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  • Jefferson Adams
    Jefferson Adams

    Could Changing Gut Bacteria Prevent Celiac Disease?

    Celiac.com 11/20/2015 - A Canadian researcher has discovered what might be a big step toward preventing celiac disease. Dr. Elena Verdú, an associate professor at the Farncombe Family Digestive Health Research Institute at McMaster University, has found that bacteria in the gut may contribute to the body's response to gluten. 

    Image: CC--Hobvias SudoneighmIf her discovery pans out, it may be possible to treat, or even prevent, celiac disease by changing the the type of bacteria in the gut. "By changing the type of bacteria in the gut, we could change the inflammatory response to gluten," says Verdú.

    So far, researchers have been unable to explain why 30 per cent of people have genes that can cause celiac disease, but only 2 to 5 per cent actually develop it. Also a mystery is why the disease develops at any age. Higher rates of celiac disease are being driven not just be better testing and awareness, but also by external triggers.

    According to Dr. Decker Butzner, a Calgary-based pediatric gastroenterologist, there are another triggering factor which we've never understood…[t]here is an environmental trigger."

    Researchers have known for some time that people with celiac disease have different types of gut bacteria than those without celiac disease, but they didn't whether the changes in gut bacteria were caused by celiac disease, or the other way around.

    Verdú's study, which found that the inflammatory response to gluten was impacted by gut microbiota, is the first study to show that it is the gut microbes are likely triggering celiac disease.

    The study appears in the American Journal of Pathology.

    Read more at TheSpec.com.



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    This is an interesting subject as I have already seen how certain gut bacteria can either greatly benefit or greatly slow peristalsis through either allowing tryptophan to be absorbed and converted into serotonin or instead cause malabsorption and breakdown of tryptophan. So proper enteric bacterial population is very important and I have found only one really great source which is Wallaby Kefir which contains several serotogenic varieties.

    On another subject I define Celiac patients as poor digesters of protein. Therefore, achlorhydria (a lack of stomach acid) couild indeed be the first domino in the ultimate indigestion of the gliaden protein , and a stomach with a low pH keeps other bacterial interlopers that do not belong from invading the intestine, a very important function, plus stomach acid enables Pepsin activation, the first step in complex protein breakdown of gliaden, and that acidity initiates brush border and pancreatic enzymes such as prolyl endopeptidase to further cleave the Gliadin protein that initiates Celiac response.

    I think this bacterial role is a valid point. There are symbiotic bacteria in the human gut which must be encouraged, while the bad dysbiotic bacteria need to be prevented such as those found in Small Intestinal bacterial overgrowth, and the stomach acid and later basic bicarbonate and digestive enzymes from the pancreas also plays an important role in segregating those bacteria......thanks

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    Fascinating. I technically don't have celiac disease. I had a positive blood test, but negative biopsy. However, in college , I had a terrible time with repeated bouts of strep throat and sinusitis, and took numerous courses of antibiotics. I now wonder if that changed my gut bacteria and started me down the road of gluten intolerance.

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    My son was hospitalized for a week and was on constant IV antibiotics during that time. About 8 months after he was discharged I was concerned that he was not gaining weight. Blood work and endoscopy w/biopsy confirmed celiac disease. My son is 17 years old, 6' 3 1/2" and weighs 145 lbs. I believe the week of constant IV antibiotics triggered his celiac disease.

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  • 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

    Jefferson Adams
    Celiac.com 03/13/2013 - To determine if the probiotic Bifidobacterium natren life start (NLS) strain might affect the treatment and clinical features of patients with untreated celiac disease, a team of researchers recently conducted an exploratory, randomized, double-blind, placebo-controlled study on the effects of Bifidobacterium infantis natren life start super strain in active celiac disease.
    The research team included E. Smecuol, H.J. Hwang, E. Sugai, L. Corso, A.C. Cherñavsky, F.P. Bellavite, A. González, F. Vodánovich, M.L. Moreno, H. Vázquez, G. Lozano, S.Niveloni, R. Mazure, J. Meddings, E. Mauriño, and J.C. Bai. They are variously affiliated with the Small Intestinal Section of the Department of Medicine in the Department of Alimentation at the Hospital de Gastroenterología "Dr. C. Bonorino Udaondo," the Department of Immunogenetics of the Hospital de Clínicas "José de San Martín" at the Universidad de Buenos Aires, the Consejo de Investigación en Salud, Ministerio de Salud in Ciudad de Buenos Aires, the Department of Gastroenterology at the Universidad del Salvador in Buenos Aires, Argentina, and the Gastrointestinal Research Group at the University of Calgary in Calgary, Alberta, Canada.
    For their study, the team enrolled 22 adult patients with two positive celiac disease-specific tests.
    Over a three week period, patients randomly received two capsules of either Bifidobacterium infantis natren life start strain super strain (Lifestart 2) (2×10 colony-forming units per capsule). All patients consumed at least 12 g of gluten per day for the duration of the test. In all, twelve patients received the bifidobacterium, while ten received the placebo.
    At the end of the trial, the team used biopsy to confirm celiac disease in all patients. The primary factor being measured was changes to intestinal permeability. The secondary factor was changes in symptoms and the Gastrointestinal Symptom Rating Scale, and in immunologic indicators of inflammation.
    Neither treatment caused significant changes in abnormal baseline intestinal permeability.
    In contrast to patients receiving the placebo, patients who received B. infantis experienced significant improvements as measured by the Gastrointestinal Symptom Rating Scale (P=0.0035 for indigestion; P=0.0483 for constipation; P=0.0586 for reflux).
    The administration of B. infantis was completely safe. Patients who received B. infantis showed lower ratios of IgA tTG and IgA DGP antibody (P=0.055 for IgA tTG and P=0.181 for IgA DGP).
    Patients who received B. infantis also had significantly higher levels of serum macrophage inflammatory protein-1β (P<0.04).
    The results indicate that B. infantis may alleviate symptoms in untreated celiac disease. The probiotic produced some immunologic changes, but did not change abnormal intestinal permeability.
    The researchers call for further study to confirm and/or expand these results.
    Source:
    J Clin Gastroenterol. 2013 Feb;47(2):139-47. doi: 10.1097/MCG.0b013e31827759ac.

    Jefferson Adams
    Celiac.com 03/24/2014 - Two new studies have confirmed colonization of gluten-degrading bacteria in the human mouth and in the upper gastrointestinal tracts respectively.
    Both studies come out of the Department of Periodontology and Oral Biology, Boston University Henry M. Goldman School of Dental Medicine in Boston, Massachusetts. The research teams included Maram Zamakhchari, Guoxian Wei, Floyd Dewhirst, Jaeseop Lee, Detlef Schuppan, Frank G. Oppenheim, and Eva J. Helmerhorst.
    Gluten is notoriously hard for mammals to digest, because gliadin proteins resist mammalian proteolytic enzymes in the gut, so researchers wanted to find sources of gluten-digesting microbial enzymes from the upper gastro-intestinal tract. These microbial enzymes have the potential to neutralize the gluten peptides that act as celiac disease triggers.
    In the first study the researchers assessed proteolytic activity in suspended dental plaque towards a) gliadin-derived paranitroanilide(pNA)-linked synthetic enzyme substrates a mixture of natural gliadins and c) synthetic highly immunogenic gliadin peptides (33-mer of α2-gliadin and 26-mer of γ-gliadin).
    In addition, they conducted gliadin zymography to establish the approximate molecular weights and pH activity profiles of the gliadin-degrading oral enzymes and performed liquid iso-electric focusing to determine overall enzyme iso-electric points.
    Their results provide the first known evidence of gluten-degrading microorganisms associated with the upper gastro-intestinal tract.
    Such microorganisms may play a hitherto unappreciated role in the digestion of dietary gluten and thus protection from celiac disease in subjects at risk.
    In the second study, the team employed a selective plating strategy using gluten agar to obtain oral microorganisms with gluten-degrading capacity. They then used16S rDNA gene sequencing to carry out microbial speciations.
    To determine enzyme activity, they used gliadin-derived enzymatic substrates, gliadins in solution, gliadin zymography, and 33-mer a-gliadin and 26-mer c-gliadin immunogenic peptides.
    They separated fragments of the gliadin peptides by RP-HPLC, and structurally characterized them using mass spectrometry. They found that strains Rothia mucilaginosa and Rothia aeria showed high gluten-degrading activity. For example, gliadins (250 mg/ml) added to Rothia cell suspensions (OD620 1.2) degraded by 50% after 30 minutes of incubation.
    Importantly, the 33-mer and 26-mer immunogenic peptides were also cleaved, primarily C-terminal to Xaa-Pro-Gln (XPQ) and Xaa-Pro-Tyr (XPY). The major gliadin-degrading enzymes produced by the Rothia strains were 70–75 kDa in size, and the enzyme expressed by Rothia aeria was active over a wide pH range (pH 3–10).
    While the human digestive enzyme system lacks the capacity to cleave immunogenic gluten, such activities are naturally present in the oral microbial enzyme repertoire.
    Taken together, these studies suggest a potential for these bacteria to fuel the development of compounds that can degrade of harmful gluten peptides that trigger celiac disease in susceptible individuals.
    Source:
    PLoS One. 2011;6(9):e24455. doi: 10.1371/journal.pone.0024455. http://www.ncbi.nlm.nih.gov/pubmed/20948997

    Jefferson Adams
    Celiac.com 08/06/2014 - Although the role of human digestive proteases in gluten proteins is quite well known, researchers don’t know much about the role of gut bacteria in the metabolism of these proteins. A research team recently set out to explore the diversity of the cultivable human gut microbiome involved in gluten metabolism.
    Their goal was to isolate and characterize human gut bacteria involved in the metabolism of gluten proteins. The team included Alberto Caminero, Alexandra R. Herrán, Esther Nistal, Jenifer Pérez-Andrés, Luis Vaquero, Santiago Vivas, José María G. Ruiz de Morales, Silvia M. Albillos and Javier Casqueiro.
    They are variously associated with the Instituto de Biología Molecular, Genómica y Proteómica (INBIOMIC), the Área de Microbiología, Facultad de Biología y Ciencias Ambientales, and the Instituto de Biomedicina (IBIOMED) Campus de Vegazana at the Universidad de León, León, Spain, and with the Departamento de Gastroenterología, Hospital de León, the Departamento de Inmunología y, Hospital de León, and with Instituto de Biotecnología (INBIOTEC) de León all in León, Spain.
    For their study, they cultured twenty-two human fecal samples, with gluten as the principal nitrogen source. They also isolated 144 strains from 35 bacterial species potentially involved in gluten metabolism in the human gut. They found 94 strains that metabolise gluten, while 61 strains showed an extracellular proteolytic activity against gluten proteins.
    In patients with celiac disease, several strains exhibited peptidasic activity towards the 33-mer peptide, an immune-triggering peptide. Most of the gluten-metabolizing strains belong to the phyla Firmicutes and Actinobacteria, mainly from the genera Lactobacillus, Streptococcus, Staphylococcus, Clostridium and Bifidobacterium.
    Their findings show that the human intestine hosts numerous bacteria that can use gluten proteins and peptides for food. These bacteria could have an important role in gluten metabolism and could give rise to new treatments for celiac disease.
    Source:
    FEMS Microbiology Ecology, Volume 88, Issue 2, pages 309–319, May 2014. DOI: 10.1111/1574-6941.12295

    Jefferson Adams
    Celiac.com 02/09/2015 - Do you suffer from persistent celiac symptoms in spite of following a strict gluten-free diet and having normal small bowel mucosa? Many celiac patients do. Moreover, typical explanations, such as accidental gluten-intake or the presence of other gastrointestinal disease, do not account for all of the symptoms in these patients.
    Recent studies have suggested that changes in intestinal microbiota are associated with autoimmune disorders, including celiac disease.
    A team of researchers recently set out to determine if abnormal intestinal microbiota may in fact be associated with persistent gastrointestinal symptoms in gluten-free celiac disease patients. The research team included Pirjo Wacklin PhD, Pilvi Laurikka, Katri Lindfors PhD, Pekka Collin MD, Teea Salmi MD, Marja-Leena Lähdeaho MD, Päivi Saavalainen PhD, Markku Mäki MD, Jaana Mättö PhD, Kalle Kurppa MD, and Katri Kaukinen MD.
    They are variously associated with the Finnish Red Cross Blood Service, Helsinki, Finland; School of Medicine, University of Tampere, Tampere, Finland; the Tampere Centre for Child Health Research at the University of Tampere and Tampere University Hospital in Tampere, Finland; the Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, in Tampere, Finland; the Department of Dermatology at Tampere University Hospital in Tampere, Finland; the Research Programs Unit of the Immunobiology, and Department of Medical Genetics at the Haartman Institute of the University of Helsinki in Helsinki, Finland; the Department of Internal Medicine at Tampere University Hospital in Tampere, and with Seinäjoki Central Hospital in Seinäjoki, Finland,
    The team used 16S rRNA gene pyrosequencing to analyze duodenal microbiota in 18 gluten-free celiac patients suffering from persistent symptoms, and 18 gluten-free celiac patients without symptoms.
    All celiac patients had been following a strict gluten-free diet for several years, and had restored small bowel mucosa and tested negative for celiac autoantibodies.
    The team rated symptoms using the Gastrointestinal Symptom Rating Scale, and found that gluten-free celiac disease patients with persistent symptoms had different duodenal bacteria than celiac patients without symptoms.
    Gluten-free celiac patients with persistent symptoms had a higher relative abundance of Proteobacteria (P=0.04) and a lower abundance of Bacteroidetes (P=0.01) and Firmicutes (P=0.05). Moreover, they had a much narrower range of bacteria types in their guts.
    The discovery that dysbiosis of microbiota is associated with persistent gastrointestinal symptoms in gluten-free celiac patients offers a new avenue of treatment for such patients.
    Source:
    Am J Gastroenterol. 2014;109(12):1933-1941.

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    I do not have any ideas except to research other autoimmune disorders.  Once you have one,  you can develop more AI issues.  Any possibility of drug side effects?  For example the FDA has a black box warning in a class of antibiotics called fluoroquinilines (e.g. Cipro by Bayer).  These can cause tendon issues.  Here is a list of autoimmune disorders.  Not all are here, but it is a start.   https://www.aarda.org/diseaselist/ Ones associated with vertigo: https://www.hindawi.c
    And he needs to be super strict in his gluten free diet! SUPER strict, not just low gluten. No cross contamination, NONE.  I am so sorry, there are no short cuts with the testing. It flat out sucks but there you have it.  Welcome to the forum!
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