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Found 7 results

  1. Celiac.com 10/21/2015 - Celiac disease has been traditionally recognized among Caucasians, with an estimated prevalence of about 1%. Latin America features a the population with European ancestry, along with native communities sharing a diverse degree of mix with European colonizers. The population of native Toba people comprises more than 60,000 individuals living with a clusters of villages in a forest called 'The Impenetrable' in Northeastern Argentina. In recent years, as a consequence of governmental food aid programs aimed at improving nutritional conditions in the community, the Toba people have undergone a drastic change in dietary habits, with wheat replacing their ancestral food sources. In general celiac disease can only occur in individuals with certain class II human leukocyte antigen (HLA) molecules – namely, HLA DQ2 and/or DQ8, but little information exists about the prevalence of HLA DQ2 and DQ8, and of celiac disease in native South Americans. The research team included Horacio Vázquez MD, María de la Paz Temprano RD, Emilia Sugai MS, Stella M Scacchi MS, Cecilia Souza MD,Daniel Cisterna MS, Edgardo Smecuol MD, María Laura Moreno MD, Gabriela Longarini MD, Roberto Mazure MD, María A Bartellini MS, Elena F Verdú MD2, Andrea González RD, Eduardo Mauriño MD, and Julio C Bai MD. They are variously affiliated with the Small Bowel Section, Department of Medicine, Hospital de Gastroenterología C Bonorino Udaondo. Buenos Aires, Argentina and the Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario. For their study, the research team set out to prospectively assess environmental, genetic and serological conditions associated with celiac disease among members of the Toba native population attending a multidisciplinary sanitary mission. Using an established questionnaire, an expert nutritionist determined daily gluten intake. The team then conducted gene typing for the human leuko-cyte antigen (HLA) class II alleles using DNA extracted from peripheral blood (HLA DQ2/DQ8 haplotype). The team then measured serum antibodies were immunoglobulin (Ig) A tissue transglutaminase (tTG) and the composite deamidated gliadin peptides/tTG Screen test. They tested positive cases for IgA endomysial antibodies. The team screened a total of 144 subjects, 55% of those female. Estimated average gluten consumption was 43 grams per day, ranging from 3 grams per day up to 185 grams per day. Genetic typing showed that 73 of 144 subjects had alleles associated with celiac disease; 69 of these subjects had alleles for HLA DQ8, while four had DQ2. Four and six subjects had antibody concentrations above the cut-off established by the authors' laboratory (>3 times the upper limit of normal) for IgA tTG and deamidated gliadin peptides/tTG screen, respectively. Four of these had concomitant positivity for both assays and endomysial anti-bodies were positive in three subjects who also presented a predispos-ing haplotype. The present study was the first to detect celiac disease in Native Americans. The native Toba ethnic population has very high daily gluten consumption, and a predisposing genetic background. This study found subjects with persistent celiac disease autoimmunity and, at least, three of them met serological criteria for celiac disease diagnosis. This study invites some questions about gluten and celiac disease in the tribe. For example, does the amount of gluten in the diet of people with genetic predisposition have an impact on the likelihood of celiac disease? Given that many of these people likely had DQ2/DQ8 positivity for many generations, did the introduction of wheat into their diets trigger their celiac disease? Much remains to be understood about celiac disease, and studies like this can be important and insightful. Source: Can J Gastroenterol Hepatol Vol 29 No X Month 2015 1
  2. Appl Environ Microbiol. 2004 Feb;70(2):1088-1096 Celiac.com 02/26/2004 - Please note that the sourdough bread used in this study is not your garden-variety sourdough bread, and as far as I know it is not commercially available. Even though this study had very promising results, it was conducted on a relatively small number of people, and larger studies need to be carried out before reaching any conclusions about the long-term safety of celiacs consuming this type of sourdough bread. -Scott Adams Researchers in Europe conducted a novel study which utilized a highly specialized sourdough lactobacilli containing peptidases that have the ability to hydrolyze Pro-rich peptides, including the 33-mer peptide, which is the main culprit in the immune response associated with celiac disease. The sourdough bread in the study was made from a dough mixture that contained 30% wheat flour and other nontoxic flours including oat, millet, and buckwheat, which was then started with the specialized lactobacilli. After 24 hours of fermentation all 33-mer peptides and low-molecular-mass, alcohol-soluble polypeptides were almost totally hydrolyzed. For the next step in the study the researchers extracted proteins fro the sourdough and used them to produce a "peptic-tryptic digest" for in vitro agglutination tests on human K 562 subclone cell. The agglutinating activity of the sourdough proteins was found to be 250 times higher that that of normal bakers-yeast or lactobacilli started breads. A double blind test was then conducted in which 17 celiac disease patients were given 2 grams of gluten-containing bread started with bakers yeast or lactobacilli. Thirteen of them showed distinct, negative changes in their intestinal permeability after eating the bread, and 4 of them did not show any negative effects. The specially prepared sourdough bread was then given to all 17 patients and none of them had intestinal permeability reactions that differed from their normal baseline values. The researchers conclude: "These results showed that a bread biotechnology that uses selected lactobacilli, nontoxic flours, and a long fermentation time is a novel tool for decreasing the level of gluten intolerance in humans."
  3. Celiac.com 04/25/2011 - Research shows that celiac disease is associated with numerous gastric abnormalities. An international research team recently set out to examine the association between rates of celiac disease and Helicobacter pylori infection in an Iranian population of 250 patients. The research team included Mohammad Rostami Nejad BS1, Kamran Rostami MD PhD, Yoshio Yamaoka MD PhD, Reza Mashayekhi MD1, Mahsa Molaei MD, Hossein Dabiri PhD, David Al Dulaimi MD, Dariush Mirsattari MD, Homayoun Zojaji MD, Mohsen Norouzinia MD, and Mohammad Reza Zali MD FACG AGAF. The team members are variously affiliated with the Research Institute of Gastroenterology and Liver Disease, Shahid Beheshti University, M.C., in Tehran, Iran, the School of Medicine, University of Birmingham in the UK, the Department of Medicine-Gastroenterology, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine in Houston, Texas, and the Department of Gastroenterology, Alexandra Hospital, Redditch, UK. For the study, the team took topsides from the gastric antrum and duodenum. They assessed morphology and histology using the updated Sydney system and modified Marsh criteria, respectively. In order to simplify the assessment of gastric lesions, the team classified gastritis in both macroscopic and microscopic stages. They screened for anti-tissue transglutaminase antibody to determine the presence of celiac disease. Of the 250 patients, 232 (93%) showed histological evidence of Helicobacter pylori infection, while 24 patients (10%) showed histological abnormalities (Marsh I to IIIc). Of the 24 patients with histological abnormalities 20 (83%) showed Helicobacter pylori infection. Of the total 250 patients, 25 patients (10%) showed positive anti-tissue transglutaminase antibody screens, nine (3.6%) of whom showed microscopic and macroscopic enteritis (Marsh I to IIIc). Clinically, there was no way to distinguish the presentation of celiac disease from those cases infected with Helicobacter pylori. Histology, even in patients with positive antibody screens, was non-specific and not useful. The results also showed a high prevalence of Helicobacter pylori infection and chronic gastritis in the study group. However, neither was associated with celiac disease, but rather, matched average rates in Western population studies. Source: Archives of Iranian Medicine, March 2011
  4. Celiac.com 03/15/2011 - For celiacs, it's not really the cinnamon bun that's the enemy. Nor the pizza crust, nor the ravioli. It's the gliadin in these foods - the alcohol-soluble portion of the gluten protein - that's the real culprit. Gliadin is the "gladiator" of the human digestive tract. When we ingest gliadin, enzymes try to break it down into a form that can be absorbed by the small intestine. But gliadin resists, fighting hard to remain intact. A regular small intestine has, like any good fortress, a protective wall: the mucosal lining of the intestine. This layer of mucus normally acts as a barrier against gliadin's assaults. But in a celiac intestine, the mucosal lining is permeable. With gliadin's destructive power enhanced by its enzyme sidekick, tissue Transglutaminase (tTG), it quickly gets past this poorly-guarded layer. Scientists are working to put their finger on exactly what makes the mucosal lining of a celiac's small intestine so permeable. Now a January study by Czech researchers found at least one thing that affects the permeability of the intestinal mucosa: gut bacteria. In this study, called "Role of Intestinal Bacteria in Gliadin-Induced Changes in Intestinal Mucosa: Study in Germ-Free Rats", researchers tied off sections of rats' intestines and introduced various kinds of bacteria to each section. They wanted to measure the effect that these bacteria had on the intestinal mucus - or more specifically, on the goblet cells that produce the intestinal mucus. To ensure that the kinds of bacteria in the rats' intestines were under experimental control, the rats had been raised from birth in germ-free conditions. They found that introducing gliadin to the intestines had the effect of decreasing the mucus-producing cells, thereby eroding the intestines' protective layer. No big surprises there - gliadin is a fighter, a digestive "gladiator", after all. But when they added strains of so-called harmful bacteria, Escherichia coli (otherwise known as E coli) or Shigella, the mucus-producing cells decreased even more. The cells first secreted massive amounts of mucus, then promptly exhausted themselves and gave up. This left the intestine looking very similar to that of a person in the early stages of celiac disease, say the researchers. But the tale did indeed have a happy ending. Along came the good bacteria, Bifidobacterium bifidum (or "Biff" for short). The mucus-producing cells in the small intestine increased when Biff was present. In fact, Biff was able to partially reverse the mucus-decreasing effects of E coli and Shigella. The researchers concluded that the composition of gut bacteria has an effect on the protective mucus of the intestines: an overgrowth of bad bacteria decreases the protective layer, while the addition of good bacteria increases the protective layer. Their study may eventually lead to treatment options for human celiacs, by finding ways to protect tender intestines from the harmful effects of gliadin. Source: PLoS One. 2011 Jan 13;6(1):e16169
  5. Celiac.com 08/25/2010 - The revolution in genetic studies continues to drive discoveries about the genetic triggers for celiac disease. In recent developments, a genome-wide association study (GWAS) has nearly doubled the number of single-nucleotide polymorphisms (SNPs) associated with celiac disease from 14 to 27, most of which contain genes related to immune functions. Doctors have known for some time now that people with genetic markers DQ2 and DQ8 are more susceptible to celiac disease than those without those gene markers. This fact points to the importance of histocompatibility complex presentation of gluten antigens to immune cells. In 2007, a landmark study established 14 celiac-associated SNPs. Recently, a team of researchers conducted a comprehensive follow-up to that study. The study team included P. C. Dubois, G. Trynka, and L. Franke. The resulting GWAS used six times more genetic samples than the 2007 study, including five European case-control data sets comprised of 4,533 celiac disease patients and 10,750 controls. In all, the team tested nearly 300,000 genes. Based on low P values (P < 5 × 10-8) and biological likelihood of candidate SNPs being related to immune function, the team selected a total of 131 single-nucleotide polymorphisms (SNPs) for replication in an independent cohort of 4918 cases and 5684 controls. Their data identify 13 additional regions associated with celiac disease. To determine the trigger gene for each potential locus, the team used three complementary, objective methods. They first used a computerized algorithm, known as GRAIL, that searches PubMed for specific terms related to various gene features. They next employed what is called expression quantitative trait locus mapping, which isolates variations that may influence the expression of the gene, rather than its protein structure and function. Lastly, they looked for co-expression of gene clusters in suspect candidate genes relative to known susceptibility loci. Each of these methods shed additional light on the association between suspect SNPs and celiac disease susceptibility. However, the authors of the study go out of their way to note that, ultimately, the authors categorized loci and predicted causal genes using their "own knowledge of celiac disease pathogenesis.” This fact, they point out, emphasizes the crucial role played by knowledgable scientists exercising their insights to reap the most benefit from ‘objective’ advanced genomic data mining technologies. This study involved genetic assessment in a very large cohort, replication in a similarly large cohort, and multiple independent approaches at refining candidate SNPs. As a result, the number of known loci of celiac disease susceptibility genes has increased from 14 to 27. Their findings also identify several new pathways of celiac disease pathogenesis that merit further investigation. The study team also notes that these findings only account for 20% of the variance in celiac disease heritability. This, they say, points to a need for additional studies regarding genetic triggers for celiac disease. Source: Nature Genetics 42, 295 - 302 (2010). doi:10.1038/ng.543
  6. GUT 2002;50:332-5 Celiac.com 03/19/2002 - According to a long term study conducted by Dr Matti Uusitupa and colleagues from the University of Kuopio, Kuopio, Finland, long-term ingestion of a moderate amount of oats in an otherwise gluten-free diet is safe for adult patients with celiac disease. In a previous study Dr. Uusitupa found no harmful effects from oats after patients ate them for 12 months, which was reflected by the patents symptoms, nutritional status, duodenal villous architecture, and mucosal mononuclear cell infiltrate, as seen in celiac patients who are in remission. The earlier study also showed that ingestion of oats did not delay recovery of mucosal damage in newly diagnosed celiacs. Dr. Uusitupas first study compared the effects of a gluten-free diet and a gluten-free diet that included oats with a randomized trial involving 92 adult celiac patients: 45 in the oats group whose intake averaged approximately 34 grams per day, and 47 patients in the control group. Patients in the oats group were allowed to eat oats freely in conjunction with an otherwise gluten free diet. After five years 35 patients in the original oats group, 23 of whom were still eating oats at least twice a week, and 28 in the control group that was on a conventional gluten free diet were examined. The results confirmed that eating oats did not cause ANY duodenal mucosal damage to the adult celiac patients in the study. Further, the patients were also examined using histological, histomorphometric, and immunological methods, and AGA, ARA, and EMA serological test results of those in the oat group showed no negative effects that could be linked to eating oats. According to Dr. Uusitupa, the high antibody levels that appeared in some of the patients that were in both groups are most likely explained by poor compliance to a gluten free diet, and the reason why celiac patients can tolerate oats must be based on structural differences between the proteins of oats, wheat, barley, and rye. The toxic portion of the harmful gluten protein lies in the ethanol soluble fraction called gliadins, whose toxicity remains after digestion. With oats, however, it is possible that the absence of specific amino acid sequences that are found in wheat gliadin but are not found in oat avenin allow oats to be tolerated by celiacs. Last, the researchers note that taking oats off of the list of forbidden cereals might improve patient compliance to the gluten-free diet by giving them more food choices.
  7. Gut. 2004 May;53(5):649-654 A multi-center Swedish study involving eight separate pediatric clinics looked at 116 children with newly diagnosed celiac disease. The group was randomized into two groups, and one group was given a standard gluten-free diet, while the other was given a standard gluten-free diet that also included oats. The study period was one year, small bowel biopsies were performed at the beginning and end of the study, and serum IgA antigliadin, antiendomysium, and antitissue transglutaminase antibodies were monitored at 0, 3, 6, and 12 months. The median intake of oats for the oat-eating group was 15g per day. By the end of the study all patients were in clinical remission for celiac disease. Neither group differed significantly from one another with regard to serology markers or small bowel mucosal architecture (including numbers of intraepithelial lymphocytes). Out of the original 116 children 93 finished the study, and significantly more younger patients withdrew from it than older patients. The researchers conclude: "This is the first randomized double blind study showing that the addition of moderate amounts of oats to a gluten-free diet does not prevent clinical or small bowel mucosal healing, or humoral immunological downregulation in coeliac children. This is in accordance with the findings of studies in adult coeliacs and indicates that oats, added to the otherwise gluten-free diet, can be accepted and tolerated by the majority of children with celiac disease."
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