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Found 12 results

  1. Celiac.com 12/22/2017 - Venture capital firms Arch Venture, and Vatera are betting big on biotech startup ImmusanT, the makers of potential celiac disease vaccine Nexvax2. Arch and Vatera have funded a $40 million B round that will support ImmusanT's development of their celiac treatment through Phase II testing. Full data are expected in mid-2019. As part of it's efforts, Arch Venture partner and former head of research at Celgene, Tom Daniel, will join the board at ImmusanT. Additionally, renowned immunologist and Arch managing director Steven Gillis will also join the board at ImmusanT. Nexvax2 is the first prong in ImmusanT's efforts to develop a treatment that creates immune system tolerance to thwart autoimmune diseases. If they are successful in tackling celiac disease, the company is looking to expand the technology to include treatments for type 1 diabetes and other ailments. Celiac disease is a great place to start, says ImmusanT CEO Leslie Williams, because scientists already know the antigen that triggers the disease. Williams says that her company has scoured 17,000 peptides to "create a hierarchy of the key components that trigger the T cell response" in celiac disease. Nexvax2 is designed to work by slowly coaxing the immune system to ignore the trigger. Patients exposed to Nexvax2 react as if they have eaten gluten, says Williams. The goal is to harness that immune reactions and to modulate it. Williams is looking to double the size of the company's tiny 7-person staff as the ImmusanT journeys through a mid-stage trial. She will then look to an expanded set of programs as well as the data to determine the best direction for the company. Williams says that all options are currently open, including another funding round, an IPO or even a strategic deal. Read more at: endpts.com
  2. Celiac.com 09/25/2017 - There are currently several efforts underway to develop successful commercial enzyme treatments for celiac disease. Efforts include looking at the digestive enzymes in plants, such as the papaya and star fruits, including such predatory plants, such as the pitcher plant. One focus has been on developing enzymes that can break down gluten before it can trigger an immune reaction. This could prove helpful to many people with celiac disease. One such enzyme under development is Latiglutenase, formerly known as ALV003. Latiglutenase is a new name for an enzyme therapy designed to be taken with meals. The idea is that a person with celiac disease would take an enzyme tablet with a meal. If the meal had mild gluten contamination, the enzyme’s two recombinant proteins would break gluten into fragments that are not toxic to the immune system, thereby preventing exposure, and symptoms. But the stomach is a notoriously difficult environment to work in, so what seems like a simple idea quite a challenge from a science and biology perspective. Seeking to explore the ability of Latiglutinase to improve symptoms, a team of researchers recently set out to test latiglutenase on celiac patients who are seropositive despite following a gluten-free diet. The research team included Jack A. Syage, Joseph A. Murray, Peter H. R. Green and Chaitan Khosla. They are variously affiliated with the Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester USA, the Celiac Disease Center at Columbia University, New York, USA, the Departments of Chemical Engineering and Chemistry, Stanford University, USA, and with ImmunogenX, Newport Beach, USA. "Though the ALV003-1221 trial was inconclusive regarding histologic improvement from latiglutenase, the evidence for symptom benefit, which is more quickly achieved, is quite convincing and clinically relevant," Joseph Murray, MD, of the Mayo Clinic in Rochester, Minn., said in a press release. In these trials, patients with celiac disease who were seropositive despite following a gluten-free diet saw major improvement in symptoms when taking latiglutenase with meals, according to a post hoc analysis of the CeliAction study. The team was really hoping to see histological improvement, but they feel satisfied that this trial shows, says Dr. Murray, that a "therapy to help patients struggling with symptoms due to celiac disease is now within reach." Stay tuned for more on efforts to develop effective enzyme treatments for celiac disease. Read more: Dig Dis Sci. 2017 Doi:10.1007/s10620-017-4687-7.
  3. Celiac.com 04/27/2017 - Celiac disease is associated with numerous chronic conditions, such as anemia and malabsorption of some critical vitamins. Changes in the gastrointestinal tract, rates of gastric emptying, and gastric pH are responsible for impaired vitamin and mineral absorption. Intestinal CYP3A4 levels may also be disrupted, which may have implications in first-pass metabolism for some drugs that are substrates for this drug metabolizing enzyme. This has led some researcher to investigate the potential impact of celiac disease on drug absorption. This would be of interest to pharmacists, since altered drug absorption can have pharmacokinetic consequences, along with the potential to impact overall drug therapy. A comprehensive review on this topic was published in 2013 by Tran et al. Another review was published in 2014. The review by Tran, et al., considered absorption studies in subjects with celiac disease, and the authors focused on a handful of drugs, including acetaminophen, aspirin, propranolol, levothyroxine, methyldopa, and some antibiotics. They reported that some reports show an altered gastrointestinal environment and sharp differences between drug absorption in patients with celiac disease, while other reports showed no absorption differences between those with and without the disease. The authors concluded that the drugs could potentially alter absorption in celiac patients, and that healthcare professionals should bear that in mind when starting drug therapy. The 2014 review of the potential impact of celiac disease on cardiovascular drug absorption considered many of the same medications previously explored by Tran et al, with a focus on cardiovascular agents. The authors warned that numerous cardiovascular drugs may alter absorption in celiac disease, but noted few published studies with strong, comprehensive data. The authors also stressed the need for more studies on celiac patients, as well as caution when initiating cardiovascular drug treatments. Available research indicates that patients with celiac disease can have altered absorption of many different drugs. Unfortunately, there still isn't much good data on altered drug absorption and disposition in celiac patients. More study will likely help illuminate the influence of celiac disease on drug disposition. The early evidence suggests that celiac disease may alter drug absorption, but studies don't yet tell us how much, or how often. The team is recommending that doctors and pharmacists consider possible absorption issues when prescribing drug treatments for people with celiac disease, and that they review the available literature on specific drugs, when possible. They also recommend increased monitoring for efficacy and adverse effects when beginning a new drug treatment regimen for celiac patients. Source: Pharmacy Times
  4. Celiac.com 03/10/2017 - PvP Biologics, a business spun out of the University of Washington, now has a $35 million deal with Takeda Pharmaceutical to develop its therapy for celiac disease. PvP Biologics is developing an enzyme that can be taken orally and survive in the harsh acidic environment of the stomach. That enzyme is called KumaMax. Under the terms of the agreement, Takeda will fund $35 million in PvP's research and development of the therapy through phase 1 clinical trials. The agreement gives Takeda Pharmaceutical the exclusive option to acquire PvP for an undisclosed fee upon successful completion. PvP Biologics has its roots in a University of Washington tech incubator program, but spun out on its own in 2016, in advance of its arrangement with Takeda. Says Adam Simpson, president and CEO of PvP Biologics, "Takeda's GI experience and capabilities are a great fit with our goal of developing a novel oral enzyme therapy to make a meaningful impact on the lives of people with celiac disease." The enzyme-driven KumaMax works by targeting gliadin, the parts of gluten that cause the autoimmune reaction leading to celiac disease. The company hopes to prevent the adverse immune reaction seen in celiac sufferers, by breaking down the gliadin. Like most similar enzyme therapies, KumaMax is not designed to be a cure for celiac disease. It is designed to help prevent adverse reactions from accidental gluten contamination. In a statement by the company, Asit Parikh, head of the gastroenterology therapeutic area for Takeda, says that "KumaMax could address a significant unmet need for celiac patients who are unable to completely avoid gluten exposure in their diets, and thus continue to experience debilitating symptoms." Read more at BizJournals.com.
  5. Celiac.com 02/07/2008 - Are we close to finding a way for people with gluten intolerance and celiac disease to safely break down and properly digest wheat gluten and protein? An article recently published in the medical journal Gut describes the results of laboratory experiments in which doctors duplicated a human digestive tract and isolated an enzyme that degrades wheat gluten and protein. Moreover, the results show that the enzyme also eliminated the toxic response to the wheat gluten and protein common in folks with gluten intolerance and celiac disease. According to the researchers, if a full-scale trial confirms the results, people with gluten intolerance and celiac disease might be able to safely stray from their strict gluten-free diets on occasion. The enzyme is prolyl endoprotease isolated from Aspergillus niger and shows the power to quickly and effectively break down gluten peptides and proteins in a simulated human digestive tract. The enzyme has a similar pH level to that of the stomach, and remains intact in the stomach’s strongly acidic conditions. The research team, led by Dr. C. Mitea from Leiden University Medical Center in the Netherlands tested the enzyme in a controlled system built to function in way that is nearly identical with the human gastrointestinal tract. According to the report, the enzyme increased the digestion speed of the glutenins and gliadins that are found in white bread, and which people with gluten intolerance and celiac disease cannot properly break down. After 90 minutes, the gluten proteins treated with the enzyme were undetectable, whereas those glutens not treated with the enzyme, remained in the stomach for at least two hours. The research team obtained similar results when they repeated the test on a fast food meal rather than just white bread alone, and showed that the enzyme treated food samples also eliminated adverse T-cell stimulatory activity that occurred in untreated samples. The tests showed that, in the same amount of time that food normally remains in the stomach, the enzyme brought about the total elimination of T-cell stimulatory peptides of gliadins and glutenins. From the test results, the research team concluded that the enzyme is a solid choice for clinical trials to determine if it can eliminate 100% of gluten toxicity. They also noted that the enzyme is readily available in industrial quantities, and thus easy to tailor into a suitable treatment should trials prove fruitful. Gut, Jan 2008; 57: 25 - 32. Editor's Note: This is not a therapy that is designed to allow celiacs to eat gluten on a daily basis. At best it will allow them to not worry about cross-contamination when eating out.
  6. Celiac.com 02/02/2013 - The possible link between the makeup of gut bacteria and celiac has been a subject of past discussion in "More Evidence Links Gut Bacteria to Celiac Disease"[1] and other articles. Certain gut bacteria appear to enhance the immune response to gluten which may contribute to the onset of celiac disease. Vitamin D may reduce or eliminate this enhanced gluten response, and, therefore, vitamin D deficiency may be a significant factor contributing to the onset and development of celiac disease.[2] "Fecal transplantation", probiotics, and vitamin D have been advocated as possible therapy, treatment, and/or preventative measures against celiac disease. While vitamin D and probiotics may have potential as preventative measures against the onset of celiac disease early in life, the option of a fecal transplant provides the actual possibility of restoring tolerance to gluten or curing celiac disease later in life following long-term intestinal mucosal recovery on a gluten-free diet. In particular, fecal transplantation might make it possible to treat refractory celiac disease which does not respond to a gluten-free diet. Fecal transplant therapy for gastrointestinal disorders was pioneered by the world reknown Australian gastroenterologist, Prof. Thomas J. Borody, M.D., and is now used most successfully for treatment of persistant C. difficile infections of the gastrointestinal tract. Fecal transplantation involves the actual transfer of screened and filtered fecal material from a healthy donor into the gut of a patient, previously treated with antibiotics to clear gut bacteria, replacing the patient's own gut bacteria with a healthy mix of donor gut bacteria. The fecal material may be administered either orally or anally, via tubes. Selecting and screening a healthy donor, usually a spouse or close relative, as well as the "disgust" factor have limited use of this therapy in past years, but its high anecdotal success rate for treating stubborn C. difficile cases is finally bringing fecal transplantation into the mainsteam of routine gastrointestinal practice. The first clinical trial of fecal transplant therapy involving 43 C. difficile patients compared to conventional vancomycin antibiotic therapy has just been published finding fecal transplantation 3 times more effective than vancomycin in resolving C. difficile infections.[3,4] To date, there does not appear any record of an attempt or clinical trial to treat celiac disease via fecal transplant therapy. A big problem preventing any significant clinical trial of fecal transplantation for celiac disease is there is no way to "standardize" the healthy donor fecal material. The mix of bacteria from every donor is unique. Each donor must also undergo careful screening for harmful fecal pathogens. But, now, recent developments may make such a clinical trial feasible. A synthetic stool substitute was successfully used to clear C. difficile infections in 2 patients as part of a "proof-of-principle" study which may lead the way to eliminate the need for individual healthy feces donors and the need for screening tests. The synthetic stool consisted of a mix of 33 bacteria species isolated from the stool of one healthy donor and cultured under simulated intestinal conditions.[5,6] Such a standardized synthetic stool potentially administered orally in capsule form could make large scale fecal transplantation clinical trials possible. An "off-the-shelf" bacteria mixture specifically developed for the treatment of celiac disease might become a reality. In the case of refractory celiac disease, a gluten-free diet does not stop the continued destruction of the intestinal mucosa. Research has not yet found the reason for refractory celiac disease, but "molecular mimicry" may be one possible cause. Celiac disease is an immune response to particular sequences of amino acids in gluten peptides called epitopes. In the absence of gluten, if there exist peptides from other sources with amino acid sequences matching or "mimicking" these gluten epitopes, the destructive immune response may continue to damage the mucosa. This is molecular mimicry in action. It is possible that some gut bacteria may express some of these epitopes on their surface, or, more likely, secrete peptides that contain these epitopes. These bacterial secretions might then coat the lining of the intestine sustaining the immune response. Secreted epitopes are the more likely cause of refractory celiac disease than bacteria surface epitopes because the immune system would eventually destroy the bacteria if bacteria surface epitopes were involved. But if the cause were the bacterial secretion epitopes, the bacteria itself would not be attacked and would continue to produce the secretions indefinitely perpetuating the mucosal damage. Fecal transplant therapy might cure refractory celiac disease by eliminating the gut bacteria producing the epitope mimicking secretions. How likely are such gut bacteria molecular mimics to exist? One study has investigated this for the case of multiple sclerosis and concluded there is a strong likelihood that "normally occurring gut bacterium" could produce epitopes that might cause MS through molecular mimicry.[7] One case of molcular mimicry between human peptides and wheat peptides has been found.[8] In the case of normal celiac disease (non-refractory celiac disease) treatable by a gluten-free diet, after some length of time on a gluten-free diet when the antibodies to gluten epitopes have cleared and when the intestinal mucosa has sufficiently healed, it may be possible to reprogram the immune system to tolerate gluten through fecal transplantation, along with vitamin D supplementation, providing a new healthy gut bacteria mix. One problem, however, is that in many cases the damage to the intestinal mucosa from celiac disease does not entirely heal.[9,10] This means that a long-term or permanent state of increased intestinal permeablity or "leaky gut" exists after beginning a gluten-free diet. "Leaky-gut" is by no means a benign condition. It puts a strain on the liver's detoxification abilities having to continually deal with toxins readily passing through the "leaky" intestinal mucosa. The toxins come from gut bacteria as well as from drugs and environmental chemicals including household products and cosmetics. Inhaled environmental toxins can be ingested when mucus expelled from the lungs is swallowed. The overload on the liver and its inability to keep up with detoxification can lead to long-term debilitating medical conditions such as wide-spread chronic pain, muscle pain and weakness, neuropathies, fatigue, dry mouth, frequent urination, swelling, allergies, and even to other autoimmune disorders[11] due to fat soluble toxins accumulating in adipose tissue where they remain causing inflammation and raising havoc indefinitely. The result is an unfavorable pro-inflammatory immune system environment which could impede any chance of restoring gluten tolerance. A promising treatment that could entirely heal the intestinal mucosa and "leaky gut" is a treatment based on a novel protein called R-spondin1. Prior to January 2009 a small San Francisco pharmaceutical company, Nuvelo, was developing an R-spondin1 therapy drug with the designation, NU206. NU206 had shown some great promise and success in lab studies. Dramatic mucosal healing was demonstrated in an experimental colitis model with mice.[12] Nuvelo's first targets were to use NU206 to heal and reduce intestinal mucosal damage from cancer chemotherapy and radiation therapy and to treat short-bowel syndrome. In December 2008 Nuvelo had actually announced results from Phase 1 clinical safety trials on 32 healthy male volunteers demonstrating administration of NU206 caused no adverse effects.[13] Unfortunately, Nuvelo, which also has other drugs in development, ran short of funding and, in January 2009, merged with a Colorado company, ARCA biopharma.[14] ARCA biopharma is dedicated to developing genetically-targeted therapies for cardiovascular diseases. [http://www.nuvelo.com/] It appears that all NU206 research and development and clinical trials were suspended with the merger. NU206, an extremely promising drug that might enable full intestinal mucosal healing and recovery in celiac disease now sits idly on a shelf with no indication clinical trials will ever resume. While there has been some very limited research on R-spondin1 in other medical applications by other scientists, there has been no new R-spondin1 research on intestinal healing since the merger. Any celiac disease interest group with access to funding for celiac disease research should consider contacting ARCA biopharma to see what efforts might be implemented to restart this very important R-spondin1 research. Sources: 1. More Evidence Links Gut Bacteria to Celiac Disease Roy S. Jamron Celiac.com 2008 Nov 6. https://www.celiac.com/articles/21685/ 2. Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease? Roy S. Jamron Celiac.com 2008 Jun 16. https://www.celiac.com/articles/21605/ 3. Fecal Transfer Proves Potent Clostridium difficile Treatment Jenni Laidman Medscape Medical News 2013 Jan 16. http://www.medscape.com/viewarticle/777772 4. Duodenal Infusion of Donor Feces for Recurrent Clostridium difficile Els van Nood, Anne Vrieze, Max Nieuwdorp, Susana Fuentes, Erwin G. Zoetendal, Willem M. de Vos, Caroline E. Visser, Ed J. Kuijper, Joep F.W.M. Bartelsman, Jan G.P. Tijssen, Peter Speelman, Marcel G.W. Dijkgraaf, Josbert J. Keller NEJM 2013 Jan 16; Published Online http://www.nejm.org/doi/full/10.1056/NEJMoa1205037 5. C difficile: Synthetic Stool Substitute Clears Infection Jenni Laidman Medscape Medical News 2013 Jan 10. http://www.medscape.com/viewarticle/777515 6. Stool substitute transplant therapy for the eradication of Clostridium difficile infection: "RePOOPulating" the gut Elaine O Petrof, Gregory B Gloor, Stephen J Vanner, Scott J Weese, David Carter, Michelle C Daigneault, Eric M Brown, Kathleen Schroeter and Emma Allen-Vercoe Microbiome 2013 Jan 9;1:3. http://www.microbiomejournal.com/content/1/1/3 7. Molecular mimicry revisited: gut bacteria and multiple sclerosis. Westall FC. J Clin Microbiol. 2006 Jun;44(6):2099-104. http://jcm.asm.org/content/44/6/2099.long 8. IgA cross-reactivity between a nuclear autoantigen and wheat proteins suggests molecular mimicry as a possible pathomechanism in celiac disease. Natter S, Granditsch G, Reichel GL, Baghestanian M, Valent P, Elfman L, Gronlund H, Kraft D, Valenta R. Eur J Immunol. 2001 Mar;31(3):918-28. http://www.ncbi.nlm.nih.gov/pubmed/11241297 9. Mucosal healing and mortality in coeliac disease. Lebwohl B, Granath F, Ekbom A, Montgomery SM, Murray JA, Rubio-Tapia A, Green PH, Ludvigsson JF. Aliment Pharmacol Ther. 2013 Feb;37(3):332-9. http://www.ncbi.nlm.nih.gov/pubmed/23190299 10. Complete recovery of intestinal mucosa occurs very rarely in adult coeliac patients despite adherence to gluten-free diet. Lanzini A, Lanzarotto F, Villanacci V, Mora A, Bertolazzi S, Turini D, Carella G, Malagoli A, Ferrante G, Cesana BM, Ricci C. Aliment Pharmacol Ther. 2009 Jun 15;29(12):1299-308. http://www.ncbi.nlm.nih.gov/pubmed/19302264 11. Chemical-induced allergy and autoimmunity Marty Bernardus Franciscus Wulferink [s.l.] : [s.n.], 2001 - Tekst. - Proefschrift Universiteit Utrecht http://igitur-archive.library.uu.nl/dissertations/1975053/inhoud.htm 12. R-spondin1, a novel intestinotrophic mitogen, ameliorates experimental colitis in mice. Zhao J, de Vera J, Narushima S, Beck EX, Palencia S, Shinkawa P, Kim KA, Liu Y, Levy MD, Berg DJ, Abo A, Funk WD. Gastroenterology. 2007 Apr;132(4):1331-43. http://www.ncbi.nlm.nih.gov/pubmed/17408649 13. Nuvelo Announces Positive Results from Phase 1 Clinical Trial of NU206 in Healthy Volunteers 2008 Dec 10. http://www.evaluatepharma.com/Universal/View.aspx?type=Story&id=172716 14. Biotechs Arca, Nuvelo complete reverse merger 2009 Jan 28. http://www.bizjournals.com/sanfrancisco/stories/2009/01/26/daily64.html
  7. Gene Ther 2003 May;10(10):835-43 Londei M, Quaratino S, Maiuri L. Institute of Child Health, University College London, London, UK. Celiac.com 05/29/2003 - This highly technical and hopeful article covers the possibility of using gene therapy to one day cure celiac disease. Here are the introduction and final words: "Gene therapy (GT) is still at the experimental stage and some recent setbacks have cooled the potential use of this therapeutic tool even in life-threatening conditions. However, this therapeutic approach has a potential, which is not limited to disease for which we have not other option. There are increasing evidence that GT will be soon used in diseases that are not life threatening. One group of diseases that can benefit from GT is the autoimmune one. Several experimental animal models have indicated the efficacy (proof of principle) of GT. In the present review, we have addressed the possibility that even extremely benign autoimmune-like diseases such as Celiac Disease (celiac disease) might one day profit from this type of therapy. We further point that in conditions such as celiac disease, where the trigger is well known and the pathogenic cascade is relatively well defined, a situation not common in autoimmunity, we can even have a better situation where to explore and use GT to control disease initiation and progression. Once the risks that are still intrinsic to GT will have been reduced the therapeutic options we outline in the present review might not appear too far from reality." "celiac disease is the prototype of diseases in which a clear role of antigen-specific T cells has been demonstrated and where their inhibition results in disease amelioration. The present therapeutic approach is the removal of the antigenic challenge: the gluten-free diet, which is effective if there is a strict compliance to the diet. It is, however, not always easy to follow such strict restrictions for all life and alternative approaches have to be considered. The use of GT is at the moment a remote hypothesis as celiac disease is a relatively benign condition, with a valid therapeutic approach and GT has intrinsic risks that have been highlighted recently. The scope of this review is, however, to indicate a future application of GT when, as they will, the present limitations and intrinsic risks of GT will be overcome."
  8. Foods derived from cereal grains (wheat, rye, barley, oats) are popular staples in our diet. In the past decade especially, a renewed enthusiasm for "whole grains", and increased dietary fiber, has lead to increased consumption of these cereals in relatively unrefined form, and often in combination, as with granola cereals, and whole wheat breads fortified with bran, coarse flours, and other additives. The argument in favor of whole grains is based on two considerations: 1) The nutrient content of whole grains and their unrefined flours is greater than refined flours. White flour has been considered by some an inferior food since it is missing some micro-nutrients. However white flours and light white bread are sometimes better tolerated than the whole grain foods. 2) The indigestible fiber in whole grains contributes to stool bulk, reduces the opportunity for constipation, and absorbs toxic or harmful molecules, which, escorted from the bowel by fiber, have less opportunity to do harm. The regulating and binding actions of grain fibber, it is argued, would reduce the incidence of bowel cancer, if eaten over a lifetime. The favorable fibers are probably better found in vegetables and fruit. While there favorable arguments for a high cereal grain intake there are major problems with these foods. Craving and compulsive eating of flour-based foods is common, especially the reward an dessert foods, containing sugar. These high-carbohydrate foods contribute the major caloric input to obese persons. The diseases clearly associated with Cereal grains or "Gluten intolerance" are the bowel disorders bearing the names,"celiac Disease", "Non-Tropical- Sprue", or "Gluten-Enteropathy", and the skin disorder, dermatitis herpetiformis. The clinical presentations of cereal-grain intolerance, which can be recognized from the history or pattern of illness alone include: Diarrhea, chronic with malabsorption, weight loss, micro-nutrient deficiencies, blood loss and anemia. Abdominal pain may be recurrent and associated with flutulence, distention, and intermittent bowel motility disturbance. Minor gluten-enteropathy may not involve diarrhea, and malabsorption may be inconspicuous or inconsistent. A nutritional anemia may be the presenting problem, although the patient will have an associated history of intermittent abdominal pain and distension. The anemia results from malabsorption iron, folic acid and/or vitamin B12. Arthritic or Fibrositic Syndromes: Aching, stiffness, and fatigue are three common symptoms which occur together in a variety of disorders, and occasionally remit completely on an elimination diet which excludes cereal-grains and other allergenic foods. Brain Disturbances: symptoms include deep, burning sensations in arms and legs, restless legs, numbness and tingling which comes on rapidly with sitting, squatting, and lying in bed; brain effects are manifest by a sense of confusion or "fuzzy-head, disorganization, irritability, and memory impairment. The occurrence of resting pain in joints, particularly the hands with slight swelling, and stiffness is the early prevention of rheumatoid arthritis; it can occur strictly as a manifestation of wheat (and other food) allergy. The activity of rheumatoid arthritis may be reduced in some patients by cereal grain and other allergenic food restriction. There are at least four mechanisms involved at the bowel level for gluten intolerance: 1) Lack of the digestive enzyme, intestinal glutaminase. 2) Antibody production to the prolamine, or a fragment of it. 3) Increased permeability of the bowel to macromolecules including the antigenic protein and its fragments. 4) Increased production and release of mediators such as histamine, seratonin, kinins, prostaglandins, and interleukins. A wheat gluten-triggered mechanism has been studied in rheumatoid arthritis patients. The clinical observation is that wheat ingestion is followed within hours by increased joint swelling and pain. Little and his colleagues studied the mechanism, as it developed sequentially, following gluten ingestion. Platelet Seratonin Release in Rheumatoid Arthritis: A study in Food Intolerant Patients. Little C. Stewart A.G., Fennesy M.R. Lancet 1983.297-9. The Gluten Proteins Gluten is a mixture of individual proteins, classified in two groups, the prolamines and the glutelins. The most troublesome component of Gluten is the Prolamine, Gliadin. It is Gliadin in wheat that causes the major problem in celiac disease, and Gliadin antibodies are most commonly found in the immune complexes, associated with major systemic disease (Unsworth, D.J., et. al., IgA Anti-Gliadin Antibodies in Celiac disease, Clin Exp Immunol. 1981: 46:286-93.Keiffer M, et. al., Wheat Gliadin Fractions and Other Cereal Antigens Reactive with Antibodies in the Sera of of Celiac Patients, Clin Exp Immunol. 1982;50:651-60). We eat the seeds of the grain plants. The seed has a bran casing, a starchy endosperm which contains 90 % of the protein, and a small germ nucleus which is the plant embryo, waiting to grow. Any flour made from the starchy endosperm contains prolamines and is potentially toxic to the grain intolerant person. If we look at the different grains we find that each has its own prolamine. The following list gives the type of prolamine each grain contains, and the percentage of protein the prolamine has in relationship to the entire grain: Wheat - Gliadin - 69% Rye - Secalinin - 30-50% Oats - Avenin - 16% Barley - Hordein - 46-52% Millet - Panicin - 40% Corn - Zien - 55% Rice - Orzenin- 5% Sorghum - Kafirin - 52% Celiac disease may serve as a model of wheat allergy. No-one should make the mistake of assuming this is the only form of wheat allergy. When wheat is the principle problem food, there is a consensus that barley, oats, and rye must be excluded as well. Millet, is intermediate in the list of offenders; corn and rice are usually tolerated when gluten prolamines are the chief and only food intolerance, although corn is a major food-allergen in its own right. Triticale is a new hybrid grain with the properties of wheat and rye, and is excluded on a gluten-free diet [bell L., Hoffer M., Recommendations for Foods of Questionable Acceptance for Patients with Celiac Disease,J.Can. Dietetic Ass'n: 1981; 42:2; 143-15]. The identity and the amount of the prolamine decides the kind of reaction that is likely to occur. It should be noted that there is considerable variability in the prolamine content of various foods made from cereal grains, and this variability is one of the many reasons why food reactions are not consistent. The usual definition of celiac disease links chronic diarrhea, with evidence of malabsorption, and changes in the surface of the small bowel. Most medical textbooks dogmatically state that an intestinal biopsy must be taken and must show typical changes before the diagnosis is made. The biopsy allows a pathologist to examine microscopically the surface of the small intestine. The surface of the small intestine is covered by a dense mat of projecting nipples called villi which shed cells containing digestive enzymes, and absorb food molecules. In long-standing celiac disease one expects the villi to be blunted and the surface to be smoothed out. While the biopsy is a useful procedure it has several drawbacks; It is a procedure with a small incidence of dangerous complication, especially bowel perforation. It is a small sample and may miss patchy or irregular bowel changes. Significant protein intolerance, and increased bowel porosity may exist despite normal appearance of the bowel lining under the microscope. Patients in remission or with intermittent symptoms may have normal biopsy results but remain exquisitely sensitive to some prolamine, or peptide fragment challenges. [bjarnson, I., et. al., Intestinal Permeability Defect in Celiac Disease, Lancet. 1983 1284-85]. The most significant test of gluten intolerance is remission of symptoms when grains are eliminated for a trial period of 3-6 weeks. I have often reviewed the history of patients with chronic diarrhea, and associated abnormalities, who have been "thoroughly investigated" in an academic center and left untreated because their biopsy result was normal. Physicians, who make therapeutic decisions solely on the basis of biopsy results are being dogmatic, not scientific, and certainly not serving the best interests of their patients who simply want to be better. Investigations which do not lead to effective therapy are of no value to patients. Diagnosis of gluten-sensitivity in all disorders may be facilitated in the near future by better immunological laboratory tests, including measurement of circulating serum antibodies directed against these proteins, and of circulating immune complexes which contain food antigens. [O'Farrelly, et. al., Alpha-Gliadin Antibody Levels: A Serological Test for Celiac Disease, 1983 Lancet; 286:2007-2010]. Better tests would permit the demonstration of increased GITPERM, and the entrance of abnormal macromolecules after test meals. Eventually the path through the body of such molecules may be studied by labeling them with isotopes, and tracking them with scanning methods like positron emission tomography. Irritable Bowel Syndrome An unexplained bowel disturbance, characterized by abdominal pain, gas, diarrhea, often alternating with constipation, is diagnosed as the "Irritable Bowel Syndrome" and too often attributed to "psychogenic causes". We recognize right away that the label "psychogenic causes" describes the lack of biological understanding more than it describes the patient's problem. The treatment usually offered includes bulk laxatives, tranquilizers mixed with antispasmodic drugs, and not infrequently, a trip to the psychiatrist, who is not likely to do a dietary history. The success rate with these methods in one study was only 12%! [Waller, S.L., Misiewicsz: Lancet 1969 ii: 753-6, Prognosis in Irritable Bowel Syndrome].Food studies are seldom undertaken in the assessment of patients with irritable bowel syndrome. Not a single patient whom I have seen with this disorder has had a food diary examined, nor any trial of exclusion diets. Dietary advice commonly-given includes "high-fibber" diets, usually increased cereal grains, which are contraindicated. Studies which allege to rule out food intolerance are poorly conducted, often basing negative results on limited, selected food challenges. Proper studies would utilize the complete methodology of diet revision therapy, and would observe patients in real-life conditions, ingesting real food over a significant period of time. The irritable bowel syndrome is at least in part a food-intolerance disorder, and the program outlined in this book will generally be helpful. In a recent study by V. Alum Jones et al, food intolerance was shown to be a major factor in causing the irritable bowel syndrome in 25 patients. This study is of particular interest because it was arranged to reveal something of the mechanism of this disorder. The results indicate that this particular presentation of food intolerance was not the result of immune events, was not associated with high blood-histamine levels, nor circulating immune complexes. Rather the disturbance seemed to be related to increased levels of Prostaglandin E2 (PGE2), synthesized and secreted by the bowel itself. Prostaglandin production is inhibited by ASA, and all of the other anti-arthritic medications, and may prevent the irritable bowel effect if taken before meals. The foods causing the irritable-bowel symptoms were (in order of frequency) Wheat...9 Corn .... 5 Milk.... 4 Coffee. 4 Tea..... 3 Citrus.. 2 All the patients found to be intolerant of wheat had normal results of intestinal biopsy. Not all wheat-induced bowel disorders are celiac disease! The important point, once again, is that the mechanisms of food intolerance are multiple and complex! The only practical way to study food intolerance is by trials of dietary revision, and challenges with real food. One interesting observation made by several of my patients is that they always got somewhat better while in hospital, having multiple tests done. Psychological factors? No. Hospital tests for gastrointestinal disorders always involve days of fasting. If you stop eating foods that are hurting you, your symptoms improve! Proper NP may avoid the waste, in terms of dollars and disappointment, that inappropriate medical investigation and treatment incurs, when a trial of appropriate DRT will often cure the "disease" under investigation. This not to deny that emotions influence bowel function, since this is clearly the case. The "Gut Brain Axis" has become a subject of specialized study because of the complexity of interaction of these two life-determining organ systems. Food selection, emotional experiences, and eating behaviors interact complexly. Anger, frustration, fear will profoundly influence food selection, appetite, digestion, and metabolism; while food selection, digestion and metabolism will determine your emotional reactivity. There is a continuous loop of causal relationships, not a one-way vector. When patients are told they have bowel dysfunction because of stress, tension, or anxiety, this is only a half truth. The other half of the truth is that patients have stress, tension, and anxiety because of bowel dysfunction. The more subjective mood-related symptoms are difficult to assess, and are attributed to "psychiatric causes" although no authority seems to know what that means! The brain effects are an expression of disorderly molecular flow through the brain. Specific nuero-active effects of grains include the circulating peptides, which have been described earlier in the book, as WMOD, and are further discussed in the last section of this chapter. Indications for Trial of Gluten Restriction NP advocates liberal gluten restrictions in a variety of circumstances, simply because the results are surprisingly good. The core diet developed by clinical trials, and described in subsequent chapters is initially free of cereal grains, since they are frequent offenders in food intolerance problems. Not only patients with bowel disorders benefit, but also people whose bowels function apparently well but suffer, fatigue, aching, swelling, and brain disturbances, expressed as mental and emotional upheavals. The specific patterns of disturbance which should invite a trial of the food-testing plan, and gluten restriction specifically are: Diarrhea, prolonged over three weeks, not associated with infections, or evidence of parasites or pathogenic bacteria in stool samples. Abdominal pain, especially if frequently recurrent, and associated with excess gas, and abdominal distensio (Irritable Bowel Syndrome). Anemia from iron, folic acid, or nutrient deficiency which is unexplained by blood loss, or dietary inadequacy, especially if associated with abdominal symptoms. Aching disorder, especially if the aching is generalized, associated with stiffness with inactivity, and dysethesiae ( odd burning, tingling sensations), and tender muscles. Any arthritic pattern, associated with diarrhea should be vigorously managed with gluten, milk, and egg restriction with careful testing of other foods for possible reactions. Fatigue, especially if associated with irritability, confusion or fuzzy-headedness, headache, and abdominal discomforts. Chronic asthma and rhinitis. Neurological symptoms which are unexplained by recognized abnormalities in physical examination and laboratory investigations. These symptoms include the above mentioned, memory disturbances, sleep disturbances, visual distortions, muscle weakness, and fasiculations (wiggly, jerking movements within muscles). A trial of gluten restriction is also appropriate in children with learning disability, schizophrenics, alcoholics, and patients with refractory mood disorders. Treatment of Grain Intolerance Exclusion of wheat, rye, barley, oats, and millet are the initial steps when gluten intolerance is suspected. The exclusion includes all the foods made with the flours of these common grains - Durham flour, Triticale, and Bugler are all excluded. The bran of these cereals is also excluded. A trial of an elimination diet lasting 3-6 weeks is sufficient to experience significant improvement in most bowel conditions. Longer periods of exclusion are required in conditions with chronic tissue inflammation, especially arthritis, and the skin disorders, eczema, and dermatitis herpetiformis, which sometimes requires an exclusion of several months before the skin condition remits completely. It is important to realize that multiple food intolerance are common and should be assumed, rather than assuming that single food intolerance's are the problem. NP does not consider it adequate therapy for a single food group to be eliminated, on the assumption that every other food will be well tolerated. Gluten restriction should be part of a more comprehensive dietary study, preferably in the form outlined in the food-testing plan. The best dietary plans are based on what is good to eat, more than what is bad to eat! No-one wants to be confronted with long lists of foods they must avoid. It is better to build a diet from scratch, emphasizing the positive. There is an entire universe of foods not related to milk, gluten-cereals, and eggs, the commonest problem foods! If improvement occurs, gluten restriction is maintained for many months at least before any effort is made to re-challenge with gluten foods. There are two exceptions, millet and oats. Millet is occasionally acceptable, early in an exclusion program although few people find it an attractive food, and it is potentially a trouble-maker. Oats is probably the best cereal to be re-introduced, and is often tolerated when wheat, rye, millet and barley are not. If gluten restriction is beneficial, oats may be tried after 2-3 months of abstinence. Some people, however, have specific and dramatic allergic reactions to oats, and acceptability must not be assumed. The major substitute for cereal grains is Rice The rice prolamine, orzenin, is different enough from gliadin to avoid immunological cross-reaction. Rice: Desirable Staple Food Rice is the staple food chosen for the core diet because it has low allergenicity, is versatile, widely available, and provides a carbohydrate caloric base to the diet. Rice comes in many varieties some of which are sufficiently different to be treated almost as separate foods. Converted white rice is preferred at the start of a core-diet program. Brown rice does contain more nutrients, and some prefer it by taste and texture; however, the husk also contains more potential problems. Rice-eating peoples generally polish their rice, removing the husk, because empirically the result is better. Again the nutritional arguments based on the nutrient content of foods outside of the body may be misleading! Brown rice may be well-tolerated, but should be introduced after tolerance for converted white rice is established. There are definite exceptions to this rule, as with all rules, since some patients do report better tolerance of selected varieties of brown rice. Rice can be utilized in a variety of forms, including rice cereals, rice pablum, puffed rice, rice-cakes, rice noodles, rice vermicelli, and rice flour (starch). Different rices vary sufficiently in taste, and texture to maintain culinary interest. Rice may be boiled with sunflower seeds, buckwheat, wild rice, other seeds, and legumes for added nutritional and culinary variety. All foods, including rice have the potential to be allergenic, however, and are not exempt from suspicion when adverse food reactions continue on a substitution diet. The most typical symptoms of rice intolerance are heavy fatigue, and chilliness. Rice may also produce the total grain syndrome, although this is uncommon in my experience. Following the core hypoallergenic diet plan, you will simply not miss cereal grains for a while, and find the variety and diversity of other vegetables, sufficient to sustain your interest and nutrition. The biggest challenge is to make the effort to choose different foods, and to prepare them attractively. Corn is less well tolerated than rice Our packaged, fast-food, and restaurant-food industries rely heavily on wheat flour to produce their products. The person on a gluten-free diet must make an extra effort to avoid these products, and to eat instead primary foods, including fresh produce, meats, fish, and rice. Most of my patients crave a carbohydrate food, if not a sugar food, then bread, buns, crackers, chips, nuts and so-on. Rice is a good alternative, being a starchy vegetable which turns sweet if you chew it for a while. Having rice available in a bowl in the refrigerator, mixed with vegetables, herbs, meats or fish offers an alternative to gluten-laden snack foods. Pasta is made with high gluten flour and is off our list of core diet foods. Again Rice is good alternative to pastas. Buckwheat Buckwheat is an interesting grain-like food to add to your diet, especially if Rice is not acceptable because of an adverse response to it. Buckwheat is not a grain, but belongs to the Polygonaceae family which includes sorrel, rhubarb and dock. Buckwheat is a seed, however, and resembles the grains in having a starchy endosperm, and can be ground into a flour, or cooked as a cereal, or prepared as rice. Buckwheat is not toxic to the celiac bowel, although some people react adversely to it. Buckwheat flour is disappointing for baking since it lacks gluten, the elastic, chewy component of bread. Other Alternatives to Cereal Grains Other starchy vegetables may stand in for grains. The potato is a starchy tuber, and potato starch can be used as a weak imitation of flour. Other roots are available, including Cassava an African vegetable which produces Arrowroot flour Tapioca is made by heating and moistening arrowroot. Flour is also made from Taro, a Japanese tuber, which is common in Hawaii where POI is a staple paste made from Taro roots. Soya beans are versatile and highly nutritious seeds which can be utilized as a flour as well. Tofu is the protein fraction of Soya beans, and is an inexpensive, nutritious food, used widely in the orient as a protein staple. It must be mixed with corn or another legume to produce a full complement of essential amino acids. The main problem with tofu is learning how to cook with it. Other legumes including, chick peas, lentils, peanuts are useful foods, on a gluten restricted diet, but have their own problems which must be considered before regular use of these foods is entertained. Each recommended food is still subject to testing, however, for each food may produce allergens or cause other problems. As with all foods in a sensitive person, the basic rule is - Find out how the food works in your body! Gluten-free diets specify food exclusions, including a variety of manufactured foods which contain Gluten. One generally can figure out what is not desirable by thinking of the probable origins of the food in question. Gluten exclusion does include malt, a barley product, and malt containing beverages (Postum, Ovaltine); beer and ale. Alcohol is usually excluded, although some tolerance may be found to selected wines, and distilled beverages. [Food for Celiacs; Campbell, J.A. : Journal of the Canadian Dietetic Ass'n., Jan '82 ; 43:1; 20-24; Gluten Free Cookbook: Leicht, L., RR#1 Box 54, Pender Island B.C. VON 2MO; Club House Foods 316 Rectory St. PO Box 788 London Ont. N6A 4Z2]. The focus of a gluten-free cookery is often on replacing gluten flour in baked goods with starches made from rice, arrowroot, potato, Soya beans, other legumes like chickpeas,and wheat starch (all the protein has been carefully removed). While baking can be done with these non-gluten "flours", the results are never as satisfying as with wheat flour. Gluten is the most desirable ingredient in flour for producing bread, and baked goods, and its absence is conspicuous. In many respects it is easier, kinder, and nutritionally wiser to forgo the baked goods in large measure and eat other foods. The task of changing your diet is very much like moving to another country and culture. You may try to bring all your old habits with you, and struggle to get all of the ingredients that you are used to forming into meals, or you can gracefully, and with a sense of adventure try the new cuisine. Certainly bakery foods are delicious and tempting, but so are creatively prepared rice, vegetable, fruit, fish, and meat meals. Even with multiple exclusions, an appealing, varied diet is within reach if you are willing to change your eating style. A book of recipes which de-emphasizes, cereal-grains, eggs, and milk is a great asset. The cookbook "Oriental Food Feasts" is full of recipe ideas from China, Japan, Indonesia, and India. One has to select recipes that utilize foods, appropriate to your dietary needs. The main thing is to be inspired to create and enjoy a new cuisine that will diminish your disturbances, sustain your interest in food, and provide balanced nutrition. [shepard, S.M., Oriental Food Feasts, Arco Publishing, Inc. New York 1979]. Vegetable selection and preparation is one of the prerequisites of a successful diet revision. The Tassajara cookbook is my favorite introduction to the subject [Tassajara Cooking; 1973 Zen Centre; San Francisco; Shambala Publications, Inc. Boulder, CO.] . Neuropsychiatry & Gluten Intolerance We have recognized that Gluten intolerance may involve the absorption of complete proteins like gliadin, or its peptide- fragments; anti-protein antibodies circulating in the blood, which form immune-complexes with the food protein, and provoke the release of mediators which may cause multiple disturbances in all body systems, and even tissue damage. These circulating problems may also influence brain function in a variety of undesirable ways. There is vague circumstantial evidence of an adverse grain effect on metal status. A family history of psychiatric problems is more common in patients with celiac disease. Celiac disease is genetically determined involving two or more concurrent genes. The genes involved are part of the immune-recognition complex, which determine the "Self" identity markers, protecting one's own cells from attack by the immune system. Celiac patients have an increased frequency of the serum histocomptability antigens (self-markers) of the HLA-B8 and HLA-Dw3 types. This genetic marker may indicate a predisposition for bowel absorption abnormalities or immunologic propensities, which result not only in celiac disease itself but other contingent abnormalities as well. Schizophrenia has been associated with gluten intolerance. The diagnosis, schizophrenia, describes a variety of differing individuals who belong to complex group of brain-disordered people. The schizophrenic brain distorts sensing, feeling, remembering, deciding, and acting. It is unlikely that schizophrenia is a single disease with a single cause. The milder, but similar brain dysfunctions which I observe commonly with gluten and other food intolerance, suggests that food allergy may play a role in schizophrenia, with gluten as a frequent triggering antigen. Dr. F.C.Dohan has consistently advocated a gluten-schizophrenia link for 20 years [Dohan, F.C., Cereals and Schizophrenia: Data and Hypothesis, 1966 Acta Psychiatr. Scand 42:125-42; Dohan, F.C. More, Celiac Disease as a Model for Schizophrenia, 1983 Biol. Psychiatry 18:561-4]. Dr. Dohan states: [" Many diseases are caused by genetically-deficient utilization of specific food substances. Perhaps the best studied example is phenyketonuria... far more common disorders, for example, atherosclerosis, and coronary heart disease, are strongly suspected of being due to genetically defective utilization of certain food constituents. " Similarly, considerable evidence indicates that the major cause of schizophrenia is the inborn inability to process certain digestion products of some food proteins, especially cereal grain glutens..."] Among Dr. Dohan's interesting an relevant recommendations is the idea of a "Gluten tolerance test". Such a test has not yet been developed, but is the sort of evaluation method that NP advocates in general. A gluten tolerance test could be initiated with routine evaluations before and after ingestion of grain foods. More sophisticated versions would measure gluten proteins and derived peptides in the blood, and would track the path of these molecules into organs, especially the brain. Finally the impact of these molecules would be evaluated by monitoring the function of the target organ in real time. I have been eager to do real-time monitoring of brain activity, topologically-computed in gluten-sensitive patients. These patients report changes in their PSYE, cognitive abilities, and emotional state which no researcher to date has documented objectively. The problem of adverse brain effects of molecules derived from food is a major under-recognized phenomenon of nutrition and molecular pathophysiology. Research in the next 10-20 years will, I am convinced, reveal a great deal about the extent, mechanisms, and importance of this consequence of eating to our mental status. Extracted from "Nutrition Therapy" by Stephen J. Gislason, MD For more information, please visit Nutramed's Web site at: http://www.nutramed.com/.
  9. Celiac.com 04/13/2011 - When people with celiac disease consume gluten, their intraepithelial lymphocytes (IELs) wreak havoc in their guts by promoting inflammation and attacking the epithelial cells lining the intestines. This autoimmune activity is mediated by arachidonic acid (AA), a cytokine produced by the IELs. But there is data that the enterocytes "the very intestinal epithelial cells attacked by the IELs" can also produce and secrete AA in response to inflammation. Do they do so in celiac disease? A recent study reported in Clinical Nutrition set out to determine just that. Using Caco-2 cells, a human intestinal epithelial cell line commonly used as an in vitro model of celiac disease, Vincentini et al. are the first to find that when these enterocytes were exposed to gliadin peptides, they did in fact generate and release arachidonic acid. Docosahexaenoic acid (DHA) is a long chain polyunsaturated fatty acid that counteracts many of the inflammatory effects precipitated by AA. When Caco-2 cells were treated with gliadin peptides and DHA, they produced much less AA (although they still made more than untreated cells). Treatment with DHA also reduced the production of other molecules involved in inflammation that were increased by exposure to gliadin, including cyclooxygenase (COX)-2, prostaglandin E2 (PGE2), and interleukin (IL)-8. PGE2 is particularly interesting, as it can increase the intestinal paracellular permeability that has been suggested to be the initial event in the pathogenesis of celiac disease. The authors suggest that by blocking the release of AA, DHA might be a tenable therapeutic option for modulating mucosal inflammation in newly diagnosed celiac patients. Source: Vincentini O, Quaranta MG, Viora M, Agostoni C, and Silano M. Docosahexaenoic acid modulates in vitro the inflammation of celiac disease in intestinal epithelial cells via the inhibition of cPLA2. Clin Nutr. 2011 Mar 19.
  10. Celiac.com 07/01/2006 - Scientists have discovered what may be a successful non-dietary therapy for celiac sprue, an inherited inflammatory disorder of the small intestine that impacts an estimated 1 in 200 people around the world. Two research studies, published in the June issue of Chemistry and Biology, pave the way for clinical testing with an oral enzyme therapy that may prevent the many symptoms and complications of this widespread disease. People with celiac sprue, also called celiac disease, cannot tolerate the protein gluten in their diet. Gluten is present in grains like wheat, barley, and rye. When gluten is ingested by a celiac patient, it sets off an inflammatory reaction that damages the small intestine, leading to malabsorption, an autoimmune-like response, and many other complications. The only effective therapy for celiac disease is complete dietary exclusion of gluten. However, the ubiquitous nature of gluten poses a constant threat to celiacs, and a majority of celiac patients who adopt a restrictive diet still exhibit structural and functional gut abnormalities. "Non-dietary therapies that allow celiac patients to safely incorporate low-to-moderate levels of gluten into their daily diet would be of considerable benefit," explains study leader Dr. Chaitan Khosla, from Stanford University and Celiac Sprue Research Foundation. "Having demonstrated earlier that certain types of enzymes can detoxify gluten, our laboratory set out to devise an optimal oral enzyme therapy for celiac sprue by borrowing from nature. In germinating barley seed, gluten serves as a nutritious storage protein that is efficiently digested by enzymes. One enzyme, EP-B2, plays a crucial role in this process by breaking gluten proteins after glutamine residues, which comprise one-third of all amino acid residues in gluten." Dr. Khoslas group used recombinant bacteria to produce a form of EP-B2 that only activates under acidic conditions similar to the conditions found in the human stomach. The researchers demonstrated that EP-B2 efficiently digested gluten protein under gastric conditions and, importantly, EP-B2 was most specific for those parts of gluten that are known to trigger celiac pathogenesis. In a second study, the researchers went on to devise an even more potent double enzyme therapy for detoxifying gluten. EP-B2 was tested in combination with another well-characterized enzyme called PEP that breaks gluten protein after proline residues. Like glutamine, proline is also abundant in inflammatory gluten peptides. At very high gluten loads, where neither PEP nor EP-B2 alone could detoxify gluten quickly enough to prevent inflammation, a PEP and EP-B2 combination completely abolished gluten immunotoxicity within ten minutes under simulated gastric and duodenal conditions. In this tag-team therapy, EP-B2 first cleaved gluten into small pieces under gastric conditions that were then easier for PEP to fully detoxify under duodenal conditions. "Our results suggest that recombinant EP-B2 should be effective as supportive therapy to help celiacs cope with the hidden gluten in everyday life, and that a two-enzyme cocktail containing PEP and EP-B2 may even allow celiacs to resume a more normal diet in the future," offers Dr. Khosla. References: Seigel et al. The researchers include Matthew Siegel, Michael T. Bethune, Jiang Xia, Alexandre Johannsen, Tor B. Stuge, and Peter P. Lee of Stanford University in Stanford, CA; Jonathan Gass, Jennifer Ehren, Gary M. Gray, and Chaitan Khosla of Stanford University in Stanford, CA and Celiac Sprue Research Foundation in Palo Alto, CA. This research was supported by a grant from the National Institutes of Health (R01 DK63158 to C.K. and Mary Hewitt Loveless, MD Pilot-Project Grant to P.P.L.). Siegel et al.: "Rational Design of Combination Enzyme Therapy for Celiac Sprue." Publishing in Chemistry & Biology 13, 649–658, June 2006 DOI 10.1016/j.chembiol.2006.04.009 www.chembiol.com Bethune et al. The researchers include Michael T. Bethune, Yinyan Tang, and Chaitan Khosla of Stanford University in Stanford, CA; Pavel Strop of Howard Hughes Medical Institute and Stanford University in Stanford, CA; Ludvig M. Sollid of University of Oslo and Rikshospitalet University Hospital in Oslo, Norway. This research was supported by R01 DK063158 to C.K. M.T.B. is a recipient of a National Institutes of Health Cellular and Molecular Biology Training Grant through Stanford University. Bethune et al.: "Heterologous Expression, Purification, Refolding, and Structural-Functional Characterization of EP-B2, a Self-Activating Barley Cysteine Endoprotease." Publishing in Chemistry & Biology 13, 637–647, June 2006 DOI 10.1016/j.chembiol.2006.04.008 www.chembiol.com. Contact: Heidi Hardman Tel: (617) 397-2879
  11. Aliment Pharmacol Ther 18(5):487-494, 2003. M. S. Goerres*, J. W. R. Meijer, P. J. Wahab*, J. A. M. Kerckhaert, P. J. T. A. Groenen, J. H. J. M. Van Krieken, C. J. J. Mulder Celiac.com 11/18/2003 - This very important Dutch study demonstrates a new and effective way of treating a subgroup of refractory celiac disease patients, those with normal intraepithelial T-lymphocytes (IELs). Considering the very poor outcome for those in the study with abnormal IELs (phenotypically immature intraepithelial T-lymphocytes defined by a lack of characteristic T-cell markers), we must hope that future research will soon yield an equally effective treatment. Here is the abstract of the study: "Introduction: Refractory coeliac disease (RCD) is a rare syndrome with a poor prognosis, defined by malabsorption due to gluten-related enteropathy after initial or subsequent failure of a strict gluten-free diet and after exclusion of any disorder mimicking coeliac disease. Patients and methods: Nineteen patients were included and treated. Based on intraepithelial T-lymphocyte(IEL) phenotyping, patients were recorded as having RCD type I with normal IELs, or RCD type II with phenotypically immature IELs defined by a lack of characteristic T-cell markers. Treatment consisted of azathioprine combined with prednisone for 1 year, which was tapered and, if possible, stopped. Results: Clinical improvement was seen in nearly all patients in both groups. Eight of 10 RCD type I patients responded histologically, and complete normalization of villi was seen in four patients. In RCD type II, 6/8 patients developed enteropathy-associated T-cell lymphoma (EATL) and 7/8 patients died. Conclusions: For the first time we report a promising therapeutic treatment option for RCD type I. In RCD type II, azathioprine and prednisone therapy (APT) is not effective, therefore we suggest that other (chemo)therapeutic agents are considered. Not all RCD type II patients presented with a monoclonal TCR?-gene rearrangement and immunohistological changes as is currently reported in the literature. Therefore, immunophenotyping seems mandatory in the work-up of RCD."
  12. Publication: Biochim Biophys Acta 1999 Jan 6;1453(1):152-60 Title: In vitro cytotoxic effect of wheat gliadin-derived peptides on the Caco-2 intestinal cell line is associated with intracellular oxidative imbalance: implications for coeliac disease. Authors: Rivabene R, Mancini E, De Vincenzi M Laboratory of Metabolism and Pathological Biochemistry, Istituto Superiore di Sanita, Rome, Italy. mbpsegr@dns.net.iss.it PMID: 9989255, UI: 99143800 Coeliac disease (celiac disease) is an inflammatory disorder of the upper small intestine in which gluten acts as an essential factor in its pathogenesis. Although it is generally accepted that cereal protein activation of the immune system is involved in celiac disease progression, a non-immunomediated cytotoxic activity of gliadin-derived peptides on the jejunal/duodenal tract cannot be excluded. In this work, considering that (a) little has been reported about the intracellular metabolic events associated with gliadin toxicity, and ( an important role for free radicals in a number of gastrointestinal disease has been demonstrated, we investigated the in vitro effects of gliadin-derived peptides on redox metabolism of Caco-2 intestinal cells during a kinetic study in which cells were exposed to peptic-tryptic digest of bread wheat up to 48 h. We found that the antiproliferative effects displayed by gliadin exposure was associated with intracellular oxidative imbalance, characterized by an increased presence of lipid peroxides, an augmented oxidized (GSSG)/reduced (GSH) glutathione ratio and a loss in protein-bound sulfhydryl groups. Significant structural perturbations of the cell plasma membrane were also detected. Additional experiments performed by using the specific GSH-depleting agent buthionine sulfoximine provide evidence that the extent of gliadin-induced cell growth arrest critically depends upon the basal redox profile of the enterocytes. On the whole, these findings seem to suggest that, besides the adoption of a strictly gluten-free diet, the possibility for an adjuvant therapy with antioxidants may be considered for celiac disease patients.
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