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    No Connection between Celiac Disease and Schizophrenia?


    Scott Adams

    Eur Psychiatry. 2004 Aug;19(5):311-4.


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    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.

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  • About Me

    In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease. In 1998 I founded The Gluten-Free Mall, Your Special Diet Superstore!, and I am the co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.

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  • Related Articles

    Scott Adams
    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.

    Scott Adams
    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.

    Scott Adams
    BMJ 2004;328:438-439 (21 February) Celiac.com 02/27/2004 – The following report is interesting, but I believe that serological studies done on those with schizophrenia would be a far better way to conduct such a study. Also, the use of such a small control group cannot accurately predict the actual incidence of schizophrenia in those with celiac disease. –Scott Adams
    According to a Danish study published in the British Medical Journal, people with celiac disease may have an increased risk of developing schizophrenia. Previous studies have also suggested an association between these two disorders. The study identified 7,997 people over age 15 who were admitted to a Danish psychiatric unit for the first time between 1981 and 1998 and were diagnosed with schizophrenia. The researchers selected 25 random controls and matched their year of birth and sex, and identified any history of celiac disease, ulcerative colitis or Crohns disease in both groups, and in their parents. A "moderately strong risk relation between coeliac disease and schizophrenia" was discovered in the data, and the researchers stress that these findings only reflect a small proportion of cases, as both disorders are rare. The prevalence of celiac disease among schizophrenics was 1.5 cases per 1,000 compared to 0.5 cases per 1,000 in the larger control group, which means that there is a three times greater risk of schizophrenia in those with celiac disease. Interestingly Crohns disease and ulcerative colitis were not associated with an increased risk of schizophrenia.
    According to Dr. Eaton: More research is needed to understand the link between celiac disease and schizophrenia. The most important question is whether treatment for celiac disease, in the form of a gluten-free diet, would benefit the small proportion of individuals with schizophrenia who are genetically prone to celiac disease but have not been diagnosed with it."

    Jefferson Adams
    Celiac.com 01/23/2013 - Can going gluten-free bring about a major improvement in mental health for some children?
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    Unimpressed with the advice, Lochner says she knew, as a mother often does, that something was, in fact, wrong with her child. In the mean time, her daughter's temper was becoming progressively more volatile. She began having behavioral episodes during the night, as well as during the day. The first time it happened, she woke up screaming hysterically at 2 a.m. Lochner found a new pediatrician for her daughter, one who took her concerns seriously.
    He ran Mary Jean through a test or screening for everything from iron deficiency to autism. At the same time, she continued to do her own research, and began to wonder if the problem might be Sensory Processing Disorder.
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    While she was investigating that possibility, s came across an article from the March 2012 Huffington Post called “Is Sensory Processing Disorder the New Black?” The article described the case of a child whose extreme behavioral symptoms disappeared after her mother put her on a gluten-free diet after consulting a nutritionist.
    For Lochman, the article hit close to home, and led her to read Kelly Dorfman’s book concerning nutritional origins of childhood illnesses: What’s Eating Your Child? Initially, Lochman says she was skeptical of claims of major behavioral improvement in children who had gone gluten-free, and regarded much of what she'd heard about gluten-free diets with some doubt.
    However, she did bring up the book with her pediatrician, and, rather than dismissing her, the doctor confirmed that gluten can cause behavioral problems in some gluten-sensitive children. He suggested that her daughter go gluten-free for a month, then back on gluten for a month, then gluten-free a second month, and that she keep a journal of her daughter's behavior.
    By doing the gluten-free trial twice, she and the doctor would be able to confidently confirm that any improvement in my daughter’s behavior was due to the removal of gluten, and not to coincidence.
    During the first month on a gluten-free diet, her daughter’s episodes decreased sharply, but Lochman was still skeptical. However, when she went back to eating gluten during the second month, the emotional outbursts and episodes came back in less than a week. By the end of that second month, she found herself looking forward to returning her daughter to the gluten-free diet for month three of the trial. In the third month, her daughter’s episodes rapidly decreased during the first two weeks. By the end of the month, they were down to only two or three times a week.
    This is when Lochman really knew something was up. She says that she thought that her daughter was seeing a major shift, if not a miracle cure. She quick to tell people how she was wrong to think that. That's because, Lochmans says that taking gluten out of her daughter's life was, in fact, a miracle cure. She says that after just six weeks on the gluten-free diet, "her daughter's 'awful screaming and flailing episodes, the ones that would last for hours and come out of nowhere, were gone. Vanished. A thing of the past. It was like she was a completely new, and different, person."
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    For her part, Kelly Dorfman notes that non-celiac gluten-sensitivity has only recently been identified as a distinct medical condition, one that resists conventional tests for diagnosing celiac disease. She says that she commonly sees patients in her practice for whom behavior and mood issues are the only symptoms of gluten intolerance.
    Dorman's new book is due to be re-released in April under a new title, Cure Your Child With Food, and includes a new chapter with more on information on 'bizarre' gluten-related effects on behavior and more.
    Read Mary Lochner's full article in the Anchorage Press.

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    Source:
    FoodProcessing.com.au

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    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

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    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.