of these foods seems a more likely explanation. Thoughtful readers may also wonder just how much insulin K was producing, at the time of her diagnosis, and just how many carbohydrates a thirty pound child needs to be healthy? It may be that GABA supplements and other chemical miracles will be unnecessary for large numbers of children who suffer from type 1 diabetes. Perhaps early diagnosis and permanent dietary adjustments will be what is needed to facilitate complete recovery for many, perhaps most, children afflicted by this insidious condition. Perhaps this case history will provide the necessary impetus to encourage undertaking controlled studies of dietary factors early in the disease process of type 1 diabetes. * While there are no carbohydrates that are essential to good health, there are essential amino acids and essential fats. Sources: de la Monte SM, Wands JR. Alzheimer's disease is type 3 diabetes-evidence reviewed. J Diabetes Sci Technol. 2008 Nov;2(6):1101-13. http://www.medicine.uottawa.ca/Students/MD/BlockOrientation/assets/documents/e_inf_week05.pdf http://www.elements4health.com/type-1-diabetes-patients-have-immune-response-to-wheat-proteins.html Scott FW, Sarwar G, Cloutier HE. Diabetogenicity of various protein sources in the diet of the diabetes-prone BB rat. Adv Exp Med Biol 1988; 246: 277–85. Scott F. Dietary initiators and modifiers of BB rat diabetes. In:Shafrir E, Renold AE, eds. Frontiers in Diabetes Research:Lessons from Animal Diabetes. London: Libbey, 1988: 34–9. Hoorfar J, Buschard K, Dagnaes-Hansen F. Prophylactic nutritional modification of the incidence of diabetes in autoimmune non-obese diabetic (NOD) mice. Br J Nutr 1993; 69: 597–607. Funda DP, Kaas A, Bock T, Tlaskalova-Hogenov H, Buschard K. Gluten-free diet prevents diabetes in NOD mice. Diabetes Metab Res Rev 1999; 15: 323–7. Bao F, Yu L, Babu S et al. One third of HLA DQ2 homozygous patients with type 1 diabetes express celiac disease-associated transglutaminase autoantibodies. J Autoimmun 1999; 13:143–8. Lampasona V, Bonfanti R, Bazzigaluppi E et al. Antibodies to tissue transglutaminase C in type I diabetes. Diabetologia 1999; 42: 1195–8. Pocecco M, Ventura A. Coeliac disease and insulin-dependent diabetes mellitus: a causal association? Acta Paediatr 1995; 84: 1432–3. Hansen D, Brock-Jacobsen B, Lund E, Bjørn C, Hansen LP, Nielsen C, Fenger C, Lillevang ST, Husby S. Clinical Benefit of a Gluten-Free Diet in Type 1 Diabetic Children With Screening-Detected Celiac Disease A population-based screening study with 2 years' follow-up Diabetes Care 29:2452-2456, 2006 Soltani N, Qiu H, Aleksic M, Glinka Y, Zhao F, Liu R, Li Y, Zhang N, Chakrabarti R, Ng T, Jin T, Zhang H, Lu WY, Feng ZP, Prud'homme GJ, Wang Q. GABA exerts protective and regenerative effects on islet beta cells and reverses diabetes.Proc Natl Acad Sci U S A. 2011 Jul 12;108(28):11692-7. Epub 2011 Jun 27. Bouzane B, Postmedia News June 28, 2011 Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
  10. Celiac.com 11/15/2016 - Do you know someone who has lived with celiac disease for over eighty years? Someone who lived on nothing but mashed bananas for a year? Someone who continued to eat gluten for over 30 years because doctors didn't know how to treat a celiac diagnosis? Someone who experienced serious physical, emotional, and family challenges as a result? Well, I met such an individual at the International Celiac Symposium in Chicago in the fall of 2013. Clara (a pseudonym) attended my poster session, The Educational, Social, and Family Challenges of Children with Celiac Disease: What Parents Should Know. As she stood before my poster with tears in her eyes she began to say, "This is me. This is me." Through a brief conversation then, and several lengthy telephone interviews that followed, she shared her incredible story with me and gave me permission to share it with you. Clara was born in 1933 on a citrus ranch in California and was the youngest of five children. She was very sick as a baby with what her family thought was a "terrible case of the flu." She lost muscle tone, had wrinkly skin, and some mornings she didn't move or even open her eyelids without the help of her mother. She looked malnourished and had a distended stomach. When she was two, her parents took her to Dr. Victor E. Stork, but he was not sure what the problem might be. A few weeks later, the doctor attended a conference where he described Clara's symptoms. He learned of another child with similar symptoms who had been diagnosed with celiac disease and fed nothing but mashed bananas. After Dr. Stork informed Clara's parents, Clara's father purchased a big hook and drove to the Long Beach docks to buy bananas. He hung bunches of bananas on their back porch to ripen and she was fed nothing but mashed bananas for over a year. What started as half a teaspoon at a time quickly grew until she was eating many bananas each day. This part of Clara's story greatly intrigued me, as I had just read the research of Sidney Haas. In the 1920s Hass successfully treated eight children who were "anorexic" from celiac disease with the banana diet while untreated children did not survive (Guandalini, 2007). Growing up, Clara was a happy child but had no appetite and didn't enjoy food. She was very small for her age and, at times, was made to stay at the dinner table until she ate everything on her plate. Clara's mother, a practical nurse, thought she might be allergic to fat. The family kept a quarter of a beef in a freezer locker 25 miles away and her mother scraped the fat off the beef before giving it to Clara. She was also made to finish her breakfast, typically oatmeal, toast, and orange juice, before going to school in the morning. Clara routinely had vomiting and diarrhea each morning, and didn't understand why this didn't happen to other children. She missed school often because she had abdominal discomfort and was weak. Clara hid in the girls' restroom during recess and physical education so she wouldn't have to participate. Since she was unsuccessful at athletics she found it easier to sit on a toilet with her feet pulled up so no one would see her. Clara continued to miss a great deal of school but was required to do her school work at home. During second grade she worked ahead, completing both second and third grade work. Consequently, she was allowed to skip third grade, which only accentuated her small size. When she entered high school people thought she was in third or fourth grade. After entering puberty at age 14 she finally acquired an appetite and began to grow much taller. At this point in her life, Clara decided that she would never be sick again. She graduated from high school in 1950, after acting in dramatic productions, serving as president of the Girls' League, and planning the ten year class reunion. Clara married at age twenty, between her junior and senior years in college. She had few symptoms during this time and was hired as a kindergarten teacher. Her husband was drafted and she taught in several different places on the west coast while he was in the service. During this time, Clara had a baby girl followed by two miscarriages. Three weeks after the birth of their second child Clara became very ill and lost her hair. They had no insurance and she lost a dramatic amount of weight. She weighed only 80 pounds and her husband had to carry her from the bed to the couch. The vomiting and diarrhea got worse and her mother had to take care of her babies. She was on heavy doses of medication and her doctors thought her gastrointestinal problems "were all in her head." Clara's speech became "jumbled" and she was not making sense. Her doctor sent her to a psychiatrist who placed her in a "sanitarium." She was hospitalized for several months where she felt very isolated and alone. Her relatives weren't told where she was and her father would not allow her mother to visit her. At the sanitarium Clara received shock treatments every three days, ten in all. Her sister offered her son's college fund to pay the sanitarium bill so that Clara would be allowed to leave. When Clara returned home she found she had lost much of her memory. She didn't remember how to hold a knife and her daughter, who was three, taught her how to tie her shoes. She was on sedatives and slept much of the time. She does not know how she took care of her children during this time. Clara and her husband had little money, so she took in ironing and taught preschool. It took them twelve years to pay off the hospital bills. It was fifteen years after this experience, and two babies later, that Clara finally got treatment for her celiac disease. She was hospitalized at UCLA Medical Center for a month while more tests and an intestinal biopsy were completed. It was 1972, and she was now 39 years old. The gastroenterologist finally confirmed the diagnosis of celiac disease and told her that she would never be able to eat pie, bread, or cake ever again. Clara was so thrilled that it was "just food" that would make a difference and not cancer. The doctor told her that there was no reason why she was still alive. Within two months she was noticing a difference and had gained weight. Clara was able to go back to teaching part-time and started teaching full-time in 1981. After her celiac diagnosis Clara did her best to avoid grains completely. One doctor told her to eat wheat germ, a product she clearly was correct in avoiding. In the 1970s she tried to make bread with rice, but her attempts were very unsuccessful. Clara started a support group in 1984 which was part of the Celiac Sprue Association. Little by little the group started receiving information on eating gluten-free, as many of these foods were readily available in Europe. By 1988 there were some gluten-free foods available in California. Clara experimented with cooking and breads and tested recipes for Carol Fenster's cookbooks. Her household today is totally gluten-free, with the exception of a loaf of bread for her husband. She and her husband traveled extensively after their retirement, visiting every state except Hawaii, along with the Caribbean and Australia. As far as lessons learned, Clara believes that people should listen to each other. She says, "If a person says, I feel horrible, someone should listen. The medical profession didn't listen to me. They said it was all in my head. If they had listened I could have been helped." It is unfortunate that her doctors didn't listen, as Clara could have been diagnosed much sooner. Willem-Karel Dicke first published an article on the importance of a gluten-free diet for the treatment of celiac disease in 1941 (Berge-Henegouwen & Mulder, 1993). Since my own celiac diagnosis came within two months of the onset of symptoms, I marvel at how someone could live for 39 years while still eating gluten. I think about the lessons to be learned from Clara's story. I consider the advancements that have been made in the diagnosis and treatment of celiac disease and the ease with which I'm able to eat gluten-free. And I send a reminder of the importance of early detection and the physical and emotional consequences that individuals like Clara face when a celiac diagnosis is delayed. References: Guandalini, S. (2007). A brief history of celiac disease. Impact, 7, (3), 1-2. Van Berge-Henegouwen, G. P., & Mulder, C.J. (1993). Pioneer in the gluten-free diet: Willem-Karel Dicke 1905-1962, over 50 year of gluten-free diet. Gut, 34, 1473-1475.
  11. Scand J Gastroenterol 1999 Feb;34(2):163-9 Kaukinen K, Collin P, Holm K, Rantala I, Vuolteenaho N, Reunala T, Maki M Dept. of Medicine, Tampere University Hospital, Finland. BACKGROUND: We investigated whether wheat starch-based gluten-free products are safe in the treatment of gluten intolerance. METHODS: The study involved 41 children and adults with coeliac disease and 11 adults with dermatitis herpetiformis adhering to a gluten-free diet for 8 years on average. Thirty-five newly diagnosed coeliac patients at diagnosis and 6 to 24 months after the start of a gluten-free diet and 27 non-coeliac patients with dyspepsia were investigated for comparison. Daily dietary gluten and wheat starch intake were calculated. Small bowel mucosal villous architecture, CD3+, alphabeta+, and gammadelta+ intraepithelial lymphocytes, mucosal HLA-DR expression, and serum endomysial, reticulin, and gliadin antibodies were investigated. RESULTS: Forty of 52 long-term-treated patients adhered to a strict wheat starch-based diet and 6 to a strict naturally gluten-free diet; 6 patients had dietary lapses. In the 46 patients on a strict diet the villous architecture, enterocyte height, and density of alphabeta+ intraepithelial lymphocytes were similar to those in non-coeliac subjects and better than in short-term-treated coeliac patients. The density of gammadelta(+)cells was higher, but they seemed to decrease over time with the gluten-free diet. Wheat starch-based gluten-free flour products did not cause aberrant up-regulation of mucosal HLA-DR. The mucosal integrity was not dependent on the daily intake of wheat starch in all patients on a strict diet, whereas two of the six patients with dietary lapses had villous atrophy and positive serology. CONCLUSION: Wheat starch-based gluten-free flour products were not harmful in the treatment of coeliac disease and dermatitis herpetiformis.
  12. Celiac.com 11/04/2016 - NIH has awarded a $3 Million grant to Dr. Betty Diamond, head of the Feinstein Institute's Center for Autoimmune and Musculoskeletal Diseases, and her colleague, Dr. Peter Gregersen, who heads the Feinstein Institute's Robert S. Boas Center for Genomics & Human Genetics, specifically to explore the relationship between a mother's autoimmunity during pregnancy and the risk of ASD in her child. Both are also researchers at the Northwell Health System's Manhasset-based R&D division. Doctors Diamond and Gregerson are following up their own previous studies that showed antibodies can lead to abnormal brain development and ASD symptoms. Also known as 'immunoglobulins,' antibodies are Y-shaped proteins produced mainly by plasma cells, white blood cells that can secrete large volumes of antibodies, and which the immune system uses to identify and neutralize pathogens including bacteria and viruses. The new study seeks to determine if increased levels of antibodies in pregnant women with autoimmune inflammatory disorders such as rheumatoid arthritis, lupus or celiac disease, leave these women at increased risk of having children on the autism spectrum. Titled "Prenatal Autoimmune and Inflammatory Risk Factors for Autism Spectrum Disorders," the new study will track 4,500 women who deliver babies at hospitals in the Northwell Health system, along with their babies, for two years. Participating mothers will receive a blood test during pregnancy to spot any potential autoimmune disease or diseases, and also to spot any elevations in immune activation, or in cell-signaling cytokine proteins. The research team will then monitor the children for signs of ASD. While researchers have already determined that autism spectrum disorders are at least partly influenced by genetics, "relatively little attention has been paid to the role of environment, and particularly the intrauterine environment," says to Gregersen. This research will help researchers to better understand the connections between a mother's autoimmunity levels during pregnancy, and the risk of later ASD in her child. Source: Feinstein Institute.org
  13. Celiac.com 09/26/2016 - Previous studies have indicated an increase in celiac disease rates in the United States, but these studies have been done on narrow populations, and did not produce results that are nationally representative. Researchers recently released an new comprehensive report, called, Time Trends in the Prevalence of Celiac Disease and Gluten-Free Diet in the US Population: Results From the National Health and Nutrition Examination Surveys 2009-2014. The research team included Hyun-seok Kim, MD, MPH; Kalpesh G. Patel, MD1; Evan Orosz, DO; Neil Kothari, MD; Michael F. Demyen, MD; Nikolaos Pyrsopoulos, MD, PhD, MBA; and Sushil K. Ahlawat, MD. They are variously affiliated with the Division of Gastroenterology and the Department of Medicine at Rutgers New Jersey Medical School in Newark. Using data from the National Health and Nutrition Examination Surveys, a team of researchers recently examined current trends in both celiac disease rates, and gluten-free diet adherence. Currently, far more people follow a gluten-free diet than have celiac disease. The numbers of people eating gluten-free food far outpace the levels of celiac disease diagnosis. This may be due to perceptions that the diet is healthier than a standard non-gluten-free diet. This research teams recent surveys examine the current trends in the prevalence of celiac disease and adherence to a gluten-free diet, including people without celiac disease, using nationally representative data from the National Health and Nutrition Examination Surveys (NHANESs) 2009-2014. The study evaluated 22,278 individuals over the age of 6 who completed surveys and blood tests for celiac disease. The subjects were interviewed directly regarding their prior diagnosis of celiac disease and adherence to a gluten-free diet. The researchers found that 106 (0.69%) individuals had a celiac disease diagnosis, and 213 (1.08%) followed a gluten-free diet but didn't have celiac disease. These results correlate to an estimated 1.76 million people with celiac disease, and 2.7 million people who follow a gluten-free diet without a diagnosis of celiac disease in the United States. Overall, the researchers found that the prevalence of celiac disease has remained steady (0.70% in 2009-2010, 0.77% in 2011-2012, and 0.58% in 2013-2014), however, those who follow a gluten-free diet but don't have celiac disease have increased over time (0.52% in 2009-2010, 0.99% in 2011-2012, and 1.69% in 2013-2014). The researchers conclude that the two might be related, as the decrease in gluten consumption could contribute to a plateau in those who are being diagnosed with celiac disease. Source: JAMA Intern Med. Published online September 06, 2016. doi:10.1001/jamainternmed.2016.5254
  14. Celiac.com 09/28/2016 - Celiac disease occurs most often in children and young adults. However, people can develop celiac disease at any age, and rates are rising even among older people. Because older people often show clinically atypical symptoms, they can sometimes experience a delay in diagnosis. Also, serological tests have a lower sensitivity and specificity in the older patients. This means that doctors only begin to suspect celiac disease in the presence of other, often vaguely associated complications, such as autoimmune disorders, fractures, and finally, malignancy, and that diagnosis must be aided by endoscopic and imaging tools. A team of researchers recently set out to assess the incidence and prevalence of celiac disease in the elderly, the patterns of clinical presentation, diagnosis, and the most frequent complications, with the aim of increasing awareness and reducing the diagnostic delay of celiac disease even in the elderly population. The research team included Maria Cappello, Gaetano C. Morreale, and Anna Licata of the Gastroenterology and Hepatology Section, DIBIMIS, University of Palermo School of Medicine, Palermo, Italy. The team's recent article highlights their findings regarding celiac rates and incidence in older patients, along with patterns of clinical presentation, diagnosis, and most frequent complications. The researchers conclude: "Despite a paucity of symptoms, such as diarrhea and weight loss, celiac disease has been increasingly recognized in the elderly. Other presentations in the elderly age group include iron deficiency anemia (often refractory to oral iron), autoimmune disorders, bone disease due to osteopenia, including fractures, malignant intestinal disease, especially lymphoma, and finally idiopathic dilated cardiomyopathy. Diagnosis may be delayed due to limited symptoms, a low index of clinical suspicion, or diagnostic difficulties related to important cognitive impairment that often affects elderly people. Although for these patients, the GFD is the key of clinical management, elderly patients sometimes are scarcely adherent to diet. Patients should be referred to specialists to ensure the better management of the disease and related complications. Micronutrients, such as iron, calcium, vitamin D supplementation, and vitamins, should be part of a modified GFD for the elderly patients. All other therapeutical interventions that limit malabsorption and avoid complications should be considered part of a management strategy." Source: Clin Med Insights Gastroenterol. 2016; 9: 41–49. doi: 10.4137/CGast.S38454 PMCID: PMC4965017
  15. Celiac.com 07/13/2016 - A really interesting study about gluten-free diets in mice just popped up over at the medical journal Diabetes, that has implications for both diabetes and celiac disease. The study found that a maternal gluten-free diet reduces inflammation and diabetes rates in the offspring of non-obese diabetic mice. The study was conducted by a research team that included Camilla H.F. Hansen, Åukasz Krych, Karsten Buschard, Stine B. Metzdorff, Christine Nellemann, Lars H. Hansen, Dennis S. Nielsen, Hanne Frøkiær, Søren Skov, and Axel K. Hansen. They are variously affiliated with the Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg, Denmark, the Department of Food Science, Faculty of Science, University of Copenhagen, Frederiksberg, the Bartholin Institute, Rigshospitalet, Copenhagen, Denmark, the Division of Toxicology and Risk Assessment, National Food Institute, Technical University of Denmark, Søborg, Denmark, and the Department of Biology, Faculty of Science, University of Copenhagen in Copenhagen, Denmark. Researchers have known for some time that early life interventions in the intestinal conditions have been shown to influence diabetes rates in mice. For example, a gluten-free diet in known to decrease type 1 diabetes incidence. Their team hypothesized that a gluten-free diet for pregnant mice only during pregnancy and lactation period would protect offspring mice against development of diabetes. The team fed pregnant non-obese diabetic (NOD) mice either a gluten-free or a standard diet, until all mice pups were weaned to standard diet. The early gluten-free mice showed significantly lower rates of diabetes and insulitis. Gut microbiota analysis by 16S rRNA gene sequencing showed significantly increased Akkermansia, Proteobacteria, and TM7 between both mothers and their offspring in the gluten-free diet group. Moreover, the gluten-free offspring showed increased pancreatic FoxP3 regulatory T cells, along with an increase in M2 macrophage gene markers and tight junction-related genes in the gut, coupled with lower intestinal gene expression of pro-inflammatory cytokines. Higher numbers of T cells in the pancreas expressing the mucosal integrin α4β7 suggests that the mechanism involve increased trafficking of gut-primed immune cells to the pancreas. This study supports the conclusion that a gluten-free diet during fetal and early postnatal life reduces development of diabetes. This may be due to changes in gut microbiota and better inflammatory and immunological conditions in the gut and pancreas. So, could it be that human mothers who eat a gluten-free diet through weening can impart the same kind of protection against diabetes? Clearly more studies need to be done until we can know for sure, but following a gluten-free diet while pregnant probably wouldn’t cause any harm to the mother or the baby. Source: Diabetes 2014 Apr; DB_131612.
  16. Celiac.com 06/10/2016 - Do all patients with potential celiac disease need a gluten-free diet? The transformation of potential celiac disease to full-blown celiac disease has been described in some western clinical studies, but there is no good data on cases in Asia. Recently, a team of researchers set out to study the short-term histological course of potential celiac disease in Indian patients. The research team included R Kondala, AS Puri, AK Banka, S Sachdeva, and P Sakhuja. They are variously affiliated with the Department of Gastroenterology and the Department of Pathology at Govind Ballabh Pant Hospital, New Delhi, India. For their study, the team identified prospective patients with potential celiac disease by screening relatives of celiac patients, patients with the diarrheal subtype of irritable bowel syndrome (IBS-D) and patients with iron deficiency anemia (IDA). They conducted endoscopy with duodenal biopsy on patients who tested positive for immunoglobulin A antibodies against tissue transglutaminase (IgA anti-tTG) Patients a Marsh-0 to Marsh-II lesion on duodenal biopsy, along with positive IgA tTG serology met the definition of celiac disease. The team retested for serology and histology at 6-month and 12 months. The team diagnosed 23 male and 34 female patients with potential celiac disease. Patients ranged from 4-73 years old, averaging 28.7 years. Of these 57 patients, 28 were identified by screening 192 first-degree relatives of 55 index cases of celiac disease, while the remaining 29 had either IBS-D or IDA. Duodenal biopsy showed Marsh-0, Marsh-I and Marsh-II changes in 28 celiac patients, 27 IBS-D patients, and 2 IDA patients. After 6 months, 12 patients became seronegative, while the remaining 45 patients continued to be seropositive at the 12-month time point. Only four patients moved to Marsh III status, while progression from Marsh-0 to either Marsh-I or Marsh-II occurred in six patients and one patient, respectively. Meanwhile, 14 patients with Marsh-I did show regression to Marsh-0. Of the two patients who were initially Marsh-II, one remained so upon follow up and one showed favorable regression to Marsh-0 status. This study shows that, even though almost 80% of the patients diagnosed have potential celiac disease continue to remain seropositive for tTG 12 months later, only 7% slipped to Marsh-III over the same time period. According to this team, these observations do not justify starting a gluten-free diet in all patients with potential celiac disease, in India. With all due respect to the research team, I wonder what would happen to these patients if they were followed over a greater time span? Would their conditions worsen? Clearly some longer term follow-up of such patients is warranted. Also, how many such patients would see an even greater regression of their symptoms and Marsh status if they followed a gluten-free diet? This study doesn’t tell us much about the possible benefits of a gluten-free diet in cases of potential celiac disease, just that, absent a gluten-free diet, some patients worsen and some improve. Source: United European Gastroenterol J. 2016 Apr;4(2):275-80. doi: 10.1177/2050640615594935.
  17. Celiac.com 01/10/2007 – Celiac disease researchers in Italy and at the Center For Celiac Research in Baltimore, Maryland have conducted a multi center, double-blind, placebo-controlled, randomized trial involving 49 adult individuals who have biopsy-proven celiac disease, and who have been on a gluten-free diet that contains less than 5mg of gluten per day for a minimum of two years. The aim of this study was to determine whether there is a safe threshold for prolonged, daily exposure to minute amounts of gluten. Subjects in the study were divided into 3 groups which were given daily capsules that contained 0mg, 5mg or 50mg of gluten. They were given biopsies and serological screening before and after a gluten challenge. One patient who was given 10mg of gluten daily did experience a clinical relapse, but at the end of the study no significant differences in the IEL count were found between the 3 groups, which lead the researchers to conclude that "(t)he ingestion of contaminating gluten should be kept lower than 50 mg/d in the treatment of celiac disease." This study is in line with past gluten threshold studies, and to help you put the amounts of gluten used in the study into perspective, and to demonstrate why the 20 ppm for naturally gluten-free products used in the Codex Alimentarius gluten-free standards is considered to be a safe threshold for those with celiac disease, the following discussion will attempt to quantify just how much gluten it takes to make 50mg. The amount of gluten contained in your average 30g slice of wheat bread is around 4.8 grams, or 4,800 milligrams (amount of gluten in wheat bread is normally 10% by weight). If you divide 4,800 by 50 it equals 96, so if divide an ordinary slice of bread into 96 pieces, that is roughly how much daily gluten, according to this study, appears to be safe for those with celiac disease. Here is a formula that can be used to determine the number of milligrams of gluten in foods based on the parts per million (ppm) of gluten in the product. The formula is: Products ppm times the number of grams of food divided by 1,000 which equals the number of milligrams. The Codex Alimentarius specifies that naturally gluten-free products contain less than 20ppm, and products that are rendered gluten-free such as Codex quality wheat starch contain less than 200ppm. Using this formula we can determine how many slices of 20ppm and 200ppm gluten-free bread a person with celiac disease would have to eat to consume 50mg of gluten. Here is the math: 20ppm x 30g/1,000 = 0.6 mg. So each slice of 20ppm gluten bread contains 0.6mg of gluten. To get 50mg of gluten per day while eating this type of bread you would have to consume 83.33 slices of it! 200ppm x 30g/1,000 = 6 mg. So each slice of 200ppm gluten bread contains 6mg of gluten. To get 50mg of gluten per day while eating this type of bread you would have to consume 8.33 slices of it. The goal of this study (and this article) is not to encourage people with celiac disease to eat gluten. The reality is that cross-contamination of supposedly gluten-free products is very common, and many of us who are on gluten-free diets still unknowingly ingest tiny amounts of gluten on a daily basis. Studies like this can help provide some sense of perspective with regard to how concerned one should be about minute gluten ingestion, and hopefully this article will help you to understand exactly what the 50mg threshold found in the study means. An article called Gluten-phobia in the Winter 2007 issue of Scott-Free Newsletter further addresses what can happen when someone takes their fear of gluten too far and lets it disrupt their life in ways that are so psychologically unhealthy that the negative effects to the author and those around her may actually rival those of the disease itself. Here are some links to additional information on this topic: FDAs Responses to Public Comments on the Draft Report Approaches to Establish Thresholds for Major Food Allergens and for Gluten in Food Detection of Cereal Proteins and DNA Using MS, ELISA, and PCR Comments by Susan Phillips Clavarino: I read with interest your remarks about the Catassi/Fasano study. As an active member of the AIC (Association of Italian Celiacs), sponsors of the study, and as the person responsible for revising the language of the text for publication…the study does raise some serious queries about background gluten contamination and its impact on the celiac intestine. When the authors remark that the IELs do not show a difference among the three groups of celiacs on long term gluten free diet (though not compared to the non celiac disease controls), they point out that the villous height/crypt depth ratio is a more valid and more sensitive marker of gluten trace contamination in celiacs on long-term dietary treatment. They also remark that "Despite the restricted criteria adopted in this study, the baseline duodenal biopsy results showed evidence of histologic damage (decreased median Vh/celiac disease count and increased median IEL count in adult celiac disease patients receiving long-term dietary treatment. Furthermore, 4 of 49 subjects had to be excluded from the protocol because severe enteropathy (obscuring the possible effects of the micro challenge) was detected at the baseline evaluation. These results confirm that an abnormal small bowel morphology persists in a significant proportion of celiac disease patients treated with a gluten-free diet, despite full resolution of their symptoms..."(due to)"... the ongoing ingestion of gluten, either deliberate or inadvertent, causing persistent inflammation in the small-intestinal mucosa..." etc. As all medically diagnosed Italian celiacs receive a free monthly allowance of naturally (i.e. no wheat starch) gluten free products containing less than 20 ppm from the Italian government health service, and as all the volunteers for the study considered themselves to be healthy (otherwise they would certainly not have volunteered), the finding that 4 out of 49 had to be excluded for severe enteropathy and that histologic damage persists in a significant proportion of adult celiac disease patients on long-term gluten-free diet, besides the other findings of the study (i.e. that 50 mg of gluten per day for only 3 months of trial results in measurable intestinal damage, while there was significant improvement in the placebo group during the strictly monitored trial) is not reassuring. In the light of the Catalan study on the amount of gluten-free dietary foods actually consumed by celiacs in Europe - together with the constant risk of involuntary background contamination and the varying degrees of individual sensitivity - the absolute maximum threshold of ppm in gluten-free products must be kept below 20 ppm. This is a very far cry from the current wording of the Codex Alimentarius which is based on the old standard of the nitrogen content in food. I hope that these words may help to clarify the importance of the work done by Profs. Catassi and Fasano, the Association of Italian Celiacs, the study by the Catalan research group (previously cited on your website), and the need for further research and information as to the impact of micro-traces of gluten on celiac disease and its complications so as to ensure that celiacs may make fully informed decisions about their dietary choices.
  18. Celiac.com 03/30/2016 - New guidelines reverse previous recommendations on infant gluten introduction to prevent celiac disease. What's going on? New evidence shows that the age of introduction of gluten into the infant diet, or the practice of introducing gluten during breast-feeding, does not reduce the risk of celiac disease in infants at risk. Two earlier studies did claim to show that the time of introduction to gluten had an impact on later development of celiac disease. Based on those studies, in 2008, ESPGHAN issued a recommendation to introduce gluten into the infant diet between 4 months and 7 months, and to introduce gluten while the infant is still being breastfed. But since then, two randomized controlled trials have shown that the age at gluten introduction does not affect overall rates, nor does it affect the incidence or the prevalence of celiac disease during childhood. The latest findings show that "primary prevention of celiac disease through nutritional interventions is not possible at the present time," says Professor Szajewska of The Medical University of Warsaw, the lead author of the new guidelines. These new guidelines say that parents may introduce gluten into their infant's diet anytime between four to twelve months of age, and that the introduction does not need to be made via breastfeeding. It remains true that, according to study data, earlier gluten introduction does cause the celiac disease to present at an earlier age. However, current evidence indicates that neither breastfeeding, nor breastfeeding during gluten introduction can reduce the risk of celiac disease. The new evidence shows no difference in celiac disease risk when gluten is introduced while the infant is still breast-feeding, compared to after weaning. Because breastfeeding has many other health benefits, doctors recommend it for all infants, regardless of celiac disease risk. The updated recommendations are based on studies of infants with known risk genes for celiac disease. However, because parents don't often know this at the time solid foods are introduced, the recommendations apply to all infants. Source: Wolters Kluwer Health, January 19, 2016
  19. Celiac.com 03/07/2016 - Even though doctors know a lot more about celiac disease than they did just a few years ago, and even though they are learning more all the time, there are still very few detailed clinical descriptions of large groups of celiac patients. Recently, a team of researchers reviewed a large Dutch cohort of celiac patients to create an overview that focused on symptom presentation, co-occurrence of immune mediated diseases and malignancies. The research team included M Spijkerman, IL Tan, JJ Kolkman, S Withoff, C Wijmenga, MC Visschedijk, and RK Weersma. They are variously associated with the Department of Gastroenterology and Hepatology, University of Groningen and University Medical Center Groningen, Groningen; the Department of Genetics, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands, and with the Department of Gastroenterology and Hepatology, Medisch Spectrum Twente, Enschede, The Netherlands. To create their overview, the team performed a retrospective study in a Dutch university and a non-university medical hospital that included only patients with biopsy proven (≥Marsh type 2 classification) celiac disease. The team selected 412 patients from 9,468 small-bowel biopsy pathology reports and financial codes. About a third of the group showed classical celiac symptoms, including diarrhea (37.4%), fatigue (35.0%), weight loss (31.6%), abdominal pain (33.3%). Around 10% showed atypical symptoms, including constipation (10.4%) and reflux (12.4%), while nearly 12% were diagnosed without any reported symptoms. About one in four patients also had immune-mediated diseases, most commonly type 1 diabetes mellitus (4.9%), microscopic colitis (4.9%), and immune mediated-thyroid disease (4.1%). Celiac patients who also had immune-mediated diseases were significantly older at the time of diagnosis, compared to those without (P=0.002). A total of 53 patients (12.9%) had malignancies, eight of whom suffered from Enteropathy Associated T-cell Lymphomas. This is the first Dutch study to describe a group of celiac patients in such detail. The study highlights the wide range of clinical variables in celiac disease, as well as the importance of screening for celiac patients for concomitant diseases. Source: Dig Liver Dis. 2016 Jan 18. pii: S1590-8658(15)30028-1. doi: 10.1016/j.dld.2016.01.006. [Epub ahead of print]
  20. Celiac.com 11/11/2015 - If you ask me, it doesn't seem that far-fetched that some people who do not have celiac disease could still have adverse reactions to gluten. However, actually proving that scientifically continues to be challenging. Take the case of the research team that recently conducted a double-blind, placebo-controlled, cross-over, gluten-challenge trial of patients with suspected non-celiac gluten sensitivity. The team wanted to try to get an idea of the number of self-diagnosed patients with non-celiac gluten sensitivity. The team enrolled 53 women and 8 men referred to two Italian centers between October 2012 and November 2013 for suspected non-celiac gluten sensitivity. The subjects were randomly assigned to receive 4.375-g gluten or rice starch per day via gastro-soluble capsules for 1 week after a 1-week run-in period, and followed by a 1-week washout period and cross-over to the other group. The team chose rice starch as the placebo because it is "the most readily absorbable of the complex carbohydrates, and thus less fermentable, in the intestinal tract." They used a daily questionnaire to chart any changes in overall symptom scores, and conducted analysis with a per-protocol approach. A total of 59 patients completed the trial, while two withdrew due to "intolerable symptoms." Overall, one week of gluten consumption increased overall symptom severity compared with one week of placebo (P = .034), including abdominal bloating (P = .04), abdominal pain (P = .047), foggy mind (P = .019), depression (P = .02) and aphthous stomatitis (P = .025). Perplexingly, the team found that "most patients showed approximately equal degrees of overall symptoms with either gluten or placebo, although overall symptoms were worsened significantly by gluten in comparison with placebo." Got that? Significant numbers of the subjects reacted to the placebo. The short conclusion is that these results "do not represent crucial evidence in favor of the existence of this new syndrome." However, and it's a big however, the results aren't quite as clear as they might appear. In an accompanying editorial, Benjamin Lebwohl, MD, from the Celiac Disease Center at Columbia University, and Daniel A. Leffler, MD, MS, from Beth Israel Deaconess Medical Center write: The "overall positive result was driven by a minority of patients, whereas the rest had no (or at most a modest) worsening compared with placebo." They add that: "These findings can be a Rorschach test of sorts, in which the viewer draws interpretations that are based on his or her prior beliefs about NCGS. … It is therefore not surprising that this trial, like its predecessors, seems only to contribute to the uncertainty about NCGS." So, basically, there's no clear word on the existence or non-existence of non-celiac gluten sensitivity, or on the number of people who might suffer from it. Stay tuned for more studies, and more information as researchers attempt to sort it all out. Source: CGHJournal.org
  21. Celiac.com 02/18/2011 - In their search for a deeper understanding of the connections between celiac disease and Crohn’s disease, scientists have begun to focus on genetic variants that trigger inflammation in the gut. A research team examining associations between celiac disease and Crohn’s disease has now confirmed four common genetic variations between the two diseases. Their discovery may help to explain why people with celiac disease suffer Crohn’s disease at higher rates than the general population. Better understanding the genetic connections will likely pave the way for new treatments for symptoms common to both conditions, such as inflammation. The study used a new method of analysis called a genome-wide association study, or GWAS. This allows researchers to look at hundreds of thousands of genetic variations, called single nucleotide polymorphisms, or SNPs, that may be involved in any one disease. The research team compared 471,504 SNPs, representing the genomes of about 10,000 people, some of whom had Crohn’s disease, some of whom had celiac disease, and others who were healthy. They found four genes that seemed to raise the risk for both diseases. Two of these genes, IL18RAP and PTPN2, had already been associated with each disease. Another, called TAGAP, had previously been identified as a risk factor in celiac disease, but was newly associated with Crohn’s disease. The fourth gene, PUS10, had been previously been tied to Crohn’s disease, celiac disease, and ulcerative colitis. Three of the four genes seem to influence immune system response to perceived threats. “The first three we can say are involved in T-lymphocyte function,” Rioux says. “They seem to have a role to play in how these cells respond to a given stimulus.” In celiac disease, gluten-induced intestinal inflammation causes damage that prevents the intestine from absorbing nutrients in food. This can cause a wide range of problems, from anemia to osteoporosis to lactose intolerance. In Crohn’s disease, inflammation of the digestive tract often causes the bowel to empty frequently, resulting in diarrhea, among other problems. Some research shows that people with one condition are more likely to have the other. One study, for example, found that more than 18.5% of people with Crohn’s disease also have celiac disease. The study has “completely changed the way we can identify genetic risk factors,” says study co-author John D. Rioux, PhD, an associate professor of medicine at the University of Montreal, in Quebec, Canada. “There are sequence differences at the genetic level that get translated down to the protein levels,” Rioux notes. “And these differences may really nudge a person toward inflammation." He adds that "we’re just in the beginning, but we hope they may elucidate a common pathway and one day help us discover treatments that correct the underlying genetic changes.” Source: Jan. 27 issue of PLoS Genetics
  22. Celiac.com 10/21/2015 - Celiac disease has been traditionally recognized among Caucasians, with an estimated prevalence of about 1%. Latin America features a the population with European ancestry, along with native communities sharing a diverse degree of mix with European colonizers. The population of native Toba people comprises more than 60,000 individuals living with a clusters of villages in a forest called 'The Impenetrable' in Northeastern Argentina. In recent years, as a consequence of governmental food aid programs aimed at improving nutritional conditions in the community, the Toba people have undergone a drastic change in dietary habits, with wheat replacing their ancestral food sources. In general celiac disease can only occur in individuals with certain class II human leukocyte antigen (HLA) molecules – namely, HLA DQ2 and/or DQ8, but little information exists about the prevalence of HLA DQ2 and DQ8, and of celiac disease in native South Americans. The research team included Horacio Vázquez MD, María de la Paz Temprano RD, Emilia Sugai MS, Stella M Scacchi MS, Cecilia Souza MD,Daniel Cisterna MS, Edgardo Smecuol MD, María Laura Moreno MD, Gabriela Longarini MD, Roberto Mazure MD, María A Bartellini MS, Elena F Verdú MD2, Andrea González RD, Eduardo Mauriño MD, and Julio C Bai MD. They are variously affiliated with the Small Bowel Section, Department of Medicine, Hospital de Gastroenterología C Bonorino Udaondo. Buenos Aires, Argentina and the Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario. For their study, the research team set out to prospectively assess environmental, genetic and serological conditions associated with celiac disease among members of the Toba native population attending a multidisciplinary sanitary mission. Using an established questionnaire, an expert nutritionist determined daily gluten intake. The team then conducted gene typing for the human leuko-cyte antigen (HLA) class II alleles using DNA extracted from peripheral blood (HLA DQ2/DQ8 haplotype). The team then measured serum antibodies were immunoglobulin (Ig) A tissue transglutaminase (tTG) and the composite deamidated gliadin peptides/tTG Screen test. They tested positive cases for IgA endomysial antibodies. The team screened a total of 144 subjects, 55% of those female. Estimated average gluten consumption was 43 grams per day, ranging from 3 grams per day up to 185 grams per day. Genetic typing showed that 73 of 144 subjects had alleles associated with celiac disease; 69 of these subjects had alleles for HLA DQ8, while four had DQ2. Four and six subjects had antibody concentrations above the cut-off established by the authors' laboratory (>3 times the upper limit of normal) for IgA tTG and deamidated gliadin peptides/tTG screen, respectively. Four of these had concomitant positivity for both assays and endomysial anti-bodies were positive in three subjects who also presented a predispos-ing haplotype. The present study was the first to detect celiac disease in Native Americans. The native Toba ethnic population has very high daily gluten consumption, and a predisposing genetic background. This study found subjects with persistent celiac disease autoimmunity and, at least, three of them met serological criteria for celiac disease diagnosis. This study invites some questions about gluten and celiac disease in the tribe. For example, does the amount of gluten in the diet of people with genetic predisposition have an impact on the likelihood of celiac disease? Given that many of these people likely had DQ2/DQ8 positivity for many generations, did the introduction of wheat into their diets trigger their celiac disease? Much remains to be understood about celiac disease, and studies like this can be important and insightful. Source: Can J Gastroenterol Hepatol Vol 29 No X Month 2015 1
  23. Celiac.com 09/16/2015 - Autoimmune disease, such as type 1 diabetes, Crohn's disease, and juvenile idiopathic arthritis, affect about 7 to 10 percent of the population in the Western Hemisphere. Using genome-wide association studies (GWASs), researchers have identified hundreds of susceptibility genes, including shared associations across clinically distinct autoimmune diseases. A team of researchers recently conducted an inverse χ2 meta-analysis across ten pediatric-age-of-onset autoimmune diseases (pAIDs) in a case-control study including more than 6,035 cases and 10,718 shared population-based controls. The research team included Yun R Li, Jin Li, Sihai D Zhao, Jonathan P Bradfield, Frank D Mentch, S Melkorka Maggadottir, Cuiping Hou, Debra J Abrams, Diana Chang, Feng Gao, Yiran Guo, Zhi Wei, John J Connolly, Christopher J Cardinale, Marina Bakay, Joseph T Glessner, Dong Li, Charlly Kao, Kelly A Thomas, Haijun Qiu, Rosetta M Chiavacci, Cecilia E Kim, Fengxiang Wang, James Snyder, and Marylyn D Richie. The are variously affiliated with The Center for Applied Genomics, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA; Medical Scientist Training Program, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA; the Department of Biostatistics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.; the Division of Allergy and Immunology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA.; the Department of Biological Statistics and Computational Biology, Cornell University, Ithaca, New York, USA; the Program in Computational Biology and Medicine, Cornell University, Ithaca, New York, USA, and the Department of Computer Science, New Jersey Institute of Technology, Newark, New Jersey, USA. For their study, the team identified 27 genome-wide significant loci associated with one or more pAIDs, mapping to in silico–replicated autoimmune-associated genes (including IL2RA) and new candidate loci with established immunoregulatory functions such as ADGRL2, TENM3, ANKRD30A, ADCY7 and CD40LG. The team functionally enriched the pAID-associated single-nucleotide polymorphisms (SNPs) for deoxyribonuclease (DNase)-hypersensitivity sites, expression quantitative trait loci (eQTLs), microRNA (miRNA)-binding sites and coding variants. They also identified biologically correlated, pAID-associated candidate gene sets on the basis of immune cell expression profiling and found evidence of genetic sharing. Network and protein-interaction analyses demonstrated converging roles for the signaling pathways of type 1, 2 and 17 helper T cells (TH1, TH2 and TH17), JAK-STAT, interferon and interleukin in multiple autoimmune diseases. Source: Nature Medicine 21, 1018–1027 (2015) doi:10.1038/nm.3933
  24. Appl Environ Microbiol. 2004 Feb;70(2):1088-1096 Celiac.com 02/26/2004 - Please note that the sourdough bread used in this study is not your garden-variety sourdough bread, and as far as I know it is not commercially available. Even though this study had very promising results, it was conducted on a relatively small number of people, and larger studies need to be carried out before reaching any conclusions about the long-term safety of celiacs consuming this type of sourdough bread. -Scott Adams Researchers in Europe conducted a novel study which utilized a highly specialized sourdough lactobacilli containing peptidases that have the ability to hydrolyze Pro-rich peptides, including the 33-mer peptide, which is the main culprit in the immune response associated with celiac disease. The sourdough bread in the study was made from a dough mixture that contained 30% wheat flour and other nontoxic flours including oat, millet, and buckwheat, which was then started with the specialized lactobacilli. After 24 hours of fermentation all 33-mer peptides and low-molecular-mass, alcohol-soluble polypeptides were almost totally hydrolyzed. For the next step in the study the researchers extracted proteins fro the sourdough and used them to produce a "peptic-tryptic digest" for in vitro agglutination tests on human K 562 subclone cell. The agglutinating activity of the sourdough proteins was found to be 250 times higher that that of normal bakers-yeast or lactobacilli started breads. A double blind test was then conducted in which 17 celiac disease patients were given 2 grams of gluten-containing bread started with bakers yeast or lactobacilli. Thirteen of them showed distinct, negative changes in their intestinal permeability after eating the bread, and 4 of them did not show any negative effects. The specially prepared sourdough bread was then given to all 17 patients and none of them had intestinal permeability reactions that differed from their normal baseline values. The researchers conclude: "These results showed that a bread biotechnology that uses selected lactobacilli, nontoxic flours, and a long fermentation time is a novel tool for decreasing the level of gluten intolerance in humans."
  25. Celiac.com 03/30/2011 - A team of medical researchers set out to compare gut permeability and mucosal immune gene expression in celiac disease and gluten sensitivity. The research team included Anna Sapone, Karen M Lammers, Vincenzo Casolaro, Marcella Cammarota, Maria T Giuliano, Mario De Rosa, Rosita Stefanile, Giuseppe Mazzarella, Carlo Tolone, Maria I Russo, Pasquale Esposito, Franca Ferraraccio, Maria Carteni, Gabriele Riegler, Laura de Magistris and Alessio Fasano. People with celiac disease suffer an adverse autoimmune reaction when they consume gluten. People with gluten-sensitivity cannot tolerate gluten and may develop gastrointestinal symptoms similar to those in celiac disease. However, for people with gluten intolerance, the overall clinical picture is usually less severe, and is not accompanied by the concurrence of tissue transglutaminase autoantibodies or autoimmune comorbidities. By examining and comparing mucosal expression of genes associated with intestinal barrier function, along with innate and adaptive immunity the team sought to better understand the similarities and differences between celiac disease and gluten sensitivity. For their study, the team enrolled a group of subjects with celiac disease, a group with gluten sensitivity, and a control group of healthy, gluten-tolerant individuals. They assessed intestinal permeability using a lactulose and mannitol probe, and collected mucosal biopsy specimens to study the expression of genes involved in barrier function and immunity. They found that gluten sensitivity, unlike celiac disease, is not associated with increased intestinal permeability. In fact, subjects with gluten sensitivity showed significantly reduced intestinal permeability compared with controls (P = 0.0308). This was accompanied with significantly increased expression of claudin (CLDN) 4 (P = 0.0286). Relative to controls, subjects with celiac disease expressed higher levels of adaptive immunity markers interleukin (IL)-6 (P = 0.0124) and IL-21 (P = 0.0572), while those with gluten sensitivity showed no higher levels. Subjects with gluten intolerance showed increased expression of the innate immunity marker Toll-like receptor (TLR) 2, but subjects with celiac disease showed no such increase (P = 0.0295). Finally, subjects with gluten intolerance showed significantly reduced expression of the T-regulatory cell marker FOXP3 relative to controls (P = 0.0325) and celiac subjects (P = 0.0293). This study supports the existence of gluten sensitivity and celiac disease as two clinically different gluten-associated disorders. The study also supports the characterization of gluten sensitivity as a condition associated with prevalent gluten-induced activation of innate, rather than adaptive, immune responses in the absence of detectable changes in mucosal barrier function. Source: BMC Medicine 2011, 9:23 doi:10.1186/1741-7015-9-2
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