Jump to content
  • Sign Up
  • Join Our Community!

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

  • Jefferson Adams
    Jefferson Adams

    Could a Virus Trigger Gluten Intolerance? Rates Double Among Finns

    Celiac.com 03/22/2010 - The main cause for gluten intolerance continues to puzzle scientists, but pathogenesis theories include both genetic susceptibility and environmental triggers, like a virus or infection.

    For the first time, scientists working with the Academy of Finland’s Research Program on Nutrition, Food, and Health have found genes in the body that are associated both with the immune system and with the body's ability to properly digest gluten in the intestinal tract.

    Gluten intolerance arises from an autoimmune reaction in the small intestine to the gluten protein found in wheat, barley and rye. Academy Research Fellow Paivi Saavalainen, a veteran researcher in hereditary risk factors for gluten intolerance, says that "some of the genes we have identified are linked with human immune defense against viruses. This may indicate that virus infections may be connected in some way with the onset of gluten intolerance.”

    Data shows that rates of celiac disease in America have increased more than 400% since World War II. Meanwhile, a Finnish scientist internationally known for his gluten research says that the number of people in Finland who suffer from gluten intolerance has doubled over the last two decades.

    Since the early 1980s, the percentage of Finns with gluten intolerance has risen from about 1 percent of adults to about 2 percent, according to Professor Markku Mäki, head of a research project in the Academy of Finland's Research Program on Nutrition, Food and Health.

    "We've already seen a similar trend emerge earlier on where allergies and certain autoimmune disorders are concerned. Screening has shown that gluten intolerance occurs in 1.5 per cent of Finnish children and 2.7 per cent of the elderly. The higher figure for older people is explained by the fact that the condition becomes more frequent with age," says Mäki.

    For the immune study, when researchers scanned the genetic maps of more than 9400 celiac patients, they found areas of immune system disturbance. Their evidence also indicated that genes connected with the inability to digest gluten were also connected with other autoimmune diseases such as type 1 diabetes and rheumatoid arthritis.

    Saavalainen and his team have succeeded in localizing risk genes in both individual patients and entire families, which adds weight to the notion that gluten intolerance is inherited.

    The researchers are hoping to use the genetic information to craft better screening tests for gluten intolerance, as up to 75% of people with gluten intolerance remain undiagnosed due to mild or atypical symptoms, and many with condition may unwittingly suffer damage to their intestinal villi. Professor Maki points out that many present first with iron deficient, or folic acid deficient, anemia.

    Source:
    Academy of Finland
     



    User Feedback

    Recommended Comments

    There are no comments to display.



    Join the conversation

    You can post now and register later. If you have an account, sign in now to post with your account.
    Note: Your post will require moderator approval before it will be visible.

    Guest
    Add a comment...

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoji are allowed.

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

    ×   Your previous content has been restored.   Clear editor

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


  • About Me

    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, science, and advanced research, and scientific methods. He previously served as Health News Examiner for Examiner.com, and devised health and medical content for Sharecare.com. Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

  • Related Articles

    Scott Adams
    W. Dickey, S.A. McMillan, D.F. Hughes
    Scandinavian Journal of Gastroenterology 1998; 33: 491-3
    Departments of Gastroenterology and Histopathology, Altnagelvin Hospital, Londonderry; Regional Immunology Service, Royal Group of Hospitals, Belfast; Northern Ireland, UK
    Background: Coeliac disease is common yet often undiagnosed because symptoms may be trivial, non-specific, or non-gastrointestinal, or because of lack of clinician awareness. Serum IgA class endomysial antibodies (EmA) have high specificity for coeliac disease and may facilitate case-finding by clinicians other than gastroenterologists. We assessed the appropriateness and diagnostic yield of requests for EmA by primary care general practitioners in a defined geographical area of Northern Ireland. Methods: We identified patients who had EmA requests by their general practitioners during 1994-1996. Individual patient questionnaires were posted to the general practitioners concerned, seeking information on indications for testing, management following the result and final diagnosis. We compared new patient diagnosis rates in two catchment areas, one served by a large district general hospital with a medical gastroenterology facility and the other by smaller hospitals without.
    Results: A total of 239 patients had coeliac profile testing by 69 of 177 general practitioners in the area. Data were available for 181 patients not previously known to have coeliac disease of whom 20 (11%) had EmA. All EmA +ve patients were referred to hospital where 19 underwent small bowel biopsy, which confirmed coeliac disease in all 19. Only 7 (35%) of the 20 had diarrhea and there was no significant difference in EmA prevalence among patients tested with and without diarrhea. Although the mean number of new patients (per 100,000 population per annum) diagnosed by biopsy was 11 at the large hospital compared with 5 elsewhere, the numbers identified by EmA in general practice for the two catchment areas were similar (2, 3). Conclusion: General practitioners have an important role in the identification of patients with coeliac disease, particularly where there is no local medical gastroenterology facility, which is facilitated by EmA testing.

    Scott Adams
    Arch Dis Child 2004;89:499-501,512-515.
    Celiac.com 09/12/2004 – According to a recent study by Italian researchers, about 1% of Italian schoolchildren have celiac disease. The scientists screened blood samples taken from 3,188 schoolchildren aged 6 to 12 years for the presence of tissue Transglutaminase (tTG). The results showed that 33 tested positive for tTG, and of those 30 were verified by follow-up biopsies, and 3 refused biopsies but also tested positive for celiac disease-related antibodies and celiac disease-associated HLA DQ2-8. Out of the 33 who tested positive only 12 had symptoms.
    The researchers believe that the subsequent treatment of these children will likely help them to avoid future autoimmune disorders associated with untreated celiac disease. They also believe that because tTG screening is less expensive and more accurate than other forms of celiac disease screening, it should be used in the future for all mass-screening programs. They conclude that future mass screening programs deserve careful consideration.

    Jefferson Adams
    Celiac.com 03/09/2009 - A team of researchers based in Finland recently demonstrated for the first time that B. lactis probiotic bacteria are capable of shielding epithelial cells from cellular damage caused by gliadin exposure.
    The research team was made up of doctors K. Lindfors, T. Blomqvist, K. Juuti-Uusitalo, S. Stenman, J. Venäläinen, M. Mäki and K. Kaukinen. They are associated with the Paediatric Research Centre for the Medical School of the Finland’s University of Tampere, the Department of Peadiatrics, and the Department of Gastroenterology and Alimentary Tract Surgery at Tampere University Hospital, and the Department of Pharmacology and Toxicology of the Finland’s University of Kuopio.    
    In people with celiac disease, wheat gliadin causes serious intestinal symptoms and damages the small-bowel mucosa. Untreated, this can leave the individual at risk of developing various cancers and numerous associated conditions. Most all of this can be reversed or prevented if detected and treated early enough.
    Currently, the only effective treatment for celiac disease is a strict life-long gluten-free diet. However, a 100% gluten-free diet is nearly impossible to maintain, with so many gluten-free products containing trace amounts of gluten. Because of this, people with celiac disease face regular gluten contamination. Also because of this, acceptable alternatives are desirable.  
    Earlier studies have indicated that probiotic bacteria might be used in sourdough fermentation to induce the hydrolysis of celiac toxic gluten in food manufacturing, and thereby benefit people with celiac disease.
    Although several studies have addressed the ability of probiotic bacteria to detoxify gliadin after an extensive incubation period, the team found none that investigated whether various live probiotic bacteria can inhibit gliadin-induced toxic effects directly on epithelial cells.
    In this study the team set out to determine whether probiotics Lactobacillus fermentum or Bifidobacterium lactis might block the toxic effects of gliadin in intestinal cell culture conditions.
    To assess the degree to which live probiotics were able to block peptic-tryptic digested gliadin-induced degradation of human colon cells Caco-2, the team measured epithelial permeability by transepithelial resistance, actin cytoskeleton arrangements by the extent of membrane ruffling and expression of tight junctional protein ZO-1.
    B. lactis inhibited the gliadin-induced increase dose-dependently in epithelial permeability, and, at higher concentrations totally eliminated the gliadin-induced reduction in transepithelial resistance.
    That is, B. lactis decreased or eliminated the compromise in cell-wall resistance caused by gliadin. This means that B. lactis overcame the mechanism that gives rise to the decreased cell resistance and the increased permeability that occurs during an adverse reaction to wheat gliadin.
    The B. lactis strain also interfered with the creation of membrane ruffles in Caco-2 cells caused by gliadin exposure. Furthermore, it also shielded the tight junctions of Caco-2 cells from the toxic effects of gliadin, as shown by the way in which ZO-1 is expressed.
    The researchers concluded that live B. lactis bacteria might achieve partial to full blockage of gliadin toxicity gluten/gliadin-induced damage in the small-intestinal mucosa of people with celiac disease, and that it merits further study concerning its potential as a dietary supplement to guard against any silent damage associated with accidental gluten-contamination in celiac disease.
    Clinical and Experimental Immunology, 152: 552–558


    Jefferson Adams
    A team of Swiss researchers recently set out to examine the nature of T cell-mediated immuno-regulation in the gastrointestinal tract. The research team was made up of doctors L. Saurer and C. Mueller of the Institute of Pathology at the University of Bern in Switzerland.
    In the human intestinal tract, just a single layer of epithelial cells divides innate and adaptive immune effector cells from a wide array of antigens. Here, the immune system faces a tall task in accepting beneficial flora and dietary antigens while preventing the dissemination of potential pathogens. When the tightly controlled process of immune system reactions breaks down, harmful inflammation and damage may result.
    In light of this, a great deal of focus has shifted toward 'conventional' regulatory CD4+ T cells, including naturally occurring and adaptive CD4+ CD25+ Foxp3+ T cells, Th3 and Tr1 cells.
    However, control mechanisms in the intestinal mucosa are highly intricate, and include adaptations of non-haematopoietic cells and innate immune cells in addition to the presence of unconventional T cells with regulatory properties such as resident TCRγδ or TCRαβ CD8+ intraepithelial lymphocytes.
    In the study, L. Saurer and C. Mueller seek to provide an overview of the present body of knowledge on standard and non-standard regulatory T cell subsets (Tregs), with particular focus on clinical data and the potential role or malfunctioning of Tregs in four major human gastrointestinal diseases, i.e. inflammatory bowel diseases, celiac disease, food allergy and colorectal cancer.
    Their data confirms most of the findings derived from experimental animal models, and has implications for clinical immunology, food allergy, immunoregulation, immunotherapy, mucosal immunology, and regulatory T cell protocols. Their findings appear in the February 2009 issue of Allergy.



  • Popular Contributors

  • Forum Discussions

    Hi Mom, I am so sorry you're getting the run around. Yes, the links worked for me too & that poor little thing! Cyclinglady gave you excellent advice. I really can't add anything to it but everything she says is right on. Keep advocating!  Read this: https://www.sjsreview.com/8752/features/sophomore-establishes-celiac-support-group/ I found how you can contact her. GenerationGF.Houston@gluten.org Here's the web page. Scroll down to the TX groups. https://gluten.org/k
    Wow!  I can say thank you in Polish, but can not spell it.  This is a bit off topic, but I will post this here and then open a new topic.   A month or so ago, a guest commented on an article that Celiac.com had published.  The guest mentioned that she has been a celiac for decades, long before the gluten free craze.  She noticed that she is now getting more gluten exposures compared to the years when there were very few gluten free processed foods on the market.  Interesting. With
    The celiac tests are: TTG IgA TTG IgG DGP IgA DGP IgG  EMA IgA And....Immunogobulin A (IgA).  This test is used only as a control test when checking for celiac disease.  If your body is not producing enough IgA, the IgA celiac tests are invalid or will not work.    You would also have a immune deficiency issues too.  But that is a separate issue.   The previous link I gave you spells out the test names which are long!  😆
×
×
  • Create New...