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Found 45 results

  1. Celiac.com 09/19/2017 - Hookworms. Intestinal parasites. They sound gross. The thought of having one's gut infected with a parasitic worm generally makes people's skin crawl. Indeed, intestinal worms, like hookworm, have a bad reputation among health experts, and have been the subject of fierce public health campaigns seeking their eradication. However, researchers have also documented the gut healing abilities of parasites like hookworm. In fact, part of how hookworms seem to work in nature is to promote an optimal gut environment in which they can thrive. In nature, the guts of people infected with hookworm are generally healthy. Could hookworms and other intestinal parasites prove key to treating and possibly eliminating diseases like celiac, and asthma? A number of clinicians and researchers feel that if they can just get the right strain of hookworm, at the right levels, they can basically eradicate celiac disease, and possibly asthma and other inflammatory diseases. When hookworms are introduced into the gut of people with celiac disease in the right amount, and kept at therapeutic levels, patients see their celiac symptoms disappear and their guts return to a healthy, normal condition. In fact, hookworms do not reproduce once inside the human gut, so if doctors put , say, 10 hookworms into a gut to treat celiac disease, there will be 10 there later, not more. In nature, the way humans build up dangerous levels of hookworm is via unsanitary environmental conditions and repeated exposure to more hookworms. Done clinically, the hookworm would present little or no danger to the human who was hosting it. While still very much in the experimental phase, researchers hope to investigate a number of strains to determine the best therapeutic levels for such disease treatments. For that, they will need FDA approval. Remember, the fecal transplant was first described in the 1950s, but took decades to catch on as a conventional treatment for gut disorders, such as c-dif bacteria, partly because it was seen as crude and somehow objectionable. But it proved to work. Really well. So much so that it's now a fairly conventional treatment. Could the hookworm follow a similar path from crude and weird to cool and effective? Could hookworms be used to cure celiac disease? Only close study will tell us for sure, and that's why the move to get FDA approval is an important one. For that, special strains of hookworm must be approved. "One of the big roadblocks is having the parasites that the FDA will allow you to infect people with," says John Hawdon, vice president of the American Society of Parasitologists and a researcher at the George Washington University. He and his colleagues are applying for permission to grow hookworm larvae to standards fit for testing in humans, which is not currently permitted in the United States. Hawdon says he anticipates a lengthy application process. Stay tuned for news on efforts to develop hookworm as a potential cure to celiac disease, asthma, and more. Sources: popsci.com iflscience.com
  2. Celiac.com 05/28/2013 - Is an intestinal biopsy always necessary to diagnose celiac disease, or can diagnosis be made without biopsy? To answer that question, a team of researchers recently set out to compare celiac disease–specific antibody tests to determine if they could replace jejunal biopsy in patients with a high pretest probability of celiac disease. The research team included Annemarie Bürgin-Wolff, Buser Mauro, and Hadziselimovic Faruk. They are variously affiliated with the Institute for Celiac Disease in Liestal, Switzerland, and Statistik Dr. M. Buser, Riehen, Switzerland. Their retrospective study included blood test data from 149 patients with celiac disease, along with 119 controls. All patients underwent intestinal biopsy, and all samples were analyzed for IgA and IgG antibodies against native gliadin (ngli) and deamidated gliadin peptides (dpgli), as well as for IgA antibodies against tissue transglutaminase and endomysium. They found that tests for dpgli were superior to ngli for IgG antibody determination: 68% vs. 92% specificity and 79% vs. 85% sensitivity for ngli and dpgli, respectively. Predictive values were also higher for dpgli than for ngli; positive (76% vs. 93%) and negative (72% vs. 83%). Regarding IgA gliadin antibody determination, sensitivity improved from 61% to 78% with dpgli, while specificity and positive predictive value remained at 97% (P less than 0.00001). A combination of four tests (IgA anti-dpgli, IgG anti-dpgli, IgA anti- tissue transglutaminase, and IgA anti-endomysium) yielded positive and negative predictive values of 99% and 100%, respectively and a likelihood ratio positive of 86 with a likelihood ratio negative of 0.00. Omitting the endomysium antibody determination still yielded positive and negative predictive values of 99% and 98%, respectively and a likelihood ratio positive of 87 with a likelihood ratio negative of 0.01. Conclusion: Antibody tests for dpgli yielded superior results compared with ngli. A combination of three or four antibody tests including IgA anti-tissue transglutaminase and/or IgA anti- endomysium enabled reliable diagnosis or exclusion of celiac disease without intestinal biopsy in 78 percent of patients. This two-step method of performing jejunal biopsy only in patients with discordant antibody results (22%) would catch all patients except those with no celiac-specific antibodies; who would then be caught through biopsy. Source: BMC Gastroenterol. 2013;13(19)
  3. Celiac.com 01/11/2017 - Researchers know that canonical Wnt/β-catenin signaling controls the homeostasis of intestinal epithelium by regulating the balance between intestinal stem cell regeneration and differentiation, but they really don't know much at all about the non-genetic mechanics of the process. One research team recently set out to test a hypothesis that the epigenetic regulator, Polycomb Repressive Complex-2 (PRC2), plays a role in Wnt-mediated epithelial homeostasis on the crypt-villus axis, and that defects in the process are implicated both in celiac disease and intestinal cancers. The research team included Mikko Oittinen, Alina Popp, Kalle Kurppa, Katri Lindfors, Markku Mäki, Minna U. Kaikkonen, and Keijo Viiri. They are variously associated with the Tampere Centre for Child Health Research, University of Tampere, Department of Pediatrics and Tampere University Hospital, Tampere, Finland, with the Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland, and with the University of Medicine and Pharmacy “Carol Davila” at the Department of Pediatrics and Institute for Mother and Child Care in Bucharest, Romania. Their study showed that PRC2 establishes repressive crypt and villus specific trimethylation of histone H3 lysine 27 (H3K27me3) signature on genes responsible for nutrient transport and cell killing in crypts and, proliferation and differentiation in mature villi, suggesting that PRC2 facilitates the Wnt-governed intestinal homeostasis. When celiac patients regularly consume gluten, PRC2 goes out-of-bounds active, and its target genes in the intestinal epithelium are negatively impacted. Colorectal adenomas, and carcinomas, also differentially express a significant set of effective intestinal PRC2 targets. This indicates that PRC2 initiates and maintains polar crypt and villus specific H3K27me3 signatures. Because H3K27me3 is a mark enriched in developmentally important genes, identified intestinal PRC2 targets are possibe imperative drivers for enterocyte differentiation and intestinal stem cell maintenance downstream to Wnt-signaling. This research also clarifies the mechanics driving crypt hyperplasia in celiac disease, and suggests that PRC2-dependent fostering of epithelial stemness is a common aspect of intestinal diseases marked by epithelial hyperplasia or neoplasia. Lastly, the team's research shows that in the gut, PRC2 represses genes having both pro-stemness and pro-differentiation functions, a fact that should be weighed when designing non-genetic therapies including PRC2 as a drug target. Source: Stem Cells 2016
  4. Celiac.com 09/15/2016 - Some doctors and clinicians have reported cases of severe sprue-like enteropathy associated with olmesartan, but, until now, no clear demonstration of an increased risk has been documented by epidemiological studies. Now, a French nationwide observational cohort study has shown a connection between severe intestinal malabsorption and the drug olmesartan, according to results presented by a team of researchers. Olmesartan is an angiotensin II receptor antagonist which has been used for the treatment of high blood pressure. Olmesartan is also sold commercially under the name Benicar. The research team included Mickael Basson, Myriam Mezzarobba, Alain Weill, Philippe Ricordeau, Hubert Allemand, Francois Alla, and Franck Carbonnel. They are variously affiliated with the French National Health Insurance Fund, Paris, France, and the Université Paris-Sud, Assistance Publique-Hôpitaux de Paris and Gastroenterology unit, Hôpitaux Universitaires Paris Sud, Le Kremlin Bicêtre, France. The team set out to assess, in a nationwide patient cohort, the risk of hospitalization for intestinal malabsorption associated with olmesartan compared with other angiotensin receptor blockers (ARB) and ACE inhibitors (ACEIs). From the French National Health Insurance claim database, they included all adult patients initiating ARB or ACEI between 1 January 2007 and 31 December 2012, with no prior hospitalization for intestinal malabsorption, no serology testing for celiac disease, and no prescription for a gluten-free diet product. Their main endpoint was incidence of hospitalization with a discharge diagnosis of intestinal malabsorption. The team included 4,546,680 patients, for a total of 9,010,303 person-years, and observed 218 events. Compared with ACEI, the adjusted rate ratio of hospitalization with a discharge diagnosis of intestinal malabsorption was 2.49 (95% CI 1.73 to 3.57, p Average length of hospital stay for intestinal malabsorption was longer in the olmesartan group than in the other groups (p=0.02). Compared with ACEI, the adjusted rate ratio of hospitalization for celiac disease was 4.39 (95% CI 2.77 to 6.96, p<0.0001). These results show that olmesartan is assoc qiated with higher rates of hospitalization for intestinal malabsorption and celiac disease. Source: Gut. doi:10.1136/gutjnl-2015-309690
  5. Celiac.com 10/11/2016 - Celiac disease is an autoimmune disease in genetically susceptible individuals and is triggered by adverse immune reactions to gluten, a protein found in wheat and other grains. Researchers led by a research group at Finland's University of Tampere, led by Keijo Viiri, PhD, recently discovered a mechanism that triggers aberrant features in celiac disease and colorectal cancer. Disturbances in this mechanism seem to trigger certain symptoms celiac disease, and possibly in colorectal cancer. The research team's recent study offers new details on the pathogenesis of the differentiation defect of the epithelium in the small intestine in celiac disease. When people with celiac disease eat gluten, they suffer intestinal mucosal damage with villus atrophy and crypt hyperplasia. At the cellular level, epithelial cells are less differentiated and hyper-proliferative leading to the malabsorption of nutrients. Researchers discovered that a certain epigenetic mechanism, called Polycomb, governs the homeostasis between the intestinal stem cells in the crypt and the differentiated epithelium in the villi. Polycomb acts by silencing genes epigenetically by methylating histone proteins that are packing the DNA. "Polycomb is well-known for its function to regulate embryonal development. We discovered that Polycomb is also able to regulate the homeostasis of the small intestine in adults. The regulation of intestinal homeostasis is a tremendous task as the epithelium of the intestine needs to be replenished completely every 4-5 days," says Academy of Finland Postdoctoral Researcher and Principal Investigator Keijo Viiri. This study demonstrates that in people with celiac disease, dietary gluten triggers excessive activity of Polycomb leading to the aberrant silencing of genes necessary for the differentiation of villus epithelium and to the concomitant differentiation defect in celiac disease. Moreover, the study demonstrates that Polycomb target genes are also dysregulated in colorectal cancer, which suggests that aberrant Polycomb activity is common in intestinal diseases entailing a differentiation defect on the intestinal epithelium. From a clinical point of view, this work provides new insight into the pathogenesis of the intestinal damage in celiac disease and provides diagnostic markers for the disease. Since Polycomb regulates only genes imperative for development, this work is also instrumental to further understand the biology of the intestinal homeostasis. Source: ScienceDaily via Suomen Akatemia (Academy of Finland)
  6. Great Smokies Diagnostic Laboratory (GSDL), a private, rapid-growth Functional Medicine Clinical laboratory, announced today receipt of 510(K) market clearance from the Food and Drug Administration (FDA) for its Intestinal Permeability test kit, utilizing the lactulose-mannitol challenge drink. Used in the non-invasive assessment of intestinal permeability, the test demonstrated its superior sensitivity as compared to the existing d-xylose test in measuring intestinal permeability, a measurement used in the diagnosis of gastrointestinal malabsorption syndromes, such as celiac disease, colitis, Crohns disease, and Irritable Bowel Syndrome. What is intestinal permeability? Intestinal permeability refers to impairment of the intestinal mucosal barrier, which is central to healthy absorption of nutrients and protection against bacterial and toxin translocation from the gastrointestinal (GI) tract to the blood stream. Disturbances in mucosal barrier function can lead to malnourishment and increased permeability (leaky gut) which can cause or contribute to disease conditions throughout the body as diverse as asthma, arthritis, and food allergies. What are gastrointestinal malabsorption syndromes? Although the Centers for Disease Control (celiac disease) has not gathered statistics specifically for malabsorption itself, tens of millions of Americans suffer from related gut mucosal integrity conditions responsible for enormous healthcare expense. Arthritis, for example, strikes over 43 million annually at a cost of more than $65 million (celiac disease), while functional gastrointestinal disorders are responsible for an estimated 2.5 to 3.5 million visits to doctors every year and some $40 million in medication expenditures (University of North Carolina Functional Gastrointestinal Disorders Center). The incidence of these health disorders and other intestinal permeability related- conditions continues to grow at an alarming rate. The growing use of non-steroidal anti-inflammatory drugs (NSAIDS), which can irritate the mucosal lining, has contributed significantly to an increase intestinal permeability worldwide. Intestinal Permeability Assessment can be used to monitor treatment of NSAID-related damage to the mucosal barrier and intestinal permeability-related to other irritants in the GI tract. An estimated 20% or more of patients taking NSAIDS develop systematic or endoscopic gastrointestinal toxicity with incidence increasing among the elderly, who account for 40-60% of NSAID users (Canadian Medical Association Journal 1996; 155: 77-88). Inflammatory and detoxification disorders, impaired healing following surgery, failure to thrive, and complications from radiation and chemotherapy for cancer have all been linked to intestinal permeability. Recent research has consistently underscored the value of Intestinal Permeability Assessment in GI disorders such as Crohns and Irritable Bowel Syndrome, as well as traumatic care, geriatric interventions, adjunctive AIDS therapy, and pediatric care, especially in the treatment of allergies and immune disorders. GSDL is the first commercial laboratory to offer Intestinal permeability testing. Utilizing state-of-the art technology, GSDL has developed a comprehensive range of functional assessments in the areas of gastroenterology, endocrinology, cardiology, nutrition/metabolism, and immunology. The laboratory conducts aggressive, ongoing research and development for innovative functional assessments.
  7. Celiac.com 10/09/2013 - This article originally appeared in the Spring 2013 issue of Journal of Gluten Sensitivity. Ron: Where do celiac disease and non celiac gluten sensitivity come from? Dr. Fine: We're talking about the dietary staple of Western Civilization, right? This is not the staple of the Asian diet or the African diet or the diet for the Americas. Not even all European populations have been eating it as long as those earliest farmers in the Middle East. We have altered the wheat so much, through hybridization and seed selection, to have more gluten and to be more favorable for farming practices, that we have to look at what gluten is ...... a highly antigenic food. It always has been. The coeliac affection was first described in 100 AD. So if we've been eating wheat, or grains, for 10, 000 years, then 8,000 years into this, gluten induced disease was written about, it was probably present long before that. The bottom line is that this is a 10,000 year old food with a 2000 year old description, so this is not a new syndrome. What could be new is that because we have hospitals and tests the resulting diseases can now be identified earlier. Before you had to be near death before anyone knew there was anything wrong with you. But we are certainly able to identify celiac disease before you are dying from it. I really think we are seeing more of an epidemic of non-celiac GS because, I believe, our immune systems are much more reactive than ever before. All autoimmune and immune diseases are on the rise. That's a fact from the NIH. The NIH has even acknowledged that there is probably an environmental component to that increase, and I agree with them. The wheat we grow now is more immune stimulating. The way I see wheat today is that it has become the poison ivy of the western diet. Poison Ivy is a plant that is highly immune stimulating but not everyone reacts to it. Not everyone gets a rash. Even if some do not react, for instance, if they rub poison ivy on their skin, you could probably biopsy the skin and see that it was stimulating an immune reaction but there may never be a rash and the person may never itch. That would be an asymptomatic immune reaction. Then, there are symptomatic people. And then, there are people who truly don't react. It is similar with eating grains. This is the food that brought us to where we are and without grains we couldn't have gotten civilization, we couldn't store food, and we couldn't have gotten all the other things that helped us become civilized. But it went awry. If you look at the Old Testament (The Torah), it says we should never mix two seeds of grain in the same field. I look at this as a warning to keep the seeds away from each other so they don't hybridize. Because when they hybridize, they also change their genetics. Wheat does not stay the same. If you cross this wheat with that wheat, instead of being haploid it becomes tetraploid and hexaploid, so modern wheat is hexaploid. Ancient wheat was haploid, with two chromosomes. So now, we've got to look at this like a public food issue. If the same food that gave us civilization is now causing disease, it's either something we've done or something that's been there all along, plus something we've done to the wheat. And, our environment is stimulating our immune systems so much now that we are reacting more to wheat. In other words, to try to say something like we've got to do something to be able to eat wheat is almost like saying 'we've got to do something so when we walk through a patch of poison ivy, we won't react.' I just don't think it makes sense to say let's find a way to eat a substance that we know is causing mental and brain problems, obesity, immune problems, gut problems, etc. They're really just empty calories anyway. There's no vital nutrients in grains. I think it's valid to ask, why are we so addicted to, or in love with, grains? Why can't we just go on from here without them? Why can't we move forward instead of trying to do everything to figure out how to stay in this current food paradigm? Ron: Maybe that is part of why the gluten free diet has become so popular lately. Dr. Fine: An interesting phenomenon we have seen is that since gluten free food and the whole gluten sensitive thing has become popular talk show material, it has been a little bit de-medicalized. That can actually pose some problems because more people are seeing it as a diet like the fifteen other diets they heard about last week. Instead of "I've got a serious problem and I need an answer, and how do I find out what's wrong with me?" That used to be what it was. People have forgotten that this is a serious medical issue. This isn't just a diet de jour. It is a diet that should be followed consistently and strictly. So maybe we should be trying to communicate where we are in this revolution. The popularizing of the gluten free diet may be harmful to some people because they will think that they have tried the diet and gotten little benefit from it, when really, they have just dabbled in the diet and have not really given it a chance to help. They may never learn that gluten really is causing their health problems because they will think that they have tried it and it didn't work for them. And they are less likely to seek objective tests for gluten sensitivity and other possible causes of their problems. It has been a kind of a mixed blessing that the gluten free diet has become so popular. At least we don't have to fight to get the truth out, but what I don't like is the idea that what used to be a highly objective, credible, medical issue ie: celiac disease and non-celiac gluten sensitivity is kind of becoming like the Atkin's diet. You know, "I'm on it. I'm off it. I'm going to go on it next week. Oh, I'm going to a birthday party so I'm going to have some cake, etc." That approach, we all know, is the absolute wrong thing to do. And I think that the people who were almost crippled by gluten, and then got better, are probably upset when somebody looks at the gluten free diet like it's the diet of the week. Ron: I know that you operate a testing laboratory but you also organize academic conferences. Dr. Fine: Yes, I've got two organizations. One is a purely educational, non-profit public organization, called the Intestinal Health Institute. My lecturing, for about 12 years now, is aimed at trying to bring about greater awareness of the health problems caused by gluten and other foods, plus intestinal and overall health. Several years ago when talking about gluten sensitivity, it was almost like getting people to see that the emperor didn't have clothes on. That has improved lately, because public and medical beliefs are changing. As a gastroenterologist in the 1980s, I saw a similar revolution in thinking take place. Somebody came out and said "Ulcer disease is not purely from too much acid. It is a disease caused by this bacterium called Helicobacter pylori." That was unbelievable within the existing paradigm. It started out with people saying: "Did you read that paper? It is absurd!" Then more information came out. Then it became controversial. When an idea becomes controversial, it is threatening something. Someone on one side is trying to protect what is, and someone on the other side has a new idea that may displace the side being protected. What I saw was a process where that idea went from being laughable, to possible. Then, fifteen years later, it became the most popular topic in gastroenterology. It went from 1985 to 2000 when Helicobacter pylori had become "the" topic. And, by the way, research goes pop too. Once a topic begins to be accepted, researchers dive in. I saw that happen at the end of the 1990's too. People with microscopic colitis, which my mentor Dr. John Fordtran had originally discovered and defined, and I researched clinically, pathologically and histopathologically. I found it to be very similar, and epidemiologically, almost identical to celiac disease. But these patients didn't have celiac disease nor did they have the markers of gliadin reactivity in their serum. Then I had this idea one day that maybe the antibodies are inside the intestine because I had heard about a researcher, Anne Ferguson, who had done some very interesting work where they had either sampled the fluid inside the intestine or flushed all the intestinal fluid out and measured antibodies, even though they weren't present in the blood. To me that made perfect sense because that's where your food is and if your immune system is ever going to secrete antibodies, as a first line of defense, it had better get those antibodies inside the intestine because that's where the bacteria are going to be invading. You can't use serum antibody testing when we know that the intestine is, indeed, the site where the problem originates. Dr. Anne Ferguson is the one who found that you can find intra-intestinal antibodies when they weren't present in the blood, so blood is an indirect measure of the presence of celiac disease. Those antibodies mainly get in blood when you have intestinal damage but if you don't, they cannot leak into the blood, it seems. It's apples and oranges. A blood test and a stool test are not the same test. IgA is a secretory antibody. It is made to be secreted into the intestinal tract, the respiratory tract, and anywhere there is a mucosa that interfaces with the world or food or a foreign antigen. That's where you see seceretory IgA and that is what we looked for. When we had the idea and played it out - and let me just say now that other people who have tried to study this, who have usually been studying it with the hypothesis that it is no good, and of course, whatever your bias in research is, you are usually going to wind up finding evidence to support that bias. Nevertheless, when we first did it, we adapted a serum method for stools, and we didn't find it either. You have to go a few steps further. But if you give up on your first try, you always miss it, and so did I. And those with a bias against it will never look any further. Anyway, so we developed a method and it was much more sensitive than finding serum positivity for anti-gliadin antibodies. You've got anti-gliadin antibodies in illnesses other than celiac disease, like irritable bowel syndrome, autoimmune diseases like microscopic colitis, chronic fatigue, and so on. So we were looking at numbers like 60% and 75% positive Vs 11% in the blood. We also found fecal gliadin antibodies in 25% of people with no symptoms at all. Still, 75% is a lot higher than 25%. So I knew that I had discovered a new paradigm. And I saw (by the way, that 25%.... at first it was 29% but it eventually averaged out to 25%) a quarter of asymptomatic people reacted positive with stool antibodies. But if you take everybody, because so many people have other diseases, like 15% of the population have irritable bowel syndrome, and nearly 15% have autoimmune disease....... when you add it all up it could be about 50% of people who are reactive to gliadin, as determined by looking for antibodies inside their intestines. Ron: How did you get started on your own? Dr. Fine: I made the transition in 2000, so our anniversary is April 1st, 2000. This is our 13th year. If you've hung around 13 years, I think, that also makes a statement. EnteroLab.com was born because I knew that what I had discovered was, well, what we're really talking about is an epidemic. At that time, I didn't know anything about the "why" or even the "what". I just knew it was a massive problem I had discovered. Maybe I could call myself the Paul Revere of gluten sensitivity. I had to be the one to get on the horse and say "gluten sensitivity is coming". I converted my academic career, which was stellar at the time.... it was very traditional.... 40 publications by the time I was 35 and I worked with what would arguably be one of the most successful researchers in the world, Dr. John Fordtran. And I went out on a limb and put my entire professional reputation and career in jeopardy because I knew this had to be brought to the world. I knew there would be a controversy. The idea, which had been in the medical literature for years..... non-celiac gluten sensitivity can be traced back to at least 1980, so we were already 20 years into that. And I thought if I bring the idea directly to the public, then, because it's a dietary treatment, they can proceed in getting better while we wait 15 to 20 years for the doctors to catch on. What I didn't know at the time is that there's a whole subset of practitioners, like chiropractors, nutritionists, and nurse practitioners, who don't seem to feel so threatened by some major new idea. They caught on quickly. They're the early adopters. Ron: You have traveled a long way since 2000 Dr. Fine: Here's the way I'm looking at what's going on now versus where we started. My observation is that every new idea, every revolutionary finding, seems to happen in two places on opposite sides of the globe. Having happened in Christchurch, New Zealand and in Dallas, Texas would qualify for that. I think Dr. Rodney Ford and I got on the track at about the same time. What I had previously been finding and, I think, what he has found was that these positive anti-gliadin antibodies in the serum, which everyone was casting off as false positives, didn't make sense. How could a quality lab test have a 10% or 12% false positive rate? That's like saying that we can't diagnose anemia without including 10% or more people who don't have it. That would be a bad test. So it didn't seem true that if anti-gliadin antibodies were part of the reaction of celiac disease, why would 10% to 12% of the population have anti-gliadin antibodies in their blood? Well, that's because they are reacting to gliadin. It is the most immunogenic food. They don't have celiac disease, either because they don't have the genes to get it, or they haven't got it yet. Fecal gliadin antibodies were this kind of intermediate thing. Ron: Are you saying that the fecal antibody does not identify a leaky gut, whereas the serum antibody does? Dr. Fine: No, it might imply that, but I wouldn't say that it says that. In fact, in a study that I did, where I looked at serum antibodies, we did permeability studies and fecal fat measurements and biopsies, and some treatment. We found abnormal permeability, as measured by a surcrose permeability test, performed by the authority on that test at the time, Dr. Jon Meddings. He found about half of those with leaky gut had the serum antibodies, not all. Ron: Is there more mainstream research that supports your findings? Dr. Fine: Well, I found a rate of about 11% serum IgG or IgA among people at a shopping center in Dallas. Dr. Marios Hadjivassiliou found IgG antibodies in about 12% of the population, and Dr. Rodney Ford tells me that he has found a rate of about 10% who are gluten sensitive. These are all congruent findings. Fecal Antibodies at 25% of asymptomatic and 60 to 75% of symptomatic people, depending on what disease or symptom you're talking about and then, because those problems are so common, the overall average, from my calculations is 50% overall...... mostly adults. Theoretically, it might be less frequent in children, but I don't have enough children's data to know. Ron: Is your testing similar to Dr. Marsh's rectal challenge testing for celiac disease? Dr. Fine: Yes. I identify one of his references in my manuscript where even siblings without DQ2 or DQ8 can be positive for a rectal challenge, even though they don't have celiac genes or get celiac disease. That's another proof that you don't have to be celiac to be gluten reactive. He did studies on that, a sibling study which was really interesting. What is your vision for future testing & treatment of celiac disease and non celiac gluten sensitivity? Dr. Fine: My lab and myself are just about finding the facts and then helping people to understand those facts. Frankly, to use a metaphor, your vision is only as good as your eyes and your glasses. If your eyes aren't good, good glasses can make your vision perfect. But if you are using the wrong glasses, ie: the wrong test, or the wrong paradigm, then you might be seeing farther than you used to see, but you are not really seeing the truth yet. Ron: Would you care to comment on the whole oats controversy? Dr. Fine: I've got a feel on oats that is a departure from the general view. We have a new test for oat protein sensitivity and it is really showing to be very helpful. We launched a more extensive food sensitivity test panel, 2 years ago, and oats is one of the antigens we included, along with rice and corn and a few meats and nuts and potatoes. What we are seeing sometimes, is people who don't have a reaction to any foods and their oats are through the roof and they are gluten sensitive. I don't know why. Just like it was all or none with celiac.... you could have something in the middle, right? Oats is the same way. It's not all or nothing. Some people are sensitive, and some people are not. We know it's the least stimulating of the four grains. That makes sense because of the biochemistry of the prolamine and glutamine residues, and a lot of antigenic glutens. However, logically, you cannot do a study of tolerating oats in anyone who doesn't tolerate oats. So anyone doing a study where the subject has to consume oats for long periods of time, that could never include someone who is sensitive to oats. The truth about studies that make this claim is that there is a very large withdrawal rate and a large component that can't qualify for the study because it made them vomit or sick in other ways. So the only thing you can conclude is that among the people who can symptomatically tolerate oats, over long periods of time, oats don't seem to cause the villous atrophy of celiac disease, which isn't the best measure anyway, to my thinking. But that does not mean that anybody with celiac disease can tolerate oats and that seems to be the message that has come down to us. We're talking about wheat, barley, and rye, and, we used to think, oats. Now we are saying oats are okay and that is just plain wrong. In fact my own gluten sensitivity became known after increasing my consumption of oats. And if you ever go into a room of gluten sensitive people and give a talk, just ask them "How many people here know that they can't eat oats?" They either get pain, gas, vomiting, or whatever. It's about 20% to 30% who will always raise their hands. To use an analogy, if people had a fear of round light fixtures, and there happened to be big, large round light fixture on the ceiling, how many people could I expect in this room right now to not be afraid of big round light fixtures? None! Those who are afraid of round light fixtures wouldn't come in the room. So nobody who can't eat oats or is afraid to eat oats is going to volunteer or succeed at staying in a study where they have to eat oats for 2 to 5 years. The only people who are going to stay in that study are the ones who want to find out they can eat oats. The researchers certainly have some reason to want to find out they can eat them. So that bias is automatically built into those studies, so the fact is that it has not been proven and people are being misled and frankly, in my opinion, everybody should wait until they get over their symptoms and then maybe do our test or try re-introducing oats. A person who doesn't eat gluten-free cannot know what an insider knows. And, they have a different agenda. They're clearly exclusively a professional. It's kind of like somebody making policy on health food who eats a horribly unhealthy diet. So I see these jaws drop in my lectures when people find out that you can't just automatically assume that you can tolerate oats. You might be able to, but you might not, and there's no way someone can Ron: Will your oats test work after years on a gluten-free diet? Dr. Fine: I don't know. That's a good question. The good thing about the stool test is that the antibodies last a lot longer. You can be gluten-free for one or two years and still we can find antibodies to the wheat gliadin in the stool. I guess that it would be the same for oats. I definitely abhor the idea of a gluten challenge for celiac disease.... especially the biopsy. I mean, the biopsy may not become abnormal for 5 years and they could still be sick. Ron: You mentioned that you follow a gluten-free diet. Can you tell me why? Dr. Fine: I've had spondyloarthropathy since I was about 14. I manage it without drugs and I have no pain. I control it just with diet. Ron: Does your lab do genetic testing? Dr. Fine: Yes, and the gene test that EnteroLab.com offers actually types the gene at the HLA locus, which means our reports indicate "this is the gene you have at the HLA-DQB1 locus".; we don't just say "yes you have the celiac gene", or "no you don't". There is data in the literature, including research I have published that identifies HLA-DQB1*0301, 0303, which are the DQ7 and DQ9 genes, respectively, and DQ1, and we know from Dr. Hadjivassiliou's research that DQ1 (including 05xx and 06xx subtypes) reacts with gluten and represent gluten sensitive genes. Of course, DQ2 and DQ8 are the main celiac HLA-DQB1 genes. The interesting thing is that, in America, it's very rare not to have one of these. Almost everybody does, actually. It just comes down to how many do you have? Which one/ones do you have? Do you have one that seems to be a more reactive one or a less reactive one? And, do you have a celiac gene or two celiac genes? Which is going to mean, if you have two celiac genes or two gluten-sensitive genes, or a celiac gene and a gluten-sensitive gene that every child you have will have at least one of them. So, we prefer our gene test over that of others that merely answers the question “ Do I or do I not have a celiac gene.” Not only is it inexpensive, at about half the price of the other lab that does it, we give you more data. I was doing genetic studies in the 90s, to figure all this information out. For instance, I met Dr. Hadjivassiliou at the International Conference on Celiac Disease at the University of Maryland in August of 2000. Dr. Fasano hosted it. I spoke before Dr. Hadjivassiliou and I showed this association with DQ1,7, or I called it 1,3 with 7 being a subtype primarily but also 9, and so he came to me and said "Well, I've seen associations with my neurologic disease with DQ1, so I'm glad someone else is finding this." So, again, it's not just the antibodies, and it's not just non-celiac gluten sensitive genes, and as far as I know, no other lab is dealing with that except us. The abnormal permeability, in my opinion, is an effect of the immune arrays going on and the primary reaction is the immune response to gluten. You could possibly say that you get altered permeability first and then you get the gluten reaction, but I don't think so. I used to study permeability in humans in vivo. You can look at my CV or go to PubMed.com and put Fine KD and you'll see some early studies about permeability where we used to measure permeability in live human subjects and it was just a given, to me, that abnormal permeability in inflammatory disorders is primarily due to the inflammation and the disruption of tissue, architecture, and the like. I think that the permeability follows the inflammation. Ron: I have dermatitis herpetiformis (DH) and I find that my skin reacts more to oats than other grains. If I eat something that is labeled “gluten-free” but contains oats, I soon find that my DH flares up. I know others with celiac disease and DH who say the same thing. I mention this oats connection in the hope that you might someday do some research to explore that connection. Dr. Fine: We are just about to launch our oat sensitivity fecal IgA test as part of a gluten sensitivity panel because it is playing a little bit different role than testing for other non-gluten foods. It's like when a sophomore seems to be stellar on a football team, they pull him up to the varsity team. So we're pulling the oat test out of the sophomore squad and putting it on the varsity because it was showing up a lot more often and I think it's in the same paradigm as the wheat gliadin separate from other foods. Even though we like to look at it as "other grains". We are seeing a lot of rice sensitivity, some corn sensitivity. Many seem to react to other grains, as I do personally. The news is that we'd like to use April 1st, 2013 as the launch date for our new gluten sensitivity panel because it is an anniversary date for us. We hope to have that new panel available about April 1st, along with a tTG test, and an anti- gliadin fecal IgA test, and maybe even another test for another dietary food antigen, which is an ASCA (anti-Saccharomyces cerevisiae antibodies). It's been associated with Crohn's disease. It's like the diagnostic screening blood test for Crohn's, but more sensitive. We and some other people have looked at it in the stool, so that's just another test that we might put in the panel to make it affordable to get all 4. Ron: Thank you for taking the time to provide our readers with such a comprehensive discussion of your work and the exciting new tests that will soon be available at your lab. Dr. Fine: You are very welcome. It was nice chatting with you. And thank you for the pioneering work that you have done as well!
  8. Celiac.com 04/19/2012 - A team of researchers examined the effect of corn, rice and amaranth gluten-free sourdoughs on the release of nitric oxide (NO) and synthesis of pro-inflammatory cytokines by duodenal mucosa biopsies of eight celiac disease patients. The research team included Maria Calasso, Olimpia Vincentini, Francesco Valitutti, Cristina Felli, Marco Gobbetti and Raffaella Di Cagno. The team used select lactic acid bacteria as starters for making corn, rice and amaranth sourdoughs. From these gluten-free sourdough matrices, they made chemically acidified doughs, without bacterial starters, and doughs started with baker’s yeast alone. They produced pepsin-trypsin (PT) digests from all sourdoughs and doughs, and used the results to the measure the recovery of biopsy specimens from eight celiac disease patients at diagnosis. They also measured the release of NO and the synthesis of pro-inflammatory cytokines interferon-γ (IFN-γ). They found that lactic acid bacteria acidified and grew well (ca. log 9.0 CFU/g) during fermentation, showing strong proteolysis on all gluten-free samples. They also found that duodenal biopsy specimens still released NO and IFN-γ when subjected to treatments with basal medium (control), PT-digest from chemically acidified doughs and PT-digest from doughs fermented with baker’s yeast alone. In fact, in every case, biopsy specimens treated with PT-digests from all gluten-free matrices with sourdough fermentation substantially reduced NO release and IFN-γ synthesis. From their results, the team concludes that sourdough fermentation might offer an easy and effective way to speed recovery from intestinal inflammation of celiac patients beginning a gluten-free diet. Source: EUROPEAN JOURNAL OF NUTRITION. DOI: 10.1007/s00394-012-0303-y
  9. Celiac.com 02/18/2013 - Currently, there are two main diagnostic tools available to would-be celiacs: biopsy and serological (antibody) tests. For the past few decades, biopsy has been the only relatively reliable (and diagnostically accepted) path to diagnosis. The problem is, biopsies are expensive and highly invasive – antibody tests would be a cheap and painless alternative, but they haven't proven themselves to be accurate enough for conclusive diagnosis. However, a recent analysis shows that antibody tests have improved a great deal in recent years and when used to test for multiple antibodies concurrently, they can be almost as effective as biopsies for diagnosing celiac disease. The study's facilitators began their restrospective analysis by collecting serum samples from 268 patients at hospitals throughout Switzerland, Germany and Austria. All included patients suffered from celiac-like symptoms and underwent both biopsy and antibody testing within 2 months of serum collection. All included patients were on gluten-containing diets at the time of testing. 149 of the patients were ultimately diagnosed with celiac disease; the other 119 showed normal intestinal mucosa and were considered celiac-free. These patients were the control group. Usually, potential celiac patients are tested for IgA anti- tTG or EMA. If the test is positive, then diagnosis is then confirmed with biopsy. However, there is still a chance that the test will throw a false positive, meaning many people are put through unnecessary biopsies. The goal of the present study was to develop a method for reducing the number of these unnecessary biopsies. It was found that when two antibody tests are used, the reliability of the tests increased substantially, weeding out a great many false positives, as well as picking up some false negatives. When three tests were used, the numbers became even more accurate – when used concurrently and all three show a positive result, the IgA anti-dpgli, igG anti-dpgli and IgA anti-tTG achieved an 87% positive likelihood and .01% negative likelihood (compared to a positive likelihood of only 7% and negative likelihood of 0.04% with just the IgA anti-tTG). Using these three tests together, only one test subject came through as a false positive, and only two came through as false negatives (compared to 16 false positives and 5 false negatives with the IgA anti-tTG only). 60 came through with discordant results (meaning at least one of the tests came back negative – in these cases, biopsy is necessary). When considering that biopsy really only has a real-world diagnostic accuracy rate of about 90%, the three test combination utilized in this study achieves strong enough numbers that biopsies are starting to look unnecessary. Biopsy still might be the surest way of detecting celiac disease, but this study shows that it is not necessary in all cases, and patients seeking celiac diagnosis have a few more tests they can ask their doctors for. Source: http://www.biomedcentral.com/1471-230X/13/19
  10. Journal of Clinical Gastroenterology 2003; 36(3):219-221 Celiac.com 03/28/2003 - A study by Antonio Tursi, M.D, et al, was recently conducted to evaluate the correlation between the degree of histologic intestinal damage in celiac patients and their level of positivity (serum value) to anti-tissue transglutaminase antibodies (anti-tTG). The study looked at 119 adult celiac patients who were diagnosed consecutively (47 men and 72 women; mean age, 28 years; range, 22-51 years), and were stratified for histologic damage according to Marsh classification. The final step was to compare their Marsh histologic intestinal damage classification with their anti-tTG serum values. Here are their results: Marsh I lesions were present in 13 patients (10.92%), Marsh II in 24 anti-tTG (20.16%), Marsh IIIa in 27 anti-tTG (22.68%), Marsh IIIb in 31 anti-tTG (26.05%) and Marsh IIIc in 24 anti-tTG (20.16%). Anti-tTG positivity was ranging from 1 of 13 anti-tTG (7.69%) in Marsh I lesions to 23 of 24 anti-tTG (95.83%) in Marsh IIIc lesions respectively (P The researchers conclude that the mean serum value in celiacs with severe enteropathy (Marsh IIIb-c lesions) was higher than in those with only slight enteropathy (Marsh I-IIIa). Further, serologic test results in the absence of histologic evaluation (biopsy) may "underestimate the real prevalence of celiac disease," thus delaying a proper diagnosis and putting patients at risk for a large variety of serious health problems.
  11. Celiac.com 05/13/2013 - Intestinal absorption capacity is currently regarded as the best way to assess overall digestive intestinal function. Earlier reference values for intestinal function in healthy Dutch adults were based on a study that was conducted in an inpatient metabolic unit setting in a relatively small series. A team of researchers recently used bomb calorimetry to measure normative values of intestinal absorption in healthy ambulant adults. The research team included N. J. Wierdsma, J. H. C. Peters, M. A. E. van Bokhorst-de van der Schueren, C. J. J. Mulder, I. Metgod & A. A. van Bodegraven They are variously affiliated with the Department of Nutrition and Dietetics, the Department of Gastroenterology, Small Bowel Unit, and the Department of Clinical Chemical Laboratory at VU University Medical Centre in Amsterdam, and the Department of Gastroenterology and Hepatology of Red Cross Hospital in Beverwijk, The Netherlands. The present study aimed to readdress and describe the intestinal absorption capacity of healthy adults, who were consuming their usual (Western European) food and beverage diet, in a standard ambulatory setting. The researchers evaluated twenty-three healthy subjects, ranging form 22–60 years old, using a 4-day nutritional diary to determine levels of nutritional intake (energy and macronutrients). They then collected fecal samples over three days to measure mean fecal losses of energy (by bomb calorimetry), fat, protein and carbohydrate. Finally, they calculated intestinal absorption capacity by determining the differences between intake and losses. They found that average (SD) daily feces production was 141 grams, of which, 49 grams (29%) was dry weight, Overall, the samples contained 891 (276) kJ [10.7 (1.3) kJ g1 wet feces; 22.6 (2.5) kJ g1 dry feces], 5.2 (2.2) g fat, 10.0 (3.8) g protein and 29.7 (11.7) g carbohydrates. Mean (SD) intestinal absorption capacity of healthy subjects was 89.4% (3.8%) for energy, 92.5% (3.7%) for fat, 86.9% (6.4%) for protein and 87.3% (6.6%) for carbohydrates. They found that average intestinal energy absorption was approximately 90%. These data serve as normative values for both stool nutrient composition and intestinal energy and macronutrient absorption in healthy adults on a regular Dutch diet in an ambulatory setting. Source: J Hum Nutr Diet. doi:10.1111/jhn.12113
  12. Celiac.com 12/12/2012 - In duodenal biopsy samples from people with active celiac disease, the transferrin receptor, CD71, is up-regulated, and promotes retro-transport of secretory immunoglobulin A (SIgA)-gliadin complexes. To better understand how interactions between SIgA and CD71 promote transepithelial transport of gliadin peptides, a team of researchers set out to determine if interactions among secretory immunoglobulin A, CD71, and transglutaminase-2 affect permeability of intestinal epithelial cells to gliadin peptides. The research team included C. Lebreton, S. Ménard, J. Abed, I.C. Moura, R. Coppo, C. Dugave, R.C. Monteiro, A. Fricot, M.G. Traore, M. Griffin, C. Cellier, G. Malamut, N. Cerf-Bensussan, and M. Heyman. They are affiliated with the Mixed Research Unit 989 of the National Institute of Health and Medical Research (INSERM UMR989) in Paris, France. For their study, the team evaluated duodenal biopsy specimens from 8 adults and 1 child with active celiac disease. The team used fluorescence-labeled small interfering RNAs against CD71 to transfect Caco-2 and HT29-19A epithelial cell lines. They used flow cytometry, immunoprecipitation, and confocal microscopy to assess interactions among IgA, CD71, and transglutaminase 2 (Tgase2). They then assessed transcytosis of SIgA-CD71 complexes and intestinal permeability to the gliadin 3H-p31-49 peptide in polarized monolayers of Caco-2 cells. To assess physical interplay between SIgA and CD71 or CD71 and Tgase2 at the apical surface of enterocytes in biopsy samples and monolayers of Caco-2 cells, the team used fluorescence resonance energy transfer and in situ proximity ligation assays. They co-precipitated CD71 and Tgase2 with SIgA, bound to the surface of Caco-2 cells. They found that SIgA-CD71 complexes were internalized and localized in early endosomes and recycling compartments, but not in lysosomes. In the presence of celiac IgA or SIgA against p31-49, transport of intact 3H-p31-49 increased significantly across Caco-2 monolayers, while soluble CD71 or Tgase2 inhibitors interfered with transport. Once it binds to apical CD71, SIgA (with or without gliadin peptides) enters a recycling pathway and avoids lysosomal degradation; this process allows apical-basal transcytosis of bound peptides. This mechanism is assisted by Tgase2 and might be involved in the pathogenesis of celiac disease. Source: Gastroenterology. 2012 Sep;143(3):698-707.e1-4. doi: 10.1053/j.gastro.2012.05.051.
  13. Celiac.com 05/30/2012 - From what we understand about celiac disease, both genetic and environmental factors play a part in its development: eople with certain genetic dispositions are more likely to develop it, but studies of twins at high risk of developing celiac disease have shown that in 25% of cases, only one of the twins will develop the disease. This indicates an environmental effect, and with more research it might be possible to discover what these environmental factors are so that parents with celiac disease can take steps to prevent their children from developing the disease themselves. Breast-feeding has already demonstrated some protective effect on infants at risk of developing celiac disease, but it is still unclear how the modulation of intestinal bacteria affects the formation of the disease. Understanding the role various strains of intestinal bacteria play in the intestine could be the key to understanding why breast-feeding helps prevent celiac disease, and perhaps why celiac disease develops at all. In the present study, 75 newborns with at least one first degree relative with celiac disease were broken into breast-feeding, formula-feeding groups, high (7-28%) and low (less than 1%) genetic risk groups, then tested at 7 days, 1 month and 4 months for prevalence and diversity of intestinal bacteria. Infants at high risk of developing celiac disease had more Bacteroides vulgatus, regardless of feeding methods while infants at low risk of developing celiac disease had more Bacteroides ovatus, Bacteroides plebeius and Bacteroides uniformis. Formula-fed infants had more Bacteroides intestinalis, Bacteroides caccae and Bacteroides plebeius, though prevalence depended on the testing stage. The most striking finding of the experiment seems to indicate that both low genetic risk of celiac disease development and breast-feeding are positively correlated with the prevalence of Bacteroides uniformis in the intestines. This might explain why breast-feeding can help protect against development of the disease, by introducing more Bacteroides uniformis into the infant's intestinal bacteria community. The implications of this research are still unclear, but a follow-up study on these infants is intended. Further research may explain how the prevalence of these bacteria in the intestine actually affects the development of celiac disease in infants. Source: http://www.ncbi.nlm.nih.gov/pubmed/21642397
  14. Celiac.com 05/23/2012 - We know from past studies that the intestinal bacteria communities of children with celiac disease differ greatly from those of healthy children, but there has been little work done to draw such a correlation with adult celiac disease sufferers. Intestinal bacteria could potentially serve as a convenient way of indexing the severity of a patient's celiac disease, but research in adults is limited. A recent study remedies this, showing that adults with celiac disease do, in fact, have different intestinal bacteria from healthy adults, which may lead to a way of testing for the severity of one's disorder based on fecal bacteria tests. Ten untreated celiac disease patients, eleven treated celiac disease patients (those on gluten-free diets for at least two years) and eleven healthy adults were tested for intestinal bacteria in fecal samples. The healthy adults were tested once under normal gluten diet conditions, and additionally, ten of them were tested again after one week of gluten-free dieting. Testing showed that untreated celiac disease patients had much more Bifidobacterium bifidum in their intestinal microbial communities than those of healthy adults. Treated celiac disease patients showed decreased levels of Bifidobacterium bifidum, as well as a reduction in the diversity of Lactobacillus and Bifidobacterium. These results most closely resembled those achieved by healthy adults. It would seem, then, that a gluten-free diet helps to balance and normalize intestinal bacteria populations. While a portion of the treated celiac disease patients displayed restored, normal intestinal bacteria, there were still differences in the presence of short-chain fatty acids. Such SCFAs would appear to correlate with celiac disease, regardless of the diet taken: healthy adults, both on gluten-free diets and on normal diets had significantly fewer SCFAs than both treated and untreated celiac disease patients. Gluten-free, healthy adults had the fewest, but treated celiac disease patients actually had the highest. We can take from this study that gluten-free diets help to lower both the presence and diversity of bacteria associated with celiac disease. A gluten-free diet does not 'fix' the presence of short-chain fatty acids in the intestines though, even though it is not entirely clear what these acids signal as to the health of the individual. Source: http://www.ncbi.nlm.nih.gov/pubmed/22542995
  15. Celiac.com 05/16/2012 - Goblet cells that line the intestine and secrete mucous are emerging as a possible target for treating inflammatory bowel disease, celiac disease and food allergies. With every meal, immune cells in the intestine stand guard against harmful bacteria but permit vitamins and nutrients to pass. The small intestine is protected from harmful pathogens by a layer of mucus secreted from goblet cells. A research team at Washington University School of Medicine in St. Louis have identified the cells that protect the intestine against food antigens, or proteins so that the immune system does not begin an attack. The discovery of goblet cells in mice shines new light on their role in the lining of the intestine, and gives scientists a potential target for treatments against inflammatory bowel disease, celiac disease and food allergies. To accomplish their task, the researchers used a new imaging technique that allows them to observe the inner workings of the intestine in a living mouse in real time. For their study, they fed marked sugar to mice and observed antigens as they were passed by goblet cells to dendritic cells. Dendritic cells play a key role in the immune system. But until now, scientists thought that intestinal goblet cells were only responsible for secreting mucus. Miller and Newberry also studied healthy human intestinal tissue from patients undergoing weight-loss surgery. Those results showed that goblet cells perform the same function in people as in mice. This indicates that the cells may be solid drug targets for treating inflammatory bowel disease and other intestinal problems. After studying normal, healthy mice, the researchers are now using the same imaging technique to look at how goblet cells and dendritic cells might function differently when inflammation or infection occurs. They also plan to study mucus-producing goblet cells in other tissues, such as the lung, to assess whether they are working the same way elsewhere in the body. Miller says the results are important because they help scientists understand that intestinal immune responses may depend as much on the ability of goblet cells to transport antigens to dendritic cells as on what the dendritic cells then do with those antigens. Source: Nature. 2012 Mar 14;483(7389):345-9. doi: 10.1038/nature10863.
  16. I have been taking probiotic supplements for a long time, but nothing has worked as well for me as Shaklee Optiflora Two-Product System with Prebiotic & Probiotic. Every since I started Shaklee's gluten-free prebiotics and probiotics I feel so much different--I feel like I have more energy. This is a high quality system that is designed to provide needed support for our digestive tracts. According to Shaklee the Optiflora Probiotic Complex uses a "patented triple layer encapsulation technology to protect live probiotics and guarantee their delivery into the intestine," which can enhance energy levels and provide excellent support for our bodies. Shaklee Optiflora Probiotic Complex contains bifidus and acidophilus, which support long-term intestinal and colon health. For those with celiac disease or other digestive issues high quality probiotics like these are a must. Shaklee Optiflora Prebiotic Complex is intended to provide a welcome environment for the friendly, beneficial bacteria that live and work in the colon. Due to the positive response my body has had to these products I plan to continue taking them long term. Visit their site for more info: http://insideout.myshaklee.com/us/en/products.php?sku=80638 Note: Articles that appearin the "Gluten-Free Product Reviews" section of this site are paid advertisements. For more information about this seeour Advertising Page.
  17. Celiac.com 10/26/2011 - In vitro and in clinical studies have shown that oxidative stress plays a role in gluten-induced toxicity, but no studies have observed this activity in living tissue. A research team set out to examine the role of nuclear factor erythroid 2-related factor2 in gliadin-mediated toxicity in human Caco-2 intestinal cells and in gliadin-sensitive human leukocyte antigen-DQ8 transgenic mice (DQ8), along with assessing the protective activity of CLA. The research team included Paolo Bergamo, Marta Gogliettino, Gianna Palmieri, Ennio Cocca, Francesco Maurano, Rosita Stefanile, Marco Balestrieri, Giuseppe Mazzarella, Chella David, and Mauro Rossi. The team had previously observed the protective role played by conjugated linoleic acid (CLA), which works by the activation of nuclear factor erythroid 2-related factor2 (Nrf2), which serves as a crucial transcription factor for the synthesis of antioxidant and detoxifying enzymes (phase 2). To assess gliadin effects in differentiated Caco-2 cells and in DQ8 mice, they fed the mice a gliadin-containing diet with or without CLA supplementation, and then combined enzymatic, immunochemical, immunohistochemical, and quantitative real-time PCR (qRT-PCR) data. In both laboratory tests, and in living tissue tests, they found gliadin toxicity accompanied by downregulation of phase 2 and elevated proteasome-acylpeptide hydrolase activity. Interestingly, in DQ8 mice intestine, gliadin did not generate severe oxidative stress extent or pathological reactions like those found in celiac patients. Moreover, the reactions that did result were mitigated by CLA. From these results, the researchers conclude that CLA offers beneficial effects against the reduction of key intestinal cytoprotective defenses. This indicates a new nutritional approach for the treatment of intestinal disease associated with altered redox homeostasis. Source: Molecular Nutrition and Food Research; Vol 55 Issue S2. DOI: 10.1002/mnfr.201100295
  18. Celiac.com 07/14/2010 - Intestinal biopsy is considered the the gold standard for celiac disease testing. However, biopsy is an invasive procedure and most people would be happy to avoid biopsy all together. Based solely on serology, a new diagnostic standard has been proposed that would no longer require intestinal biopsy for celiac disease diagnosis in some patients. Researchers performed duodenal biopsy and serology in six-hundred and seventy-nine adults who were at high risk and low risk for celiac disease. They tested blood samples to detect antibodies to tissue transglutaminase (tTG) and deamidated gliadin peptide (DGP). The goal of researchers was to establish the diagnostic performance of various serological tests for diagnosing celiac disease in patients with varying pretest results. In this study, they hope to find potential serological algorithms to decrease the requirement for biopsy. One-hundred and sixty-one consecutive adults with undiagnosed, but suspected intestinal disorders were selected as the high-risk group to be evaluated for celiac disease. Five-hundred and eighteen patients who had been referred for routine upper gastrointestinal endoscopy due to non-specific symptoms such as indigestion, were randomly selected for the low-risk group. Prevalence of celiac disease was found in 39.1% of the high-risk group, and 3.3% of the low-risk group. Of the high-risk patients, all individual assays demonstrated a high diagnostic efficacy, while the low-risk group demonstrated a lower diagnostic efficacy. The serological findings of this study demonstrated that the algorithm used for individual assays allows patients to avoid biopsy with a negative serology; and positive serology results would require a patient to undergo biopsy. The DGF/tTG Screen assay may very well be recognized as the best preliminary test for celiac disease. The combination of two tests which include a DGP/tTG screening, may have the ability to identify celiac disease correctly in various clinical situations, which would allow biopsy to be avoided in the vast majority of cases. Although the findings were significant for this study, small bowel histology is still deemed the gold standard for accurate celiac disease diagnosis. Further validation of the algorithms is necessary to confirm the findings of this study before new diagnostic guidelines can be considered. Source: World J Gastroenterol. 2010 Jul 7;16(25):3144-52.
  19. Celiac.com 12/22/2010 - A recent evaluation of the safety and efficacy of small intestinal release mesalamine (SIRM) for symptom relief in refractory celiac disease (RCD) shows that SIRM seems to be a safe and effective treatment option, though larger tests are needed to know for certain. The research team conducting the evaluation included Shailaja Jamma, MD, Daniel A. Leffler, MD, Melinda Dennis, RD, Robert M. Najarian, MD, Detlef B. Schuppan, MD, Sunil Sheth, MD, and Ciaran P. Kelly, MD, They set out to evaluate the safety and efficacy of small intestinal release mesalamine (SIRM) for symptom relief in refractory celiac disease. There are currently no adequate clinical therapies for patients with refractory celiac disease and corticosteroid and/or immunosuppressants treatments are of limited use due to side effects. SIRM has been shown to reduce local inflammation, and it is well tolerated. For the study, the team looked at records of the refractory celiac disease patients who received SIRM in an open-label therapeutic trial. Data included patient demographics, disease characteristics, dose and duration of SIRM therapy, and patient response. The team then categorized each response as complete, if symptoms resolved completely, partial if symptoms improved at least 50%, and non-responsive if symptoms improved less than 50%. The team treated four patients with SIRM alone and six patients with a combination of SIRM and oral budesonide. After four weeks, half of the patients showed complete response, while 10% showed a partial response. Two of the six patients were able to discontinue budesonide. One patient discontinued SIRM after complaining of headaches. These initial results indicate that SIRM seems to be a safe and efficacious treatment option in patients with refractory celiac disease, though a larger, more comprehensive study is needed to confirm these results. Source: J Clin Gastroenterol 2010 Sep 24. doi: 10.1097/MCG.0b013e3181f42401
  20. American Journal of Clinical Pathology, April 2000 - A New Method of Quantitative Fecal Fat Microscopy and its Correlation with Chemically Measured Fecal Fat Output, by Kenneth Fine, M.D. and Frederick Ogunji Ph.D (Celiac.com 07/09/2000) Patients with gluten sensitivity should be evaluated for nutrient malabsorption because if present, this means there is small intestinal damage and institution of a gluten-free diet is imperative to prevent osteoporosis and other nutrient deficiency syndromes. Furthermore, a test at the time of diagnosis serves as a baseline to be compared to later if needed. For more than 50 years, the primary method used to assess for the presence of small intestinal damage and nutrient malabsorption in patients with celiac disease has been a 72-hour quantitative stool collection. However, because this method requires that patients accurately collect all the stools they pass for 3 days (missed stools lead to falsely low results), the test is logistically difficult for medical centers unaccustomed to the procedure, and the voluminous specimens usually are abhorred by patients and laboratory technicians. It poses obvious problems for children who cannot or will not collect all their stools, as well as for patients with chronic diarrhea, who may have bowel movement frequencies reaching 15 or more per day and/or fecal volumes as high as 2 or 3 liters per day. For these reasons, physicians evaluating patients with suspected or proven gluten sensitivity often avoid tests for intestinal malabsorption altogether. Recently, researchers at the Intestinal Health Institute in Dallas, Texas have developed a new method for quantitating fecal fat excretion that requires collection of only a single stool specimen. Development of this method was based on the fact that as more fat is malabsorbed, the fat globules in stool become more numerous and larger. In a study published in the April 2000 issue of the American Journal of Clinical Pathology entitled A New Method of Quantitative Fecal Fat Microscopy and its Correlation with Chemically Measured Fecal Fat Output, Kenneth Fine, M.D. and Frederick Ogunji Ph.D. tested 180 patients and found a highly statistically significant linear correlation between quantitative fecal fat microscopy (the new method) and chemically measured fecal fat output (the old method). They also showed that their microscopic analysis of just one stool gives comparable results to analysis of an entire 3-day collection. These researchers have, thus, shown that a dedicated quantitative analysis of one stool under a microscope can detect the rise in fecal fat due to intestinal malabsorption (or pancreatic maldigestion) as accurately as 3-day stool collections, making this latter test a thing of the past for most patients. This new stool test for intestinal malabsorption and other celiac-testing is available for order online from a laboratory set up by Drs. Fine and Ogunji to serve the needs of celiac patients. It is called EnteroLab and can be accessed at http://www.enterolab.com/.
  21. Celiac.com 04/13/2010 - A team of clinicians recently described a case of immune modulation by non-Hodgkin lymphoma in a patient with two primary intestinal T-Cell lymphomas and long-standing celiac disease. F. Mühr-Wilkenshoff, M. Friedrich, H. D. Foss, M. Hummel, M. Zeitz, and S. Daum made up the research team. They are variously affiliated with the Medical Clinic I, Gastroenterology, Rheumatology and Infectious Diseases, and with the Department of Pathology, Charité of the Campus Benjamin Franklin of University Medicine Berlin, Germany. About 20–30% of all non-Hodgkin lymphomas (NHLs) are gastrointestinal in nature. Of these gastrointestinal lymphomas, about 20–30% occur in small intestine The clinical team recently reported the case of a 72-year-old patient who had been diagnosed with celiac disease when he was 52-years old. The man had not followed a gluten-free diet, yet showed no evidence of enteropathy or celiac-associated antibodies, but still developed a jejunal T-cell lymphoma. Doctors resected the lymphoma due to perforation and treated the patient with four courses of IMVP-16. The patient began and maintained a strict gluten-free diet. Two years later, the patient appeared with weight loss and a clonally divergent refractory sprue type II with loss of antigen (CD8; T-cell receptor-) expression in intraepithelial lymphocytes. At this time, he showed high titers of celiac-associated antibodies, although he was on a strict GFD. The research team notes that the missing enteropathy under a gluten-containing diet supports the idea of immune suppression in malignant diseases, especially non-Hodgkin lymphoma. They also note that the fact that, even while maintaining a strict gluten-free diet, the patient developed refractory sprue type II, an early form of another independent T-cell lymphoma, along with celiac-associated antibodies, suggests that clonal intraepithelial lymphocytes might be stimulating antibody production. Thus, they conclude that isolated detection of celiac-associated antibodies in patients with celiac disease does not prove that patients have deviated from their gluten-free diets. Source: Digestion 2010;81:231–234 DOI: 10.1159/000269810
  22. Celiac.com 03/19/2010 - Celiac disease is a chronic inflammatory disorder of the gut triggered by an adverse immune response to dietary gluten proteins in genetically susceptible individuals. One of the first ways the body responds to offending proteins in an adverse celiac disease response is by producing mucous via IgA secretion in an effort to neutralize offending antigens and pathogens. A team of researchers recently sought to better document the relationships between immunoglobulin-coated bacteria and bacterial composition in feces of celiac disease patients, untreated and treated with a gluten-free diet (GFD) and healthy controls. The research team included Giada De Palma, Inmaculada Nadal, Marcela Medina, Ester Donat, Carmen Ribes-Koninckx, Miguel Calabuig, and Yolanda Sanz. They observed that intestinal dysbiosis and reduced immunoglobulin-coated bacteria are associated with celiac disease in children. Both untreated and treated celiac disease patients showed markedly lower levels of IgA, IgG and IgM-coated fecal bacteria compared to healthy controls. Celiac disease patients showed substantially reduced ratio of Gram-positive to Gram-negative bacteria compared to control subjects. Untreated celiac disease patients showed less abundant group proportions (P<0.050) of Bifidobacterium, Clostridium histolyticum, C. lituseburense and Faecalibacterium prausnitzii than did healthy controls. Untreated celiac disease patients showed more abundant group proportions (P<0.050) of Bacteroides-Prevotella than in control subjects. Both untreated and treated celiac disease patients showed significantly impoverished (P<0.050) levels of IgA coating the Bacteroides-Prevotella compared with healthy controls. From these results, the research team concluded that intestinal dysbiosis plays a role in reduced IgA-coating bacteria in celiac disease patients. This offers a fresh perspective into the possible relationships between the gut microbiota and the host defenses in celiac disease patients. Source: BMC Microbiology 2010, 24 February
  23. Celiac.com 03/05/2010 - A team of researchers recently studied therelationship between increased levels of antigliadin antibodies andintestinal barrier gene variants. The research team included V.M. Wolters, B. Z. Alizadeh, M. E. Weijerman, A. Zhernakova, I. M. vanHoogstraten, M. L. Mearin, M. C. Wapenaar, C.Wijmenga, M. W. Schreurs.They are affiliated with the Department of Pediatric Gastroenterology,UMC Utrecht, Utrecht, The Netherlands. Numerous genes may affectintestinal barrier function, including MAGI2, MYO9B, and PARD3, whichhave a close association with celiac disease. Gauging intestinalpermeability is tough to do, so researchers can test indirectly byusing antibodies against gliadin and Baker's yeast (anti-Saccharomycescerevisiae antibodies). The goal of the study was to determinewhether intestinal permeability, represented by antibodies againstgliadin, was connected to MAGI2, MYO9B, and PARD3. The teamanalyzed patients with Down syndrome, a population with suspectedincreased intestinal permeability. The team examined connectionsbetween AGA and ASCA. The team genotyped 126 Down syndromepatients for six single-nucleotide polymorphisms in MAGI2 (rs1496770,rs6962966, rs9640699), MYO9B (rs1457092, rs2305764), and PARD3(rs10763976). They then performed an allele dosage associationof these risk genes and AGA levels. They also found a strongcorrelation between AGA and ASCA (p < 0.01). Subjects withone or more risk genotypes showed lower average AGA levels (trend testp = 0.007) and made up a larger number of patients with normal AGAlevels (p = 9.3 x 10(-5)). Celiac-associated risk genotypesare associated with lower AGA values rather than higher AGA values.This all means that, regarding the increased prevalence of elevated AGAin patients with Down syndrome, there are other immunologic factors atplay. These may involve altered induction and/or maintenance oftolerance. Source: Hum Immunol. 2010 Feb 3.
  24. Celiac.com 04/27/2006 - Liver abnormalities have been found in a high percentage of celiacs when first diagnosed, around 42% according to some studies. Gluten toxicity and increased intestinal permeability have both been suspected as a cause of liver abnormalities. Serious liver disorders, including cirrhosis, have been found in association with a number of celiac disease cases which appear to resolve upon treatment and maintaining a gluten-free diet. It is not clear whether some damage to the liver may remain long term even after maintaining a gluten-free diet. Below is an interesting study (Hepatology. 2006 Mar 23;43(4):837-846) of the effects of induced liver cirrhosis on the intestinal mucosa which results in oxidative stress and an alteration of intestinal permeability, intestinal bacteria makeup, and bacterial overgrowth. Hence not only does damage to the intestine in response to gluten often result in bacterial overgrowth, but damage to the liver by gluten may also contribute to bacterial overgrowth and mucosal alterations. Damage to the liver caused by celiac disease may also have other consequences, as the liver plays many important roles including storage and production of important compounds and proteins and the removal of fat soluble toxic substances. As we are increasingly exposed to endocrine disrupting xenobiotic environmental chemicals and toxic substances, a dysfunctional livers inability to remove fat soluble toxic substances may leave celiacs more susceptible to adverse effects from these chemicals which can accumulate in adipose (fatty) tissue. In the Winter 2006 issue of Scott Adams' Celiac.com Newsletter, I discuss in detail, in Unraveling Fibromyalgia, how a dysfunctional liver and fat soluble toxic substances accumulating in innervated and vascularlized adipose tissue in the vicinity of joints may be the cause of fibromyalgia. Bacterial overgrowth has also been found in association with fibromyalgia. But clearly, lesser degrees of fatigue, muscle and joint pain, thyroid disorders, and other symptoms could also result from liver dysfunction caused by celiac disease. The inability of the liver to remove xenobiotic chemicals may also increase the risk of breast and other cancers. Recently a new review on liver disorders and celiac disease has appeared (See below - World J Gastroenterol 2006 March 14;12(10): 1493-1502 and 1503-1508): Liver Damage and the Intestinal Mucosa. One cannot ignore the secondary effects and symptoms that liver damage may add to those symptoms caused by glutens effect on the intestinal mucosa. Those unexplained aches and pains and other symptoms and disorders which have frequently been reported by some celiacs may be a result of liver dysfunction. Some notes: Elevated liver enzymes are the result of liver enzymes released by damaged liver cells. The article cites one study stating A gluten-free diet for 1 to 10 years resulted in complete normalization of liver chemistry tests in 95% patients. Normal liver chemistry tests DO NOT necessarily mean that the liver is functioning normally and that no damage remains. See: Special Considerations in Interpreting Liver Function Tests - http://www.aafp.org/afp/990415ap/2223.html Referenced Abstracts: Hepatology. 2006 Mar 23;43(4):837-846 Intestinal mucosal alterations in rats with carbon tetrachloride-induced cirrhosis: Changes in glycosylation and luminal bacteria. Natarajan SK, Ramamoorthy P, Thomas S, Basivireddy J, Kang G, Ramachandran A, Pulimood AB, Balasubramanian KA. The Wellcome Trust Research Laboratory, Department of Gastrointestinal Sciences, Christian Medical College, Vellore, India. Spontaneous bacterial peritonitis is a major cause of mortality after liver cirrhosis. Altered permeability of the mucosa and deficiencies in host immune defenses through bacterial translocation from the intestine due to intestinal bacterial overgrowth have been implicated in the development of this complication. Molecular mechanisms underlying the process are not well known. In order to understand mechanisms involved in translocation of bacteria, this study explored the role of oxidative stress in mediating changes in intestinal mucosal glycosylation and luminal bacterial content during cirrhosis. CCl(4)-induced cirrhosis in rats led to prolonged oxidative stress in the intestine, accompanied by increased sugar content of both intestinal brush border and surfactant layers. This was accompanied by changes in bacterial flora in the gut, which showed increased hydrophobicity and adherence to the mucosa. Inhibition of xanthine oxidase using sodium tungstate or antioxidant supplementation using vitamin E reversed the oxidative stress, changes in brush border membrane sugar content, and bacterial adherence. In conclusion, oxidative stress in the intestine during cirrhosis alters mucosal glycosylation, accompanied by an increased hydrophobicity of luminal bacteria, enabling increased bacterial adherence onto epithelial cells. This might facilitate translocation across the mucosa, resulting in complications such as spontaneous bacterial peritonitis. World J Gastroenterol 2006 March 14;12(10):1503-1508 Hepatobiliary and pancreatic disorders in celiac disease Hugh James Freeman Free full text: http://www.wjgnet.com/1007-9327/12/1503.asp A variety of hepatic and biliary tract disorders may complicate the clinical course of celiac disease. Some of these have been hypothesized to share common genetic factors or have a common immunopathogenesis, such as primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune forms of hepatitis or cholangitis. Other hepatic changes in celiac disease may be associated with malnutrition resulting from impaired nutrient absorption, including hepatic steatosis. In addition, celiac disease may be associated with rare hepatic complications, such as hepatic T-cell lymphoma. Finally, pancreatic exocrine function may be impaired in celiac disease and represent a cause of treatment failure. World J Gastroenterol 2006 March 14;12(10):1493-1502 Gut flora and bacterial translocation in chronic liver disease John Almeida, Sumedha Galhenage, Jennifer Yu, Jelica Kurtovic, Stephen M Riordan Free full text: http://www.wjgnet.com/1007-9327/12/1493.asp Increasing evidence suggests that derangement of gut flora is of substantial clinical relevance to patients with cirrhosis. Intestinal bacterial overgrowth and increased bacterial translocation of gut flora from the intestinal lumen, in particular, predispose to an increased potential for bacterial infection in this group. Recent studies suggest that, in addition to their role in the pathogenesis of overt infective episodes and the clinical consequences of sepsis, gut flora contributes to the pro-inflammatory state of cirrhosis even in the absence of overt infection. Furthermore, manipulation of gut flora to augment the intestinal content of lactic acid-type bacteria at the expense of other gut flora species with more pathogenic potential may favorably influence liver function in cirrhotic patients. Here we review current concepts of the various inter-relationships between gut flora, bacterial translocation, bacterial infection, pro-inflammatory cytokine production and liver function in this group.
  25. Celiac.com 10/16/2009 - A team of researchers recently set out to investigate the ability of a polymeric binder to reverse the toxic effects induced by gliadin in human intestinal cells and gliadin-sensitive HCD4-DQ8 mice. The team was made up of Maud Pinier, Elena F. Verdu, Mohamad Nasser–Eddine, Chella S. David, Anne Vézina, Nathalie Rivard, and Jean–Christophe Leroux. The team neutralized gliadin through complexation to a linear copolymer of hydroxyethylmethacrylate (HEMA) and sodium 4-styrene sulfonate (SS). They then examined the ability of the polymeric binder to mitigate the damaging effect of gliadin on cell-cell contact in IEC-6, Caco-2/15, and primary cultured differentiated enterocytes. They used gliadin-sensitive HLA-HCD4/DQ8 transgenic mice to measure the effectiveness of the polymeric binder in averting gliadin-triggered intestinal barrier dysfunction. They found that Poly(hydroxyethylmethacrylate-co-styrene sulfonate) [P(HEMA-co-SS)] complexed with gliadin in a fairly precise manner. Exposing intestinal cells to gliadin caused major changes in both cell structure and cell to cell contacts. By complexing the gliadin with P(HEMA-co-SS) the researchers were able to prevent these undesirable changes. More importantly, the P(HEMA-co-SS) inhibited gliadin digestion by gastrointestinal enzymes, which minimized the development of peptides that trigger immune adverse immune reactions. By co-administering P(HEMA-co-SS) with gliadin to HLA-HCD4/DQ8 mice, researchers were able to eliminate gliadin-triggered changes in the gut barrier and lower intraepithelial lymphocyte and macrophage cell counts. From these results, the team concludes that polymeric binders can prevent in vitro gliadin-induced epithelial toxicity and intestinal barrier dysfunction in HCD4/DQ8 mice. Such polymeric binders might play a significant role in the treating people with gluten-induced disorders. Source: GASTROENTEROLOGY 2009;136:288–298
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