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Found 9 results

  1. 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.
  2. Celiac.com 11/13/2018 - Ubiquitin is highly conserved across eukaryotes and is essential for normal eukaryotic cell function. The bacterium Bacteroides fragilis is part of the standard human gut microbiome, and the only bacterium known to encode a homologue of eukaryotic ubiquitin. The B. fragilis gene sequence points to a previous horizontal gene transfer from a eukaryotic source. The sequence encodes a protein (BfUbb) with 63% identity to human ubiquitin, which is exported from the bacterial cell. Is molecular mimicry of human ubiquitin by gut microbe linked to autoimmune diseases like celiac disease? A team of researchers recently set out to determine if there was antigenic cross‐reactivity between B. fragilis ubiquitin and human ubiquitin and also to determine if humans produced antibodies to BfUbb. The research team included L. Stewart, J. D. M. Edgar, G. Blakely and S. Patrick. They are variously affiliated with the School of Biological Sciences, University of Edinburgh, Edinburgh, UK; the School School of Biological Sciences, Queen’s University Belfast, Belfast, UK; the Regional Immunology Laboratory, Belfast Health and Social Care Trust, Belfast, UK; and the Wellcome‐Wolfson Institute for Experimental Medicine, Queen’s University Belfast, Belfast, UK. Molecular model comparisons of BfUbb and human ubiquitin predicted likely structural similarity with 99.8% confidence. The team used linear epitope mapping to identify cross-reacting epitopes in BfUbb and human ubiquitin. Also, at least one epitope of BfUbb does not cross‐react with human ubiquitin. The team used enzyme‐linked immunosorbent assay to compare the reaction of human serum to BfUbb and human ubiquitin from 474 subjects among four groups: (1) newly autoantibody‐positive patients, (2) allergen‐specific immunoglobulin (Ig)E‐negative patients, (3) ulcerative colitis patients and (4) healthy volunteers. The team’s data show that the exposure to BfUbb into the human immune system triggers the creation of IgG antibodies. Patients referred for first‐time autoimmune disease testing are more likely to have a high levels of antibodies to BfUbb than are healthy volunteer subjects. From this, the team concludes that molecular mimicry of human ubiquitin by BfUbb could be a trigger for autoimmune disease. Finding and understanding potential triggers for autoimmune conditions helps to take us one step further to understanding and potentially curing celiac disease. Stay tuned for further developments in their arena. First published: 04 August 2018 https://onlinelibrary.wiley.com/doi/full/10.1111/cei.13195
  3. Hello I made this account tonight because I am need of help by those with more experience than me. Basically since June I've been feeling horrible every morning throughout the entire day. My main symptoms were extreme nausea (no vomiting), stomach pain, constipation, and diarrhea. I was in and out of the doctors doing blood work and taking medicines for other things like ibs and gastritis until we started to think about a month and a half later that it could be celiac or a gluten insensitivity. My typical day was wake up around 9 am, feel nauseous, eat little while drinking water, and feel okay enough to fall asleep around 3 pm for a few hours and wake up feeling better with almost no nausea at all. After seeing a Gastroenterologist and having extensive blood work done, everything came back looking normal (beginning of august). We kept up with gluten free diet while taking protonix and eventually things started to turn around. I was waking up less nauseous and it would only last a few hours or a couple compared to all day. It ended up getting better to the point where i woke up later than 8 or 9 am with finally no nausea or hunger pains and i would be able to eat a fair amount throughout the day and not have any symptoms besides occasional bloating. Something happened last thursday where I woke up with nausea and it lasted a couple hours. It has been the same thing since then and even today was one of my worst days with eating little and nausea being present after eating any meal no matter how small. I never use to get nausea at night and for the past two days i have had it for a couple hours before bed. I canceled my endoscopy that was scheduled for the 27th this monday about a week prior to that date because i had felt so much better but now i regret it. We think ive been glutened but i keep a food journal and i havent been eating anything different than before i had made great progress. Does anyone else have this problem? Does this sound like ive been glutened? Something feels different and although i havent been officially diagnosed celiacs I just dont understand why id be feeling this way after making such great progress. This all comes when im starting up school and an internship and is very inconvenient and depressing. I have my own utensils and cookware that I use and I am extra paranoid and safe about making sure my areas in the kitchen are gluten free and clean. Does anyone have any tips or knowledge about this? Should I call up my doctor again? The nausea was so bad this summer i couldnt work and couldnt do anything besides pace around the house while sipping water with the air conditioner running. Im really hoping i can go back to feeling the way i felt just a week ago so that i can start up my internship and make it to school everyday. I appreciate any and all feedback!
  4. Celiac.com 07/25/2018 - Several recent research articles have emphasized the connection between intestinal autoimmune diseases, such as Crohn's disease with dysbiosis or an imbalance in the microbiota composition in the gut. However, little is known about the role of the microbiota in autoimmune pathologies affecting other tissues than the intestine. A team of researchers recently set out to examine the role played by gut microbiota in the pathogenesis of non-intestinal autoimmune diseases, such as Grave's diseases, multiple sclerosis, Type-1 diabetes, systemic lupus erythematosus, psoriasis, schizophrenia, and autism spectrum disorders. They wanted to see if microbiota can influence and determine the function of cells of the immune system. In their report, the team discusses how metabolites derived from bacteria could be used as potential therapies for non-intestinal autoimmune diseases. The report was reviewed by Richard Eugene Frye of Phoenix Children's Hospital, United States, and Matej Oresic at the University of Turku in Finland. The report was edited by Marina I. Arleevskaya of Kazan State Medical Academy in Russia. The authors conclude: "The current evidence supports the notion that changes or alterations of the microbial species that form part of the intestinal microbiota will affect the balance of Tregs and Th17 cells at the intestine, which could modify the immune response of non-intestinal autoimmune diseases. The experimental evidence suggesting that the cytokines secreted from Treg and Th17 will determine and influence non-intestinal autoimmune responses. It could also be possible that cells of the immune system located at the intestine could to move other organs to establish or modify an autoimmune response. The major message of this review is that the abundant data support the notion that the intestine is a critical organ the appropriate immune balance and for the prevention of non-intestinal autoimmune diseases. The key point is that by modifying the intestinal microbiota of a patient that suffers non-intestinal autoimmune disease it might be possible to improve the outcome of such illness." For more on the role of microbiota in influencing immune cell function and promoting individual wellbeing, read the full report in Frontiers in Microbiology. The research team included Maria C. Opazo, Elizabeth M. Ortega-Rocha, Irenice Coronado-Arrázola, Laura C. Bonifaz, Helene Boudin, Michel Neunlist, Susan M. Bueno, Alexis M. Kalergis, and Claudia A. Riedel. They are variously affiliated with the Laboratorio de Biología Celular y Farmacología, Departamento de Ciencias Biológicas, Facultad de Ciencias Biológicas, Millennium Institute on Immunology and Immunotherapy, Universidad Andres Bello, Santiago, Chile; Facultad de Medicina, Millennium Institute on Immunology and Immunotherapy, Universidad Andres Bello, Santiago, Chile; Laboratorio de Inmunobiología, Facultad de Medicina, Departamento de Biología Celular y Tisular, Universidad Nacional Autónoma de México, Mexico City, Mexico; Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Millennium Institute on Immunology and Immunotherapy, Pontificia Universidad Católica de Chile, Santiago, Chile; Unidad de Investigación Médica en Inmunoquímica Hospital de Especialidades Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City, Mexico; Institut National de la Santé et de la Recherche Médicale U1235, Institut des Maladies de l'Appareil Digestif, Université de Nantes, Nantes, France; and the Departamento de Endocrinología, Facultad de Medicina, Pontificia Universidad, Metropolitana, Chile.
  5. I got test results back from a leaky gut/gut immunity and candida stool and saliva test. Here are the results: I have very low slgA (gut immunity) and a very high yeast colonization in my mouth. The gut immunity is the main one i'm concerned about and have always suspected. I met with nutritionist yesterday and she put me on a food plan and gave me a supplement with the mixture of prebiotics, probiotics and digestive enzymes in them and also an iron supplement. I've been on it since yesterday and actually feel a bit worse today so i'm getting worried already. I really want this to work. She seemed confident i could heal my gut in no time though. Is there anyone who's gone through a similar situation that i can talk to or just anyone with some knowledge on this sort of thing?
  6. Celiac.com 03/14/2017 - Recent studies of adult celiacs have suggested that complete, not just partial, mucosal recovery and healing is possible, but, in many cases, may take longer than is currently understood. Recently Dr. Hugh James Freeman of the Department of Medicine, Gastroenterology, University of British Columbia, Vancouver, BC, Canada, conducted a study to assess healing time in celiac patients. In this study, 182 patients (60 males, 122 females) referred for evaluation of symptoms, including diarrhea and weight loss, were selected only if initial biopsies showed characteristic inflammatory changes with severe architectural disturbance. All patients were treated with a strict gluten-free diet, and diet compliance was regularly monitored. Up to 90% or more of patients showed a complete mucosal response or healing, many within 6 months. However, most patients required up to 2 years for full healing and recovery to take place in the gut. In this evaluation, women in each of 4 different age ranges showed better mucosal response and healing than men, while elderly celiacs had lower rates overall. Such factors should be considered before labeling a patient with "non-responsive" disease. However, celiacs who are diagnosed later, start a gluten-free diet later, and who have inflammatory changes with persistent gut damage may be at increased risk for a later small bowel complication, including lymphoma. The overall good news here is that full mucosal healing can and does occur in most people with celiac disease. Some people may take longer to heal, but the evidence shows that most do eventually heal. Source: International Journal of Celiac Disease, 2017, Vol. 5, No. 1, xx. DOI:10.12691/ijcd-5-1-4
  7. Celiac.com 11/25/2017 - We have long known that gluten intolerance, both celiac disease and gluten sensitivity, are highly associated with neurological symptoms. Migraines, ataxia (unstable gait), seizures, schizophrenia – the list is long. But a recent research study just published last month sheds some new light on exactly what the mechanism may be. Understanding why these debilitating symptoms occur as a result of a gluten intolerance will, hopefully, go a long way toward increased awareness among the lay public and clinicians alike. It is certainly true that too many millions of Americans suffer the effects of a gluten intolerance unknowingly. They only know that they feel unhealthy but have no idea that gluten is the culprit. The digestive tract is sometimes called the second brain. Some say that is because it is second in importance to the brain. After all, if the food that is consumed doesn't turn into fuel that can effectively feed the 10 trillion cells in the body, those cells will be unable to perform their job and keep the body healthy. In fact, poor digestion is absolutely linked to poor health and increased onset of degenerative disease. This article in Current Pain and Headache Reports looks at another possibility for naming the digestive tract the second brain, and it simply stems from anatomy. The digestive tract actually has a ‘mind of its own'; more correctly, it has a nervous system of its own, called the enteric nervous system. ‘Enteric' simply means having to do with the intestine. This nervous system, according to research, is very similar to the brain housed in the head in that it is bathed in similar chemicals (called neurotransmitters – which, interestingly enough, are mostly produced in the gut!). It sends and receives impulses and records experiences and is influenced by emotions. Some proof of the latter: Have you ever been nervous and had diarrhea? This particular study stated that experiencing ‘adverse events' created a state of hypervigilance (a state of being overly responsive - not a good thing) in the nervous system which was associated with migraines and IBS. Such ‘hypervigilance' was previously only associated with the central nervous system – the one attached to the brain in the head. This group of researchers suggests that the initiation of hypervigilance may very likely lie in the enteric nervous system also. What this means is that if the small intestine is genetically sensitive to gluten and gluten is ingested, it could set off a nervous system response that could create disabling diseases, such as migraines and IBS, but likely others as well. The take-away message is that it is truly critical to diagnose gluten intolerance as soon as possible. Once that hurdle is surmounted it then needs to be followed with a program of nutrition, lifestyle and diet that will ensure healing of the small intestine and a ‘calming' of the hypervigilant nervous system. You may sometimes hear this referred to as healing a leaky gut. Here at HealthNOW we often see this clinically in patients who seem intolerant to many different foods and can't seem to enjoy stable improvement of their symptoms, even after they eliminate gluten from their diet. The reason for this insufficient improvement is that a comprehensive follow-up program is missing – a program that addresses what we call the Secondary Effects of Gluten. This entails evaluating for any other food sensitivities, cross reactive foods, a tendency towards autoimmune disease, the presence of any infectious organisms, healing the leaky gut, balancing the probiotic population, and more. While increasing awareness of the presence of gluten intolerance is absolutely critical, neglecting the secondary effects, as mentioned above, can result in long-term ill health that is truly preventable. Have you experienced such symptoms? Have you removed gluten but are only partially healthier? I'd love to hear from you. To your good health.
  8. Celiac.com 02/01/2017 - More and more evidence shows a connection between gut inflammation and type 1 diabetes (T1D). A team of researchers recently set out to assess gut inflammatory profiles and microbiota in patients with T1D, and to compare them with healthy controls (CTRL) and with celiac disease patients as gut inflammatory disease controls. The research team included Silvia Pellegrini, Valeria Sordi, Andrea Mario Bolla, Diego Saita Roberto Ferrarese, Filippo Canducci, Massimo Clementi, Francesca Invernizzi, Alberto Mariani, Riccardo Bonfanti, Graziano Barera, Pier Alberto Testoni, Claudio Doglioni, Emanuele Bosi, and Lorenzo Piemonti. They are affiliated with the Diabetes Research Institute at the IRCCS San Raffaele Scientific Institute in Milan, Italy. The team evaluated inflammatory status and microbiome composition in biopsies of the duodenal mucosa from 19 patients with T1D, 19 with celiac disease, and 16 healthy control subjects, recruited at San Raffaele Scientific Institute, in Milan, Italy, between 2009 and 2015. They assessed inflammation by gene expression study and immunohistochemistry and used 16S rRNA gene sequencing to analyze microbiome composition. Compared to CTRL and celiac disease patients, the team found an increased expression of CCL13, CCL19, CCL22, CCR2, COX2, IL4R, CD68, PTX3, TNFα and VEGFA genes in T1D patients. The immunohistochemical analysis confirmed T1D specific inflammatory status was mainly marked by increased monocyte/macrophage lineage infiltration, compared to healthy and celiac disease control tissues. The T1D duodenal mucosal microbiome also proved to be different from the control groups. This was mainly marked by increased Firmicutes, and Firmicutes/Bacteroidetes ratio and a reduction in Proteobacteria and Bacteroidetes. The expression of genes specific for T1D inflammation was associated with the excess of specific bacteria in duodenum. This study shows that patients with T1D show specific abnormalities in gut inflammation and microbiota. Greater knowledge of the complex pathogenesis of T1D will likely provide new directions for therapies targeting the gut. Look for more studies in this area in the near future, as scientists look to nail down specific treatments to prevent gut inflammation. Source: The Journal of Clinical Endocrinology & Metabolism. DOI: https://doi.org/10.1210/jc.2016-3222
  9. Celiac.com 01/02/2017 - New research shows that a group of proteins in wheat, called ATIs, may be responsible for activating inflammation in such disorders as celiac disease, multiple sclerosis, asthma, and rheumatoid arthritis. Scientists also believe that the proteins may promote the development of non-celiac gluten sensitivity. The findings were presented at UEG Week 2016 in Vienna in Vienna, Austria, a meeting organized by United European Gastroenterology for specialists to communicate the latest research in digestive and liver diseases. One group of proteins found in wheat - amylase-trypsin inhibitors (ATIs) - has been shown to trigger an immune response in the gut that can spread to other tissues in the body. ATIs are plant-derived proteins that inhibit enzymes of common parasites - such as mealworms and mealybugs - in wheat. Interestingly, ATIs also have an important role in metabolic processes that occur during seed development. The finding that ATIs may promote inflammation in the and beyond the gut, is a major step forward in understanding the mechanics of celiac disease and/or gluten-intolerance. Stay tuned for more news on this and other breaking stories in celiac disease research. Read more at MedicalNewsToday.com.
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