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    Barley Enzymes Effectively Digest Gluten in Rats


    Scott Adams

    Celiac.com 09/12/2006 – A recent study by researchers at Stanford University has found that barley endoprotease EP-B2 is effective at digesting gluten in rats, and should be studied further as an “adjunct to diet control” in human celiac disease patients. This new finding adds to Stanford’s growing body of work on enzyme therapy as a possible treatment for those with celiac disease, and may one day lead to a effective treatment.


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    Effect of barley endoprotease EP-B2 on gluten digestion in the intact rat.
    J Pharmacol Exp Ther. 2006 Sep;318(3):1178-86.
    Gass J, Vora H, Bethune MT, Gray GM, Khosla C.
    Stanford University.

    Abstract:

    "Celiac Sprue is a multi-factorial disease characterized by an intestinal inflammatory response to ingested gluten. Proteolytically resistant gluten peptides from wheat, rye and barley persist in the intestinal lumen, and elicit an immune response in genetically susceptible individuals. Here we demonstrate the in vivo ability of a gluten-digesting protease ("glutenase") to accelerate the breakdown of a gluten-rich solid meal. The proenzyme form of endoprotease B, isoform 2 from Hordeum vulgare (EP-B2) was orally administered to adult rats with a solid meal containing 1 g gluten. Gluten digestion in the stomach and small intestine was monitored as a function of enzyme dose and time by HPLC and mass spectrometry. In the absence of supplementary EP-B2, gluten was solubilized and proteolyzed to a limited extent in the stomach, and was hydrolyzed and assimilated mostly in the small intestine. In contrast, EP-B2 was remarkably effective at digesting gluten in the rat stomach in a dose and time dependent fashion. At a 1:25 EP-B2:gluten dose, the gastric concentration of the highly immunogenic 33-mer gliadin peptide reduced by more than 50-fold within 90 min, with no overt signs of toxicity. Evaluation of EP-B2 as an adjunct to diet control is therefore warranted in celiac patients."


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  • Related Articles

    Scott Adams
    Dig Dis Sci 1999;44:2344-2349.
    Celiac.com 04/10/2000 - Dr. Carme Farre, of Hospital Sant Joan de Deu, in Barcelona, Spain, and his multi-center colleagues, report in the November issue of Digestive Diseases and Sciences that both serologic markers and the human lymphocyte antigen class II extended DQ2 (HLA-DQ2) haplotype are useful markers for screening first-degree relatives of patients with celiac disease for the disorder. These markers are more reliable predictors of celiac disease than other clinical features, which are absent from one third of relatives of people with celiac disease.
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    Jefferson Adams
    Celiac.com 09/10/2007 - A study published recently in the journal of Alimentary Pharmacology and Therapeutics shows that the paracellular permeability inhibitor AT-1001 effectively reduces intestinal barrier dysfunction, proinflammatory cytokine production, and gastrointestinal symptoms in people who have celiac disease. At present, a lifetime devoted to following a strict gluten-free diet is the backbone of current treatment for celiac disease. However, as researchers have come to know more about celiac disease, they’re insights are leading to developments that offer more effective prognosis and treatment of the disease.
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    Destiny Stone
    Celiac.com 03/26/2010 - Mass screening studies among the general population for celiac disease show a prevalence of approximately 0.5-1.0% in adults and in children. Yet, despite the growing numbers of newly diagnosed celiac disease patients, most cases still remain undiagnosed and therefore, untreated. In part, the masses of misdiagnosed or undiagnosed  celiac disease  patients are a result of the variety of disguises  celiac disease can have. Celiac disease can manifest into a multitude of symptoms including, but by no means exclusive to, malabsorption syndrome, diarrhea, anemia, infertility and osteoporosis.
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    Source:

    http://www.ncbi.nlm.nih.gov/pubmed/20047580

    Melissa Reed
    Celiac.com 08/19/2014 - It is common for many people with celiac disease to have vitamin deficiencies. Eating a wide variety of foods such as meat, fish, eggs and vegetables can assist in with fixing those deficiencies. Children need vitamins to promote growth, development and good immune health. As adults we need them to prevent disease and stay healthy.
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    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
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    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
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    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
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    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
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    Source:
    Alimentary Pharmacology & Therapeutics

    Jefferson Adams
    Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
    A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.
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    They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage.
    The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
    Source:
    Gut. 2017 Feb;66(2):250-257. &nbsp;doi: 10.1136/gutjnl-2015-310148.