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  • Scott Adams
    Scott Adams

    Untreated Celiacs at Increased Risk of Cerebral Hypoperfusion

    Am J Med 2004;116:312-317.

    Italian researchers have concluded that as many as 73% of patients with untreated celiac disease have at least one brain region that is hypoperfused (the blood vessels are damaged), although the condition is rare in the non-celiac and treated celiac disease populations. Dr. Giovanni Addolorato, from the Catholic University in Rome, and colleagues looked at 15 untreated and 15 treated (on gluten-free diets) celiac disease patients and compared them with 27 healthy controls. They found that 11 (73%) of the untreated celiac disease patients exhibited hypoperfusion in at least one cerebral region, when only one treated patient and no controls had the problem. Additionally they found that in 7 of the 26 brain regions that they looked at, blood flow was significantly lower in untreated patients than in controls, and no blood flow differences were detected between the treated group and the control group.

    According to the researchers the cause of the vascular brain damage in celiac disease is unclear at this point, but it may be related to the increased intestinal blood flow, and/or endothelial inflammation caused by the autoimmune disease, perhaps involving antigliadin antibodies or unidentified neurotoxic antibodies.


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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.

  • Related Articles

    Scott Adams
    Nerve Disease and Celiac Disease
    Celiac.com 02/08/1996 - The article was based on a study published in the same weeks Lancet which was conducted by Dr. Marios Hadjivassiliou and colleagues at the Royal Hallamshire Hospital in Sheffield, England. Dr. Hadjivassiliou tested patients with various undiagnosed neurological symptoms and found that 57% of them tested positive to gluten sensitivity. Specifically, they tested positive for gliadin antibodies, which means they have gluten sensitivity and not necessarily celiac disease. Sixteen percent of the patients were found to have full blown celiac disease, which is far higher than the estimated .004% level found in the normal population. Five percent of the patients with previously diagnosed neurological disorders such as Parkinsons disease were found to have the gliadin antibodies present compared to 12% of a healthy control group.
    According Dr. Hadjivassilious theory, many neurological ailments could be caused when the anti-gliadin antibodies mistakenly attack neural tissue and destroy it. The fact that some celiac patients with neural damage never fully heal helps to support Dr. Hadjivassilious theory, because neural tissue repairs itself very slowly, if at all. Further, Dr. Hadjivassiliou states in the article that celiac disease seems to be much more common than was previously thought (1 in 250 people). When one includes the people who test positive for the gliadin antibody (this means they have gluten-sensitivity and are not necessarily celiacs), the amount could be much higher than 1 in 250. Based on his study, Dr. Hadjivassiliou recommends that patients who exhibit any type of neural disorders be tested for gluten sensitivity and celiac disease.

    Jefferson Adams
    Celiac.com 09/02/2008 - Thanks to a team of  researchers based in Great Britain, doctors may soon have a powerful new diagnostic tool to help them in their efforts to combat the damage caused by celiac disease. Their new discovery concerns people with celiac disease who may also develop neurological disorders.
    The research team was made up of Marios Hadjivassiliou, MD, Pascale Aeschlimann, BSc, Alexander Strigun, MSc, David Sanders, MD, Nicola Woodroofe, PhD, and Daniel Aeschlimann, PhD.  The team recently investigated the nature of gluten sensitivity by isolating a unique neuronal transglutaminase enzyme and examining whether it is the focus of the immune response in celiac patients with neurological dysfunction.
    About one in ten people with celiac disease also suffer from associated neurological disorders, mainly from a condition involving the cerebellum called gluten ataxia, and another involving the peripheral nerves called gluten neuropathy. For many people celiacs with gluten ataxia, their neurological problems are their sole symptom. Only about 1 out of 3 people with gluten ataxia and celiac disease will show classic intestinal damage when given a biopsy. This can make proper diagnosis difficult for them. Also, there’s presently no reliable way to predict which people with gluten intolerance might develop neurological problems.
    Most people familiar with celiac disease know that gastrointestinal discomfort is one of the most common symptoms. The antibody most commonly associated with such discomfort is called anti-transglutaminase 2 IgA. This is one of the main antibodies that doctors commonly look for when evaluating possible cases of celiac disease. Anti-TG2 antibodies are pretty much exclusive to people with celiac disease, and are associated with both untreated clinically symptomatic celiac disease, and with the latent form of the disease. This makes the presence of anti-TG2 antibodies an excellent diagnostic indicator of celiac disease.
    Anti-TG2, however, may not be the best indicator in every case of celiac disease. One example is in cases of dermatitis herpetiformis, which is an external skin reaction to gluten. Most people with dermatitis herpetiformis have a persistent itchy skin rash, and while the majority of cases show intestinal damage with a biopsy, patients rarely experience intestinal discomfort associated with classic celiac disease.1 There is also reliable data that point to a role that anti-TG3 plays in cases of dermatitis herpetiformis.2 This indicates that the nature of a given individual’s immune response may determine how celiac disease manifests itself within that individual.
    That hypothesis seems to be born out by the research team’s discovery that another antibody, called anti-transglutaminase 6 IgG and IgA response is widespread in gluten ataxia, completely outside of any intestinal symptoms. These antibodies are not found in healthy control patients or in patients with neurological conditions that had clear genetic causes. Both groups showed no anti-TG6 in their blood samples.
    The research team took blood samples from 20 patients with newly diagnosed celiac disease before the patients began a gluten-free diet. The team confirmed the presence of celiac disease with duodenal biopsy and made sure the patients had no patients had no evidence of neurological problems.
    The team then took blood samples from 34 patients with Gluten Ataxia, which they defined as otherwise sporadic idiopathic ataxia with positive IgG and/or IgA anti-gliadin antibodies.
    The also took samples from another17 patients with peripheral idiopathic neuropathy (PN) who tested positive for anti-gliadin antibodies. These 17 patients tested negative for anti-MAG and anti-GM1 and had no evidence of intestinal damage on biopsy.
    The team used three separate control groups. The first was a group with genetic ataxia, which included 18 patients with ataxia that was genetic in nature, or with a clear family history of autosomal dominant ataxia. The second control group of 14 patients included cases of diseases that were immune-mediated, but not tied to gluten-sensitivity (such as vasculitis, viral cerebellitis, paraneoplastic ataxia, GAD ataxia). Lastly, the team used blood samples from 19 healthy individuals as another control group.
    The research team used recombinant human transglutaminases to develop ELISA and inhibition assays with which they measured blood samples of patients with gluten sensitive gastrointestinal and neurological disorders, along with several control groups that included unrelated inherited or immune conditions, for the presence and specificity of autoantibodies.
    The team found that the blood samples of patients with celiac disease and gluten ataxia contain IgA and IgG class antibodies to TG6 that are not present in the healthy control patients or in patients with neurological conditions that had clear genetic causes.
    At present, doctors test for celiac disease by checking the HLA type, and looking for the presence of anti-gliadin and anti-transglutaminase 2 antibodies. The results of this study indicate that the presence of anti-transglutaminase 6 can help to pinpoint patients with gluten sensitivity that may be at risk of developing neurological disease.
    Forthcoming: Annals of Neurology
    Footnotes:
    1. Marks J, Shuster S, Watson AJ. Small bowel changes in dermatitis herpetiformis. Lancet 1966; 2:1280-1282.
    2. Sárdy M, Kárpáti S, Merkl B, Paulsson M, and Smyth N. Epidermal transglutaminase (TGase3) is the autoantigen of Dermatitis Herpetiformis. J Exp Med 2002; 195:747-757.


    Jefferson Adams
    Celiac.com 02/09/2009 - Doctors are recommending simple, low-cost blood tests to screen for celiac disease in patients who have Restless Leg Syndrome (RLS) with low serum ferritin, but who otherwise show no clear cause for iron deficiency.
    Low iron reserves are a known risk factor Restless Leg Syndrome, as blood iron levels below 45-50ng/mL have been tied to more severe expressions of RLS. In fact, iron levels are so important to assessing RLS, that it is now common for doctors to test blood ferritin levels when first assessing Restless Leg Syndrome. Celiac disease is a common genetic disorder of the immune system that can cause iron deficiency.
    Doctors S. Manchanda, C.R. Davies, and D. Picchietti of the College of Medicine at the University of Illinois at Urbana-Champaign recently set out to determine if celiac disease might play a role in iron deficiency in patients with Restless Leg Syndrome.
    The doctors evaluated a series of four patients with Restless Leg Syndrome and blood ferritin below 25ng/mL, who had shown positive blood tests for celiac disease. Doctors confirmed celiac disease for all four patients via duodenal biopsy and positive reaction to a gluten-free diet. In each case, Restless Leg Syndrome symptoms improved, with two patients discontinuing Restless Leg Syndrome medication and two responding positively without medication.
    The doctors are recommending simple, low-cost blood tests to screen for celiac disease in patients who have Restless Leg Syndrome with low serum ferritin, but who otherwise show no clear cause for iron deficiency.
    They also note that diagnosis and treatment of celiac disease is likely to improve the outcome for those patients with Restless Leg Syndrome, as well as to better identify people at risk for the significant long-term complications associated with celiac disease.
    Restless Leg Syndrome is just the latest neurological disorder to show a connection to celiac disease. Stay tuned as more information  becomes available.

    Source: Sleep Med. 2009 Jan 10. PMID: 19138881

    Jefferson Adams
    Can Going Gluten-free Protect You From Brain Disease?
    Celiac.com 03/20/2014 - No one wants a brain disease, and some recent books on the effects of gluten-free diets are suggesting that a gluten-free diet might actually protect you from brain diseases.
    One such book is Grain Brain: The Surprising Truth About Wheat, Carbs, and Sugar — Your Brain's Silent Killers, by David Perlmutter, M.D., a practicing neurologist.
    Symptoms of celiac disease are known to include intestinal difficulties associated with an adverse immunological response triggered by gluten. This response, which leads to inflammation in the gut, can happen elsewhere in the body too.
    According to Perlmutter, inflammation is at the root of many diseases and complications, including, brain decay.
    According to Perlmutter, gluten can lead to inflammation in the brain, which he believes leads to conditions like dementia and Alzheimer's.
    Perlmutter says that gluten, by triggering the immune system, causes inflammation in the brain, which promotes the brain's glycation by circulating blood sugar. Gram for gram, wheat raises blood sugar levels more than sugar itself.
    Perlmutter encourages strong dietary changes that have drawn some criticism. Specifically, he has recommended an intake of 60 or fewer grams of carbohydrate per day.
    Some point out potential negative health consequences of a high-fat, low-carb diet, both in healthy people and for those with specific conditions, like adrenal or thyroid issues.
    However, Perlmutter's take on brain glycation, in which gluten triggers an immune response in certain people, contributing to inflammation, and to inflammatory disease, such as diabetes and Alzheimer's, may have some foundation. 
    Perlmutter is a reputable neurologist, so his opinion and insight go beyond anecdotal evidence and speculation. It will be interesting to see how much of his perspective is borne out by science. Meantime, Perlmutter certainly makes for interesting, thought-provoking reading.
    What's your experience? Has going gluten-free made an impact on your brain function and awareness?
    Read more at: Celiac.com and at Medical Express.com.

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