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Found 5 results

  1. Celiac.com 12/28/2018 - Beyond a few teaser studies, we don’t know enough about whether the individual micro-biome might play a role in the development of celiac disease and inflammatory bowel disease. Top celiac researcher Alessio Fasano, together with colleague G. Serena, recently presented an overview of current knowledge regarding the contribution of the individual micro-biome to celiac disease and inflammatory bowel disease. Their discussion includes a particular focus on how probiotics may be used as potential preventive therapy for CIDs. They are both affiliated with the Mucosal Immunology and Biology Research Center and Division of Pediatric Gastroenterology and Nutrition, Massachusetts General Hospital for Children - Harvard Medical School, Boston, MA, USA. As part of their presentation, they write that, globally, cases of chronic inflammatory diseases (CIDs) are undergoing a steep rise. This rise, together with limited effective strategies for slowing these disease explosions demands deeper knowledge of their physical mechanisms in order to reduce the adverse effects of the diseases on children. Several cross-sectional studies have shown a connection between intestinal microbial imbalance and active disease. Unfortunately, they note, these studies do not demonstrate any connection between changes in microflora as a factor in disease development, and so do not suggest any promising directions to explore for possible treatments. Fasano and Serena say that additional studies are needed to show conclusively whether intestinal dysbiosis plays a part in triggering CIDs. Furthermore, given the complexity of the microflora interaction with the host, it is necessary to design a systems-level model of interactions between the host and the development of disease by integrating micro-biome, metagenomics, metatranscriptomics, and metabolomics with either clinical or environmental data. In their overview, Fasano and Serena discuss the current knowledge regarding the contribution of the individual microbiome to celiac disease and inflammatory bowel disease. Their discussion includes a particular focus on how probiotics may be used as potential preventive therapy for CIDs. The article includes a paywall, but you may find it at: Adv Exp Med Biol. 2018 Dec 20. doi: 10.1007/5584_2018_317
  2. Celiac.com 12/10/2018 - More and more people are eating gluten-free for non-medical reasons. These days, people with celiac disease make up a small percentage of overall gluten-free food sales. However, the effects of eliminating or reducing wheat, barley and rye ingredients from the diets of in healthy adults have not been well studied. A team of researchers recently set out to assess the effects of a gluten-free diet in healthy adults. To make their assessment, the researchers conducted a randomized, controlled, cross-over trial of 60 middle-aged Danish adults with no known diseases. The trial included two 8-week assessments comparing a low-gluten diet of 2 grams of gluten per day, and a high-gluten diet of 18 grams of gluten per day, separated by a washout period of at least six weeks with habitual diet including 12 grams of gluten per day. Compared with a high-gluten diet, the data show that a low-gluten diet triggers slight changes in the intestinal microbiome, increases food and drink intake and postprandial hydrogen exhalation, and reduces self-reported bloating. The team’s data indicate that results of a low-gluten diet in non-celiac adults are likely triggered by qualitative changes in dietary fiber. Studies like this are important for understanding the effects of a gluten-free diet in both celiacs and non-celiacs alike. Better understanding of a gluten-free diet will help doctors, celiac patients, and healthy individuals to make better, more informed dietary decisions. Source: Nature Communications; volume 9, Article number: 4630 (2018) The research team included Lea B. S. Hansen, Henrik M. Roager, Nadja B. Søndertoft, Rikke J. Gøbel, Mette Kristensen, Mireia Vallès-Colomer, Sara Vieira-Silva, Sabine Ibrügger, Mads V. Lind, Rasmus B. Mærkedahl, Martin I. Bahl, Mia L. Madsen, Jesper Havelund, Gwen Falony, Inge Tetens, Trine Nielsen, Kristine H. Allin, Henrik L. Frandsen, Bolette Hartmann, Jens Juul Holst, Morten H. Sparholt, Jesper Holck, Andreas Blennow, Janne Marie Moll, Anne S. Meyer, Camilla Hoppe, Jørgen H. Poulsen, Vera Carvalho, Domenico Sagnelli, Marlene D. Dalgaard, Anders F. Christensen, Magnus Christian Lydolph, Alastair B. Ross, Silas Villas-Bôas, Susanne Brix, Thomas Sicheritz-Pontén, Karsten Buschard, Allan Linneberg, Jüri J. Rumessen, Claus T. Ekstrøm, Christian Ritz, Karsten Kristiansen, H. Bjørn Nielsen, Henrik Vestergaard, Nils J. Færgeman, Jeroen Raes, Hanne Frøkiær, Torben Hansen, Lotte Lauritzen, Ramneek Gupta, Tine Rask Licht and Oluf Pedersen. They are variously affiliated with the National Food Institute; the Department of Biotechnology and Biomedicine, Technical University of Denmark; the Department of Bio and Health Informatics; the Department of Chemical and Biochemical Engineering at the Technical University of Denmark in Lyngby, Denmark; the Department of Plant and Environmental Sciences; the Department of Nutrition, Exercise and Sports; the Department of Nutrition, Exercise and Sports; and the Department of Veterinary Disease Biology, Faculty of Science, University of Copenhagen in Frederiksberg, Denmark; the Department of Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark; the Department of Clinical Biochemistry, Copenhagen University Hospital Hvidovre in Hvidovre, Denmark; the Department of Radiology, Bispebjerg Hospital in Copenhagen, Denmark; the Department of Autoimmunology & Biomarkers, Statens Serum Institut in Copenhagen, Denmark; the Department of Biology and Biological Engineering, Chalmers University of Technology in Gothenburg, Sweden; the School of Biological Sciences, The University of Auckland in Auckland, New Zealand; the Bartholin Institute, Rigshospitalet in Copenhagen, Denmark; the Research Centre for Prevention and Health, The Capital Region of Denmark in Frederiksberg, Denmark; the Research Unit and Department of Gastroenterology, Herlev and Gentofte Hospital, the Capital Region of Denmark in Herlev, Denmark; with Clinical-Microbiomics A/S in Copenhagen, Denmark; the Department of Microbiology and Immunology, KU Leuven–University of Leuven, Rega Institute; and VIB, Center for Microbiology in Leuven, Belgium; with Biostatistics, Department of Public Health, University of Copenhagen in Copenhagen, Denmark; the Laboratory of Genomics and Molecular Biomedicine, Department of Biology; the Novo Nordisk Foundation Center for Basic Metabolic Research; the Department of Radiology, Bispebjerg Hospital, Copenhagen, Denmark; and the Department of Biomedical Sciences; and the department of Biostatistics at the Department of Public Health at the University of Copenhagen, Copenhagen, Denmark.
  3. I recently returned to the US after a decade in China where I was unconsciously following a gluten-free diet. Rice, meat, vegetables and rarely any bread, etc. After returning to the US in June 2017, I suddenly developed a lot of celiac symptoms. In September, I had my microbiome analyzed and the results were consistent with celiac according to a few studies. But there isn't a ton of research out there. My question is...Did anyone's doctor look at that as an indicator of celiac? I haven't had the blood test or biopsy done, but I do feel better after going gluten-free for 10 days and a lot of symptoms have subsided.
  4. Celiac.com 12/25/2017 - In the very near future, your personal microbiome may be the key to creating a customized treatment for celiac disease. That's because new advances in genome studies are promising to help create a customized, individual approach for treating numerous disorders, including celiac disease. Such individualized treatments may also help to reduce adverse events, and decrease health care costs. So far, a similar approach for optimizing preventive and therapeutic approaches in cancer using human genome sequencing has proven successful. Writing in the Mayo Clinic Proceedings, ad team of researches expounded on this approach. The research team included Purna C. Kashyap, Nicholas Chia, PhD, Heidi Nelson, MD, Eran Segal, PhD, and Eran Elinav, MD, PhD. They are variously affiliated with the Enteric Neuroscience Program, Department of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN; the Department of Surgery, Mayo Clinic, Rochester, MN; the Department of Computer Science at the Weizmann Institute of Science in Rehovot, Israel and with the Department of Immunology, at the Weizmann Institute of Science in Rehovot, Israel. Your personal microbiome is the sum total of all the microbes that reside within and upon you, along with all their genetic elements. Using genome sequencing allows doctors to design highly personal, highly focused treatments and therapeutic strategies. In their review for the Mayo Clinic Proceedings, the team highlights the importance of the microbiome in all aspects of human disease, including pathogenesis, phenotype, prognosis, and treatment response. The microbiome also plays a crucial role as a diagnostic and therapeutic biomarker. The team's report describes the role to be played by next-generation sequencing in helping to provide precision microbial identification of infectious diseases, and helping to elucidate the nature and function of microbial communities. Basically, as we further unlock the human genome, we can begin to better understand the role played by the myriad microbes that make up the human microbiome. As we unlock the role of various parts of the microbiome, look for major advances and refinements to diagnosing, treating, and even conquering conditions like celiac disease, and many others. And, with advances coming at breakneck speed, look for this to happen sooner, rather than later. Source: PlumX Metrics - mayoclinicproceedings.org
  5. Celiac.com 09/16/2016 - Great news about poop transplants: They work! And now doctors kind of understand how and why they work. This is good news about a humor provoking, but very serious matter. Clostridium difficile infection is one of the most common health care-associated infections, and up to 40% of patients suffer from recurrence of disease following standard antibiotic therapy. C. difficile infection has proven to be very difficult to treat. Fecal microbiota transplantation (FMT) has been successfully used to treat recurrent C. difficile infection. Doctors hypothesize that FMT promotes recovery of a microbiota capable of colonization resistance to C. difficile. However, they didn't really understand how it worked. Recently, a research team investigated changes in the fecal microbiota structure following FMT in patients with recurrent C. difficile infection, and imputed a hypothetical functional profile based on the 16S rRNA profile, using a predictive metagenomic tool. After FMT, they also noted increased relative abundance of Bacteroidetes and decreased abundance of Proteobacteria. The research team included Anna M. Seekatz, Johannes Aas, Charles E. Gessert, Timothy A. Rubin, Daniel M. Saman, Johan S. Bakken, and Vincent B. Young. They are variously affiliated with the Department of Internal Medicine, Division of Infectious Diseases, Department of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan, USA; Essentia Health, Department of Gastroenterology, Duluth, Minnesota, USA; Essentia Institute of Rural Health, Duluth, Minnesota, USA; and St. Luke's Hospital, Section of Infectious Diseases, Duluth, Minnesota, USA. Their results showed that, after transplantation, fecal microbiota of recipients was more diverse, and more similar to the donor profile, than the microbiota before transplantation. Additionally, they observed differences in the imputed metagenomic profile. In particular, amino acid transport systems were over-represented in samples collected prior to transplantation. These results Indicate that functional changes accompany microbial structural changes following this therapy. Further identification of the specific microbiota, and functions that promote colonization resistance, may help to create better treatment methods for C. difficile infection. Source: mBio. 2014 May-Jun; 5(3): e00893-14. Published online 2014 Jun 17. doi: 10.1128/mBio.00893-14. PMCID: PMC4068257
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