Jump to content
Celiac Disease FAQ | This site uses cookies GDPR notice. Read more... ×
  • Sign Up

Search the Community

Showing results for tags 'response'.



More search options

  • Search By Tags

    Type tags separated by commas.
  • Search By Author

Content Type


Celiac Disease & Gluten-Free Diet Forums

  • Diagnosis & Recovery, Related Disorders & Research
    • Calendar of Events
    • Celiac Disease Pre-Diagnosis, Testing & Symptoms
    • Post Diagnosis, Recovery & Treatment of Celiac Disease
    • Related Disorders & Celiac Research
    • Dermatitis Herpetiformis
    • Gluten Sensitivity and Behavior
  • Support & Help
    • Coping with Celiac Disease
    • Publications & Publicity
    • Parents' Corner
    • Gab/Chat Room
    • Doctors Treating Celiac Disease
    • Teenagers & Young Adults Only
    • Pregnancy
    • Friends and Loved Ones of Celiacs
    • Meeting Room
    • Celiac Disease & Sleep
    • Celiac Support Groups
  • Gluten-Free Lifestyle
    • Gluten-Free Foods, Products, Shopping & Medications
    • Gluten-Free Recipes & Cooking Tips
    • Gluten-Free Restaurants
    • Ingredients & Food Labeling Issues
    • Traveling with Celiac Disease
    • Weight Issues & Celiac Disease
    • International Room (Outside USA)
    • Sports and Fitness
  • When A Gluten-Free Diet Just Isn't Enough
    • Food Intolerance & Leaky Gut
    • Super Sensitive People
    • Alternative Diets
  • Forum Technical Assistance
    • Board/Forum Technical Help
  • DFW/Central Texas Celiacs's Events
  • DFW/Central Texas Celiacs's Groups/Organizations in the DFW area

Celiac Disease & Gluten-Free Diet Blogs

There are no results to display.

There are no results to display.

Categories

  • Celiac.com Sponsors
  • Celiac Disease
  • Safe Gluten-Free Food List / Unsafe Foods & Ingredients
  • Gluten-Free Food & Product Reviews
  • Gluten-Free Recipes
    • American & International Foods
    • Gluten-Free Recipes: Biscuits, Rolls & Buns
    • Gluten-Free Recipes: Noodles & Dumplings
    • Gluten-Free Dessert Recipes: Pastries, Cakes, Cookies, etc.
    • Gluten-Free Bread Recipes
    • Gluten-Free Flour Mixes
    • Gluten-Free Kids Recipes
    • Gluten-Free Recipes: Snacks & Appetizers
    • Gluten-Free Muffin Recipes
    • Gluten-Free Pancake Recipes
    • Gluten-Free Pizza Recipes
    • Gluten-Free Recipes: Soups, Sauces, Dressings & Chowders
    • Gluten-Free Recipes: Cooking Tips
    • Gluten-Free Scone Recipes
    • Gluten-Free Waffle Recipes
  • Celiac Disease Diagnosis, Testing & Treatment
  • Celiac Disease & Gluten Intolerance Research
  • Miscellaneous Information on Celiac Disease
    • Additional Celiac Disease Concerns
    • Celiac Disease Research Projects, Fundraising, Epidemiology, Etc.
    • Conferences, Publicity, Pregnancy, Church, Bread Machines, Distillation & Beer
    • Gluten-Free Diet, Celiac Disease & Codex Alimentarius Wheat Starch
    • Gluten-Free Food Ingredient Labeling Regulations
    • Celiac.com Podcast Edition
  • Journal of Gluten Sensitivity
    • Spring 2019 Issue
    • Winter 2019 Issue
    • Autumn 2018 Issue
    • Summer 2018 Issue
    • Spring 2018 Issue
    • Winter 2018 Issue
    • Autumn 2017 Issue
    • Summer 2017 Issue
    • Spring 2017 Issue
    • Winter 2017 Issue
    • Autumn 2016 Issue
    • Summer 2016 Issue
    • Spring 2016 Issue
    • Winter 2016 Issue
    • Autumn 2015 Issue
    • Summer 2015 Issue
    • Spring 2015 Issue
    • Winter 2015 Issue
    • Autumn 2014 Issue
    • Summer 2014 Issue
    • Spring 2014 Issue
    • Winter 2014 Issue
    • Autumn 2013 Issue
    • Summer 2013 Issue
    • Spring 2013 Issue
    • Winter 2013 Issue
    • Autumn 2012 Issue
    • Summer 2012 Issue
    • Spring 2012 Issue
    • Winter 2012 Issue
    • Autumn 2011 Issue
    • Summer 2011 Issue
    • Spring 2011 Issue
    • Spring 2006 Issue
    • Summer 2005 Issue
  • Celiac Disease & Related Diseases and Disorders
    • Lists of Diseases and Disorders Associated with Celiac Disease
    • Addison's Disease and Celiac Disease
    • Anemia and Celiac Disease
    • Anorexia Nervosa, Bulimia and Celiac Disease
    • Arthritis and Celiac Disease
    • Asthma and Celiac Disease
    • Ataxia, Nerve Disease, Neuropathy, Brain Damage and Celiac Disease
    • Attention Deficit Disorder and Celiac Disease
    • Autism and Celiac Disease
    • Bacterial Overgrowth and Celiac Disease
    • Cancer, Lymphoma and Celiac Disease
    • Candida Albicans and Celiac Disease
    • Canker Sores (Aphthous Stomatitis) & Celiac Disease
    • Casein / Cows Milk Intolerance and Celiac Disease
    • Chronic Fatigue Syndrome and Celiac Disease
    • Cognitive Impairment and Celiac Disease
    • Crohn's Disease and Celiac Disease
    • Depression and Celiac Disease
    • Dermatitis Herpetiformis: Skin Condition Associated with Celiac Disease
    • Diabetes and Celiac Disease
    • Down Syndrome and Celiac Disease
    • Dyspepsia, Acid Reflux and Celiac Disease
    • Epilepsy and Celiac Disease
    • Eye Problems, Cataract and Celiac Disease
    • Fertility, Pregnancy, Miscarriage and Celiac Disease
    • Fibromyalgia and Celiac Disease
    • Flatulence (Gas) and Celiac Disease
    • Gall Bladder Disease and Celiac Disease
    • Gastrointestinal Bleeding and Celiac Disease
    • Geographic Tongue (Glossitis) and Celiac Disease
    • Growth Hormone Deficiency and Celiac Disease
    • Heart Failure and Celiac Disease
    • Infertility, Impotency and Celiac Disease
    • Inflammatory Bowel Disease and Celiac Disease
    • Intestinal Permeability and Celiac Disease
    • Irritable Bowel Syndrome and Celiac Disease
    • Kidney Disease and Celiac Disease
    • Liver Disease and Celiac Disease
    • Lupus and Celiac Disease
    • Malnutrition, Body Mass Index and Celiac Disease
    • Migraine Headaches and Celiac Disease
    • Multiple Sclerosis and Celiac Disease
    • Myasthenia Gravis Celiac Disease
    • Obesity, Overweight & Celiac Disease
    • Osteoporosis, Osteomalacia, Bone Density and Celiac Disease
    • Psoriasis and Celiac Disease
    • Refractory Celiac Disease & Collagenous Sprue
    • Sarcoidosis and Celiac Disease
    • Scleroderma and Celiac Disease
    • Schizophrenia / Mental Problems and Celiac Disease
    • Sepsis and Celiac Disease
    • Sjogrens Syndrome and Celiac Disease
    • Skin Problems and Celiac Disease
    • Sleep Disorders and Celiac Disease
    • Thrombocytopenic Purpura and Celiac Disease
    • Thyroid & Pancreatic Disorders and Celiac Disease
    • Tuberculosis and Celiac Disease
  • The Origins of Celiac Disease
  • Gluten-Free Grains and Flours
  • Oats and Celiac Disease: Are They Gluten-Free?
  • Frequently Asked Questions
  • Celiac Disease Support Groups
    • United States of America: Celiac Disease Support Groups and Organizations
    • Outside the USA: Celiac Disease Support Groups and Contacts
  • Celiac Disease Doctor Listing
  • Kids and Celiac Disease
  • Gluten-Free Travel
  • Gluten-Free Cooking
  • Gluten-Free
  • Allergy vs. Intolerance
  • Tax Deductions for Gluten-Free Food
  • Gluten-Free Newsletters & Magazines
  • Gluten-Free & Celiac Disease Links
  • History of Celiac.com
    • History of Celiac.com Updates Through October 2007
    • Your E-mail in Support of Celiac.com 1996 to 2006

Find results in...

Find results that contain...


Date Created

  • Start

    End


Last Updated

  • Start

    End


Filter by number of...

Joined

  • Start

    End


Group


AIM


MSN


Website URL


ICQ


Yahoo


Jabber


Skype


Interests


Location

Found 20 results

  1. Celiac.com 02/29/2016 - Previous studies have shown that oat proteins trigger an adverse anti-33-mer monoclonal antibody reaction that is proportional to the immune responses in terms of T-cell proliferation. Although there has been some research regarding the impact of these varieties on the adaptive response, researchers still don't know very much about the role of the dendritic cells. A research team recently set out to characterize different oat fractions and to study their effect on dendritic cells from celiac patients. The research team included Isabel Comino, David Bernardo, Emmanuelle Bancel, María de Lourdes Moreno, Borja Sánchez, Francisco Barro, Tanja Šuligoj, Paul J. Ciclitira, Ángel Cebolla, Stella C. Knight, Gérard Branlard and Carolina Sousa. They are variously affiliated with the Departamento de Microbiología y Parasitología, Facultad de Farmacia, Universidad de Sevilla, Sevilla, Spain; the Gastroenterology Unit, Antigen Presentation Research Group, Imperial College London & St Mark′s Hospital, Harrow, United Kingdom; the Hospital Universitario de La Princesa and Instituto de Investigación Sanitaria Princesa (IIS-IP), Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Madrid, Spain; the INRA UMR-1095, Clermont-Ferrand, France; the Nutrition and Bromatology Group, Department of Analytical and Food Chemistry, Food Science and Technology Faculty, University of Vigo-Ourense Campus, Ourense, Spain; the Instituto de Agricultura Sostenible (CSIC), Córdoba, Spain; the Division of Diabetes and Nutritional Sciences, King's College London, Gastroenterology, The Rayne Institute, St Thomas' Hospital, London, United Kingdom; and the Biomedal S.L., Sevilla, Spain. The team first isolated protein fragments from oat grains and then analyzed them using SDS–PAGE. They then characterized several proteins in the prolamin fraction using immunological and proteomic tools, as well as Nano-LC-MS/MS. These proteins were very similar to α- and γ-gliadin, and showed reactive sequences to anti-33-mer antibody, indicating their potential for causing adverse immune reactions. Furthermore, the team found that some of the newly identified oat peptides triggered a range of immune responses on circulating dendritic cells from celiac patients, as compared with healthy controls. This is the first study to show that newly identified oat peptides can trigger a range of stimulatory responses on circulating dendritic cells from celiac patients, which highlights the potential of these oat peptides to trigger adverse immune responses in people with celiac disease. Source: Food & Nutrition Research eISSN 1654-661X
  2. Celiac.com 12/07/2016 - Refractory celiac disease (RCD) is a form of celiac disease that does not respond to treatment with gluten-free diet, and often involves greater risk of complications. The guts of many RCD patients over-produce effector cytokines, which are supposed to amplify the tissue-destructive immune response. However, it remains unclear if the RCD-associated mucosal inflammation is sustained by defects in counter-regulatory mechanisms. A team of researchers recently set out to determine whether RCD-related inflammation is marked by high Smad7, an intracellular inhibitor of transforming growth factor (TGF)-β1 activity. The research team included S Sedda, V De Simone, I Marafini, G Bevivino, R Izzo, OA Paoluzi, A Colantoni, A Ortenzi, P Giuffrida, GR Corazza, A Vanoli, A Di Sabatino, F Pallone, and G Monteleone. They are variously affiliated with the Department of Systems Medicine at the University of Rome "Tor Vergata," the First Department of Internal Medicine at the Fondazione IRCCS Policlinico San Matteo of the University of Pavia, and with the Department of Molecular Medicine at San Matteo Hospital at the University of Pavia in Pavia, Italy. The team evaluated Smad7 in duodenal biopsy samples of patients with RCD, patients with active celiac, patients with inactive celiac disease and healthy controls by Western blotting, immunohistochemistry and real time-PCR. In the same samples, they used ELISA and immunohistochemistry to assess TGF-β1 and phosphorylated (p)-Smad2/3, respectively. They evaluated pro-inflammatory cytokine expression in RCD samples cultured with Smad7 sense or antisense oligonucleotide. Smad7 protein, but not RNA, expression was increased in RCD, as compared to active and inactive celiac patients and healthy controls. This increased expression was associated with defective TGF-β1 signaling, as marked by diminished p-Smad2/3 expression. TGF-β1 protein content did not differ among groups. Knockdown of Smad7 in RCD biopsy samples reduced IL-6 and TNFα expression. These results show that, in RCD, high Smad7 associates with defective TGF-β1 signaling, and sustains inflammatory cytokine production. These results suggest a novel mechanism by which amplifies mucosal cytokine response in RCD, and suggest that treatments targeting Smad7 might be helpful in RCD. Source: Immunology. 2016 Nov 14. doi: 10.1111/imm.12690.
  3. Celiac.com 11/03/2016 - Refractory celiac disease type II (RCDII) often transforms into an enteropathy-associated T-cell lymphoma (EATL), a serious condition that requires intensive treatment. Current treatment strategies for RCDII include cladribine(2-CdA) and autologous stem cell transplantation (auSCT). A team of researchers recently set out to assess long-term survival in refractory celiac disease type II, and to define clear prognostic criteria for EATL development comparing two treatment strategies. They also wanted to evaluate histological response as prognostic factor. The research team included P Nijeboer, RLJ van Wanrooij, T van Gils, NJ Wierdsma, GJ Tack, BI Witte, HJ Bontkes, O Visser, CJJ Mulder, and G Bouma. They are variously affiliated with the Department of Gastroenterology, the Department of Nutrition and Dietetics, the Department of Epidemiology and Biostatistics, the Department of Pathology, and the Department of Haematology at VU University Medical Centre in Amsterdam, The Netherlands. For their study, they retrospectively analyzed 45 patients. All patients received 2-CdA, after which they were either closely monitored (monotherapy, n=30) or received a step-up approach, including auSCT (step-up therapy, n=15). Ten patients (22%) developed EATL, nine of whom had received monotherapy. Absence of histological remission after monotherapy was associated with EATL development (p=0.010). A total of 20 patients (44%) died, with an average survival of 84 months. Overall survival (OS) in the monotherapy group was far better in those with complete histological remission compared to those with without histological remission. The monotherapy patients, who achieved complete histological remission, showed comparable EATL occurrence and OS as compared to the step-up therapy group (p=0.80 and p=0.14 respectively). Histological response is an accurate parameter to evaluate the effect of 2-CdA therapy and this parameter should be leading in the decisions whether or not to perform a step-up treatment approach in RCDII. Source: United European Gastroenterology Journal, April 2016; DOI: 10.1177/2050640616646529
  4. Celiac.com 05/30/2016 - People with HLA genes have the highest risk factor for developing autoimmune disorders. The vast majority of people with celiac disease carry the HLA DQA1*05 and DQB1*02 alleles, both of which encode the DQ2.5 molecule. A research team recently set out to examine the implications for anti-gluten T cell response of the preferential expression of HLA-DQ2.5 genes associated with celiac disease with respect to non-predisposing HLA genes. The research team included L Pisapia, A Camarca, S Picascia, V Bassi, P Barba, G Del Pozzo, and C Gianfrani. They are variously affiliated with the Institute of Protein Biochemistry-CNR, the Institute of Genetics and Biophysics-CNR in Naples, Italy, and the Institute of Food Sciences-CNR in Avellino, Italy. In order to activate pathogenic CD4+ T lymphocytes, that is, to trigger active celiac disease, it is necessary for the body to form complexes between DQ2.5 and gluten peptides on antigen-presenting cells (APCs). It is widely accepted by clinicians that the DQ2.5 genes establish the different intensities of anti-gluten immunity, depending on whether they are in a heterozygous or a homozygous configuration, that is, whether both genes are activated, or only one gene is activated. The research team's recent study shows that, in celiac patients, HLA DQA1*05 and DQB1*02 gene expression is much higher than expression of non-celiac-associated genes. This, in turn, impacts protein levels and causes a comparable cell surface exposure of DQ2.5 heterodimers between DQ2.5 homozygous and heterozygous celiac patients. As a consequence, the magnitude of the anti-gluten CD4+ T cell response is strictly dependent on the antigen dose, and not on the DQ2.5 gene configuration of APCs. These findings are important, because they support the idea that the expression of DQ2.5 genes is an important risk factor in celiac disease. The preferential expression of DQ2.5 alleles observed in this study offers a new explanation of why these genes are so frequently associated with celiac disease and with other autoimmune disorders. Source: J Autoimmun. 2016 Apr 12. pii: S0896-8411(16)30029-4. doi: 10.1016/j.jaut.2016.03.016.
  5. Celiac.com 07/01/2015 - Children with celiac disease show an impaired immune response to the hepatitis B vaccine, and neither a gluten-free diet, nor additional vaccine boosters seem to change that, according to research presented at the 33rd Annual Meeting of the European Society for Paediatric Infectious Diseases. Although a number of studies have documented this reduced response, most have been limited by low numbers of patients with celiac disease, and/or lower numbers of control patients, said Maria José Pérez, MD, from Henares Hospital in Coslada, Spain. Two of those prior studies that implicated gluten in the impaired vaccine response, showed that celiac patients who follow a gluten-free diet have a hepatitis B vaccine response that is similar to that in the general population after celiac patients switch to a gluten-free diet. In their study, Dr. Pérez and her colleagues looked at the immune response to the vaccine in children with celiac disease. The team evaluated 214 children with celiac disease and 346 control patients who had completed the hepatitis B vaccine regimen in the first year of life. All patients were vaccinated before gluten was introduced into their diets. They measured gluten antibody levels for each child to determine vaccine response. Kids who showed levels of hepatitis B surface antibody under 10 mUI/mL were defined as non-responsive to the vaccine. Overall, non-response was 8% higher in children with celiac disease than in control subjects (68.7% vs 60.7%). For children younger than 5 years, this difference was a whopping 20%, with a rate of 50.0% for celiac children, compared with 30.1% for the control group (P = .015). In children with celiac disease, the researchers found no relation between level of antibody and time since the last intake of gluten. So, one important takeaway is that gluten consumption or avoidance does not change the immune response to hepatitis B vaccine in patients with celiac disease. Over time, levels of antibody decreased in both groups, so doctors assessing immune response to hepatitis B vaccine should factor in the amount of time elapsed since vaccination, says Dr. Pérez. The prospective study involved 72 children with celiac disease who were vaccinated in the first year of life and whose antibody levels were below 10 mUI/mL. The researchers found no change in levels after the children received a single vaccine booster. In light of these results, the research team advises that children with celiac disease and undetectable levels of antibody be revaccinated with a full series of the vaccine. Source: 33rd Annual Meeting of the European Society for Paediatric Infectious Diseases (ESPID): Abstracts 463 and 464 and poster MPW06. Presented May 15, 2015.
  6. Hi there, My wife was recently diagnosed with Celaic and we are a newly gluten free household. We've done well so far, but there's a learning curve about what to do when out and about, and all the crooks and crannies that gluten can be hiding. I'm wondering what to do when she starts to have a reaction from something or other. Her primary symptoms are: Migraines & headaches Weariness / exhaustion Brain Fog Bloating & gas General digestive distress Neck / back pain I want to have a roadmap of things to do when this happens to reduce the duration of her reaction and feel less helpless. Are there things that make you feel better when you (or someone you love) has been glutened? If you suspect or find out after the fact that there was gluten in something you ate, do you have tricks or tips to dealing with it? Thanks!
  7. Below is Ron Hoggan's reply the editor of the Montreal Gazette regarding the article: "Is gluten really something that most people should avoid?" Dear Health Editor: Mr. Dunning represents corn as a choice for bread-making prior to the advent of wheat, rye, and barley cultivation. However, the evidence suggests that corn was not yet available 10 to 15 thousand years ago when wheat, the earliest of these three grains, was first cultivated so it wasn’t available more than 20 thousand years ago when wild barley was first exploited ( 1 ). The evidence also indicates that corn was not available in the Near East, where wheat was first cultivated, as corn was a New World food developed by Mesoamerican indigenous peoples ( 2 ) half a world away. In short, corn was not a discarded option for bread making when and where gluten grains were first cultivated. Perhaps Mr. Dunning should be forgiven such a relatively minor mistake. After all, he is a journalist, not a cereal scientist. However, as he is identified, in the article in question, as a science writer and a critical analyst, that should set the bar a little higher. Surely we may expect him to conduct basic research in an area by at least glancing at some of the peer reviewed reports on this topic. The one time he does this, he harkens to a report on autism as a tool for arguing against the connection between ADHD and gluten*. For instance, he decries the adoption of a gluten free diet by those without celiac disease, gluten induced neuropathy, or wheat allergy. Yet more than 90% of those with celiac disease currently go undiagnosed in the USA (3) and the average delay between onset of symptoms and diagnosis is 11 years (4). Here in Canada, we have very long delays before most of us can get to see a gastroenterologist, so our delays to diagnosis may be even longer. This suggests that our rates of diagnosis are even lower than those of the USA. Perhaps Mr. Dunning’s querulous rhetoric could be more constructively directed at these long delays and the alarming rates of under-diagnosis of celiac disease. In the interim, it seems very sensible for those with undiagnosed celiac disease to follow a gluten free diet and experience the improved health and quality of life which Mr. Dunning admits are available to these individuals through a gluten free diet. This is an issue that might be revisited when our health care system is providing a timely diagnosis to at least a majority of cases of celiac disease. Recent research has also shown that those with non-celiac gluten sensitivity, which afflicts about 12% of the general population ( 5), experience even higher rates of morbidity and early mortality than those with celiac disease (6 ). Yet this group is either entirely ignored in Mr. Dunning’s article, or, more likely, it is the unstated focus of his attack. Mr. Dunning also seems to be unaware that humans lack the full compliment of enzymes necessary for full digestion of gluten proteins thus making many of the constituent amino acids beyond our ability to metabolize when he states that gluten is “a protein that your body uses.” He further asserts that there is no good reason to avoid gluten if one does not have one of the three conditions he lists. Yet my own work suggests that the morphine-like opioids derived from gluten grains may be a contributing factor in several types of malignancy ( 7). I was pleased to read that Mr. Dunning had at least glanced at data on gluten sensitive idiopathic neuropathy, but chagrined to read his speculation regarding the prevalence of this condition. I have devoted many years to the study of gluten’s impact on human health and have yet to read any work suggesting its prevalence. Perhaps Mr. Dunning could at least hint at his source when making such contentious claims. Nonetheless, there is clear evidence that a majority of those who experience gluten sensitive idiopathic neuropathy (5) do so in the presence of non-celiac gluten sensitivity, an autoimmune dynamic. Closer to home, our own Scott Frazer has demonstrated that consumption of gluten proteins is a potent force behind the development of many cases of type 1 diabetes (8). Reports of the causal connection between gluten consumption and autoimmune disease abound in the peer reviewed literature and are too numerous to warrant citing. Mr. Dunning also asserts “there is no evidence that incidence of disease increased worldwide once wheat became a staple.” The field of Archaeology differs dramatically with Mr. Dunning’s claim. In general, it is quite well established that pre-agricultural, hunter-gatherers were much taller and had stronger bones than their descendants who adopted agriculture (9). For instance, a common finding in the skeletal remains of early farmers is a condition of porotic hyperostosis (10). Mr. Dunning also seems to be unaware that fats, per gram, provide more than twice the energy available in either carbohydrates or proteins and this ignores the added weight of indigestible fibre. The increased caloric density of fats is a principle that most students learn in high school Biology classes. Yet Mr. Dunning asserts that bread was a source of high energy and light weight. While science requires scepticism and criticism to function, polemic rhetoric based on personal bias generates more heat than light. Mr. Dunning’s report is rife with errors and emotion. Publication of such dogma does little to enhance either the Gazette’s or Mr. Dunning’s credibility. Newspapers are given considerable credence as many readers, myself included, assume that journalists are exercising due diligence in checking their facts prior to publication of these reports. It is only when I read an article such as this one, that is deeply flawed and falls within my area of expertise, that my faith in journalists and the media is undermined. *note: The only report I could find that fits the meagre description provided by Mr. Dunning is one that involved 15 children who were studied over a 12 week period (11). If this is, indeed, the study Mr. Dunning referred to, it hardly provides conclusive evidence of anything beyond the obvious need for more comprehensive study in this area. His use of these data as a springboard for his absolutist claims seems highly questionable, to say the least. Sincerely, Ron Hoggan, Ed. D. Royal Roads University, Continuing Studies co-author: Dangerous Grains ISBN: 978158333-129-3 www.dangerousgrains.com editor: Journal of Gluten Sensitivity www.celiac.com editor/co-author: Cereal Killers http://tiny.cc/s7neg Sources: http://en.wikipedia.org/wiki/Wheat http://en.wikipedia.org/wiki/Maize Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago S, Elitsur Y, Green PH, Guandalini S, Hill ID, Pietzak M, Ventura A, Thorpe M, Kryszak D, Fornaroli F, Wasserman SS, Murray JA, Horvath K. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study. Arch Intern Med. 2003 Feb 10;163(3):286-92 Green PHR, Stavropoulos SN, Panagi SG, Goldstein SL, Mcmahon DJ, Absan H, Neugut AI. Am J Gastroenterol. 2001 Jan;96(1):126-31 Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71. Anderson LA, McMillan SA, Watson RG, Monaghan P, Gavin AT, Fox C, Murray LJ. Malignancy and mortality in a population-based cohort of patients with celiac disease or "gluten sensitivity". World J Gastroenterol. 2007 Jan 7;13(1):146-51. Hoggan R. Considering wheat, rye, and barley proteins as aids to carcinogens. Med Hypotheses. 1997 Sep;49(3):285-8. http://www.ohri.ca/profiles/scott.asp Lutz W. [The carbohydrate theory]. Wien Med Wochenschr. 1994;144(16):387-92. Wright L, Chew F, Porotic Hyperostosis and Paleoepidemiology: A Forensic Perspective on Anemia among the Ancient Maya. Am Anthro. 1998 Dec; 100: 924-939. Elder JH, Shankar M, Shuster J, Theriaque D, Burns S, Sherrill L. The gluten-free, casein-free diet in autism: results of a preliminary double blind clinical trial. J Autism Dev Disord. 2006 Apr;36(3):413-20.
  8. Celiac.com 06/07/2013 - A number of studies have indicated that people with celiac disease have an inadequate response to hepatitis B vaccination. In an effort to better understand the issue, a team of researchers recently set out to assess hepatitis B vaccination response in relation to gluten exposure status in patients with celiac disease. The research team included F. Zingone, P. Capone, R. Tortora, A. Rispo, F. Morisco, N. Caporaso, N. Imperatore, G. De Stefano, P. Iovino, and C. Ciacci. They are affiliated with the Department of Medicine and Surgery at the University of Salerno in Salerno, Italy. To measure the gluten exposure status at the time of vaccination, they compare three groups of patients, along with a control group. In all, the study included 163 celiac patients. Group A contained 57 patients exposed to gluten, including patients vaccinated as 12-year-old adolescents, for whom celiac disease diagnosis was established after vaccination. Group B contained 46 patients not exposed to gluten, including patients vaccinated as 12-year-old adolescents and on a gluten-free diet at the time of vaccination. Group C was composed of 60 infants, including those vaccinated at birth. Group D included 48 healthy, vaccinated, non-celiac subjects. The researchers then compared the response of celiac patients to hepatitis B vaccination with the response by healthy subjects. They found that 43.9% of patients in group A, 34.8% of patients in group B, 58.3% of patients in group C, and 8.3% of patients in group D showed inadequate response to hepatitis B immunization. Overall, group A versus group D, P less than 0.001; group B versus group D, P = 0.002; group C versus group D, P = 0.001, while they found no significant difference for group A versus group B and group A versus group C. This study suggests that gluten exposure does not influence the response to hepatitis B immunization, and that the human leukocyte antigen likely plays the main immunological role in poor responses to hepatitis B-vaccinated celiac patients. Source: Clin Vaccine Immunol. 2013 May;20(5):660-2. doi: 10.1128/CVI.00729-12. Epub 2013 Feb 27.
  9. Celiac.com 08/13/2012 - Research has indicated that giving small amounts of wheat-rich food to people with celiac disease, who are on a gluten-free diet, will trigger interferon (IFN)-γ-secreting T cells in the bloodstream. These T cells react to gluten, and can be easily detected. However, very little is known about how this procedure might be reproduced in the same patient groups that underwent two, or more, gluten challenges. A team of researchers recently set out to assess the reproducability of this short wheat challenge method for detecting immune an response to gluten. The research team included A. Camarca, G. Radano, R. Di Mase, G. Terrone, F. Maurano, S. Auricchio, R. Troncone, L. Greco, C. Gianfrani. They are affiliated with the Institute of Food Sciences-CNR, Avellino Department of Paediatrics and European Laboratory for the Investigation of Food-Induced Diseases, University of Naples, Naples, Italy. They evaluated fourteen celiac patients in remission who consumed wheat bread for 3 days, along with thirteen patients who underwent a second gluten challenge after 3-10 months on a strict gluten-free diet. The team then analyzed the immune reactivity to gluten in peripheral blood by detecting IFN-γ both before and 6 days after patients began a a gluten-inclusive diet. They found that gliadin-specific IFN-γ-secreting CD4(+) T cells increased significantly by day 6 of the first challenge. These cells arose as prevalently human leucocyte antigen (HLA)-DQ restricted and with a phenotype of gut homing, as suggested by the expression of β7-integrin. They also saw a reaction to gliadin after the second wheat consumption, although the responses varied by individual at each challenge. The study showed that a short wheat challenge offers a non-invasive approach to investigate the gluten-related immune response in peripheral blood of people who are sensitive to gluten. Moreover, the study showed that the procedure can be reproduced in the same subjects after a gluten wash-out of at least 3 months. The results of this study mean that we can likely expect this procedure to find its way into clinical practice in the future. Source: Clinical and Experimental Immunology. 2012 Aug;169(2):129-36. doi: 10.1111/j.1365-2249.2012.04597.x.
  10. Celiac.com 06/15/2012 - Diagnosing celiac disease can be challenging for doctors if a patient has already started a gluten-free diet, and/or when test results are inconsistent. A research team set out to evaluate the in vitro gliadin challenge in such patients. Researchers included Raffaella Tortora MD; Ilaria Russo PhD; Giovanni D De Palma MD; Alessandro Luciani PhD; Antonio Rispo MD; Fabiana Zingone MD; Paola Iovino MD; Pietro Capone MD; and Carolina Ciacci MD They are variously affiliated with the Department of Clinical and Experimental Medicine at Federico II University of Naples in Naples, Italy; the Department of Surgery, Endoscopy Unit at Federico II University of Naples in Naples, Italy; the Institute of Pediatrics at the University of Foggia in Foggia, Italy; and the University of Salerno, School of Medicine, Gastroenterology at Campus di Baronissi in Salerno, Italy. For their study, the team included 57 patients without celiac disease (negative controls), 166 patients with untreated celiac disease and 55 patients with celiac disease following a gluten-free diet (positive controls), and 59 patients with difficult diagnosis. The team conducted duodenal biopsies on all patients which provided the data for diagnosing the celiac disease and for the in vitro evaluation of the gliadin-induced mucosal expression of seven inflammatory markers: PY99, ICAM-1 (intercellular cell adhesion molecule), HLA-DR, CD3, CD25, CD69, and transglutaminase 2 IgA. As part of their diagnostic work-up for celiac disease, the team included a test for specific serum antibodies. The team asked patients in the difficult diagnosis group to discontinue their gluten-free diets to that they could test for antibodies under untreated conditions. To maintain statistical accuracy, the team used the area under the receptor-operated curve (ROC) to analyze the results. They found that HLA-DR was most accurate in diagnosing celiac disease on negative controls and positive controls, excluding patients on a gluten-free diet (area under ROC=0.99). Test accuracy did not increase by combining HLA-DR data with data of other markers. The results were similar in the 39 patients of the difficult diagnosis group who underwent the test for celiac disease-specific antibodies under untreated conditions. Finally, the results showed that in vitro response of mucosal HLA-DR to gliadin is an accurate tool for diagnosing celiac disease, including in patients with difficult diagnosis. Source: The American Journal of Gastroenterology. 2012;107(1):111-117.
  11. Celiac.com 03/28/2012 - A clinical research team wanted to determine if adding ascorbate (vitamin C) to gliadin-stimulated biopsy culture could reduce the mucosal immune response to gliadin in people with celiac disease. The research team included D. Bernardo, B. Martínez-Abad, S. Vallejo-Diez, E. Montalvillo, V. Benito, B. Anta, L. Fernández-Salazar, A. Blanco-Quirós, J. A. Garrote, and E. Arranz. They are affiliated with the Mucosal Immunology Lab of the Department of Paediatrics & Immunology at Spain's Universidad de Valladolid-CSIC. Their quest was fueled by the understanding that the IL-15/NF-κB axis plays a key role in celiac disease. Because ascorbate is known to inhibit effects on NF-κB, the IL-15/NFκB axis looks like a good possible molecular target for reducing gliadin-induced inflammation in celiac disease. For their study, the team conducted in vitro gliadin challenges (100 μg/ml) on duodenal biopsy explants from treated patients with celiac disease. Challenges were conducted with and without 20mM ascorbate. As an internal control, the team used an extra tissue explant in basal culture. The team then measured secretion levels of nitrites (3h), and IFNγ, TNFα, IFNα, IL-17, IL-13, and IL-6 (24h) on the supernatants. They measured IL-15 using western-blot on whole protein duodenal explants. When the team added ascorbate to in vitro culture gliadin-challenged biopsies, they found that the ascorbate blocked secretion of nitrites (p=0.013), IFNγ (p=0.0207), TNFα (p=0.0099), IFNα (p=0.0375), and IL-6 (p=0.0036), as compared with samples from culture that received no ascorbate. They also found that the addition of ascorbate reduced cytokine secretion to levels even lower than those observed in basal cultures (IFNγ: p=0.0312; TNFα: p=0.0312; IFNα: p=0.0312; and IL-6: p=0.0078). Moreover, the gliadin-challenge triggered IL-15 production in biopsies from treated celiac disease patients, while IL-15 was completely blocked in the cultures that received ascorbate. Interestingly, ascorbate completely blocked IL-15 production even in the only treated celiac disease-patient who showed basal IL-15 production. From these results, the team concludes that ascorbate reduces the mucosal inflammatory response to gluten in an in vitro biopsy culture. As such, ascorbate might offer supplementary benefits in future celiac disease therapy. Source: Allergol Immunopathol (Madr). 2012 Jan-Feb;40(1):3-8.
  12. Celiac.com 03/08/2012 - Eating gluten-free for an entire lifetime is no easy task. Many people with celiac disease and gluten-sensitivities would love an alternative to a gluten-free diet, and a number of companies are looking to develop alternative therapies that would enable people to consume gluten without suffering damage. Even though nearly all drug-development programs include gluten challenges, very little is known about the duration of gluten challenge and gluten dosage. That is, how quickly does gluten cause damage, and at what dosages? A team of researchers recently studied the ways in which antibodies respond and mucosa change when the small bowel is exposed to gluten in people with celiac disease. The study team included Marja-Leena Lähdeaho, Markku Mäki, Kaija Laurila, Heini Huhtala, and Katri Kaukinen. To assess the amount of gluten-exposure needed to cause some small-bowel mucosal deterioration, the team conducted a gluten-challenge on twenty-five adult celiac patients. Each patient received either a low (1-3 g) or moderate (3-5g) doses of gluten daily for 12 weeks. The team assessed patient symptoms, including small-bowel morphology, densities of CD3+ intraepithelial lymphocytes (IELs) and celiac serology. Their results showed that both moderate and low amounts of gluten induced small-bowel damage in 67% of celiac patients. However, moderate gluten doses also caused mucosal inflammation and gastrointestinal symptoms in seven patients that lead to their premature withdrawal from the study. Interestingly, 22% of patients who developed significant small-intestinal damage showed no symptoms. The team concludes that, for most people with celiac disease, even low amounts of gluten can cause significant mucosal changes. However, since many people with celiac disease show no such response, sample sizes must be large enough to be statistically significant. Source: BMC Gastroenterology. 2011;11(129).
  13. Recently I have noticed a trend in articles that demonize the gluten-free diet, and imply that there is something unhealthy or even dangerous about it. Here is an example of one that I forwarded to Dr. Ron Hoggan: http://www.post-gazette.com/pg/11017/1118230-114.stm and below is his response to its author: Dear China Millman, Thank you for your interesting article on gluten-free dieting. I was very pleased to read that you include patients with non-celiac gluten sensitivity among those who should follow a gluten free diet. I assume that you have arrived at your estimate of 20 million who are afflicted with wheat allergy, non-celiac and celiac gluten sensitivity using Dr. Fasano’s estimate that 6 to 7 percent of Americans have what you refer to as this “milder form of gluten intolerance”. There are other estimates. For instance, Dr. Kenneth Fine did random blood draws at a shopping center in Dallas, Texas and found an 11% rate of gluten sensitivity. Congruently, Dr. Marios Hadjivassiliou has reported rates as high as 12% in the United Kingdom and Dr. Rodney Ford reports a prevalence estimate of 10% in New Zealand. Each investigator used different methods to arrive at their estimate, and each method is likely to underestimate the true prevalence of non-celiac gluten sensitivity. For instance, they all rely on a single class of antibody reaction against a single sub-group of proteins found in gluten grains. Thus, Dr. Fasano’s estimate may be unduly conservative as it is substantially lower than others have found in similar populations and the testing used to arrive at Dr. Fasano's estimate also carries all of the other limitations mentioned above. As for the notion that non-celiac gluten sensitivity is milder than celiac disease, Anderson et al, in their study titled “Malignancy and mortality in a population-based cohort of patients with coeliac disease or ‘gluten sensitivity’ World J Gastroenterol 2007 January 7; 13(1): 146-151, report a higher rate of malignancy and early mortality among those with non-celiac gluten sensitivity than among those with celiac disease. This finding may be the result of the common recommendation that patients ignore test results that show non-celiac gluten sensitivity, as many physicians believe that such results are “non-specific” and do not warrant a gluten free diet. However, it may also reflect that non-celiac gluten sensitivity is a more serious illness than celiac disease. It may also reflect something entirely different than these two interpretations, but it does make a very good case for the need for more research in this very neglected area. As for the comments by Heather Mangieri and the American Dietetics Association, they might benefit from reading studies such as the one by Dr. Cheng et al titled “Body Mass Index in Celiac Disease Beneficial Effect of a Gluten-free Diet” in the 2009 Journal of Clinical Gastroenterology. They found that, after diagnosis with celiac disease, about half of the overweight and obese patients lost weight. Given the conservative data you report, suggesting that at least 90% of American cases of celiac disease go undiagnosed, there can be little doubt that a large portion of those with undiagnosed celiac disease who are overweight or obese would be likely to lose weight. The number who would lose weight should be greater among those who chose to follow a gluten free diet to lose weight, as some of those who are diagnosed with celiac disease do not comply with the diet. If one accepts the proposition that those with non-celiac gluten sensitivity, IBS, and IBD often have similarly problematic reactions to gluten, the number of Americans who could lose weight and live healthier, and therefore happier, lives (eating a gluten free diet) rises exponentially. On a personal level, my mother lost 66 pounds during her first years on a gluten free diet. Now, some 15 years later, she has lost almost 100 pounds. I doubt that she would still be alive had she not undertaken the gluten free diet purely on the basis of test results suggestive of non-celiac gluten sensitivity. In the current context of excessive under-diagnosis of celiac disease and limited understandings of the dynamics by which a gluten free diet causes weight loss among celiac patients, and an enormously greater number of Americans who have non-celiac gluten sensitivity, it is difficult to understand why anyone would be cautioned against following a gluten free diet with weight loss as their objective. Whether these individuals are undiagnosed celiac patients, have undiagnosed non-celiac gluten sensitivity, or they find that a gluten free diet is helping them to achieve their body mass objectives, there is little legitimate cause to "warn" people away from a gluten free diet. Overall, your article does raise awareness of gluten as a potential health threat, so its overall impact is positive despite the misinformation that a gluten free diet does not help with weight loss. Sincerely, Ron Hoggan, Ed. D. Royal Roads University, Continuing Studies
  14. I wrote this response below to address a recent New York Times article: Confirming a Diagnosis of Celiac Disease. Celiac.com 01/13/2010 - The problem with current diagnosis criteria for celiac disease is that it takes a certain degree of damage to intestinal villi in order to get a formal diagnosis. Since celiac disease with villi damage are just one manifestation of a much broader and more widespread problem--gluten sensitivity--many people who could still develop serious health problems if they continue to eat gluten, will go undiagnosed under the current definition of celiac disease. The reality of gluten sensitivity is that around 7 to 12% of the US population test positive for antibodies which are an indicator that their immune system is mounting a response to gliadin, the part of gluten that causes the reaction in those who are sensitive. Many of these people may never get flattened villi, however, many may end up with other conditions that are triggered by gluten exposure in sensitive individuals, for example nerve damage (ataxia), liver problems, diabetes, thyroid issues, etc.. In the past 10 years the diagnostic criteria for celiac disease have been changed significantly to include various degrees of villi damage (Marsh Criteria), and as a result, more people are now being properly diagnosed. In the next 10 years I predict that blood tests alone will replace the use of all biopsy results to diagnose celiac disease, as they are a far more sensitive indicator of gluten sensitivity. Once this happens we will finally reach a point where those affected can be properly treated and avoid the risk of the many disorders that have been associated with sensitive individuals who eat gluten, some of which are described here.
  15. Celiac.com 11/02/2009 - When it comes to health and wellness, probiotics are the new black. Their role in promoting beneficial gut bacteria and in mediating adverse gut reactions is gaining a great deal of attention and study among the nutrition and health-minded. This is also true in the field of celiac disease research, where the role of probiotic strains in positively influencing various immune reactions within the gut is drawing clinical study and a good deal of interest. A number of strains of probiotic bacteria are important in regulating certain activities in gut-associated lymphoid tissue. By better understanding exactly what factors control probiotic-driven immuno-modulation, researchers hope to improve their role in the treatment, or even prevention, of specific immune-mediated diseases. A team of Italian researchers recently set out to examine the effects of various strains of Lactobacillus spp. and Bifidobacterium lactis in transgenic mice expressing the human DQ8 heterodimer, a HLA molecule linked to celiac disease. The research team was made up of R. D'Arienzo, F. Maurano, P. Lavermicocca, E. Ricca, and M. Rossi of the Institute of Food Sciences, CNR, in Avellino, Italy. The team used live mice mucosally immunized with the gluten component gliadin. To support their efforts, the team conducted in vitro analysis on immature bone marrow-derived dendritic cells (iBMDCs). Their results revealed that all strains up-regulated surface B7-2 (CD86), indicating DC maturation, but with varying intensity. No probiotic strain triggered significant levels of IL-10 or IL-12 in iBMDCs, whereas Lactobacillus paracasei and Lactobacillus fermentum basically induced TNF-alpha expression. Notably, when probiotic bacteria were co-administered in live mice with mucosa immunized with the gluten component gliadin, each of these strains increased the antigen-specific TNF-alpha secretion. The results indicate that probiotics promote strain-specific reactions that support, rather than suppress, the innate and adaptive immune systems of live mice with gluten antigen sensitivity. Using live mice models to better understand the role of probiotic bacteria in mediating immune response to gliadin and other food proteins provides important insight into how such immune responses may be mediated in humans. Such insights will help to speed better treatments for celiac disease and possibly other food-triggered immune reactions. This study supports the notion that Lactobacillus spp. and Bifidobacterium lactis strains may be helpful in promoting better gut health for sufferers of celiac disease. However, further research in humans is needed for conclusive evidence. Source: Cytokine. September 5th, 2009.
  16. Celiac.com 04/10/2006 - This study looks at innate immune response to gliadin. The innate immune system responds to gliadin inducing zonulin release and increasing intestinal permeability and may be a factor in the onset of celiac disease, but I question if this leads ultimately to the Ag-specific adaptive immune response seen in patients with celiac disease. This innate response fails to explain why one identical twin may have celiac disease and not the other. Both of the twins as well as people not even susceptible to celiac disease would presumably have this same innate response to gliadin. I again urge celiac disease researchers to consider gluten-internalizing bacteria as the necessary trigger for the onset of celiac disease. The presence or absence of such bacteria does indeed offer an explanation as to why one twin gets celiac disease and not the other. Zonulin does not. In the commercial supplement product, Glisodin, the properties of gliadin have, in fact, already been used for the last few years to facilitate the delivery of the antioxidant enzyme superoxide dismutase (SOD) protecting it from digestive acids and getting it through the intestinal mucosa, probably taking advantage of the zonulin effect. Aware of celiac disease, the developer of Glisodin tried to use other peptides as a carrier of SOD, but the only gliadin was effective. Unfortunately, this denies celiacs the benefit of using Glisodin to treat oxidative stress. Abstract of Study: J Immunol. 2006 Feb 15;176(4):2512-21. Gliadin Stimulation of Murine Macrophage Inflammatory Gene Expression and Intestinal Permeability Are MyD88-Dependent: Role of the Innate Immune Response in Celiac Disease. Thomas KE, Sapone A, Fasano A, Vogel SN. Department of Microbiology and Immunology. Recent studies have demonstrated the importance of TLR signaling in intestinal homeostasis. Celiac disease (celiac disease) is an autoimmune enteropathy triggered in susceptible individuals by the ingestion of gliadin-containing grains. In this study, we sought to test the hypothesis that gliadin initiates this response by stimulating the innate immune response to increase intestinal permeability and by up-regulating macrophage proinflammatory gene expression and cytokine production. To this end, intestinal permeability and the release of zonulin (an endogenous mediator of gut permeability) in vitro, as well as proinflammatory gene expression and cytokine release by primary murine macrophage cultures, were measured. Gliadin and its peptide derivatives, 33-mer and p31-43, were found to be potent inducers of both a zonulin-dependent increase in intestinal permeability and macrophage proinflammatory gene expression and cytokine secretion. Gliadin-induced zonulin release, increased intestinal permeability, and cytokine production were dependent on myeloid differentiation factor 88 (MyD88), a key adapter molecule in the TLR/IL-1R signaling pathways, but were neither TLR2- nor TLR4-dependent. Our data support the following model for the innate immune response to gliadin in the initiation of celiac disease. Gliadin interaction with the intestinal epithelium increases intestinal permeability through the MyD88-dependent release of zonulin that, in turn, enables paracellular translocation of gliadin and its subsequent interaction with macrophages within the intestinal submucosa. There, the interaction of gliadin with macrophages elicits a MyD88-dependent proinflammatory cytokine milieu that facilitates the interaction of T cells with APCs, leading ultimately to the Ag-specific adaptive immune response seen in patients with celiac disease.
  17. Celiac.com 09/25/2009 - Scientists at the Ottawa Hospital Research Institute and the University of Ottawa have uncovered what looks to be an important clue regarding the causes of type 1 diabetes. A research team led by Dr. Fraser Scott recently screened 42 patients with type 1 diabetes and found that nearly half showed an abnormal immune response to wheat proteins. Dr. Scott is a Senior Scientist at the Ottawa Hospital Research Institute and Professor of Medicine at the University of Ottawa. The research team includes Dr. Majid Mojibian, Dr. Habiba Chakir, Dr. David E. Lefebvre, Jennifer A. Crookshank, Brigitte Sonier and Dr. Erin Keely. In most people, the immune system functions normally, identifying and attacking dangerous foreign visitors, like viruses and bacteria, without harming healthy body tissue or other benign molecules, including food molecules in the digestive tract. The breakdown of this process contributes to the development of various autoimmune diseases and allergies. In the case of Type 1 diabetes, the immune system wrongly targets the cells of the pancreas, the organ responsible for regulation of blood sugar. Globally, diabetes afflicts nearly 250 million people. Type 1 diabetes, the most severe form of the disease, makes up about 10 percent, or about 25 million, of that worldwide total. There is currently no cure for Type 1 diabetes, and sufferers require daily insulin injections can help control blood sugar levels. Dr. Scott’s results offer the first suggestions that T cells in the immune systems of type 1 diabetics are also more likely to have adverse immune reactions to wheat. His results also suggest that such over-reaction is tied to genes associated with type 1 diabetes. According to Dr. Scott, the research suggests that "people with certain genes may be more likely to develop an over-reaction to wheat and possibly other foods in the gut and this may tip the balance with the immune system and make the body more likely to develop other immune problems, such as type 1 diabetes.” Dr. Scott adds that the immune system has to find "the perfect balance to defend the bodyagainst foreign invaders without hurting itself or over-reacting to theenvironment and this can be particularly challenging in the gut, wherethere is an abundance of food and bacteria.” In side comments that accompany the paper, diabetes expert Dr. Mikael Knip of Finland suggest that the team's results "add to the accumulating concept that the gut is an active player in the diabetes disease process.” Earlier animal models studies by Dr. Scott have shown that a wheat-free diet can reduce the risk of developing diabetes, but he notes that more research is needed to confirm the association and to assess possible effects of diet changes in humans. More research is also needed to examine possible connections to celiac disease, an autoimmune disease associated with adverse immune reactions to wheat proteins that has significant associations with diabetes. This research project was funded by the Juvenile Diabetes Research Foundation and the Canadian Institutes of Health Research. Source: Diabetes - August 2009
  18. Celiac.com 07/30/2009 - Here is Dr. Ron Hoggan's response to Slate's unfortunate article "Throwing Out the Wheat" which was written by Daniel Engber: Dear Mr. Engber, You represented Dr. Fasano as saying: “For every patient whose intestinal biopsy turns up positive, he says, nine or 10 more test clean but commit to going gluten-free all the same.” This ratio is well established in the medical and scientific literature. The rate of gluten sensitivity, as measured by IgA and IgG antibodies against gliadin, (a protein family that is a sub-group of gluten) constitutes about 10% to 12% of the general population. That is about ten times the rate of celiac disease found in the general population. These anti-gliadin antibodies (AGA) clearly demonstrate that gliadin proteins or derivative peptides are reaching the bloodstream and sensitizing the immune system to this foreign (non-self) protein. Many of these gluten sensitive individuals experience all of the same signs and symptoms as celiac patients. Similarly, you state: “Since there's no way to "prove" a case of gluten-intolerance in the lab...” This is grossly inaccurate. Although many practitioners will state that AGA are non-specific, I doubt that any of them would argue against the statement that the presence of AGA clearly indicates that gliadin or its fractions have managed to get into the bloodstream. When they say AGA are non-specific, they simply mean that these antibodies are not associated with any specific disease. They seem to be found in a wide range of autoimmune diseases, cancers, and behavioral/psychiatric disorders. You also say: “If you're paying more attention to what you eat, there's a good chance your symptoms will lessen. That's not because gluten or red meat or another food is damaging your small intestine; it's because eating less makes it easier for your gut to recover.” This assertion is based on a flawed assumption. Gluten-free foods are much more calorie-dense than those made with gluten. Thus, a common mistake made by those beginning a gluten-free diet is to eat about the same quantities they are used to eating. For instance, if one is in the habit of taking two sandwiches in their lunch, they are likely to pack two gluten free sandwiches. Since the gluten-free bread is much more nutrient dense. Increased nutrient densities apply to pasta, baked goods, and almost all gluten-free substitutes. Thus, the switch to eating a gluten-free diet usually leads to eating less, not more, as you claim in the above statement. Later you state: “Chances are you'll have reduced your total intake of carbs, and thus the amount of α-amylase in your gut.” For the reasons stated above, this is also inaccurate. You go on to say: “In other words, the mere fact of being on a gluten-free diet could make you more sensitive to grains and cereals—which would only reinforce your conviction that you're gluten-intolerant.” I am not aware of any data indicating a reduction of alpha almylase in the context of a gluten free diet. I would be amazed if you can find any such data. It reflects an assumption about the production and function of amylase that appears indefensible to me. The low carb craze has followed a very different path to the media, and began with a fellow named Banting in the 1800s whose doctors suggested a low carb diet to him as a means of losing weight. It worked, and he published a pamphlet about it. It saw a resurgence in the form of a ketogenic diet in the 1920s, at Johns Hopkins, as a treatment for epilepsy. Subsequent development of anti-seizure medications during the 1930s left the treatment without any patients, so it was abandoned until 1997 with the airing of First Do No Harm, a movie about one child’s plight and his parents’ struggle to find a treatment for his life threatening seizures. Meanwhile, research suggested that the growth of insulin sensitive tumors might be stalled by a ketogenic diet, and various case reports and subsequent clinical trials both support that perspective and indicate that most folks won’t maintain such a boring diet. The gluten-free diet was suggested by a concerned mom in 1932 and it was fully 18 years before Dr. Willem Karel Dickie’s doctoral thesis would be accepted and the world would begin to treat celiac disease with a gluten free diet. I won’t bore you with the details of this evolution but there are many twists and turns to the story of gaining acceptance of a gluten-free diet for the effective treatment of celiac disease. Both of these developments occurred quite separately. The two things they have in common are: 1. They both gained popular notice and support through the Internet, and; 2. They both defied conventional medical wisdom when they were first considered. Your graph simply identifies the impact that the Internet has had on democratizing health care. Your ill-informed attack on a gluten free diet is regrettable because it suggests it is a fad diet rather than a therapeutic one. At best, that will make it more difficult for people to get cooperation when trying to look after their own health by avoiding gluten. At worst, it will dissuade people from sticking to their diets if they believe your false assertion that gluten sensitivity cannot be identified in a lab. It can be, and is, on a very regular basis. Your information on celiac disease was mostly well researched and solid, but you clearly did not put any thought or effort into finding out about gluten sensitivity (often called gluten intolerance). I wish you would correct some of this misinformation, as it is really misleading and potentially harmful. Daniel Engber responded to the above email insisting that “it's impossible to prove gluten intolerance in the lab.” And that “Many of the strongest advocates for those with this condition describe it as one that can only be diagnosed by process of elimination. Or, to be more specific, by an elimination/reintroduction test.” He also challenged me asking if “All those who have AGA are gluten-intolerant?” Then he said that he just doesn’t believe it. Here is my reply: July 31, 2009 Hi Daniel, Thanks for your response. I don't know who these "strongest advocates" are, but your information about elimination/reintroduction testing being the only way gluten sensitivity is absolutely inaccurate. Check with any reputable blood testing lab that does IgA and/or IgG anti-gliadin antibody testing. They will set you right on this score. The presence of AGA in the bloodstream is clear, incontrovertible evidence that the body is mounting an immune response against gluten. This antibody reflects a delayed-type food sensitivity that is sometimes erroneously called an allergy. This is gluten sensitivity. It may be transient, chronic, or permanent, but there can be no doubt that it reflects the condition that is referred to as gluten intolerance. Not everyone who is gluten sensitive will show these antibodies but, yes, everyone who shows these antibodies is gluten sensitive. It is a basic principle of immunology that elevated selective antibodies reflect prior or current exposure of these antigens to the bloodstream. You must have spoken with Alessio Fasano to get that quote. Just ask him about AGA testing. He will tell you the same thing I'm telling you. I have discussed these and related matters with him at some length. I think you are mistaken in your claim that you linked to anything that Joe Murray said. I'll be very surprised if he has said anywhere that a gluten-free diet leads to eating less (although he has repeatedly said it can cause weight loss in the context of celiac disease). Could you tell me where this link appears? Nonetheless, even if the volume of food consumed is less (more on that in a moment) the increased caloric density would very likely be offset by the significant increase in caloric density of gluten-free foods. While Dr. Murray has treated and spoken with many more celiac than I have, I'd be willing to wager that I have observed many more of them while eating. :-) Apparently I misunderstood your thesis. I took you to say that public awareness of low-carb/Atkin's dieting and gluten sensitivity followed a largely parallel path because they are both pop culture trends that reflect a kind of hysteria about nutrition that is not based on science. Thus, I offered some data showing that the rise in public awareness of these two nutritional perspectives are based on scientific insights and the rapid increase of public awareness of these issues in 2004 and 2006-2008 was probably the result of improved access to information on the Internet in combination with scientific discoveries during those periods. I should have detailed the discovery and development of serological tests for celiac disease and gluten sensitivity as well as the research that began to reverse the vilification of saturated fats at about the same time. (snip) The vast majority of those eating a gluten-free are eating a very high carb diet. On this issue your article is quite misled and misleading. Please take the time to respond again, as I am most interested in that link to Joe Murray's comments. I also urge you to look at the significance and nature of AGA serum antibodies. Gluten sensitivity is readily demonstrated by these simple blood tests. Best Wishes, Ron Monday, August 03, 2009 4:50 PM Dan replied admitting that he had not, after all, linked to an article by Joe Murray. The link he apparently intended to put in was the following: http://www.montanaceliacsociety.com/physiciansmanual.htm I responded with the following message: Mon 8/3/2009 9:02 PM Hi Dan, I gave you the wrong url. Please try this one: https://www.celiac.com/gluten-free/index.php?showtopic=60511 I'm wondering how you can continue to assert "it's impossible to prove gluten intolerance in the lab" when I have given you ample information to the contrary as well as directing you to blood testing labs (Great Smokies, Immuo, Imco Diagnostics, etc. etc.) that will verify my assertion. There is also a wealth of information in the peer reviewed medical literature supporting what I'm saying. I'd be happy to provide a list of relevant research reports if you are interested. You don't mean to suggest that this quote from Joe Murray somehow justifies your above assertion do you? Just pick up a telephone and give him a call. I'm very confident that he will not support your notion that gluten sensitivity cannot be identified in the lab. Do remember that Dr. Murray is a sub-specialist in celiac disease. He may not be a big fan of assertions of non-celiac gluten sensitivity, but he won't deny that the AGA blood tests establish immune sensitization and hence, gluten sensitivity. Rodney Ford and Marios Hadjivassiliou are a couple of other world renowned researchers who are reporting AGA as a significant marker of serious disease in the absence of celiac disease. Your assertion that "it's impossible to prove gluten intolerance in the lab" was the lynchpin of your entire article. Without it, you may have to acknowledge that you have just discredited a group of people who, on the basis of solid science, are trying to improve their health. Yet you have set back their relationships with skeptical family members and friends based on your inadequate research. I really do think that you owe these people a retraction or at least a statement that mitigates some of the damage your article is doing. Sincerely, Ron Tuesday, August 04, 2009 3:14 AM Dan responded saying that he thought we were having a semantic argument. It became clear to me that he was confusing gluten sensitivity with gluten sensitive enteropathy – which is another name for celiac disease. He thought I was talking about latent celiac disease. He insisted again that gluten intolerance is not defined by any standard such as celiac disease is. He went on to say: “If you want to define "gluten intolerance" and/or "gluten sensitivity" so it applies to some subgroup of those who suffer from symptoms related to gluten, that's fine with me. I'm using the phrase "gluten intolerance" to describe all those who experience relief from the gluten-free diet without having been diagnosed with celiac.” I responded with the following: From: Ron Hoggan, Ed. D. Tue 8/4/2009 11:01 AM To: Daniel Engber Subject: RE: Throwing Out the Wheat Hi Dan, It sounds like you may be confusing gluten sensitive enteropathy with gluten sensitivity. The former is a descriptive name for celiac disease, while the latter indicates an immune system sensitized to gliadin. Selective antibodies are produced in response to foreign proteins or peptides that have breached a barrier (skin or mucosal) and are now present in the bloodstream or imbedded in self tissues. The immune system reacts as if these foreign proteins were bacterial invaders. (In fact, they are cytotoxic and neurotoxic but that is not at issue here (1, 2). If there was only one event during which gliadin proteins or peptides reached the circulation, as might be the case during a bout of flu, for instance, AGA levels usually diminish quite quickly. Thus, when a person shows elevated levels of AGA, the condition is usually chronic. It indicates that they are leaking gliadin proteins and/or peptides into the bloodstream. Celiac disease only afflicts between 10% and 15% of these people with elevated AGA. Serological tests for celiac disease identify endomysium antibodies (EMA) and tissue transglutaminase (tTG). There is no debate about the foregoing. It is common knowledge and is accepted by the vast majority of researchers and practitioners working in this area. The controversy comes in when we ask what elevated AGAs mean. Many claim that it is a non-specific finding. That is, AGAs are not diagnostic for celiac disease or any other currently recognized disease. They are much more common among those with autoimmune diseases, AIDS, and several other groups, but they do not provide any clues that will help diagnose a particular illness. AGAs are also found in some apparently healthy individuals. The only condition for which they fairly specific is what is often called a "leaky gut". However, most practitioners do not recognize increased intestinal permeability as a disease entity. There is no debate regarding the connection between elevated AGAs and leakage of gliadin into the body. In the past, the debate has been about whether AGAs are diagnostic for any disease and whether a leaky gut is an issue of any real concern. However, in the late 90s, researchers at U. Maryland, working to develop a cholera vaccine, found a protein messenger called zonulin. As its presence increases in the intestinal lumen, it relaxes the tight junctions between gut epithelial cells (3). Zonulin is overproduced by some individuals in response to gluten ingestion. It turns out that those with celiac disease, type 1 diabetes, and a variety of autoimmune diseases are particularly inclined to produce excessive quantities of zonulin in response to gluten ingestion (4). Similarly, Marios Hadjivassiliou and his neurological research group at the Royal Hallamshire Hospital in Sheffield have found that AGA are elevated in more than half of all patients with neurological disease of unknown origin and only about a third of those have celiac disease. The remaining two thirds are simply gluten sensitive, as identified by AGA (5). Variation in zonulin production, from one individual to another, is likely the factor that determines gluten sensitivity. Gluten sensitivity does not identify celiac disease, latent celiac disease, or any other enteropathy that I'm familiar with. It identifies an immune system sensitized to gluten. Avoidance of gluten in such cases can help to avoid developing additional autoimmunity, just as it sometimes does in celiac disease, but current evidence suggests that it will usually not reverse it once that autoimmunity has begun. The use of Rodney Ford's term "gluten syndrome"(2) might well have saved us considerable cyber ink, as we might have been able to begin by disagreeing about the value of a gluten free diet across the gluten syndrom spectrum, rather than taking several emails to determine that you were equating gluten sensitivity with celiac disease. Best Wishes, Ron Sources: Paganuzzi AS, Zucco F, Cardelli M, de Angelis I, Mattei R, Pino A, Rocca E, Zampaglioni F.Cytotoxic effects of wheat gliadin-derived peptides.Toxicology. 1985 Dec;37(3-4):225-32. Ford RP.The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29. Drago S, El Asmar R, Di Pierro M, Grazia Clemente M, Tripathi A, Sapone A, Thakar M, Iacono G, Carroccio A, D'Agate C, Not T, Zampini L, Catassi C, Fasano A. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines.Scand J Gastroenterol. 2006 Apr;41(4):408-19. Visser J, Rozing J, Sapone A, Lammers K, Fasano A. Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Ann N Y Acad Sci. 2009 May;1165:195-205. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71. Clemente MG, De Virgiliis S, Kang JS, Macatagney R, Musu MP, Di Pierro MR, Drago S, Congia M, Fasano A. Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function.Gut. 2003 Feb;52(2):218-23. Note: I should have added that since Dan was using the phrase gluten intolerance “to describe all those who experience relief from the gluten-free diet without having been diagnosed with celiac,” he has defeated his own argument. If a person has symptoms and they get relief from a gluten free diet, they would have to be pretty self destructive, foolish, or self-indulgent to go back to eating gluten. In a private email I received from another person, he said: “After reading his original article I had the distinct feeling that a girlfriend of his (or friend/relative) had gone on a gluten-free diet and had recently dumped him--maybe because he wasn't so supportive of this change...but I don't have any proof... ” I am most inclined to agree with this poster’s suspicions. Finally, I forwarded a copy of the letter titled: “Is gliadin really safe for non-coeliac individuals? Production of interleukin 15 in biopsy culture from non-coeliac individuals challenged with gliadin peptides” by D Bernardo1, J A Garrote2, L Fernández-Salazar3, S Riestra4, E Arranz5 from Gut 2007;56:889-890; doi:10.1136/gut.2006 These investigators report that “gluten elicits its harmful effect” on all the individuals they studied, not just those with celiac disease. I believe that Jefferson Adams has written a detailed account of this research that appears elsewhere on celiac.com. Although Mr. Engber declined to give me permission to publicly post his emails, and hence, his side of this discussion, I have invited Dan to respond to the above on celiac.com, as I would like to give him every opportunity to either provide some evidence to support his unfortunate claims about non-celiac gluten sensitivity, or to retract his damaging comments in the original article he penned. Although I have been a little rough on him, I do hope he will present his side of this debate, as it is of great importance to many individuals who must negotiate with friends and relatives to safeguard their health. These people would not dream of casually scattering rat poison on food to be served to a loved one. However, they seem to feel imposed upon by those who are gluten sensitive, because they do not want gluten scattered on their food. This attitude is just as inappropriate and sometimes, just as dangerous as scattering rat poison on food. Sincerely, Ron Hoggan
  19. Celiac.com 10/12/2007 - The presence of gluten serves to activate HLA-DQ2/DQ8-restricted intestinal specific T-cells. Currently, the only treatment for celiac disease is a strict gluten-free diet. A team of Italian researchers recently conducted a study to determine whether a new enzyme strategy might offer promise in abolishing adverse gluten-associated activity. The team used mass spectrometry to analyze enzyme modifications of immuno-dominant a-gliadin peptide P56-58 and modeling studies to determine the extent of peptide binding to HLA-DQ2.The team treated wheat flour with microbial transglutaminase and lysine methylesther. They then extracted, digested and deaminated the gliadin. They used biopsy specimens from 12 adults with known celiac disease to generate gliadin-specific intestinal T-cell lines (iTCLs), which they then challenged in vitro with various antigen solutions. The results showed that tissue TG-mediated transamidation with lysine methylesther of P56-58, or gliadin in alkaline conditions inhibited the interferon expression in iTCLs. Gastroenterology, Volume 133, Issue 3, September 2007; p780-789
  20. TI- Proba prowokacyjna u dzieci z nietolerancja biaLek mleka krowiego i glutenu: ocena reakcji klinicznych i zmian w bLonie sluzowej jelita cienkiego. AU- Kaczmarski M CS- Kliniki Chorob Zakaznych Dzieci AM w BiaLymstoku. JN- Pol Tyg Lek; 45 (8-9) p161-5 PY- Feb 19-26 1990 AB- Provocation test (re-introduction of the noxious protein) was carried out in two groups of patients: (a) with intolerance to the cow-milk proteins (41 children) treated with milk-free diet for 6-24 months, and ( with gluten intolerance (26 children) treated with gluten-free diet for 6-36 months. The following parameters were compared: type and frequency of the clinical symptoms seen in these patients prior to the introduction of allergen-free diet. Moreover, the type of observed morphological changes in the small intestine mucosa following provocation test were analyzed in the groups of 7 patients. A two-year elimination of milk from the diet produces milk tolerance in about 61% patients; clinical symptoms in the remaining children are diversified. Re-introduction of gluten with the diet (provocation test) produces recurrence of gluten intolerance in 96% of children treated with gluten-free diet for 2-3 years. Recurrence of the disease was accompanied by the atrophy of the intestinal villi.
×