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Celiac.com 11/06/2023 - Celiac disease is a condition where the body cannot properly process gluten. It is primarily known as a gastrointestinal disorder, but it can also lead to various neurological and psychiatric issues. Often, children receive diagnoses of neurological symptoms, such as epilepsy, attention-deficit hyperactivity disorder (ADHD), restless leg syndrome (RLS), and peripheral neuropathy, without identifying the root cause. Recent research delved into the neurological manifestations of gluten-related disorders and the influence of a gluten-free diet on these conditions, with a particular focus on pediatric patients. A team of researchers recently set out to review the pathological manifestations of gluten-related neuro-psychiatric disorders, and the impact of gluten-free diet in children. The research team included Prajwala Nagarajappa, Sree Mahathi Chavali, and Maneeth Mylavarapu. They are variously affiliated with the Department of Public Health, Adelphi University in Garden City, New Jersey, USA; the Department of Pediatrics, Graduate from GSL Medical College, Charlotte, USA; and the Mysore Medical College and Research Institute in Mysore, India. Many of these pediatric patients experience neuropsychiatric symptoms with no apparent cause. However, these symptoms might be linked to celiac disease, as studies show that antibody levels could be indicators. What's striking is that these neurological manifestations can often be managed, or even eliminated, with a gluten-free diet. Comprehensive Literature Review on Neuropathological Manifestations and the Impact of a Gluten-Free Diet To explore these issues, researchers conducted a comprehensive literature review, sourcing studies from major databases like PubMed and Google Scholar. They sought studies providing individual-level data on neuropathological manifestations and the impact of a gluten-free diet on extra-intestinal celiac disease symptoms. Their research protocol was registered in the International Prospective Register of Systematic Reviews (PROSPERO). The inclusion criteria covered prospective studies, observational studies, and case reports on pediatric patients with biopsy-confirmed celiac disease, serologically positive celiac disease, celiac disease with neuropsychiatric symptoms, and research reporting the effects of a gluten-free diet. After a stringent quality assessment to ensure minimal bias, 20 studies were included for discussion. In six studies, patients with neuropsychiatric symptoms had positive serological findings and more severe biopsy results. Seven studies explored the positive influence of a gluten-free diet, and five of these reported statistically significant results. The findings of this study underscore the role of gluten in the severity of neuropsychiatric symptoms in celiac disease. The research strongly indicates that a gluten-free diet can significantly impact the prognosis of this disease. Furthermore, neuropsychiatric symptoms without accompanying gastrointestinal manifestations are more frequently observed in pediatric patients. The study provides clear evidence of a substantial association between gluten and various neurological conditions, including neuropathy, ADHD, epilepsy, and RLS. These conditions can potentially benefit from a gluten-free diet. Given these insights, the study suggests that guidelines should incorporate a combination of serological, biopsy, and imaging techniques for early detection and the initiation of a gluten-free diet. Moreover, the research supports introducing gluten-free diet as a primary preventive measure in the pediatric population. By addressing the significance of gluten in pediatric neurological conditions, this study aims to raise awareness about this frequently misdiagnosed, but manageable disease. Read more in DOI: 10.7759/cureus.47062

Celiac.com 04/20/2016 - I am likely to be accused of gluten heresy. That is because I propose that celiac disease and gluten sensitivity usually coexist. By this I mean that they are not mutually exclusive entities. In other words, most people who have celiac disease are also gluten-sensitive. Many people who are gluten-sensitive are likely to develop celiac disease with continued gluten exposure (depending on their genetic markers). My observations show that the distinction between celiac disease and gluten-sensitivity (the gluten syndrome) is blurred. The purpose of published algorithms and decision trees are designed to separate out celiac disease from other gluten-illnesses. I suggest that this thinking is flawed. For example, most flow charts go something like this: (See Flow Chart 1 at left). People are selected for celiac-blood-tests for a number of reasons. If your blood tests are positive (and usually if you carry a DQ2/8 gene), then you get an endoscopy to confirm/deny the diagnosis. This allows you to be categorized either Yes-celiac disease or Not-celiac disease. There is no overlap. This is an "us-and-them" scenario. However, isolating YES-celiac disease from every other gluten problem does not take into account that people who have gluten-gut-damage may well have other manifestations of gluten-related disorders. Such simplistic algorithms (decision trees) strike problems at every decision point. Such as: Who should be tested? Who should be re-tested? When should these tests be done? At what age? On how much gluten? What tests should be done? What are the cut-off levels? How important is carrying the DQ2/8 genes? What about sero-negative celiac disease? How accurate are endoscopic biopsies? Who interprets the Marsh scale? How long should a gluten challenge be? Such simplistic algorithms (decision trees) also do not give satisfactory answers to the following questions: Why do 10% of people with celiac disease have little or no symptoms, despite having severe small bowel damage (villous atrophy)? This group is called "asymptomatic" celiac disease. Villous atrophy alone cannot account for the majority of gluten-related symptoms. Why do half of the people with celiac disease have autonomic nervous system dysfunction? This is the disturbance of the automatic nerve activity of your internal organs. This cannot be directly attributed to villous atrophy. Why do most people with celiac disease have some brain/mental upset, including the pervasive brain-fog? Many people have neurological disease from gluten but do not have established celiac disease. How can so many "extra-intestinal manifestations" of celiac disease be attributed to intestinal gut damage alone? I am sure that you will have witnessed strong feelings from the defenders of 'celiac-disease-is-a-stand-alone illness'. For instance, read these two opposing comments from Facebook: A. "I find it hard to believe that gluten intolerant people (or gluten avoiders) are as strict as us who have celiac disease." B. "I am gluten intolerant (suspected Celiac but I refuse to eat gluten in order to be tested properly) … I am incredibly strict on what I eat." The world of gluten is not black and white! But there remains a tension between those who have "biopsy-proven" celiac disease, and those people who are "gluten-intolerant". However, there is a cross-over between gluten-sensitivity/intolerance and celiac disease. There is no sharp dividing line – there is lots of grey! I would like to see the support groups of both celiac disease and gluten sensitivity work together with a focus on their common ground. This is already happening in some countries. Both groups promote an accurate diagnosis and a strict gluten-free diet. But I call into question the accuracy of current diagnostic methodology. Another comment from Facebook is a good example of these blurred lines: "I had an endoscopy and I have some small intestine damage: increased intraepithelial lymphocytes, shortened villi and duodenitis. The gastroenterologist said I had gluten-sensitivity but because I was not celiac (wasn't Marsh stage 3a), he said that I didn't need to be quite as careful with gluten. But I know I am super sensitive - even a small piece of chocolate with gluten in it makes me sick for a few weeks. I suspect that I either didn't have enough gluten before the endoscopy, or I am in the early stages of developing it." This is what I conclude: Both groups (people with celiac disease, and people with gluten sensitivity/intolerance) come under the umbrella category of gluten-related disorders. The term non-celiac gluten-sensitivity (NCGS) excludes those with evidence of intestinal damage from gluten. But with time and continued gluten ingestion, some of these people will develop celiac disease. NCGS is part of the gluten-related disorders spectrum (see my book: www.glutenrelateddisorder.com). Both groups have an identical list of possible symptoms. They are both equally harmed by gluten. They are indistinguishable from each other without blood tests and/or endoscopy. For both groups, my recommendation is to be zero gluten. Avoidance of cross-contamination is crucial for everyone. Both groups can be exquisitely sensitive to gluten. Some celiacs experience no symptoms from gluten, making it more of a challenge for them to remain gluten-zero. Some gluten-sensitive people do not yet have overt symptoms but are developing an inflammatory state. Many people who are gluten-sensitive produce antibodies to gluten, AGA (anti-gliadin-antibodies). There is a large literature on this. AGA-positive people are more likely to develop gluten-illnesses. AGA tests are recommended in the Fasano paper the "spectrum of gluten related disorders", for the celiac and gluten sensitivity work-up (particularly for neurological disorders). I use them on a day-to-day basis in my Clinic, and so do many other practitioners. More wheat/gluten harmful proteins have yet to be identified. Early in the development of celiac disease, the person can have significant symptoms, and they may have elevated AGA antibodies, but they may have no evidence yet of intestinal damage. At this stage these two conditions are indistinguishable. How early can you diagnose celiac disease? Do you have to wait until there is substantial intestinal damage so that you can make the classic diagnosis with villous atrophy? Or do you keep on eating gluten until the damage has occurred? Or do you go strictly gluten zero and not know if you are gluten sensitive or have early celiac disease? The HLA gene (DQ2/DQ8) cannot be used as a casting vote. It is my recommendation to abandon gluten as early as possible and not wait until you have substantial intestinal damage, which may never heal. Not only is the gluten intolerant community (this includes celiac disease) confused about gluten-illness. Also, the medical fraternity is confused. The science and clinical issues are rapidly developing whilst most medical practitioners are still looking for the classic celiac with weight loss, malabsorption, and a bloated tummy (and are using an out-of-date simplistic algorithm). Many people request celiac tests of their GPs but are denied the test. The community is much more aware of gluten related disorder than medical practitioners. Yes, there are a lot of issues to think about. These gluten-illnesses are complicated to diagnose. My prediction is that increasing numbers of people will adopt a gluten zero diet. However, almost certainly it is much more than the substance gluten that is making us sick. It will take a long time to unravel all of these strings. Most people are after an easy answer, or a drug, or a vaccine. But I'm sure that it is going to become even more complicated as we learn more. These complexities do not show up in a simplistic algorithm. The way for an individual to solve this is to adopt a gluten-zero diet, lifelong.

Celiac.com 02/16/2016 - About two years ago, as a result of two comprehensive review articles written by research scientists, Anthony Samsel and Stephanie Seneff, the term "glyphosates" made media headlines. Based on more than 200 citations, their reviews concluded that long term exposure to glyphosates via ingestion (in food and water) and/or inhalation seems to parallel the incidence and clinical features of celiac disease and may contribute to a number of diseases including autism, cancer, Parkinson's Disease, Alzheimer's Disease, infertility, depression, inflammatory bowel disease, Multiple Sclerosis, cancer, allergies, eosinophilic esophagitis (EOE), obesity, and kidney disorders. In case you don't already know, glyphosate (an organophosphate) is the active chemical ingredient in Monsanto's trademarked herbicide called RoundUp, which in the last 15 or more years has become very popular and is used throughout the world. It is largely used in "no-till non-organic production systems" as a desiccant (drying agent) for many genetically engineered (GE) food crops, especially those considered "RoundUp Ready" such as corn, soy, canola, cotton, sugar beets and alfalfa. RoundUp Ready foods are genetically engineered to resist being killed by RoundUp. While wheat is not a genetically engineered food crop, RoundUP is used on all non-organic wheat crops to produce a greater yield and reduce any rye grass weeds. The glyphosates in the RoundUp kill weeds by disrupting the shikimate pathway in the plant. I once used RoundUp to kill some weeds in my yard thinking that it was safe and nontoxic. It was thought then that humans and animals could not be affected by this weed-killing herbicide because humans and animals don't possess the shikimate pathway, only plants and bacteria do. That was until Samsel and Seneff set me straight. The bacteria in the human gut, which outnumbers the cells in our body, do have shikimate pathways. Glyphosates suppress the enzyme necessary for the shikimate pathway to produce aromatic amino acids such as tyrosine, tryptophan and phenylalanine. This happens in plant cells, too, where reduced levels of other amino acids have been discovered including serine, glycine and methionine. What does this mean for we humans? These amino acids are precursors to neurotransmitters (found in the gut and in the brain). Tryptophan alone is necessary for the production of serotonin, "the happy hormone." An impaired supply of serotonin frequently found in celiac disease causes depression. Impaired serotonin receptors in the gut sets the stage for inflammatory bowel disease. So besides blocking the shikimate pathway for the production of nutrients in foods, glyphosates seem to reduce the overall bioavailability of nutrients in the foods we eat. I have been a regular advocate for taking a daily multi vitamin and mineral, contending that the food we eat may lose nutrients from farm to table. Low and behold, Samsel and Seniff's review substantiated my contention. They cite two studies, which showed multiple mineral depletions in soybean crops treated with glyphosates. The depleted nutrients in the soybeans mirrored those frequently found in celiac disease, including cobalamin (B12), iron, molybdenum, selenium and sulfur. The authors hypothesize that the association between celiac disease and autoimmune hypothyroid disease may be due to a selenium deficiency. Samsel and Seniff suspect that chelation in the gut due to glyphosate ingestion may further account for deficiencies in cobalt, molybdenum and iron in these foods. This confirms yet another contention of mine that a single nutrient can indeed disrupt a whole system. The chelation of cobalamin in the gut is suspected to contribute to neurodegeneration and heart disease; the synergistic dynamic of molybdenum deficiency altering the body's supply of sulfate can have the consequence of cancer, anemia and insulin resistance. The authors purport that glyphosates disruption of the sulfur transport in the body is "the most important consequence of glyphosate's insidious slow erosion of health." The health of the human intestinal tract is affected by glyphosate ingestion and inhalation. Citing a study on the effects of glyphosates on predatory fish, Samsel and Seneff's review showed that glyphosates cause damage to the intestinal mucosal folds and microvilli similar to what is seen in celiac disease. Beneficial gut bacteria are killed, allowing the pathogenic (disease-causing) bacteria to proliferate, producing a state of bacterial dysbiosis (microbial imbalance). With reductions in the beneficial Bifidobacteria and Lactobacillus bacteria, the breakdown of both gluten and phytase are impaired, leading to the inability to digest gluten. The pathogenic bacteria such as E. Coli and C. Difficile can lead to kidney failure and inflammation. These authors argue that other digestive pathologies, such as pancreatitis, fatty liver disease and EOE are due to impaired CYP function in the liver. Could there also be a link between the high rates of small intestinal bacterial overgrowth (SIBO) and gut dysbiosis caused by glyphosate disruption of these enzymes? Glyphosates disruption of CYP enzymes in the liver occurs with celiac disease. These enzymes are involved in detoxification of xenobiotics (foreign chemical substances), so theoretically a reduction of CYP enzymes slows detoxification. Vitamin D3 and cholesterol synthesis and regulation of retinoic acid are also a part of the CYP enzyme system. It has puzzled me at times, that some of my patients do not respond to high dose vitamin D supplementation. The concept that glyphosates effect on CYP enzyme inhibition results in inadequate vitamin D activation in the liver could be a mystery solved. CYP enzymes are also important in bile acid production, gallbladder and pancreatic function. Samsel and Seneff hypothesize that glyphosate "disrupts the transport of sulfate from the gut to the liver and pancreas", resulting in bile acid insufficiency and gall bladder disease. Excess retinoic acid as a result of glyphosate exposure is similarly found in celiac disease and has been linked to reproductive disorders. How can we avoid glyphosate exposure? The obvious answer is not to use this herbicide to kill weeds in your yard. In the best interest of health, eat organic foods as much as possible, avoid the "the dirty 15" and genetically engineered foods. Check out your local farmer's market and buy from certified organic farmers. Eat animal products fed with non- genetically engineered foods. If you eat wheat, choose organic wheat. Glyphosates cannot be washed off of food, and there is yet no known way of detoxifying glyphosates from the body. The authors suggest eat garlic or soak in an Epsom salts bath to ensure adequate sulfur intake. Sea salt is a natural way to include minerals in your diet along with eating vegetables. Maria Larkin, M.Ed, RDN/LD owns Better Gut Better Health, LLC, a nutrition counseling practice in Durham and Portsmouth, NH. She is a registered dietitian and functional medicine provider, specializing in gastrointestinal concerns, food allergies and sensitivities. Website: www.bettergutbetterhealth.com. References: Samsel, A. and Seneff, S. Glyphosate's Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to Modern Diseases. Entropy, 2013: 15 (4): 1416-1463. Samsel, A. and Seneff, S. Glyphosate, pathways to modern diseases II: Celiac sprue and gluten intolerance. Interdisciplinary Toxicology, 2013: 6 (4): 159-184.

Celiac.com 09/24/2010 - A team of researchers recently found that people with celiac disease, even those following a gluten-free diet, also commonly suffer from sleep disorders that are related to depression, anxiety and fatigue. Since anxiety and depression both occur at higher rates in people with celiac disease than in the general population, the researchers were curious to see how celiac disease might affect quality of sleep. The research team included F. Zingone, M. Siniscalchi, P. Capone, R. Tortora, P. Andreozzi, E. Capone, and C. Ciacci. They are affiliated with the Department of Clinical and Experimental Medicine at Federico II University of Naples in Italy. In addition to finding that sleep disorders commonly affect people with celiac disease, regardless of gluten-free status, they also found that sleep disorders are less common in celiacs who score higher on quality of life scales, while those with low quality of life scores suffer at higher rates. For their study, the team evaluated people celiac disease at diagnosis, celiacs on a gluten-free diet at follow-up, and a group of healthy control subjects. All patients completed the Pittsburgh Sleep Quality Index (PSQI), SF36, Zung and Fatigue scales and State-Trait Anxiety Inventory (STAI). Their results showed that people with celiac disease at diagnosis and those following a gluten-free diet showed higher PSQI scores than did healthy volunteers (P < 0.001). PSQI scores were no lower for those following a gluten-free diet than for the others with celiac disease (P = 0.245). People with celiacs disease at diagnosis and those on a gluten-free diet scored similarly on the other tests, but differed sharply from the healthy control subjects. Patients who had higher individual scores for overall physical and mental fitness (r = −0.327, P = 0.002, and r = −0.455, P < 0.001, respectively) had higher overall PSQI scores. Factors influencing sleep quality were depression (r = 0.633, P < 0.001), fatigue (r = 0.377, P < 0.001), state anxiety (r = 0.484, P < 0.001) and trait anxiety (r = 0.467, P < 0.001). So, if you or someone you love has celiac disease, be prepared to address sleep issues, and maybe consider doing everything possible to ensure a good night's rest. Source: Alimentary Pharmacology & Therapeutics. DOI: 10.1111/j.1365-2036.2010.04432.x

Celiac.com 08/01/2017 - Although autoimmune disorders are not widely associated with Parkinson disease, there is increasing evidence for a link between immunity and neurodegenerative disorders. Indeed, both innate and adaptive immunity have been implicated in neurodegenerative disorders. A team of researchers recently set out to examine the connection between immunity and neurodegenerative disorders. The research team included Nikolaus R. McFarland, MD, PhD; Karen N. McFarland, PhD; and Todd E. Golde, MD, PhD. They are variously associated with the Center for Movement Disorders and Neurorestoration, Department of Neurology, College of Medicine, University of Florida, Gainesville, the Center for Translational Research in Neurodegenerative Disease, College of Medicine, University of Florida, Gainesville, the McKnight Brain Institute, University of Florida, Gainesville, and the Department of Neuroscience, College of Medicine, University of Florida, Gainesville. One of the more interesting examples the researchers examined is TREM2, a member of the immunoglobulin receptor superfamily that expresses itself in microglia and tissue macrophages, and which has gene variants associated increased Alzheimer ’s risk. They also took a look at other TREM2 variants that are linked to the development of polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy, a dementia associated with bone cystic lesions. Another example with less clear biological significance is the reproducible genetic association between a single-nucleotide polymorphism (SNP) in the locus and type 1 diabetes. We are at the very beginning of a research effort to better understand the connection between immunity and neurodegenerative disorders. It may take a while, but the results of these efforts will likely help researchers design better diagnostic and treatment regimes. Source: JAMA Neurol. Published online June 5, 2017. doi:10.1001/jamaneurol.2017.0843

Celiac.com 12/23/2013 - Symptoms of celiac disease negatively impact the social activities and emotional states of some patients. A team of researchers recently set out to assess rates of altered eating behavior in celiac patients. The research team included V. Passananti, M. Siniscalchi, F. Zingone, C. Bucci, R. Tortora, P. Iovino, and C. Ciacci. They are variously affiliated with the Department of Clinical and Experimental Medicine at University Federico II of Naples, Italy, and with the Department of Medicine and Surgery, University of Salerno, Baronissi Campus, in Salerno, Italy. The researchers evaluated 100 celiac adults and 100 control subjects of statistically similar gender, age, and physical activity. The researchers had both celiac patients and control subjects complete a dietary interview and the Binge Eating Staircases, Eating Disorder Inventory (EDI-2), Eating Attitudes Test, Zung Self-Rating Depression Scale, State Trait Anxiety Inventory Forma Y (STAI-Y1 and STAI-Y2), and Symptom Check List (SCL-90). The results showed that, compared with the control group, celiac patients had higher STAI-Y1 and STAI-Y2, Somatization, Interpersonal, Sensitivity, and Anxiety scores of the SLC-90. EDI-2 differed in pulse thinness, social insecurity, perfectionism, inadequacy, aceticisms, and interpersonal diffidences between celiac disease patients and healthy female controls, whilst only in interceptive awareness between celiac disease patients and healthy male controls. Celiac patients with gastrointestinal symptoms showed dependently higher EAT-26 scores. The EAT26 showed a connection between indices of diet-related disorders in both celiac disease, and the feminine gender after controlling for anxiety and depression. Eating disorders appear to be more frequent in young celiac women than in celiac men and in healthy control subjects. Overall, these results indicate that pathological eating behavior in celiac adults may be due to celiac disease itself, rather than the gastrointestinal related symptoms or psychological factors. Source: Gastroenterology Research and Practice Volume 2013 (2013), Article ID 491657

Celiac.com 07/30/2012 - A number of studies have found higher rates of lymphoma in people with celiac disease. However, few studies make any distinction between lymphoproliferative disorders (LPDs). A team of researchers recently investigated rates of various lymphoproliferative disorders in patients with celiac disease. The research team included L.A. Leslie, B. Lebwohl, A.I. Neugut, J. Gregory Mears, G. Bhagat, and P.H. Green. They are affiliated with the Department of Medicine at Columbia University Medical Center in New York, NY. The team wanted to assess rates of LPD subtypes in celiac disease patients, describe patterns of celiac disease presentation in patients who develop LPD, and compare survival in patients with various LPD subtypes. To do so, they carried out a retrospective cohort study of adults with biopsy-proven celiac disease seen at a US referral center from 1981 to 2010. They also identified patients with comorbid LPD, and calculated standardized incidence ratios (SIR) for each LPD subtype. They began with a study group of 1,285 patients with celiac disease. The group contained 40 patients with LPD [sIR = 6.48, 95% confidence interval (CI) = 4.62-8.64] including 33 with non-Hodgkin lymphoma (NHL, SIR = 6.91, 95% CI = 4.26-8.28). Rates of NHL subtypes including enteropathy-associated T-cell (EATL, n = 12), non-EATL T-cell (SIR = 22.43, 95% CI = 7.08-46.41), diffuse large B-cell (SIR = 5.37, 95% CI = 1.93-10.52), mantle cell (SIR = 32.21, 95% CI = 6.07-78.97), and marginal zone (SIR = 37.17, 11.73-76.89), lymphoma were substantially higher among patients diagnosed with celiac before LPD (n = 24, NHL SIR = 4.47, 95% CI = 2.86-6.44). Patients who developed LPD were usually older at time of celiac diagnosis (57.9 ± 15.5 versus 42.5 ± 17.4 years, P < 0.0001) and more likely to present with diarrhea (60.0% versus 39.8% P = 0.016), abdominal pain (17.5% versus 5.5% P = 0.0046), and/or weight loss (12.5% versus 4.0%, P = 0.028). EATL patients had a shorter average survival than non-EATL NHL patients (3.2 versus 15.0 years, P = 0.016). Overall, rates of LPD are higher in celiac disease patients, and those diagnosed at an older age, who present with symptoms of malabsorption, are more likely to be diagnosed with LPD. Source: Am J Hematol. 2012 Apr 26. doi: 10.1002/ajh.23237.

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