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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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    NO SIGNS OF GENETIC OVERLAP BETWEEN PTSD AND AUTOIMMUNE CONDITIONS


    Jefferson Adams

    Celiac.com 06/20/2016 - Are there genetic correlations between PTSD and mental disorders or immune-related disorders? What role does genetics play in PTSD, if any? A team of researchers recently set out to discover genetic loci associated with the lifetime risk for PTSD in 2 groups from the Army Study to Assess Risk and Resilience in Service members (Army STARRS).


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    The research team included Murray B. Stein, MD, MPH, Chia-Yen Chen, ScD; Robert J. Ursano, MD; Tianxi Cai, ScD; Joel Gelernter, MD; Steven G. Heeringa, PhD; Sonia Jain, PhD; Kevin P. Jensen, PhD; Adam X. Maihofer, MS; Colter Mitchell, PhD; Caroline M. Nievergelt, PhD; Matthew K. Nock, PhD; Benjamin M. Neale, PhD; Renato Polimanti, PhD; Stephan Ripke, MD5; Xiaoying Sun, MS; Michael L. Thomas, PhD; Qian Wang, PhD; Erin B. Ware, PhD; Susan Borja, PhD; Ronald C. Kessler, PhD; Jordan W. Smoller, MD, ScD; for the Army Study to Assess Risk and Resilience in Service-members (STARRS).

    They are variously affiliated with the Department of Psychiatry, and the Department of Family Medicine and Public Health, UCSD, La Jolla, the Psychiatry Service of the Veterans Affairs San Diego Healthcare System, San Diego, California, the Department of Psychiatry at Massachusetts General Hospital and Harvard Medical School, Boston, the Stanley Center for Psychiatric Research, Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, the Department of Psychiatry, Uniformed Services University of the Health Sciences in Bethesda, Maryland, the Harvard T. H. Chan School of Public Health, Boston, Massachusetts, the Department of Psychiatry, Genetics, and Neurobiology at Yale University in New Haven, Connecticut, the Institute for Social Research, University of Michigan, Ann Arbor, the Department of Psychology, Harvard University, Cambridge, Massachusetts, the Department of Computational Biology and Bioinformatics, Graduate School of Arts and Sciences at Yale University, New Haven, Connecticut, the National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, and with the Department of Health Care Policy, Harvard Medical School, Boston, Massachusetts

    The study looked at subjects from two coordinated genome-wide association studies of mental health in the US military.

    The first study, the New Soldier Study (NSS), included 3,167 unique patients with PTSD and 4,607 trauma-exposed control subjects. The NSS data were collected from February 1, 2011, to November 30, 2012.

    The second study, the Pre/Post Deployment Study (PPDS), included 947 unique patients with PTSD and 4,969 trauma-exposed control subjects. The PDDS data were collected from January 9 to April 30, 2012.

    The primary analysis compared lifetime DSM-IV PTSD cases with trauma-exposed controls without lifetime PTSD. Data were analyzed from March 18 to December 27, 2015. The team used logistic regression models to conduct association analyses for PTSD among European, African, and Latino Americans by study, followed by meta-analysis. They also estimated heritability, genetic correlation and pleiotropy with other psychiatric and immune-related disorders.

    The NSS population of 7,774 patients was just over 80% male, and about 21 years old, while the PPDS population of 5,916 patients was 94.4% male, and about 26.5 years old.

    A genome-wide significant locus was found in ANKRD55 on chromosome 5 (rs159572; odds ratio [OR], 1.62; 95% CI, 1.37-1.92; P = 2.34 × 10−8) and persisted after adjustment for cumulative trauma exposure (adjusted OR, 1.64; 95% CI, 1.39-1.95; P = 1.18 × 10−8) in the African American samples from the NSS.

    They also found a genome-wide significant locus in or near ZNF626 on chromosome 19 (rs11085374; OR, 0.77; 95% CI, 0.70-0.85; P = 4.59 × 10−8) in the European American samples from the NSS. They did not find any similar results for either single-nucleotide polymorphism in the corresponding ancestry group from the PPDS sample, in other ancestral groups, or in transancestral meta-analyses.

    Overall, they saw no significant evidence for single-nucleotide polymorphism–based heritability, and they found no significant genetic correlations between PTSD and 6 mental disorders or 9 immune-related disorders.

    They did find significant evidence of a single-gene linking PTSD and rheumatoid arthritis and, to a lesser extent, psoriasis.

    Beyond that, they didn't find not much to support any connection to specific gene locations.

    The researchers are calling for additional studies "to replicate the genome-wide significant association with ANKRD55—associated in prior research with several autoimmune and inflammatory disorders—and to clarify the nature of the genetic overlap observed between PTSD and rheumatoid arthritis and psoriasis."

    Source:


    Image Caption: Drill sergeants in competition. Photo: CC--US Army
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  • Related Articles

    Dr. Vikki Petersen D.C, C.C.N
    This article originally appeared in the Spring 2009 edition of Journal of Gluten Sensitivity.
    Celiac.com 03/02/2009 - Patients with depression are told they have a chemical imbalance.  If someone else in their family is also depressed, the “gene card” is played.  “Your depression is genetic”, they are told.
    I have been in practice for over 20 years and I find the above data to be false.  Consistently we find patients who are suffering from depression and anxiety to be gluten sensitive. How could a food cause depression?  Let’s take a look.
    After the digestive tract, the most commonly affected system to be affected by gluten is the nervous system. It is thought that depression can be caused by gluten in one of two ways.  
    The first area addresses the inflammatory changes gluten can cause. A gluten sensitive individual’s immune system responds to the protein gliadin.  Unfortunately, that protein is similar in structure to other proteins present in the body, including those of the brain and nerve cells. A cross reactivity can occur whereby the immune system “confuses” proteins in the body for the protein gliadin.  This is called cellular mimicry and the result is the body attacking it’s own tissues with inflammation resulting. When inflammation happens in the brain and nervous system, a variety of symptoms can occur, including depression. Research shows us that patients with symptoms involving the nervous system suffer from digestive problems only 13% of the time.  This is significant because mainstream medicine equates gluten sensitivity almost exclusively with digestive complaints.
    In a study examining blood flow to the brain, 15 patients with untreated celiac disease were compared to 15 patients treated with a gluten-free diet for a year.  The findings were amazing. In the untreated group, 73% had abnormalities in brain circulation by testing while only 7% in the treated group showed any abnormalities. The patients with the brain circulation problems were frequently suffering from anxiety and depression as well.
    In addition to circulation problems, other research looks at the association between gluten sensitivity and its interference with protein absorption.  Specifically the amino acid tryptophan can be deficient. Tryptophan is a protein in the brain responsible for a feeling of well-being and relaxation. A deficiency can be correlated to feelings of depression and anxiety.
    Our society is too willing to accept a “chemical imbalance” as an explanation for their symptoms and instead of getting to the root cause of the condition, simply swallow a pill – a pill that in the case of anti-depressants has very dangerous and sometimes lethal side effects.
    The frequency with which we are able to successfully taper patients off their anti-depressants is considered “unbelievable” to many mainstream doctors, yet we do it regularly.  How is that possible?  We actually diagnose the root cause of the depression.  Frequently the culprit is gluten, and in such cases a gluten-free diet is the main path to recovery.


    Jefferson Adams
    Celiac.com 04/29/2009 - A team of researchers based at UK's prospective University of Highlands and Islands (UHI) have found a link between gluten and schizophrenia. According to their latest findings, proteins found in the gluten of wheat, rye and barley might play a role in triggering schizophrenia in people with a genetic risk for the condition, or in worsening symptoms in people who have the disease.
    The research team has been looking into the role played by gluten in schizophrenia and diabetes, as well as hunting for connections between the two disorders. Their research showed that the bodies of certain schizophrenia sufferers could not properly processes gluten, which led to tissue damage.
    As a result of these and other findings, researchers now consider genetic risk factors, together with environmental triggers, to be central to development of both schizophrenia and diabetes. Gluten is one such example.
    According to senior researcher and reader in genetics, Dr. Jun Wei, more than one-third of all people with schizophrenia show "high levels of antibodies against wheat gluten," and may experience some improvement in symptoms with a gluten-free diet.
    Though the studies are still in their early stages, the hypothesis is encouraging, because, as noted by head of UHI department of diabetes and cardiovascular science, Prof Ian Megson, if it is correct, "a simple change in diet might prevent these diseases...in some individuals."
    The research is part of two comprehensive studies at UHI into the connections between schizophrenia and diabetes, and the role played by gluten, and is supported by a £300,000 grant from the Schizophrenia Association of Great Britain (SAGB).
    It would be interesting to see more research done on the connection between celiac disease and schizophrenia, as other studies have indicated that there is a link.

    Source: BBC News


    Dr. Ron Hoggan, Ed.D.
    This article originally appeared in the Winter 2010 edition of Journal of Gluten Sensitivity.
    Celiac.com 10/06/2010 - Do you know where LSD comes from? It is made from gluten grains.  In 1938 Albert Hofmann, a Swiss chemist, discovered LSD, having refined it from a mold that grows on grains.  However, it was not until 1943 that he discovered its psycho-active properties.  In his own words Hofmann states: “I synthesized the diethylamide of Iysergic acid with the intention of obtaining an analeptic.” The expectation of such a drug was based on its source—ergot—which grows on gluten grains and causes ergotism, also known as ergotoxicosis, ergot poisoning, holy fire, and Saint Anthony’s Fire. 
    This poisonous mold has long been known to infect gluten grains.  It was to prevent the development of these molds that the Romans invented central heating systems.  They stored their grains on the lowest floor of residences and other buildings that were centrally heated and well ventilated.  Their fears of ergot were based on the powerful and bizarre symptoms that developed in people who ate grains that had become moldy with ergot.  Some afflicted individuals began to hallucinate, often becoming so mentally disturbed that they injured or killed themselves.  Others experienced loss of blood circulation to their extremities which became gangrenous.  Their digits and limbs sometimes fell off before these people died.  Some experienced a combination of these two sets of symptoms.  Animals sometimes display similar symptoms after consuming moldy grains. 
    Familiar with the vaso-constricting nature of ergot, Dr. Hofmann was trying to develop a stimulant drug that, in combination with another drug refined from ergot, could be used to halt hemorrhaging following childbirth.  Hofmann experienced an accidental dosing of LSD.  Here are some of his comments from his laboratory notes:

    Last Friday, April 16, 1943, I was forced to stop my work in the laboratory in the middle of the afternoon and to go home, as I was seized by a peculiar restlessness associated with a sensation of mild dizziness.  On arriving home, I lay down and sank into a kind of drunkenness which was not unpleasant and which was characterized by extreme activity of imagination.  As I lay in a dazed condition with my eyes closed (I experienced daylight as disagreeably bright) there surged upon me an uninterrupted stream of fantastic images of extraordinary plasticity and vividness and accompanied by an intense, kaleidoscope-like play of colors.  This condition gradually passed off after about two hours. From http://www.psychedelic-library.org/hofmann.htm. Several days later Dr. Hofmann intentionally ingested 250 µg of LSD which he hypothesized would be a threshold dose.  Here is what he said about his second ingestion:
    April 19, 1943: Preparation of an 0.5% aqueous solution of d-lysergic acid diethylamide tartrate. 4:20 P.M.: 0.5 cc (0.25 mg LSD) ingested orally.  The solution is tasteless. 4:50 P.M.: no trace of any effect.  5:00 P.M.: slight dizziness, unrest, difficulty in concentration, visual disturbances, marked desire to laugh... At this point the laboratory notes are discontinued: The last words were written only with great difficulty.  I asked my laboratory assistant to accompany me home as I believed that I should have a repetition of the disturbance of the previous Friday.  While we were cycling home, however, it became clear that the symptoms were much stronger than the first time.  I had great difficulty in speaking coherently, my field of vision swayed before me, and objects appeared distorted like images in curved mirrors.  I had the impression of being unable to move from the spot, although my assistant told me afterwards that we had cycled at a good pace.  http://www.psychedelic-library.org/hofmann.htm The difficulty Hofmann experienced with speaking coherently is reminiscent of a 1988 case report from Massachusetts General Hospital in which a patient was admitted for investigation of bowel complaints.  While in the hospital he became unable to speak coherently.  Eventually diagnosed with celiac disease, he was placed on a gluten free diet.  After several months on the diet, his speech was fully returned.  But I’m getting ahead of myself.  We were talking about Hofmann’s discovery.  LSD arrived in the USA in 1948 and was used to gain a better understanding of the schizophrenic experience:

    In psychiatry, the use of LSD by students was an accepted practice; it was viewed as a teaching tool in an attempt to enable the psychiatrist to subjectively understand schizophrenia.  http://en.wikipedia.org/wiki/History_of_LSD These students who tried LSD apparently failed to consider that the connection between the symptoms of LSD ingestion and schizophrenia might be due to a common source—psycho-active peptides from gluten grains.  About a decade after LSD had crossed the Atlantic, and from a very different research perspective, Dr. Curtis Dohan began investigating the possibility that gluten grains might be a factor in schizophrenia.  He had found that people with celiac disease and those with schizophrenia both excrete increased quantities of specific groups of indoles in their urine.  Some such indoles are known to be psychoactive and some psychoactive alkaloids also contain such indoles. 
    Having learned about this connection between celiac disease and schizophrenia, Dr. Dohan then undertook a study in which he examined hospital admission rates for schizophrenia both during periods of plenty and during World War II grain shortages.  He found that there was, indeed, a reduction in admissions during grain shortages, which normalized when ample grains became available again. 
    Dohan’s next step, along with several colleagues, was to design and conduct a single-blind cross-over study of schizophrenic patients in a locked ward.  They found that symptoms of schizophrenia abated on a gluten-free, dairy-free diet.  These same patients relapsed on re-introduction of these foods.  These data were published in The British Journal of Psychiatry in 1969.  Dohan’s findings were replicated and published in the January1976 issue of Science by Man Mohan Singh and Stanley Kay.
    Three years later, Christine Zioudrou and her colleagues demonstrated the presence of psychoactive peptides in the incomplete digests of gluten grains, including some with morphine-like properties, which they named “exorphins”.  Subsequent research by Fukudome and Yoshikawa has shown that there are five separate sequences from gluten grains that have psycho-active properties.  They named these exorphins A4, A5, B4, B5, and C. 
    At some point in this process, Dohan may have learned about the pseudo-hallucinations sometimes reported in celiac patients.  The primary difference between the schizophrenic’s hallucinations and those associated with celiac disease is that the celiac patient can exercise conscious control to stop them.  The schizophrenic appears unable to do this. 
    As he continued to accumulate more such data, Dohan went on to publish 16 more papers and letters over the next twenty years demonstrating an impressive body of evidence to support his suspicion that psychoactive peptides from gluten and possibly dairy proteins had a powerful impact on many cases of schizophrenia.  Yet, to an even greater extent than today, most people simply could not believe that such supposedly healthful foods as gluten grains and dairy products could be causing illness.  It was probably this paradigm that helped lead to subsequent publications and a period of dormancy in this area of research. 
    Several reports of very small numbers of schizophrenic patients, chronic patients, which Dohan had specifically identified as unlikely to respond to the diet, showed no benefit from a gluten-free diet.  Other studies were improved through double-blinding but weakened by extremely limited dietary control, permitting visitors to bring food to patients participating in that study, essentially abrogating the value of the entire study.  Some researchers ignored Dohan’s assertions that celiac disease could serve as a model for studying schizophrenia.  They chose, instead, to produce data that discredited the possibility that schizophrenia is identical to celiac disease by showing that most schizophrenic patients do not show signs of malabsorption.  Other work, conducted in the same vein, showed that celiac antibodies are not found in most schizophrenic patients. 
    Despite all the powerful evidence compiled by Dohan and others, this wave of studies and letters discredited Dohan’s work by contradicting notions that Dohan had never voiced.  For instance, he never expressed the notion that schizophrenia was celiac disease.  He simply asserted that there were compelling similarities and a small but significant overlap between schizophrenia and celiac disease, suggesting the need to explore gluten as a possible contributing factor in schizophrenia.  Considerable data support that notion but Dohan’s vigorous and persistent pursuit of this important discovery was soon depicted as a personal quest.  For instance, in a private email with one of Dohan’s contemporaries, Dohan was repeatedly called “unscientific.” Yet, fifteen years later, this same researcher has since participated in a published study that supports Dohan’s hypothesis. 
    Fortunately for all of us, the last dozen years have seen a resurgence of interest in the gluten hypothesis regarding schizophrenia, beginning with a case report by De Santis et al.  They described a patient with schizophrenia and a SPECT scan showing abnormal blood flow patterns in the brain typical of schizophrenia.  This patient developed symptoms of celiac disease and was placed on a gluten free diet.  Not only did this patient’s celiac symptoms disappear, her/his symptoms of schizophrenia disappeared and blood flow patterns in her brain normalized.  The gluten-free diet was the only plausible explanation for these changes.  
    A list of reports suggest important reasons to investigate the impact of gluten on our brains.  For instance, Dr. Knivsburg reported the discovery of two cases of celiac disease and one of milk protein sensitivity among 15 dyslexic children.  That is a huge increased incidence over the general population.  Similarly, Dr. Kozlowska found that almost 70% of celiac children have ADHD that normalizes on a gluten-free diet.  The Massachusetts General Hospital case study mentioned earlier reported celiac-associated aphasia that resolved on a gluten free diet.  Dr. Hu and colleagues report a laundry list of cognitive impairments in association with celiac disease including amnesia, acalculia, confusion, and personality changes.  Many of these disabilities wax and wane according to the gluten content of the diet. 
    However, the notion of gluten-driven cognitive deficits, including learning disabilities, and behavioral abnormalities in association with non-celiac gluten sensitivity, has only recently gotten some research attention.  For instance, Alexandra Blair of The TimesOnline in the United Kingdom reported on an informal study conducted at a small school for dyslexic children in Northumberland.  They got some startlingly positive improvements in students’ performance after placing them on a gluten free diet.  Dr. Marios Hadjivassiliou et al.  at the Royal Hallamshire Hospital in Sheffield, U.K.  have repeatedly reported that a majority of patients with neurological disease of unknown origin are also gluten sensitive while only about one third of these patients have celiac disease. 
    Kalaydjian et al.  reviewed the medical literature to about 2005 and called for large, controlled studies of the connection between gluten and schizophrenia because it is clear that some schizophrenic patients benefit enormously from a gluten free diet.  Similarly, earlier this year, Kraft et al.  reported on a schizophrenic patient who was diagnosed at seventeen years of age.  Fifty three years later, at her doctor’s suggestion, she undertook a ketogenic diet to lose weight.  Not only did she lose weight, she also lost all signs and symptoms of schizophrenia. 
    As 2009 comes to a close, two more publications have made this year into something of a turning point for this research.  Cascella et al.  state that “Our results confirm the existence of a subgroup of patients with antibody characteristics associated with the presence of a specific immune response to gluten.”
    Similarly, Samaroo et al.  report that their findings “….  indicate that the anti-gliadin immune response in schizophrenia has a different antigenic specificity from that in celiac disease…” they go on to assert that the genetic HLA markers for celiac disease were not found in the schizophrenic patients they studied. 
    At the most basic level, we know that gluten causes increased intestinal permeability among a wide range of genetically susceptible individuals.  We also know that substances from moldy grains will cause schizophrenic symptoms in any of us.  It is not a great leap to suggest that, in the context of gluten-induced increased intestinal permeability, similarities in hallucinations, altered brain perfusion, and a range of cognitive deficits found in schizophrenia, celiac disease, and gluten sensitivity might all be rooted in the commonest food in our diets from which hallucinogenic drugs can be produced. 
    Institutional nutrition and food programs for the needy and/or homeless include large proportions of inexpensive gluten-laden foods.  Such diets, often provided charitably for those at the lowest socio-economic strata, are at least self-defeating.  Further, such foods are often consumed at this economic level despite visible molds growing on them.  I have heard stories of homeless persons scavenging through dumpsters located at or near bakeries.  There can be little doubt that such eating practices perpetuate the very psychiatric conditions that have reduced many of these people to a state of homelessness. 


    Jefferson Adams
    Celiac.com 10/03/2011 - A number of studies show that people with celiac disease have higher risk of depression and death from external causes, but there are no conclusive studies on death from suicide.
    A research team set out to more deeply examine the risk of suicide in people with celiac disease. The team included J. F. Ludvigsson, C. Sellgren, B. Runeson, N. Långström, and P. Lichtenstein. They are affiliated with the Department of Paediatrics at Örebro University Hospital in Sweden.
    The team examined suicide risk in individuals with celiac disease where the small intestinal biopsy showed no villous atrophy.
    For their study, the team collected biopsy data from all 28 clinical pathology departments in Sweden for 29,083 individuals diagnosed during 1969-2007 with celiac disease with Marsh 3 villous atrophy, with inflammation without villous atrophy (Marsh 1-2; n=13,263), or with positive celiac disease serology, but normal mucosa (Marsh 0, n=3719).
    The team used Cox regression to calculated hazard ratios for suicide as recorded in the Swedish Cause of Death Register.
    The team found that people with celiac disease have a higher risk for suicide compared to general population control subjects (HR=1.55; 95%CI=1.15-2.10; based on 54 completed suicides).
    The results showed that suicide was more common among those who suffered from inflammation (HR=1.96; 95%CI=1.39-2.77), but the team found no such increase in people who showed positive celiac disease serology, but normal mucosa. (HR=1.06; 95%CI=0.37-3.02).
    Overall, the team found a slightly higher risk of suicide in patients with celiac disease than in the general population. The increased risk is one that merits attention from doctors, when treating patients with celiac disease.
    Source:

    Dig Liver Dis. 2011 Aug;43(8):616-22.

    Jefferson Adams
    Celiac.com 05/04/2012 - Some studies have shown that people with untreated celiac disease can have higher rates of psychiatric disorders, but little study has been made to determine whether people with psychiatric disorders have higher rates of celiac disease.
    To answer that question, a team of researchers recently studied celiac disease in patients with chronic psychiatric disorders. The research team included Manouchehr Khoshbaten, Mohammad Rostami Nejad, Nasrin Sharifi, Ali Fakhari, Mahdyar Golamnejad, Sayed Hassan Hashemi, Pekka Collin, and Kamran Rostami
    The team set out to assess rates of celiac disease in Iranian patients suffering from chronic depression or schizophrenia.
    For their study, they screened 200 Iranian inpatient men with in chronic phase of depressive disorders or schizophrenia, along with another 200 age-matched healthy male subjects, for celiac disease using anti-tissue transglutaminase IgA antibodies. The average patient age was 37 years.
    This study found that one (1%) schizophrenic and two (2%) depressive patients tested positive for anti-tissue transglutaminase IgA antibodies. They noted that duodenal biopsy was not possible in these male patients.
    In the control group one (0.5%) individual was positive for anti-tissue transglutaminase IgA antibodies, but had normal duodenal histology. Theere was no statistical difference between patients and control group.
    Celiac disease serology is not significantly higher in schizophrenic and depressive inpatients than in the general population.
    Based on this observation, they do not advocate systematic blood screening in such patients, but they do advocate increased alertness to the possibilities of celiac disease in those patients.
    Source:
    Gastroenterology and Hepatology

  • Recent Articles

    Jefferson Adams
    Celiac.com 04/20/2018 - A digital media company and a label data company are teaming up to help major manufacturers target, reach and convert their desired shoppers based on dietary needs, such as gluten-free diet. The deal could bring synergy in emerging markets such as the gluten-free and allergen-free markets, which represent major growth sectors in the global food industry. 
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    Morris says the joint partnership will allow Catalina to “enhance our dataset and further increase our ability to target shoppers who are currently buying - or have shown intent to buy - in these emerging categories,” including gluten-free, allergen-free, and other free-from foods.
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    Source:
    fdfworld.com

    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.
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    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