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    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, science, and advanced research, and scientific methods. He previously served as Health News Examiner for Examiner.com, and devised 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 "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

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    Jefferson Adams
    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.

    Jefferson Adams
    Celiac.com 06/01/2015 - Earlier research on celiac disease and neuropathy has been hampered by the use of inpatient data, low study power, and lack of information on neuropathic characteristics.
    A team of researchers recently set out to accurately assess both relative and absolute risk of developing neuropathy in a nationwide population-based sample of patients with biopsy-verified celiac disease. The research team included Sujata P. Thawani, MD, MPH; Thomas H. Brannagan III, MD; Benjamin Lebwohl, MD, MS; Peter H. R. Green, MD; and Jonas F. Ludvigsson, MD, PhD.
    They are variously affiliated with the Peripheral Neuropathy Center at the Neurological Institute of Columbia University College of Physicians and Surgeons, the Celiac Disease Center in the Department of Medicine at Columbia University College of Physicians and Surgeons in New York, New York, with the Department of Medical Epidemiology and Biostatistics at the Karolinska Institutet in Stockholm, Sweden, and with the Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden.
    For their study, the team collected data on small-intestinal biopsies conducted at Sweden’s 28 pathology departments from 1969 to 2008. They compared the risk of neuropathy in a total of 28 ,232 celiac disease patients, all with villous atrophy, Marsh 3, against results from 139, 473 age- and sex-matched non-celiac control subjects.
    They used Cox proportional hazards regression to estimate hazard ratios (HRs), and 95% confidence intervals (CIs), for neuropathy as defined by relevant International Classification of Diseases codes in the Swedish National Patient Register; including both inpatient and outpatient data.
    They found that patients with biopsy-verified celiac disease faced a 2.5 times higher risk of developing neuropathy (95% CI, 2.1-3.0; P < .001). Celiac patients also had an increased risk of developing chronic inflammatory demyelinating neuropathy (2.8; 1.6-5.1; P = .001), autonomic neuropathy (4.2; 1.4-12.3; P = .009), and mononeuritis multiplex (7.6; 1.8-32.4; P = .006).
    However, the team found no association between celiac disease and acute inflammatory demyelinating polyneuropathy (0.8; 0.3-2.1; P = .68).
    The team found a significantly increased risk of neuropathy in patients with celiac disease, and they are recommending that doctors screen patients with neuropathy for celiac disease.
    Source:
    JAMA Neurol. Published online May 11, 2015. doi:10.1001/jamaneurol.2015.0475

    Jefferson Adams
    Celiac.com 11/02/2015 - People with celiac disease frequently report cognitive symptoms when they are exposed to gluten, and clinicians have documented cognitive deficits in some patients with newly diagnosed celiac disease. A team of researchers recently set out to determine whether patients with celiac disease have an increased risk of dementia.
    The research team included Benjamin Lebwohl, José A. Luchsinger, Daniel E. Freedberg, Peter H.R. Green, and Jonas F. Ludvigsson. They are variously affiliated with the Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA; the Department of Medical Epidemiology and Biostatistics, Karolinska University Hospital and Karolinska Institute, Stockholm, Sweden; the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA; the Department of Epidemiology, Mailman School of Public Health, Columbia University Medical Center, New York, NY, USA; and the Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    For their study, the team used a population-based database of adults aged 50 years and older with histologically proven celiac disease; that is, patients showing duodenal/jejunal villous atrophy. The database included patients from all 28 pathology departments in Sweden.
    The team compared the incidence of a subsequent dementia diagnosis to those of age- and gender-matched controls.
    In all, the team reviewed data on 8,846 patients with celiac disease, and 43,474 control subjects, with a median age of 63 years; 56% were female. Over an average follow-up time of 8.4 years, 4.3% of celiac disease patients were diagnosed with dementia, compared with 4.4% of control subjects (HR 1.07; 95% CI 0.95–1.20).
    Even though the data showed an increased risk of dementia in the first year following celiac diagnosis (HR 1.73; 95% CI 1.15–2.61), the risk did not continue through entire the follow-up period. Moreover, the increased risk was restricted to celiac patients with vascular dementia (HR 1.28; 95% CI 1.00–1.64), and was not present for Alzheimer’s dementia (HR 1.12; 95% CI 0.91–1.37).
    Overall, people with celiac disease do not show any increased risk for dementia, though subgroup analysis suggests that they may have a higher risk for vascular dementia.
    Source:
    Iospress.com

    Jefferson Adams
    Celiac.com 12/28/2015 - Immune-mediated cerebellar ataxias include gluten ataxia, paraneoplastic cerebellar degeneration, GAD antibody associated cerebellar ataxia, and Hashimoto's encephalopathy.
    Despite the identification of an increasing number of immune-mediated cerebellar ataxias, there is no proposed standardized therapy.
    Recently, a research team set out to develop guidelines for treatment of immune-mediated cerebellar ataxias.
    The research team included H. Mitoma, M. Hadjivassiliou, and J. Honnorat. They are variously associated with the Department of Medical Education at Tokyo Medical University in Tokyo, Japan; the Academic Department of Neurosciences at Royal Hallamshire Hospital, Sheffield, UK; the University Lyon 1; INSERM, UMR-S1028, CNRS, UMR-5292, Lyon Neuroscience Research Center, Neuro-Oncology and Neuro-Inflammation Team, 7; and the National Reference Centre for Paraneoplastic Neurological Diseases, Hospices Civils de Lyon, Hôpital neurologique in Bron, France.
    For their study, the team evaluated the efficacies of immunotherapies in reported cases using a common scale of daily activity.
    Their resulting analysis focuses on the importance of removing autoimmune triggers (e.g., gluten or cancer), evaluating immunotherapy (e.g., corticosteroids, intravenous immunoglobulin, immunosuppressants), and adjusting according to each sub-type.
    Source:
    Cerebellum Ataxias. 2015 Nov 10;2:14. doi: 10.1186/s40673-015-0034-y. eCollection 2015.

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    Wanted to give a dosing idea with b-vitamins, magnesium, and vitamin D. I take 1tbsp each of Liquid Health Energy & Stress and Neurological Support with 1 drop 2000iu vitamin D twice daily in a warm beverage before meals. Magnesium can vary and what is best depends on your bowel habits. If you do not have Diarrhea, and you do not use the restroom at least once a day then you need magnesium Citrate (Natural Vitality Calm) dosed to tolerance. Starting with 2g (1/4tsp), up the dose another
    I used to use Oil of Olay sensitive skin, but when I got a Nima Sensor it tested positive for gluten and I switched to Jergens Daily moisture fragrance free. Nima isn't meant for testing non food products, but I can't take the risk.  
    OMG I’ve having the same issue with dairy, sugars, even natural sugars like fruits! I’m following this thread. I really thought I was the only one! Thanks for asking it. My dr says I just need to go a good 6 months gluten/sugar/dairy free to “reset my system” and it should help. We’ll see. Good luck to you sir!   AJ
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