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  • About Me

    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, and science. He previously served as Health News Examiner for Examiner.com, and provided health and medical content for Sharecare.com.

    Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book Dangerous Grains by James Braly, MD and Ron Hoggan, MA.

  • Related Articles

    Jefferson Adams
    Brain Abnormalities in Patients with Celiac Disease and Neurological Issues
    Celiac.com 09/17/2012 - Many aspects of celiac disease simply have not been well studied, so they remain poorly understood. For example, researchers have not done enough study on people with celiac disease to understand if they show any readily available serological markers of neurological disease.
    To better understand this issue, a research team recently assessed the amount of brain abnormality in patients with celiac disease, along with looking into MR imaging sequences as biomarkers for neurological dysfunction.
    The study team included S. Currie, M. Hadjivassiliou, M.J. Clark, D.S. Sanders, I.D. Wilkinson, P.D. Griffiths, and N. Hoggard, of the Academic Unit of Radiology at University of Sheffield, Royal Hallamshire Hospital, in Sheffield, UK.
    For their study, they conducted a retrospective examination of a consecutive group of 33 patients with biopsy proven celiac disease, who had been referred for neurological opinion. The group ranged in age from 19 to 64 years old, with an average of 44±13 years.
    Researchers divided the group into subgroups based on their main neurological complaints of balance disturbance, headache and sensory loss.
    They used 3T MR to evaluate variations in brain grey matter density, cerebellar volume, cerebellar neurochemistry and white matter abnormalities (WMAs) between celiac patients and control subjects.
    The results showed that the celiac patients had a significantly lower cerebellar volume than did control subjects. Celiac patients had 6.9±0.7% of total intracranial volume, compared with 7.4±0.9% for control subjects (p<0.05).
    Celiac patients also showed significantly less grey matter density in multiple brain regions, both above and below the tentorium cerebelli, compared with the control subjects (p<0.05).
    The data showed that 12 (36%) patients demonstrated WMAs unexpected for the patient's age, with the highest incidence occurring in the headache subgroup.
    This group of patients averaged nearly double the number of WMAs per MR imaging session than the subgroup with balance disturbance, and six times more than the subgroup with sensory loss.
    The MR images of celiac patients who have neurological symptoms show significant brain abnormality on MR imaging, which means that MR imaging may serve as valuable biomarkers of disease in celiac patients.
    Source:
    J Neurol Neurosurg Psychiatry. 2012 Aug 20.

    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.

    Jefferson Adams
    Celiac.com 10/27/2014 - There have been a few reports tying cortical myoclonus with ataxia to celiac disease. Such reports also suggest that the former is unresponsive to a gluten-free diet.
    A team of researchers recently set out to determine if there is any significant connection between the two conditions. The research team included Ptolemaios G. Sarrigiannis, Nigel Hoggard, Daniel Aeschlimann, David S. Sanders, Richard A. Grünewald, Zoe C. Unwin, and Marios Hadjivassiliou.
    They are variously associated with the Departments of Gastroenterology, Neurology, Neurophysiology and Neuroradiology at Royal Hallamshire Hospital, in Sheffield, UK, and with the College of Biomedical and Life Sciences at Cardiff University in Cardiff, UK.
    The team presented detailed electro-clinical characteristics of a new syndrome of progressive cortical hyperexcitability with ataxia and refractory celiac disease. Regular follow ups of over 600 patients with neurological manifestations due to gluten sensitivity revealed 9 patients with this syndrome.
    They found that all nine patients, six men and three women, experienced asymmetrical irregular myoclonus involving one or more limbs and sometimes face. This was often stimulus sensitive and became more widespread over time. Three patients had a history of Jacksonian march, and five had at least one secondarily generalized seizure. Electrophysiology showed evidence of cortical myoclonus. Three showed a phenotype of epilepsia partialis continua at onset.
    All patients showed clinical, imaging and/or pathological evidence of cerebellar involvement. All patients followed a strict gluten-free diet, and most successfully eliminated gluten-related antibodies. However, all patients still showed evidence of enteropathy, suggests that refractory celiac disease is to blame.
    During the study, two patients died from enteropathy-associated lymphoma and one from status epilepticus. Five patients were treated with mycophenolate and one in addition with rituximab and IV immunoglobulins. These patients showed improvement of ataxia and enteropathy, but continued to suffer the effects of myoclonus.
    These results indicate that myoclonus ataxia might be the most common neurological manifestation of refractory celiac disease.
    The clinical involvement, apart from ataxia, covers the whole clinical spectrum of cortical myoclonus.
    Source:
    Cerebellum & Ataxias 2014, 1:11. doi:10.1186/2053-8871-1-11

    Jefferson Adams
    Israeli Researchers Propose Link Between Gluten and ALS
    Celiac.com 04/23/2015 - It's well-known that many people with celiac disease experience neuropathy and other nerve disorders. Now, a team of Israeli researchers are cautiously proposing a link between gluten reactions and ALS.
    The research team, from the Tel Aviv Medical Center, believes that the gluten sensitivity seen in people with celiac disease might have a connection with ALS, or amyotrophic lateral sclerosis. Their study linking tissue transglutaminase 6 antibodies to ALS is the first study to document a connection between ALS and antibodies to a particular enzyme. Also known as Lou Gehrig's disease, ALS is a progressive disease that attacks nerve cells and pathways in the brain and spinal cord, eventually causing paralysis.
    In the study, researcher Vivian Drory and her team found antibodies to an enzyme produced in the brain, called tissue transglutaminase 6 (TG6), in 23 out of 150 patients with ALS, but in only five of 115 healthy volunteer subjects. Furthermore, ALS patients showed higher concentrations of those antibodies.
    It's well documented that people with celiac disease produce antibodies to another transglutaminase, TG2, when they eat gluten, a protein in wheat, barley and rye. Interestingly, nearly half (45%) of patients with celiac disease also produce antibodies to TG6, even when they have no neurological symptoms.
    Droury's team set out to evaluate the prevalence of celiac disease-related antibodies and HLA antigen alleles, as well as TG6 antibodies, in patients with ALS and healthy individuals serving as controls to determine whether a neurologic presentation of a gluten-related disorder mimicking ALS might occur in some patients.
    They conducted a case-control study in an ALS tertiary center, where they measured serum levels of total IgA antibodies, IgA antibodies to transglutaminase 2 (TG2) and endomysium, along with IgA and IgG antibodies to deamidated gliadine peptide and TG6 and performed HLA antigen genotyping in 150 consecutive patients with ALS and 115 healthy volunteers of similar age and sex.
    Study subjects did not have any known autoimmune or gastroenterologic disorder, and none was receiving any immunomodulatory medications.
    The team found that ALS patients with antibodies to TG6 showed the classic picture of ALS and the typical rate of disease progression. The volunteers with antibodies to TG6 showed no signs of any disease.
    All patients and control group participants were seronegative to IgA antibodies to TG2, endomysium, and deamidated gliadine peptide. Twenty-three patients (15.3%) were seropositive to TG6 IgA antibodies as opposed to only 5 controls (4.3%) (P = .004). The patients seropositive for TG6 showed a classic picture of ALS, similar to that of seronegative patients.
    The team tested fifty patients and 20 controls for celiac disease-specific HLA antigen alleles; 13 of 22 TG6 IgA seropositive individuals (59.1%) tested seropositive for celiac disease-related alleles compared with 8 (28.6%) of the 28 seronegative individuals (P = .04).
    Average levels of IgA antibodies to TG6 were 29.3 (30.1) in patients and 21.0 (27.4) in controls (P = .02; normal, <26). Average levels of IgA antibodies to TG2 were 1.78 (0.73) in patients and 1.58 (0.68) in controls (normal, <10). In a subset of study participants, mean levels of deamidated gliadin peptide autoantibodies were 7.46 (6.92) in patients and 6.08 (3.90) in controls (normal, <16).
    None of the ALS patients or volunteers had the antibodies to TG2 that are commonly associated with celiac disease, but the ALS patients were more likely to show the genetic mutations that put them at risk for celiac disease.
    Drory said her team has begun to study TG6 antibody levels in patients newly diagnosed with ALS, and they will be testing the effects of a gluten-free diet in some of those that test positive. However, theirs is just one report, and Drory expects it will be at least a couple of years before the team has any solid results. Her team is also inviting further input from other centers, and study of their data.
    In the meantime, she warns ALS patients against adopting a gluten-free diet without "clear evidence of antibodies," because any imbalance of diet might prove harmful. It's also worth remembering that an association is not the same as a cause. At least one earlier study concluded that there was no association between TG6 antibodies and either neurological disease or gluten itself.
    The possibility of a link between celiac disease and a degenerative nerve disease like ALS is interesting, to say the least. The findings of this team will likely invite more examination of any connection between gluten reactions and nerve disorders, so stay tuned for any follow-up news.
    Source:
    JAMA Neurol. 2015 Apr 13. doi: 10.1001/jamaneurol.2015.48.

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