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      Frequently Asked Questions About Celiac Disease   04/07/2018

      This Celiac.com FAQ on celiac disease will guide you to all of the basic information you will need to know about the disease, its diagnosis, testing methods, a gluten-free diet, etc.   Subscribe to Celiac.com's FREE weekly eNewsletter   What are the major symptoms of celiac disease? Celiac Disease Symptoms What testing is available for celiac disease?  Celiac Disease Screening Interpretation of Celiac Disease Blood Test Results Can I be tested even though I am eating gluten free? How long must gluten be taken for the serological tests to be meaningful? The Gluten-Free Diet 101 - A Beginner's Guide to Going Gluten-Free Is celiac inherited? Should my children be tested? Ten Facts About Celiac Disease Genetic Testing Is there a link between celiac and other autoimmune diseases? Celiac Disease Research: Associated Diseases and Disorders Is there a list of gluten foods to avoid? Unsafe Gluten-Free Food List (Unsafe Ingredients) Is there a list of gluten free foods? Safe Gluten-Free Food List (Safe Ingredients) Gluten-Free Alcoholic Beverages Distilled Spirits (Grain Alcohols) and Vinegar: Are they Gluten-Free? Where does gluten hide? Additional Things to Beware of to Maintain a 100% Gluten-Free Diet What if my doctor won't listen to me? An Open Letter to Skeptical Health Care Practitioners Gluten-Free recipes: Gluten-Free Recipes
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    MORE EVIDENCE LINKS GUT BACTERIA TO CELIAC DISEASE


    Roy Jamron

    Celiac.com 11/06/2008 - Previously, the possible link between gut bacteria and celiac disease has been discussed in "Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease?"[1] A 5-year European study, DIABIMMUNE, is currently underway focusing on some 7000 children, from birth, investigating the development of intestinal bacterial flora and its influence on the development of the human immune system and autoimmune disease, including celiac disease.[2] Hopefully, this study will provide some much needed answers. Now a Spanish group of scientists has produced further evidence supporting a possible role for gut bacteria in the pathogenesis of celiac disease by investigating whether gut microflora present in the feces of celiac disease patients participates in the pro-inflammatory activity of celiac disease.[3]


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    The makeup of fecal microflora in celiac disease patients differs significantly from that of healthy subjects. To determine whether gut microflora is a participant in the pro-inflammatory milieu of celiac disease, the Spanish research team incubated cultures of peripheral blood mononuclear cells from healthy adults with fecal microflora obtained from 26 active celiac disease children, 18 symptom-free celiac disease children on a gluten-free diet, and 20 healthy children. The scientists additionally investigated possible regulatory roles of Bifidobacterium longum ES1 and B. bifidum ES2 obtained from the feces of healthy individuals, co-incubating the Bifidobacterium with the test subject fecal microflora and the peripheral blood mononuclear cell culture.

    Fecal micrflora from both active and, notably, treated, symptom-free celiac children caused a significant increase in pro-inflammatory cytokine production and a decrease in anti-inflammatory IL-10 production in the peripheral blood mononuclear cell cultures compared to the fecal microflora from healthy children. However, cultures co-incubated with the Bifidobacterium strains exhibited a suppression of the pro-inflammatory cytokine production and an increase in IL-10 production. IL-10 is a cytokine which promotes immune tolerance.

    The scientists concluded that the makeup of the gut flora of celiacs may contribute to pro-inflammation in celiac disease, possibly in a synergy with gliadin, and that certain strains of Bifidobacterium appear to suppress and reverse pro-inflammatory effects and offering therapeutic opportunities for the treatment of celiac disease.

    It would have been interesting if the scientists had also investigated the effect of adding vitamin D to the fecal microflora and the peripheral blood mononuclear cell cultures. It is likely the addition of vitamin D might also have resulted in a suppression of pro-inflammatory cytokine production and an increase in IL-10 production. This is borne out by experiments with Mycobacterium tuberculosis and its culture filtrate antigen in peripheral blood mononuclear cell cultures where the addition of vitamin D resulted in a suppression of pro-inflammatory cytokine production and an increase in IL-10 production.[4] It is possible that celiac disease may be entirely prevented in infancy by routinely administrating prophylactic doses of vitamin D and probiotics containing specific strains of Bifidobacterium before gluten is introduced into the infant's diet. The vitamin D and Bifidobacterium strains may provide an IL-10 anti-inflammatory environment in which the immune system learns to respond tolerantly to gluten, forever preventing the onset of celiac disease.

    The fact that certain strains of fecal Bifidobacterium from healthy individuals appear to suppress celiac disease inflammation brings to mind the concept of "fecal bacteriotherapy" or "fecal transplant", a therapy developed and used in practice by the world reknown Australian gastroenterologist, Prof. Thomas J. Borody, M.D., known best for his development of a triple-antibiotic treatment for H. pylori and ulcerative colitis.[5] Fecal bacteriotherapy involves transplanting feces from a healthly, screened donor into an ailing patient with a persistant bacterial gastrointestinal disorder whose own gut flora has first been reduced or eliminated with antibiotics. The fecal microflora from the healthy donor reseeds the gut of the ailing patient with a healthy mix of intestinal microflora curing the gastrointestinal disorder. The Bifidobacterium research done by the Spanish researchers suggests that fecal bacteriotherapy might be an option to treat or cure celiac disease in adults, replacing gut flora causing intolerance to gluten with a healthy mix of gut flora that encourages tolerance to gluten.

    Sources

    [1] Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease?
    Roy S. Jamron
    https://www.celiac.com/articles/21605/

    [2] European Study Will Focus On Relation Of Gut Bacteria to Autoimmune Disease in Children
    Roy S. Jamron
    https://www.celiac.com/articles/21607/

    [3] Journal of Inflammation 2008, 5:19.
    Bifidobacterium strains suppress in vitro the pro-inflammatory milieu triggered by the large intestinal microbiota of coeliac patients.
    Medina M, De Palma G, Ribes-Koninckx C, Calabuig M, Sanza Y.
    http://www.journal-inflammation.com/content/pdf/1476-9255-5-19.pdf

    [4] J Clin Immunol. 2008 Jul;28(4):306-13.
    Regulatory role of promoter and 3' UTR variants of vitamin D receptor gene on cytokine response in pulmonary tuberculosis.
    Selvaraj P, Vidyarani M, Alagarasu K, Prabhu Anand S, Narayanan PR.
    http://www.springerlink.com/content/d67236620021j84u/

    [5] Prof. Thomas J. Borody, M.D., Bio and Publication List http://www.cdd.com.au/html/hospital/clinicalstaff/borody.html http://www.cdd.com.au/html/expertise/publications.html



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    Dear Mr. Jamron, After 2 years of a gluten free diet

    my health remained very bad. That is when I learned about heavy metal toxicity. When the gut barrier isn't strong anymore,there is no good protection anymore and we get stuff in our system which is very bad for our health. I don't believe bacteria are THE CAUSE or THE CURE for celiac disease. The reason people with celiac disease have different bacteria in their gut is because the immune system is not working correctly anymore because of the toxins and heavy metals. When these toxins and heavy metals are removed, perfect health will be regained, BUT the celiac disease will remain.

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    Thanks Roy for that. It makes me feel so much better about my banging on about gut dysbiosis and rogue bacteria being behind so many health issues. Celiac is just one condition among many and just the tip of the iceberg. I am sure a lot more will come out on this subject.

     

    It's encouraging when you get information that proves you are on the right track. Now I have a little more evidence to back up my belief.

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    Guest Michelle Grace

    Posted

    Very informative and interesting. Makes absolute sense to me. I have long believed there are many factors contributing to the disorder/disease. Thanks for the article.

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    Guest MaryClare

    Posted

    Healthy intestinal flora from birth on will provide a strong defense and immune system that will be much more likely to keep at bay many auto-immune disorders.

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    Thanks for this article. I'm pretty firmly convinced that expression of the celiac genes is primarily facilitated by a gut that is out of balance -- too much bad bacteria, not enough good. Curses to all those dozens of antibiotics I took as a child!!

     

    I suspect it would do all celiacs good to follow the GAPS diet for some time, as a means to heal the gut. Alas, it's pretty challenging to do in the real world, without a very high level of motivation...

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  • Related Articles

    Roy Jamron
    This article appeared in the Summer 2008 edition of Celiac.com's Scott-Free Newsletter.
    Celiac.com 06/16/2008 - Do vitamin D deficiency, gut bacteria, and timing of gluten introduction during infancy all combine to initiate the onset of celiac disease? Two recent papers raise the potential that this indeed may be the case. One paper finds that when transgenic mice expressing the human DQ8 heterodimer (a mouse model of celiac disease) are mucosally immunized with gluten co-administered with Lactobacillus casei bacteria, the mice exhibit an enhanced and increased immune response to gluten compared to the administration of gluten alone.[1] A second paper finds that vitamin D receptors expressed by intestinal epithelial cells are involved in the suppression of bacteria-induced intestinal inflammation in a study which involved use of germ-free mice and knockout mice lacking vitamin D receptors exposed to both friendly and pathogenic strains of gut bacteria.[2] Pathogenic bacteria caused increased expression of vitamin D receptors in epithelial cells. Friendly bacteria did not.
    If one considers these two papers together, one notices: (1) Certain species of gut bacteria may work in conjunction with gluten to cause an increased immune response which initiates celiac disease; (2) The presence of an adequate level of vitamin D may suppress the immune response to those same gut bacteria in such a way as to reduce or eliminate the enhanced immune response to gluten caused by those gut bacteria, thus preventing the onset of celiac disease.
    Vitamin D has recently been demonstrated to play a role in preserving the intestinal mucosal barrier. A Swedish study found children born in the summer, likely introduced to gluten during winter months with minimal sunlight, have a higher incidence of celiac disease strongly suggesting a relationship to vitamin D deficiency.[3] Recent studies found vitamin D supplementation in infancy and living in world regions with high ultraviolet B irradiance both result in a lower incidence of type 1 diabetes, an autoimmune disease closely linked to celiac disease.[4][5]
    Gut bacteria have long been suspected as having some role in the pathogenesis of celiac disease. In 2004, a study found rod-shaped bacteria attached to the small intestinal epithelium of some untreated and treated children with celiac disease, but not to the epithelium of healthy controls.[6][7] Prior to that, a paper published on Celiac.com[8] first proposed that celiac disease might be initiated by a T cell immune response to "undigested" gluten peptides found inside of pathogenic gut bacteria which have "ingested" short chains of gluten peptides resistant to breakdown. The immune system would have no way of determining that the "ingested" gluten peptides were not a part of the pathogenic bacteria and, thus, gluten would be treated as though it were a pathogenic bacteria. The new paper cited above[1] certainly gives credence to this theory.
    Celiac disease begins in infancy. Studies consistently find the incidence of celiac disease in children is the same (approximately 1%) as in adults. The incidence does not increase throughout life, meaning, celiac disease starts early in life. Further, in identical twins, one twin may get celiac disease, and the other twin may never experience celiac disease during an entire lifetime. Something other than genetics differs early on in the childhood development of the twins which initiates celiac disease. Differences in vitamin D levels and the makeup of gut bacteria in the twins offers a reasonable explanation as to why one twin gets celiac disease and the other does not. Early childhood illnesses and antibiotics could also affect vitamin D level and gut bacteria makeup. Pregnant and nursing mothers also need to maintain high levels of vitamin D for healthy babies.
    Sources:
    [1] Immunol Lett. 2008 May 22.
    Adjuvant effect of Lactobacillus casei in a mouse model of gluten sensitivity.
    D'Arienzo R, Maurano F, Luongo D, Mazzarella G, Stefanile R, Troncone R, Auricchio S, Ricca E, David C, Rossi M.
    http://dx.doi.org/10.1016/j.imlet.2008.04.006
    [2] The FASEB Journal. 2008;22:320.10. Meeting Abstracts - April 2008.
    Bacterial Regulation of Vitamin D Receptor in Intestinal Epithelial Inflammation
    Jun Sun, Anne P. Liao, Rick Y. Xia, Juan Kong, Yan Chun Li and Balfour Sartor
    http://www.fasebj.org/cgi/content/meeting_abstract/22/1_MeetingAbstracts/320.10
    [3] Vitamin D Preserves the Intestinal Mucosal Barrier
    Roy S. Jamron
    https://www.celiac.com/articles/21476/
    [4] Arch Dis Child. 2008 Jun;93(6):512-7. Epub 2008 Mar 13.
    Vitamin D supplementation in early childhood and risk of type 1 diabetes: a systematic review and meta-analysis.
    Zipitis CS, Akobeng AK.
    http://adc.bmj.com/cgi/content/full/93/6/512
    [5] Diabetologia. 2008 Jun 12. [Epub ahead of print]
    The association between ultraviolet B irradiance, vitamin D status and incidence rates of type 1 diabetes in 51 regions worldwide.
    Mohr SB, Garland CF, Gorham ED, Garland FC.
    http://www.springerlink.com/content/32jx3635884xt112/
    [6] Am J Gastroenterol. 2004 May;99(5):905-6.
    A role for bacteria in celiac disease?
    Sollid LM, Gray GM.
    http://dx.doi.org/10.1111/j.1572-0241.2004.04158.x
    [7] Am J Gastroenterol. 2004 May;99(5):894-904.
    Presence of bacteria and innate immunity of intestinal epithelium in childhood celiac disease.
    Forsberg G, Fahlgren A, Hörstedt P, Hammarström S, Hernell O, Hammarström ML.
    http://dx.doi.org/10.1111/j.1572-0241.2004.04157.x
    [8] Are Commensal Bacteria with a Taste for Gluten the Missing Link in the Pathogenesis of Celiac Disease?
    Roy S. Jamron
    https://www.celiac.com/articles/779/


    Jefferson Adams
    This article originally appeared in the Spring 2009 edition of Journal of Gluten Sensitivity.
    Celiac.com 05/15/2010 - Willem-Karel Dicke was born in 1905, in Dordrecht, Holland, and died Utrecht in 1962.  Dicke was a Dutch pediatrician, the first clinician to develop the gluten-free diet, and to prove that certain types of flour cause relapses in celiac disease patients.
    From 1922 until 1929, Dicke studied medicine in Leiden.  He then specialized in pediatrics in Juliana Children’s Hospital in The Hague from 1929 until 1933.  In 1936, at just 31 years of age, he was named medical director of the hospital. 
    In the 1940s and 1950s he went on to formally establish the gluten-free diet, forever changing treatment methods and clinical outcomes of children suffering from celiac disease.  By 1952, Dicke recognized that the disease is caused by the ingestion of wheat proteins, not carbohydrates. 
    From the late 1880s into the 1920s and 30s, doctors like R. A. Gibbons, Sidney Haas and others pioneered the use of specialty diets to treat celiac disease.  Diets such as the banana diet, the fruit diet, the carbohydrate diet (fruit, puree of potatoes or tomatoes), the beefsteak diet, the milk diet had all been tried, with some success.
    In his now seminal 1950 thesis on celiac disease and wheat-free diet, Dicke lays out the results of the detailed dietary study he conducted over several years at the Juliana Children’s Hospital on a patient with celiac disease.
    The study likely had its earliest beginnings at the advent of Dicke’s promotion to medical director, if not slightly before.  From the testimony of Dicke’s wife in 1991, we know that Dicke was convinced of the beneficial effect of wheat free diet even before 1940.  She confirmed that between 1934 and 1936, Dicke began to conduct experiments with wheat free diets confirming Christopher Booth’s comments in The Lancet, Feb 25, 1989:
    “It was a young mother’s statement of her celiac child’s rash improving rapidly if she removed bread from the diet that alerted his interest,” when Dicke was a pediatrician in The Hague in 1936.
    Dicke published his first report on a wheat-free diet in Het Nederlands Tijdschrift voor Geneeskunde in 1941.  (W. K. Dicke: A simple diet for Gee-Herter’s Syndrome).  At the time, celiac was still called Gee-Herter’s syndrome.  It reads, in part:
    “In recent literature it is stated that the diet of Haas (Banana-diet) and Fanconi (fruit and vegetables) gives the best results in the treatment of patients suffering from coeliac disease.  At present (World War II) these items are not available.  Therefore, I give a simple diet, which is helping these children at this time of rationing.  The diet should not contain any bread or rusks.  A hot meal twice a day is also well tolerated.  The third meal can be sweet or sour porridge (without any wheat flour).”
    In the Netherlands, the last winter of World War II, the winter of 1944/45 became known as the ‘Winter of Hunger.’ 
    Delivery of regular food staples, such as bread, was largely disrupted, especially in the western part of the country.  This meant that people had to turn to uncommon foods, such as tulip bulbs, for sustenance.  It was during this time that Dicke became even more convinced that eating less grain, along with unusual foods, such as tulip bulbs, improved the clinical condition of his patients. 
    Dicke’s next major confirmation came when Allied planes started dropping bread in the Netherlands, and these same children began to deteriorate rapidly. 
    After World War II, Dicke conducted a series of experiments with standardized diets were performed on four children in the Wilhelmina Children’s Hospital in Utrecht and in one child in the Juliana Children’s Hospital in The Hague.  These experiments involved excluding or adding wheat or rye flour over long periods in the diets of these children with coeliac disease. 
    In Dicke’s post-war experiments, children were challenged with different cereals under a strict dietary protocol with measurement of total fecal output, fecal fat content, and the fat absorption coefficient was calculated.
    Dicke worked closely with biochemist J. H. van de Kamer of the Netherlands Central Institute for Nutritional Research TNO in Utrecht, who developed the first accurate and easily available method for measure fecal fat content in wet feces.  Dicke also worked closely with H. A. Weyers, a pediatrician from the Wilhelmina Children’s Hospital in Utrecht, who developed a method that used the coefficient of fat absorption to analyze fecal fat excretion in children with celiac disease.
    Based on these findings Dicke concluded in his 1950 thesis that wheat flour, but not well-purified wheat starch (amylum), and also rye flour, triggered the anorexia, the increased fecal output, and the streatorrhea common in celiac patients.  Dicke presented his doctoral thesis on the subject at the University of Utrecht in 1950.
    Dicke’s 1950 thesis refers to a celiac disease patient he treated in 1936.  The patient’s symptoms disappeared and he returned to normal weight and growth patterns after following a strict wheat free diet in the hospital.  However, each time the boy went home and was unable to maintain a wheat free diet, he suffered a decline in his growth curve. 
    Dicke charted these advances and reversals over four long-term admissions.  Each time the trend towards normal growth was restored.  In his thesis, Dicke presents several growth curves of children treated with a wheat free diet.  In long term studies over several years he shows that, with a wheat free diet, these children gain weight, reaching normal growth patterns when compared with age matched controls.  At the end of chapter 3 of his thesis he concludes that:
    “- if certain types of meal, such as wheat and rye are replaced in the daily diet, the patient improves;
    - acute attacks of diarrhea, do not occur, provided these types of meal are not given;
    - after a latent period which can vary in length, deterioration and acute attacks of diarrhea re-occur, if the objectionable types of meal are added to the diet too soon....”
    In 1953, together with van de Kamer and Weyers, he subsequently published Coeliac disease IV “An investigation into the injurious constituents of wheat in connection with their action on patients with coeliac disease.”
    They wrote that the alcohol soluble or the gliadin component of the water insoluble protein of wheat was responsible for the fat malabsorption in patients with celiac disease. 
    Although these findings were quickly confirmed by researchers in Britain, Scandinavia, and Germany, some researchers, especially in America, questioned the wisdom of a gluten free diet.
    After the establishment of the intestinal biopsy technique for the diagnosis of celiac disease, it became apparent that a wheat free diet should be maintained for long periods before an adequate response occurred, as Dicke had predicted. 
    In 1954, Dr. Dicke, Charlotte Anderson, and a number of their colleagues, confirmed these findings, and described the damage to the lining of the small intestine as being directly related to celiac disease.
    In 1957 he was appointed a professor of Utrecht University and became a medical director of Wilhelmina Children’s Hospital.
    To honor Willem Karel Dicke, Netherland’s Society of Gastroenterology established a gold medal in his name, to be presented to pioneering researchers in the field.  Willem Dicke himself was named as the recipient of the first gold Dicke Medal.
    Dr. Dicke died in 1962 of cerebrovascular disease.  He was just 57 years old.
    Jefferson Adams is a freelance writer living in San Francisco.  His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden’s Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
    Sources:

    Willem Dicke.  Brilliant Clinical Observer and Translational Investigator.  Discoverer of the Toxic Cause of Celiac Disease, by David Yan and Peter R.  Holt , M.D. DOI: 10.1111/j.1752-8062.2009.00167.x GUT 1993; 34:1473-1475 Mulder, C.  “Pioneer in Glutenfree diet: Willem Karel Dicke 1905-1962 Over 50 Years of Gluten Free Diet.”  appended to: English translation by C.  Mulder June 1, 1993 of  Dicke, W.K.  “Coeliac Disease  Investigation of Harmful Effects of Certain Types of Cereal on Patients Suffering from Coeliac Disease.” Ph.  D.  Thesis, State University of Utrecht, 1950

    Gryphon Myers
    Celiac.com 07/04/2012 - It is becoming increasingly clear that celiac disease (or some form of gluten sensitivity) affects many more people in the world than estimates from the past few decades suggested. In the 1950s, celiac disease was estimated as affecting 1 in 8000 individuals worldwide, while today that number has grown to 1 in 100. Seeking to explain why this sizable portion of our population cannot tolerate gluten, Professor David Sanders, who is a Consultant Gastroenterologist at the Royal Hallamshire Hospital and University of Sheffield, looks to evolution for answers.
    It is hard to think of a world without bread, as even Ancient Romans harvested grain. But wheat is actually a new food for us: it was only widely introduced into the human diet roughly ten thousand years ago, which is a very small percentage (0.4%) of the 2.5 million years our species has walked the planet.
    So what were we eating that other 99.6% of our life as a species? We ate things that are edible raw, without the need for processing or refinement (which wheat is not). Our ability to process grains to an edible form was a technological development that did not occur until a relatively recent chapter in our history.
    In a sense, then, our ingenuity is ahead of our biology. As Dr. Sanders says, “... it makes sense that our bodies are still adapting to this food, and more specifically, the gluten it contains.” After millions of years of what is essentially gluten-free dieting, our bodies might be ill-equipped to process gluten, as it is still a relatively foreign substance.
    Source:
    http://www.science20.com/news_articles/being_glutenfree_determined_evolution_says_gastroenterologist-91578

    Jefferson Adams
    Celiac.com 05/12/2014 - Currently, researcher know almost nothing about the natural history and evolution of celiac disease in ancient populations.
    But, a set of recently unearthed bones from ancient Rome show signs of a struggle with celiac disease, and may help researchers to better understand the natural history and evolution of the condition.
    Researchers believe the bones are those of an 18 to 20-year old upper class Roman woman, who likely had celiac disease or gluten intolerance, as her skeleton reveals signs of malnutrition and osteoporosis and her attempts to manage it by changing her diet.
    DNA analysis has confirmed that the woman carried two copies of an immune system gene variant strongly associated with celiac disease. Although celiac disease can be influenced by numerous environmental factors, the gene variant is found in nearly all contemporary celiac populations.
    The combination of genetic risk factors and malnutrition in someone likely to have good access to nutritious food, make celiac disease a reasonable diagnosis, says Gabriele Scorrano, a biological anthropologist at the University of Rome Tor Vergata.
    An article about the study appears in Nature, and the study itself appears in the American Journal of Physical Anthropology.

  • Recent Articles

    Jefferson Adams
    Celiac.com 04/19/2018 - Previous genome and linkage studies indicate the existence of a new disease triggering mechanism that involves amino acid metabolism and nutrient sensing signaling pathways. In an effort to determine if amino acids might play a role in the development of celiac disease, a team of researchers recently set out to investigate if plasma amino acid levels differed among children with celiac disease compared with a control group.
     
    The research team included Åsa Torinsson Naluai, Ladan Saadat Vafa, Audur H. Gudjonsdottir, Henrik Arnell, Lars Browaldh, and Daniel Agardh. They are variously affiliated with the Institute of Biomedicine, Department of Microbiology & Immunology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; the Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden; the Department of Pediatric Gastroenterology, Hepatology and Nutrition, Karolinska University Hospital and Division of Pediatrics, CLINTEC, Karolinska Institute, Stockholm, Sweden; the Department of Clinical Science and Education, Karolinska Institute, Sodersjukhuset, Stockholm, Sweden; the Department of Mathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden; the Diabetes & Celiac Disease Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden; and with the Nathan S Kline Institute in the U.S.A.
    First, the team used liquid chromatography-tandem mass spectrometry (LC/MS) to analyze amino acid levels in fasting plasma samples from 141 children with celiac disease and 129 non-celiac disease controls. They then crafted a general linear model using age and experimental effects as covariates to compare amino acid levels between children with celiac disease and non-celiac control subjects.
    Compared with the control group, seven out of twenty-three children with celiac disease showed elevated levels of the the following amino acids: tryptophan; taurine; glutamic acid; proline; ornithine; alanine; and methionine.
    The significance of the individual amino acids do not survive multiple correction, however, multivariate analyses of the amino acid profile showed significantly altered amino acid levels in children with celiac disease overall and after correction for age, sex and experimental effects.
    This study shows that amino acids can influence inflammation and may play a role in the development of celiac disease.
    Source:
    PLoS One. 2018; 13(3): e0193764. doi: & 10.1371/journal.pone.0193764

    Jefferson Adams
    Celiac.com 04/18/2018 - To the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service animals.
    If you’ve flown anywhere lately, you may have seen them. People flying with their designated “emotional support” animals. We’re not talking genuine service animals, like seeing eye dogs, or hearing ear dogs, or even the Belgian Malinois that alerts its owner when there is gluten in food that may trigger her celiac disease.
    Now, to be honest, some of those animals in question do perform a genuine service for those who need emotional support dogs, like veterans with PTSD.
    However, many of these animals are not service animals at all. Many of these animals perform no actual service to their owners, and are nothing more than thinly disguised pets. Many lack proper training, and some have caused serious problems for the airlines and for other passengers.
    Now the major airlines are taking note and introducing stringent requirements for service animals.
    Delta was the first to strike. As reported by the New York Times on January 19: “Effective March 1, Delta, the second largest US airline by passenger traffic, said it will require passengers seeking to fly with pets to present additional documents outlining the passenger’s need for the animal and proof of its training and vaccinations, 48 hours prior to the flight.… This comes in response to what the carrier said was a 150 percent increase in service and support animals — pets, often dogs, that accompany people with disabilities — carried onboard since 2015.… Delta said that it flies some 700 service animals a day. Among them, customers have attempted to fly with comfort turkeys, gliding possums, snakes, spiders, and other unusual pets.”
    Fresh from an unsavory incident with an “emotional support” peacock incident, United Airlines has followed Delta’s lead and set stricter rules for emotional support animals. United’s rules also took effect March 1, 2018.
    So, to the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service and emotional support animals.
    Source:
    cnbc.com

    admin
    WHAT IS CELIAC DISEASE?
    Celiac disease is an autoimmune condition that affects around 1% of the population. People with celiac disease suffer an autoimmune reaction when they consume wheat, rye or barley. The immune reaction is triggered by certain proteins in the wheat, rye, or barley, and, left untreated, causes damage to the small, finger-like structures, called villi, that line the gut. The damage occurs as shortening and villous flattening in the lamina propria and crypt regions of the intestines. The damage to these villi then leads to numerous other issues that commonly plague people with untreated celiac disease, including poor nutritional uptake, fatigue, and myriad other problems.
    Celiac disease mostly affects people of Northern European descent, but recent studies show that it also affects large numbers of people in Italy, China, Iran, India, and numerous other places thought to have few or no cases.
    Celiac disease is most often uncovered because people experience symptoms that lead them to get tests for antibodies to gluten. If these tests are positive, then the people usually get biopsy confirmation of their celiac disease. Once they adopt a gluten-free diet, they usually see gut healing, and major improvements in their symptoms. 
    CLASSIC CELIAC DISEASE SYMPTOMS
    Symptoms of celiac disease can range from the classic features, such as diarrhea, upset stomach, bloating, gas, weight loss, and malnutrition, among others.
    LESS OBVIOUS SYMPTOMS
    Celiac disease can often less obvious symptoms, such fatigue, vitamin and nutrient deficiencies, anemia, to name a few. Often, these symptoms are regarded as less obvious because they are not gastrointestinal in nature. You got that right, it is not uncommon for people with celiac disease to have few or no gastrointestinal symptoms. That makes spotting and connecting these seemingly unrelated and unclear celiac symptoms so important.
    NO SYMPTOMS
    Currently, most people diagnosed with celiac disease do not show symptoms, but are diagnosed on the basis of referral for elevated risk factors. 

    CELIAC DISEASE VS. GLUTEN INTOLERANCE
    Gluten intolerance is a generic term for people who have some sort of sensitivity to gluten. These people may or may not have celiac disease. Researchers generally agree that there is a condition called non-celiac gluten sensitivity. That term has largely replaced the term gluten-intolerance. What’s the difference between celiac disease and non-celiac gluten-sensitivity? 
    CELIAC DISEASE VS. NON-CELIAC GLUTEN SENSITIVITY (NCGS)
    Gluten triggers symptoms and immune reactions in people with celiac disease. Gluten can also trigger symptoms in some people with NCGS, but the similarities largely end there.

    There are four main differences between celiac disease and non-celiac gluten sensitivity:
    No Hereditary Link in NCGS
    Researchers know for certain that genetic heredity plays a major role in celiac disease. If a first-degree relative has celiac disease, then you have a statistically higher risk of carrying genetic markers DQ2 and/or DQ8, and of developing celiac disease yourself. NCGS is not known to be hereditary. Some research has shown certain genetic associations, such as some NCGS patients, but there is no proof that NCGS is hereditary. No Connection with Celiac-related Disorders
    Unlike celiac disease, NCGS is so far not associated with malabsorption, nutritional deficiencies, or a higher risk of autoimmune disorders or intestinal malignancies. No Immunological or Serological Markers
    People with celiac disease nearly always test positive for antibodies to gluten proteins. Researchers have, as yet, identified no such antobodies or serologic markers for NCGS. That means that, unlike with celiac disease, there are no telltale screening tests that can point to NCGS. Absence of Celiac Disease or Wheat Allergy
    Doctors diagnose NCGS only by excluding both celiac disease, an IgE-mediated allergy to wheat, and by the noting ongoing adverse symptoms associated with gluten consumption. WHAT ABOUT IRRITABLE BOWEL SYNDROME (IBS) AND IRRITABLE BOWEL DISEASE (IBD)?
    IBS and IBD are usually diagnosed in part by ruling out celiac disease. Many patients with irritable bowel syndrome are sensitive to gluten. Many experience celiac disease-like symptoms in reaction to wheat. However, patients with IBS generally show no gut damage, and do not test positive for antibodies to gliadin and other proteins as do people with celiac disease. Some IBS patients also suffer from NCGS.

    To add more confusion, many cases of IBS are, in fact, celiac disease in disguise.

    That said, people with IBS generally react to more than just wheat. People with NCGS generally react to wheat and not to other things, but that’s not always the case. Doctors generally try to rule out celiac disease before making a diagnosis of IBS or NCGS. 
    Crohn’s Disease and celiac disease share many common symptoms, though causes are different.  In Crohn’s disease, the immune system can cause disruption anywhere along the gastrointestinal tract, and a diagnosis of Crohn’s disease typically requires more diagnostic testing than does a celiac diagnosis.  
    Crohn’s treatment consists of changes to diet and possible surgery.  Up to 10% of Crohn's patients can have both of conditions, which suggests a genetic connection, and researchers continue to examine that connection.
    Is There a Connection Between Celiac Disease, Non-Celiac Gluten Sensitivity and Irritable Bowel Syndrome? Large Number of Irritable Bowel Syndrome Patients Sensitive To Gluten Some IBD Patients also Suffer from Non-Celiac Gluten Sensitivity Many Cases of IBS and Fibromyalgia Actually Celiac Disease in Disguise CELIAC DISEASE DIAGNOSIS
    Diagnosis of celiac disease can be difficult. 

    Perhaps because celiac disease presents clinically in such a variety of ways, proper diagnosis often takes years. A positive serological test for antibodies against tissue transglutaminase is considered a very strong diagnostic indicator, and a duodenal biopsy revealing villous atrophy is still considered by many to be the diagnostic gold standard. 
    But this idea is being questioned; some think the biopsy is unnecessary in the face of clear serological tests and obvious symptoms. Also, researchers are developing accurate and reliable ways to test for celiac disease even when patients are already avoiding wheat. In the past, patients needed to be consuming wheat to get an accurate test result. 
    Celiac disease can have numerous vague, or confusing symptoms that can make diagnosis difficult.  Celiac disease is commonly misdiagnosed by doctors. Read a Personal Story About Celiac Disease Diagnosis from the Founder of Celiac.com Currently, testing and biopsy still form the cornerstone of celiac diagnosis.
    TESTING
    There are several serologic (blood) tests available that screen for celiac disease antibodies, but the most commonly used is called a tTG-IgA test. If blood test results suggest celiac disease, your physician will recommend a biopsy of your small intestine to confirm the diagnosis.
    Testing is fairly simple and involves screening the patients blood for antigliadin (AGA) and endomysium antibodies (EmA), and/or doing a biopsy on the areas of the intestines mentioned above, which is still the standard for a formal diagnosis. Also, it is now possible to test people for celiac disease without making them concume wheat products.

    BIOPSY
    Until recently, biopsy confirmation of a positive gluten antibody test was the gold standard for celiac diagnosis. It still is, but things are changing fairly quickly. Children can now be accurately diagnosed for celiac disease without biopsy. Diagnosis based on level of TGA-IgA 10-fold or more the ULN, a positive result from the EMA tests in a second blood sample, and the presence of at least 1 symptom could avoid risks and costs of endoscopy for more than half the children with celiac disease worldwide.

    WHY A GLUTEN-FREE DIET?
    Currently the only effective, medically approved treatment for celiac disease is a strict gluten-free diet. Following a gluten-free diet relieves symptoms, promotes gut healing, and prevents nearly all celiac-related complications. 
    A gluten-free diet means avoiding all products that contain wheat, rye and barley, or any of their derivatives. This is a difficult task as there are many hidden sources of gluten found in the ingredients of many processed foods. Still, with effort, most people with celiac disease manage to make the transition. The vast majority of celiac disease patients who follow a gluten-free diet see symptom relief and experience gut healing within two years.
    For these reasons, a gluten-free diet remains the only effective, medically proven treatment for celiac disease.
    WHAT ABOUT ENZYMES, VACCINES, ETC.?
    There is currently no enzyme or vaccine that can replace a gluten-free diet for people with celiac disease.
    There are enzyme supplements currently available, such as AN-PEP, Latiglutetenase, GluteGuard, and KumaMax, which may help to mitigate accidental gluten ingestion by celiacs. KumaMax, has been shown to survive the stomach, and to break down gluten in the small intestine. Latiglutenase, formerly known as ALV003, is an enzyme therapy designed to be taken with meals. GluteGuard has been shown to significantly protect celiac patients from the serious symptoms they would normally experience after gluten ingestion. There are other enzymes, including those based on papaya enzymes.

    Additionally, there are many celiac disease drugs, enzymes, and therapies in various stages of development by pharmaceutical companies, including at least one vaccine that has received financial backing. At some point in the not too distant future there will likely be new treatments available for those who seek an alternative to a lifelong gluten-free diet. 

    For now though, there are no products on the market that can take the place of a gluten-free diet. Any enzyme or other treatment for celiac disease is intended to be used in conjunction with a gluten-free diet, not as a replacement.

    ASSOCIATED DISEASES
    The most common disorders associated with celiac disease are thyroid disease and Type 1 Diabetes, however, celiac disease is associated with many other conditions, including but not limited to the following autoimmune conditions:
    Type 1 Diabetes Mellitus: 2.4-16.4% Multiple Sclerosis (MS): 11% Hashimoto’s thyroiditis: 4-6% Autoimmune hepatitis: 6-15% Addison disease: 6% Arthritis: 1.5-7.5% Sjögren’s syndrome: 2-15% Idiopathic dilated cardiomyopathy: 5.7% IgA Nephropathy (Berger’s Disease): 3.6% Other celiac co-morditities include:
    Crohn’s Disease; Inflammatory Bowel Disease Chronic Pancreatitis Down Syndrome Irritable Bowel Syndrome (IBS) Lupus Multiple Sclerosis Primary Biliary Cirrhosis Primary Sclerosing Cholangitis Psoriasis Rheumatoid Arthritis Scleroderma Turner Syndrome Ulcerative Colitis; Inflammatory Bowel Disease Williams Syndrome Cancers:
    Non-Hodgkin lymphoma (intestinal and extra-intestinal, T- and B-cell types) Small intestinal adenocarcinoma Esophageal carcinoma Papillary thyroid cancer Melanoma CELIAC DISEASE REFERENCES:
    Celiac Disease Center, Columbia University
    Gluten Intolerance Group
    National Institutes of Health
    U.S. National Library of Medicine
    Mayo Clinic
    University of Chicago Celiac Disease Center

    Jefferson Adams
    Celiac.com 04/17/2018 - Could the holy grail of gluten-free food lie in special strains of wheat that lack “bad glutens” that trigger the celiac disease, but include the “good glutens” that make bread and other products chewy, spongey and delicious? Such products would include all of the good things about wheat, but none of the bad things that might trigger celiac disease.
    A team of researchers in Spain is creating strains of wheat that lack the “bad glutens” that trigger the autoimmune disorder celiac disease. The team, based at the Institute for Sustainable Agriculture in Cordoba, Spain, is making use of the new and highly effective CRISPR gene editing to eliminate the majority of the gliadins in wheat.
    Gliadins are the gluten proteins that trigger the majority of symptoms for people with celiac disease.
    As part of their efforts, the team has conducted a small study on 20 people with “gluten sensitivity.” That study showed that test subjects can tolerate bread made with this special wheat, says team member Francisco Barro. However, the team has yet to publish the results.
    Clearly, more comprehensive testing would be needed to determine if such a product is safely tolerated by people with celiac disease. Still, with these efforts, along with efforts to develop vaccines, enzymes, and other treatments making steady progress, we are living in exciting times for people with celiac disease.
    It is entirely conceivable that in the not-so-distant future we will see safe, viable treatments for celiac disease that do not require a strict gluten-free diet.
    Read more at Digitaltrends.com , and at Newscientist.com

    Jefferson Adams
    Celiac.com 04/16/2018 - A team of researchers recently set out to investigate whether alterations in the developing intestinal microbiota and immune markers precede celiac disease onset in infants with family risk for the disease.
    The research team included Marta Olivares, Alan W. Walker, Amalia Capilla, Alfonso Benítez-Páez, Francesc Palau, Julian Parkhill, Gemma Castillejo, and Yolanda Sanz. They are variously affiliated with the Microbial Ecology, Nutrition and Health Research Unit, Institute of Agrochemistry and Food Technology, National Research Council (IATA-CSIC), C/Catedrático Agustín Escardin, Paterna, Valencia, Spain; the Gut Health Group, The Rowett Institute, University of Aberdeen, Aberdeen, UK; the Genetics and Molecular Medicine Unit, Institute of Biomedicine of Valencia, National Research Council (IBV-CSIC), Valencia, Spain; the Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire UK; the Hospital Universitari de Sant Joan de Reus, IISPV, URV, Tarragona, Spain; the Center for regenerative medicine, Boston university school of medicine, Boston, USA; and the Institut de Recerca Sant Joan de Déu and CIBERER, Hospital Sant Joan de Déu, Barcelona, Spain
    The team conducted a nested case-control study out as part of a larger prospective cohort study, which included healthy full-term newborns (> 200) with at least one first relative with biopsy-verified celiac disease. The present study includes 10 cases of celiac disease, along with 10 best-matched controls who did not develop the disease after 5-year follow-up.
    The team profiled fecal microbiota, as assessed by high-throughput 16S rRNA gene amplicon sequencing, along with immune parameters, at 4 and 6 months of age and related to celiac disease onset. The microbiota of infants who remained healthy showed an increase in bacterial diversity over time, especially by increases in microbiota from the Firmicutes families, those who with no increase in bacterial diversity developed celiac disease.
    Infants who subsequently developed celiac disease showed a significant reduction in sIgA levels over time, while those who remained healthy showed increases in TNF-α correlated to Bifidobacterium spp.
    Healthy children in the control group showed a greater relative abundance of Bifidobacterium longum, while children who developed celiac disease showed increased levels of Bifidobacterium breve and Enterococcus spp.
    The data from this study suggest that early changes in gut microbiota in infants with celiac disease risk could influence immune development, and thus increase risk levels for celiac disease. The team is calling for larger studies to confirm their hypothesis.
    Source:
    Microbiome. 2018; 6: 36. Published online 2018 Feb 20. doi: 10.1186/s40168-018-0415-6