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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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    CELIAC DISEASE IN PATIENTS WITH CHRONIC PSYCHIATRIC DISORDERS


    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.


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    Photo: CC -Jessia HimeTo 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:


    Image Caption: Photo: CC -Jessia Hime
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    Guest SandraB

    Posted

    Given a rate of celiac thought to be about 1 in 100 (in the UK) a study of 200 against a control of 200 is quite small, surely. 1,000 would give better odds of coming up with a useful recommendation. Even so, three celiacs had been missed amongst the psychiatric patients whose mental state probably improved on going gluten free. If countries cannot afford routine testing, then relatives need to be made aware that they can test privately and why they should.

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    Guest Kevin

    Posted

    There is no reliable test for gluten sensitivity; yet. Therefore all those researches are useless. It does need to be rocket science to figure out that zonulin is the culprit. That is the reason for most human health and neurological disorders. I am just wondering, when you "professionals" will let the public know that gluten is poison for most people?

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    Guest Jen

    Posted

    Interesting article. My husband, who has celiac disease has mental health issues and is on medication for it. My mother has celiac disease and is bi-polar. My husband's mother has not been diagnosed with celiac disease but we feel she has it because she is on seizure medications, has fibromyalgia, and hydroensephilitus, and arthritis....plus she is extremely moody (sorry that is the only way I can describe it.) I am not saying all celiac disease patients are psychiatric patients. And vice versa. But, I too have celiac disease and when I accidentally get glutened, depression hits usually pretty soon after physical symptoms. I think it is a study that needs to be done soon!!! More extensively. Maybe other countries, nationalities need to be studied.

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    Guest Mabel W

    Posted

    I desperately wish my parents and siblings who have health issues ranging from stomach pain to bipolar would just even try the gluten challenge. I have celiac, diagnosed by blood test, by my Lupus doctor. I was told they should get tested but when I tried to tell them, they aren't interested. They just say they can't afford testing and they don't think they could eat gluten free anyway. I try to tell them the benefits of doing it and the dangers of not doing it of they have it, all to no avail. Any hope for such folks? More research would be helpful I think.

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    admin

    The following was written by Dr. Kalle Reichelt who is a leading celiac disease researcher at the Pediatric Research Institute in Oslo, Norway. Please direct any questions regarding this article to him at: K.L.Reichelt@rh.uio.no
    What most people ignore is that both peptides and trace (biologically significant amounts) amounts of proteins are taken up across the gut mucosa (1,2). Because one molecule of gluten contains at least 15 opioid sequences it is quite clear that this could cause a problem. Increased peptide excretion is found in the urine of celiacs before treatment (3) (Reichelt et al in prep). This is confirmed by a series of papers that demonstrate intact food proteins in mothers milk (4-7). A Canadian group has confirmed that gluten does change a brain enzyme and monoamine levels in cats (8). Their findings a significant even though cats are not gluten eating animals. There is increasing evidence that components from food can indeed cause serious psychiatric (9-12) and neurological (13-16) diseases. Even rheumatoid arthritis may have a link to food proteins (17), and it well established that stress increases gut permeability. Nobody denies the possibility of reactive depression, but there is little reason why this could not be made worse by dietary factors. Because antibodies are indeed induced by peptides it may even be so that dietary peptides by mimicry to endogenous cell surface peptide sequences, may be responsible for many autoimmune diseases (18).
    References:
    Gardner MLG (1994) Physiology of the gastrointestinal tract. Edit: LR Johnson. Raven press 3rd edit. pp 1795-1820. Husby S et al (1985) Scand J Immunol 22:83-92. Klosse JA et al (1972) Clin Chim Acta 42:409-422. Kilshaw PJ and Cant AJ (1984) Inter. Arch Allergy Appl Immunol 75:8-15. Axelsson I et al (1986) Acta paed Scand 75:702-707. Stuart CA et al (1984) Clin Allergy 14:533-535. Troncone R et al (1987) Acta paed Scand 76:453-456. Thibault L et al (1988) J Clin Biochem Nutr. 4:209-221. Hallert C et al (1982) Psychic disturbances in adult celiac disease III.Reduced central monoamine metabolism and signs of depression. Scand J Gastroenterol 17:25-28. Singh MM and Kay SR (1976) Wheat gluten as a pthogenic factor in schizophrenia. Science 191:401-402. Dohan FC and Grasberger JC (1973) relapsed schizophrenics: earlier discharge from the hospital after cereal-free, milk-free diet. Amer J Psychiat 130:685-686. Reichelt KL et al (1990) The effect of gluten free diet on glycoprotein attached urinary peptidee excretion and behaviour in schizophrenics. J Orthomol Med 5:223-239. Gobbi G et al (1992) Celiac disease, epilepsy and cerebral calcifications. The Lancet 340:439-443. Paul K-D et al (1985) EEG-Befunde Zoeliakikranken Kindern in Abh{ngigkkeit von der Ern{hrung. Z Klin Med 40:707-709. Kahn A et al (1987) Difficulty of initiating sleep associated with cows milk allergy in infants. Sleep 10:116-121. Hadjivassiliou M et al (1996) Does cryptic gluten sensitivity play a part in neurological illness? The Lancet 347:369-371. Kjeldsen-Kragh J et al (1991) Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. The Lancet 338:899-902. Karjalainen J et al (1992) Bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. New Eng J Med 327:302-307.

    admin

    Celiac.com 09/01/2002 - Patients with celiac disease are 20 times more likely than the general population to have epilepsy and often have associated cerebral and cerebellar calcifications imaged by CT and MRI. Depression, dementia, and schizophrenia are all also common in persons with untreated celiac disease. Cerebellar degeneration with resulting ataxia (gluten-associated ataxia) is a known entity in Europe, and the National Institutes of Health (NIH) is currently recruiting subjects with ataxia to examine them for gluten sensitivity and celiac disease. Focal white matter lesions in the brain recently have been reported to occur in children with celiac disease and are thought to be either ischemic in origin as a result of vasculitis or caused by inflammatory demyelination. Parents of children with celiac disease have reported behavioral changes such as irritability, separation anxiety, emotional withdrawal, and autistic-like behaviors that all seemed to improve on a GFD. Although not scientifically validated, the GFD is now also being advocated for children with autism by several groups. Whether or not children with autism are at a higher risk for celiac disease or celiac children have a higher incidence of autism remains to be proven. However, children with Down syndrome, who often have autistic-like behaviors, are at higher risk for celiac disease. It has been hypothesized that gluten may be broken down into small peptides that may cross the blood-brain barrier and interact with morphine receptors, leading to alterations in conduct and perceptions of reality.
    The serologic tests can be divided into 4 different types of antibodies: antigliadin (AGA), antireticulin, antiendomysium (AEA), and antitissue transglutaminase (tTG). Each antibody varies widely in its sensitivity, specificity, and positive and negative predictive values (Table 2).
    Table 2 (from Pietzak et al, 2001, compiled data from multiple studies)

    Test Sensitivity Specificity PPV NPD AGA IgG 57-100 42-98 20-95 41-88 AGA IgA 53-100 65-100 28-100 65-100 AEA IgA* 75-98 96-100 98-100 80-95 Guinea pig tTG† 90.2 95 Human tTG† 98.5 98 * Patients older than 2 years of age.
    † IgG +IgA antibodies.

    The AEA IgA immunofluorecent antibody is an excellent screening test for celiac disease, with both a high sensitivity and specificity. This antibody was discovered in the early 1980s and rapidly gained use as part of a screening celiac panel by commercial laboratories in combination with AGA IgG and AGA IgA. Its major drawbacks are that it may be falsely negative in children under the age of 2 years, in patients with IgA deficiency, and in the hands of an inexperienced laboratory. Also, the substrate for this antibody was initially monkey esophagus, making it expensive and unsuitable for screening large numbers of people. Recently, the human umbilical cord has been used as an alternative to monkey esophagus. However, the subjective nature of the AEA assay may lead to false-negative values and unacceptable variability between laboratories.
    Because tTG had been first described as the autoantigen of celiac disease in 1997, it has been used to develop innovative diagnostic tools. The tTG IgA ELISA test is highly sensitive and specific, using either the commercially available guinea pig tTG or human recombinant tTG. The tTG assay correlates well with AEA-IgA and biopsy. However, it represents an improvement over the AEA assay because it is inexpensive and rapid (30 minutes), is not a subjective test, and can be performed on a single drop of blood using a dot-blot technique. Therefore, this test is ideally suited for mass screenings and in the future could be performed in the general practitioners office, much like the now routine finger-stick hematocrit.
    For the reasons outlined above, the IgA class human anti-tTg antibody, coupled with the determination of total serum IgA, currently seems to be the most cost-effective way to screen for celiac disease. AEA should be used as a confirmatory, pre-biopsy test, whereas AGA determinations should be restricted to the diagnostic work-up of younger children and patients with IgA deficiency, using the guidelines in Table 3.
    Table 3
    Probability of celiac disease based on three antibodies in combination
    AEA IgA AGA IgA AGA IgG Interpretation + + + Celiac disease 99% probable + - + probable + + - Celiac disease probable + - - Celiac disease probable - + + Celiac disease less likely* - - + Celiac disease less likely* - + - Celiac disease less likely - - - Celiac disease very unlikely+ * If patient is IgA sufficient: AGA IgG > 100 warrants work-up of enteropathy.
    + If patient is on a gluten-containing diet.
    Celiac disease: AEA, antiendomysium antibodies: AGA, antigliadin antibodies.

    admin

    Eur Psychiatry. 2004 Aug;19(5):311-4. Celiac.com 09/12/2004 - Israeli researchers conducted a study designed to determine whether or not an association exists between celiac disease and schizophrenia. Past studies have indicated that such a connection may exist. The researchers screened 50 consecutive patients over 18 years old who were diagnosed with schizophrenia and their matched controls for celiac-specific anti-endomysial IgA antibodies. All patients also completed a detailed questionnaire. There were no significant differences between the groups in gender, Body Mass Index (BMI) or country of birth, and the mean age of the study group was significantly higher than the controls. All tests for anti-endomysial antibodies in both groups were negative, and the researchers concluded that "In contrast to previous reports, we found no evidence for celiac disease in patients with chronic schizophrenia as manifested by the presence of serum IgA anti-endomysial antibodies. It is unlikely that there is an association between gluten sensitivity and schizophrenia"
    Celiac.com Comments on this Study:
    This was a relatively small study that did not include other celiac disease screening methods, such as IgG (antigliadin antibody), tTG (tissue Transglutaminase), or intestinal biopsies. A recent study has shown that only 77% of those with total and 33% of those with partial villous atrophy actually have positive blood tests for celiac disease, so many cases of celiac disease may be missed by using only blood tests to screen for it. Further, about 4% of celiacs are anti-endomysial IgA deficient, so anyone in this subclass would have been missed in the study. Given such a small number of people in the study--50--if even one celiac were missed it would greatly affect the outcome of the study. Both groups should have been given much more comprehensive celiac disease screening to ensure that no cases of celiac disease were missed.
    In the article by Dr. Hadjivassiliou titled Gluten Sensitivity as a Neurological Illness he says:

    The introduction of more celiac disease specific serological markers such as anti-endomysium and more recently transglutaminase antibodies may have helped in diagnosing celiac disease but their sensitivity as markers of other manifestations of gluten sensitivity (where the bowel is not affected) is low. This certainly reflects our experience with patients with gluten sensitivity who present with neurological dysfunction. Endomysium and transglutaminase antibodies are only positive in the majority but not in all patients who have an enteropathy. Patients with an enteropathy represent only a third of patients with neurological manifestations and gluten sensitivity. Antigliadin antibodies unlike endomysium and transglutaminase antibodies are not autoantibodies. They are antibodies against the protein responsible for gluten sensitivity.
    Only one third of the patients with neurological disorders associated with gluten sensitivity have villous atrophy on duodenal biopsy. Even some with biochemical markers of malabsorption such as low serum vitamin B12, low red cell folate, or vitamin D concentrations had normal conventional duodenal histology. These cases may illustrate the patchy nature of bowel involvement in coeliac disease and the inaccurate interpretation of duodenal biopsies by inexperienced histopathologists. Preliminary data based on staining of the subpopulation of T cells in the small bowel epithelium suggests that these patients have potential celiac disease. There are, however, patients where the immunological disorder is primarily directed at the nervous system with little or no damage to the gut. Our practice is to offer a gluten-free diet to these patients unless the HLA genotype is not consistent with susceptibility to gluten intolerance (that is, other than HLA DQ2, DQ8, or DQ1). All patients are followed up and any clinical response is documented.

    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. 


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    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