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Celiac.com 12/29/2016 - Researchers have documented a reduction of gastrointestinal symptoms in untreated celiac disease patients after oral administration of Bifidobacterium infantis Natren Life Start super strain (NLS-SS). The reduction of symptoms was not connected with and changes in intestinal permeability or serum levels of cytokines, chemokines, or growth factors. That led the team to hypothesize that the benefits observed in celiac patients treated with B. infantis may be connected to the modulation of innate immunity. A team of researchers recently set out to investigate the potential mechanisms of a probiotic B. infantis Natren Life Start super strain on the mucosal expression of innate immune markers in adult patients with active untreated celiac disease compared with those treated with B. infantis 6 weeks and after 1 year of gluten-free diet. The research team included Maria I. Pinto-Sanchez, MD, Edgardo C. Smecuol, MD, Maria P. Temprano, RD, Emilia Sugai, BSBC, Andrea Gonzalez, RD, PhD, Maria L. Moreno, MD, Xianxi Huang, MD, PhD, Premysl Bercik, MD, Ana Cabanne, MD, Horacio Vazquez, MD, Sonia Niveloni, MD, Roberto Mazure, MD, Eduardo Maurino, MD, Elena F. Verdu´, MD, PhD, and Julio C. Bai, MD. They are variously affiliated with the Medicine Department, Farcombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada; Small Intestinal Section, Department of Medicine; Department of Alimentation, Dr. C. Bonorino Udaondo Gastroenterology Hospital and Research Institute at the Universidad del Salvador in Buenos Aires, Argentina. They first used immunohistochemistry to assess the numbers of macrophages and Paneth cells, and the expression a-defensin-5 in duodenal biopsies. They found that a gluten-free diet reduces duodenal macrophage counts in celiac patients more effectively than B. infantis. In contrast, B. infantis decreases Paneth cell counts and expression of a-defensin-5 in celiac disease (P< 0.001). The results identify differential innate immune effects of treatment with B. infantis compared with 1 year of gluten-free diet. The team is calling for further study to determine synergistic effects of gluten-free diet and B. infantis supplements in celiac disease. Source: salvador.academia.edu
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Celiac.com 07/13/2016 - A really interesting study about gluten-free diets in mice just popped up over at the medical journal Diabetes, that has implications for both diabetes and celiac disease. The study found that a maternal gluten-free diet reduces inflammation and diabetes rates in the offspring of non-obese diabetic mice. The study was conducted by a research team that included Camilla H.F. Hansen, Åukasz Krych, Karsten Buschard, Stine B. Metzdorff, Christine Nellemann, Lars H. Hansen, Dennis S. Nielsen, Hanne Frøkiær, Søren Skov, and Axel K. Hansen. They are variously affiliated with the Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg, Denmark, the Department of Food Science, Faculty of Science, University of Copenhagen, Frederiksberg, the Bartholin Institute, Rigshospitalet, Copenhagen, Denmark, the Division of Toxicology and Risk Assessment, National Food Institute, Technical University of Denmark, Søborg, Denmark, and the Department of Biology, Faculty of Science, University of Copenhagen in Copenhagen, Denmark. Researchers have known for some time that early life interventions in the intestinal conditions have been shown to influence diabetes rates in mice. For example, a gluten-free diet in known to decrease type 1 diabetes incidence. Their team hypothesized that a gluten-free diet for pregnant mice only during pregnancy and lactation period would protect offspring mice against development of diabetes. The team fed pregnant non-obese diabetic (NOD) mice either a gluten-free or a standard diet, until all mice pups were weaned to standard diet. The early gluten-free mice showed significantly lower rates of diabetes and insulitis. Gut microbiota analysis by 16S rRNA gene sequencing showed significantly increased Akkermansia, Proteobacteria, and TM7 between both mothers and their offspring in the gluten-free diet group. Moreover, the gluten-free offspring showed increased pancreatic FoxP3 regulatory T cells, along with an increase in M2 macrophage gene markers and tight junction-related genes in the gut, coupled with lower intestinal gene expression of pro-inflammatory cytokines. Higher numbers of T cells in the pancreas expressing the mucosal integrin α4β7 suggests that the mechanism involve increased trafficking of gut-primed immune cells to the pancreas. This study supports the conclusion that a gluten-free diet during fetal and early postnatal life reduces development of diabetes. This may be due to changes in gut microbiota and better inflammatory and immunological conditions in the gut and pancreas. So, could it be that human mothers who eat a gluten-free diet through weening can impart the same kind of protection against diabetes? Clearly more studies need to be done until we can know for sure, but following a gluten-free diet while pregnant probably wouldn’t cause any harm to the mother or the baby. Source: Diabetes 2014 Apr; DB_131612.
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Celiac.com 07/28/2014 - One angle being tried by researchers to treat celiac disease involves oral peptides. These are orally administered drugs that would prevent an adverse gluten reaction in people with celiac disease who are following a gluten-free diet. The drugs are intended to prevent adverse reactions from minor gluten contamination or exposure. In a recent update from the Mayo clinic, Joseph Murray, MD, confirms that larazotide acetate, a first-in-class oral peptide, has ”met the study's primary end point of a reduction in GI symptoms.” Dr. Murray presented the results from the study as a late-breaking abstract at Digestive Disease Week 2014. In a celiac disease reaction, the epithelial tight junctions that control paracellular permeability are compromised, and gut permeability increases. This is partly due to an inflammatory immune response to the entrance of gluten peptides into the intestinal lamina propria through these tight junctions. Larazotide acetate prevents tight-junction opening and reduces gluten uptake, inhibiting gluten- and cytokine-induced intestinal permeability and inflammation in vivo. This randomized, parallel, double-blind, placebo-controlled, multicenter trial was conducted at 74 sites in North America. The aim was to evaluate the effect of larazotide acetate on GI signs and symptoms in patients with celiac disease. Source: Medscape.com
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Celiac.com 07/23/2012 - At 2012 Digestive Diseases Week in San Diego, California, Alvine Pharmaceuticals, Inc. announced the publication of data from Phase 2A trial of its main celiac disease compound, ALV003. The results show that ALV003, orally administered to celiac disease patients on a gluten free diet, significantly reduces gluten-triggered intestinal mucosal damage. For the trial, 41 adults with clinically proven celiac disease who had followed a gluten-free diet for at least one year were randomly given ALV003 or a placebo each day for six weeks. During that time, they also received 2g of gluten in the form of bread crumbs. Participants received a small bowel biopsy prior to randomization and again, at the end of the six week challenge. The results showed that the study met its primary endpoint of a clinically and statistically meaningful reduction in intestinal mucosal damage in celiac patients on a gluten-free diet. Damage was measured by the ratio of the villus height to crypt depth, or Vh:celiac disease between the ALV003 and placebo treated groups over the six week study period. Secondary endpoints included change in intraepithelial lymphocyte (IEL) density, gastrointestinal symptoms as measured by Gastrointestinal Symptom Rating Scale (GSRS) scores, celiac serologies, safety and tolerability. Each subject received small bowel biopsy at the start of the trial, and again after six weeks of daily gluten challenge. When researchers compared biopsy results from 34 patients, they found significantly less small intestinal mucosal damage in patients treated with ALV003 than in placebo-treated patients (p=0.013). Placebo-treated patients suffered worse damage and symptoms. Most often, these included abdominal distention, flatulence, eructation, abdominal pain and diarrhea. The published data shows that: Biopsy results for patients who received ALV003 had significantly reduced small intestinal mucosal damage compared with placebo-treated patients (p=0.0133). For placebo-treated patients, IELs, including CD3+ and CD3+ aB and subsets, which measure cellular inflammation responses, were significantly higher, but were mostly normal in the ALV003-treated patients. ALV003-treated patients had better overall GSRS scores and scores for indigestion and abdominal pain symptoms, compared with placebo-treated patients, though the results were not statistically significant. Patients reported no serious adverse events, however, placebo-treated patients reported more regular and consistent non-serious adverse. Such events that occurred in 10 percent or more patients included abdominal distention, flatulence, eructation, diarrhea, nausea, headache and fatigue. Celiac-disease blood tests revealed no significant changes between the ALV003 and placebo-treated patients, though results did show positive trends for tissue transglutaminase and deamidated gliadin peptide antibody titers in the ALV003-treated group, which indicates improved immune response. Daniel Adelman, M.D., Alvine's Senior Vice President and Chief Medical Officer, says that the trial results represent the first time that any such treatment for celiac disease has met its pre-specified primary endpoint of providing protection against damage from gluten-exposure in celiac disease patients, with data that is both clinically and statistically significant. Such a drug could help to protect gluten-free celiac disease patients against accidental gluten contamination. The company plans to initiate a Phase 2B trial later this year. Read the abstract of the presentation (Sa1342) on the DDW website. Review information on Alvine's current clinical trial titled "Evaluation of Patient Reported Outcome Instruments in Celiac Disease Patients" at the NIH website.
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Celiac.com 02/17/2009 - Texas AgriLife Research scientist Dr. Nancy Turner has recently discovered that a microscopic compound commonly found in plant-based foods reduces inflammation and prevents the formation of cancerous lesions in the colon. The tiny molecule, called quercetin, is easily absorbed when people eat fruits and vegetables, and so requires no specialized supplements or drugs. Quercetin is a tiny, but powerful compound that is easily absorbed from onions, peppers, tomatoes and most other common produce. According to Turner, nearly all plant-based foods offer "some level of quercetin," including "fun things like wine." Previous laboratory research has shown quercetin to be effective in reducing rates of colon cancer, but Turner's study is the first to illuminate the mechanism by which quercetin works its magic. These results offer researchers another line of inquiry into other inflammatory bowel diseases such as Crohn's and celiac disease, as it's quite likely that quercetin can offer some measure of protection against those conditions as well. According to Turner, the levels of quercetin used in the study are comparable to those "achieved in diets around the world such as...the Mediterranean-style diets." As such, reaching such levels in American diets is "not an unachievable goal," she said. In the study, Turner's research team observed the responses of rats to quercetin-supplemented diets. Some of the rats were in the early stages of colon cancer formation, while others were cancer-free. In people, as in animal models, early colonic lesions represent some of the very first pre-cancerous changes that can be seen visually. These so called "aberrant crypts," are thought to mark or predict tumor formation. Earlier studies have shown quercetin to reduce the number of these crypts, but Turner "wanted to know how it might be protecting." Cancer is commonly understood as uncontrolled cell growth, but researchers are now realizing that the normal action of cell death, a process called "apoptosis," plays a crucial role in allowing cancer to develop. Healthy bodies generally maintain equilibrium between the generation of new cells and sloughing off cells that have completed their job. Quercetin seems to play a beneficial role in both cases. It decreases the number of cells being generated in the colon [and] increases the number of cells that were undergoing apoptosis. In all, quercetin helps to maintain a normal number of cells. The research team then turned its attention to the relatively new discovery that inflammation is one of the prime instigators of colon cancer. The team focused on two enzymes, called Cox-1 and Cox-2. Cox-1 is a standard protein that the body usually exhibits. But Cox-2 has a potential role in a number of diseases. Turner explains that Cox-2 is an "inducible protein that is expressed in the body when there is some kind of external stimulus to a cell." Scientists consider high levels of Cox-2 "as being a bad thing." Research shows that not only are elevated levels of Cox-2 present in colon cancer, but that the Cox-1 levels become elevated before Cox-2 levels rise. According to Turner, it seems that Cox-1 exerts some sort of influence over whether Cox-2 expression. Both the control groups and the carcinogen-injected groups that consumed dietary quercetin had lower levels of both Cox-1 and Cox-2, suggests that there may be chance for quercetin to prevent tumor growth. Clearly, further study is needed to better understand the links. But Turner encourages people to consume lots of fruits and vegetables. She points out that, in addition promising benefits for colon cancer, quercetin has demonstrated positive influence in fighting other chronic ailments such as cardiovascular disease. *Turner's research was funded by the U.S. Department of Agriculture . Source: http://agnews.tamu.edu/showstory.php?id=972
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