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    Parkinson's Disease, Seizures, Slow Recovery from Concussion


    Dr. Ron Hoggan, Ed.D.


    • Journal of Gluten Sensitivity Spring 2014 Issue


    Image Caption: Concusssion study. Image: CC--University of the Fraser Valley

    Celiac.com 11/10/2016 - So far, 2014 has been a challenging new year for me. I was reminded of some events that happened almost fifty years ago. Based on that reminder, I resolved to contact a former girlfriend, both to suggest that she get testing for celiac disease, and to apologize for some insensitive things I said and did when I was 17. She was a year younger than me and one grade behind me in school. She was very slender and exceedingly self-conscious about having what she called "a chest like a boy". (She may have been experiencing delayed development, as is sometimes seen in celiac disease.) Every new place we visited, she went looking for the washroom as soon as she could. Movie theatres, restaurants, libraries, everywhere we went, she found the washroom first. She even did that the first time she was at my mother's house, which occasioned an uncharitable comment from my mom.


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    Pat was also troubled by some microscopic hair that was growing on her upper lip. It sounds silly now, but these things were important to her at the time. I remember telling her that nobody could see her "moustache" without a magnifying glass. Nonetheless, she put Nair on it and, for at least one day, had the brightest red upper lip I have ever seen. She said it was too sore to put makeup on, so it really drew a lot of unwanted attention. Until meeting my wife, I never knew anyone who was as honest about who she was. I regret that I didn't appreciate her as much as I should have, but that was partly due to my age.

    Time passed, way led onto way, and life happened. Forty nine years later, there I was, looking for her on Facebook and other social media. I tracked her through old phone numbers, family members, and I even searched the title on her parents' home. I was full of excitement about re-connecting with my old friend, a person with whom I had shared those last innocent days of adolescence. Our friendship had been cut short because her dad was transferred to a city more than 600 miles away, and she was annoyed with me because I had said and done some insensitive things. We never even wrote to each other. I used to talk about her with my students, explaining our mutual fascination with literature. I thought about her often, but never, until this year, considered contacting her.

    After about a month of searching, I eventually found her. Much to my dismay, I was almost a year too late. She had passed away on March 10th of 2013, at the age of 64. At the time of her death, she was in the process of being evaluated for Parkinson's disease. She was at home when she experienced her last, massive seizure, which resulted in brain death. Both of her daughters are heartbroken over Pat's sudden, unexpected passing. Already a widow, Pat had left this world before I took the time and made the effort to be in touch with her again. I was filled with sadness, disappointment, and regret when I first reached one of her daughters and confirmed that she was the person I had known. I still wonder, if I had gotten in touch a decade earlier, would she still be alive? Would a gluten-free diet have helped her? I'll never know, but the relevant literature does seem to suggest that a gluten-free diet may have helped (1, 2).

    Then, a week or so ago, I received an email from a concerned mom. Her athletic, teen-aged son was recovering from a brain concussion he had sustained. His friends who had sustained similar concussions, at other times, reported having recovered more quickly. His mom began to wonder if her son's slow recovery could be the result of his celiac disease, despite more than a decade of strict compliance with the diet. I didn't know. I could only offer the suggestions that he try daily supplementation with medium chain triglycerides, and a ketogenic diet, as they seem to have stopped my life-long tremors. I also suggested that he try avoiding dairy and soy as well, based on research I did 14 years ago for my grandson.

    This concerned mom also mentioned, "I generally find doctors are dismissive of the idea that celiac is linked to any issues outside the digestive tract, unless it's malnutrition-related, and they tend to think everything should be hunky-dory if you just follow the gluten-free diet." She went on to say that "It gets kind of old being thought of as the silly, overprotective mom."

    Neurological researchers have long known about a correlation between a variety of neurological ailments and gluten sensitivity, with or without celiac disease (3). We also know that neurological symptoms are commonly found among more than half of patients with celiac disease (4). Also, despite modern diagnostic protocols and technology, we are still seeing some overlap between celiac disease and both amyotrophic lateral sclerosis (5) and multiple sclerosis (6) as well as other neurological illnesses. For instance, the increased presence of the gene named Parkinson's disease 7 (PARK7) has been found in the duodenal mucosa of untreated children with celiac disease and may be implicated in the alteration of the permeability of their intestinal barriers (7). This further suggests an important link between gluten sensitivity and Parkinson's disease. This gene may predispose to the appearance of this most distressing disease later in life.

    Many people with celiac disease continue to experience neurological symptoms, despite compliance with a gluten-free diet. This may suggest that the neurodegenerative dynamics, once initiated by gluten ingestion, may continue, either in the absence of gluten or in response to trace amounts of gluten (10). I also started to wonder if the cellular and immune system clean-up processes that follow brain injuries might initiate some of the same damaging autoimmune processes in the brain? They might also occur in response to other dietary factors which may trigger autoimmune dynamics that mimic reactions to gluten, or maybe there is some other, unknown factor that triggers the brain damage.

    One research group on the leading edge of the investigation of gluten sensitivity in relation to neurological illnesses reports that, "Incomplete elimination of gluten from the diet may be enough to abolish gastrointestinal symptoms with recovery of the small bowel mucosa but is insufficient to arrest the state of heightened immunological responsiveness resulting in neuronal injury" (10). So, when it comes to even tiny amounts of gluten, they may be enough to perpetuate gluten induced neurological illnesses. There may also an agent in the environment that is causing a cross reaction. This area really needs more investigation, as baby boomers threaten alarmingly increased rates of all forms of dementia.

    We already know that people with celiac disease are at much greater risk of developing neurological diseases than the general population (13). These ailments range from headaches to learning disabilities to movement disorders to tic disorders, to seizures, to sensory disorders (4) and many who have non-celiac gluten sensitivity also experience a high rate of neurological disease (3). Does that also mean that young athletes with celiac disease will take longer to recover from head injuries?

    Does it also mean, given the slow acceptance of gluten as a factor in many common neurological illnesses (11) that people like my former high school flame will never be told about the neuro-protective benefits of a gluten-free diet or a ketogenic diet? Surely, resistance to the well established data showing neurological manifestations of gluten sensitivity as a scientific fact (12) is more emotional than rational. A gluten-free diet and/or a ketogenic diet should be offered to those people regardless of whether their neurologist is either resistant to, or not staying current with, his/her professional literature. But they cannot offer what they do not know or have developed some bias against. Dr. David Perlmutter has done an excellent job of getting the word out to the general public, with his recent book titled Grain Brain, but there is much more work to do.

    People who are gluten sensitive, and are therefore at greater risk of developing neurological disease, might be well advised to look carefully at the benefits of a high fat, ketogenic diet, and the benefits of supplementing with medium chain triglycerides and Omega 3 fatty acids (14). Equally, they might be well advised to avoid the pro-inflammatory omega 6 and omega 9 fatty acids, as well as limiting the amounts of polyunsaturated fats they eat, which are also pro-inflammatory 14). I find that I feel my best when I am in mild, diet-induced ketosis (about 15 mg/dl as measured in morning urine, with Ketostix, which are inexpensive and available at most drug stores). There are a number of good books that explore the fine points of a high fat, ketogenic diet. These include The Art and Science of Low Carbohydrate Living by Volek and Phinney, The Ketogenic Diet by Lyle McDonald, and many others.

    Finally, when considering a gluten-free diet for neurological ailments, it is important to recognize that 20 parts per million may be far too much gluten to consume. The maximum threshold to qualify as gluten-free under the United Nations Codex Alimentarius Commission and many other regulatory agencies, including the FDA, is 20 parts per million. Without further research, especially in the field of neurology and gluten sensitivity, we will never know what, if any, levels of gluten are safe to consume.

    Regardless of the nature of your neurological ailment, whether it is Parkinson's disease, or seizures, or multiple sclerosis, or amyotrophic lateral sclerosis, or brain cancer, or almost any other kind of cancer (15), or even if you are just slow recovering from a neurological injury, the positive results of dietary interventions might offer you a whole new lease on life.

    Sources:

    1. http://www.medscape.com/viewarticle/770593
    2. Currie S, Hadjivassiliou M, Clark MJ, Sanders DS, Wilkinson ID, Griffiths PD, Hoggard N. Should we be ‘nervous' about coeliac disease? Brain abnormalities in patients with coeliac disease referred for neurological opinion. J Neurol Neurosurg Psychiatry. 2012 Dec;83(12):1216-21.
    3. Matheson NA. Letter: Food faddism. Am J Clin Nutr. 1975 Oct;28(10):1083.
    4. Zelnik N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2004 Jun;113(6):1672-6.
    5. Brown KJ, Jewells V, Herfarth H, Castillo M, White matter lesions suggestive of amyotrophic lateral sclerosis attributed to celiac disease. AJNR Am J Neuroradiol. 2010 May;31(5):880-1
    6. Batur-Caglayan HZ, Irkec C, Yildirim-Capraz I, Atalay-Akyurek N, Dumlu S. A case of multiple sclerosis and celiac disease. Case Rep Neurol Med. 2013;2013:576921.
    7. Vörös P, Sziksz E, Himer L, Onody A, Pap D, Frivolt K, Szebeni B, Lippai R, GyÅ‘rffy H, Fekete A, Brandt F, Molnár K, Veres G, Arató A, Tulassay T, Vannay A. Expression of PARK7 is increased in celiac disease. Virchows Arch. 2013 Sep;463(3):401-8.
    8. Hadjivassiliou M, Grünewald RA, Lawden M, Davies-Jones GA, Powell T, Smith CM. Headache and CNS white matter abnormalities associated with gluten sensitivity. Neurology. 2001 Feb 13;56(3):385-8.
    9. Hadjivassiliou M, Sanders DS, Grünewald RA, Woodroofe N, Boscolo S, Aeschlimann D. Gluten sensitivity: from gut to brain. Lancet Neurol. 2010 Mar;9(3):318-30
    10. Hadjivassiliou M, Grünewald RA, Davies-Jones GA. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3.
    11. Tengah P, AJ Wills. Questions and Answers About the Neurology of Gluten Sensitivity. Pract Neurol 2003;3:354-357
    12. Hadjivassiliou M, Grünewald R. The Neurology of Gluten Sensitivity: science Vs conviction. Pract Neurol 2004;3:4, 124-126.
    13. Hadjivassiliou M, Grünewald R. Gluten sensitivity as a neurological illness. Neurol Neurosurg Psychiatry. May 2002; 72(5): 560–563.
    14. http://www.omegascience.org/product_ingredients/coconut_oil.aspx
    15. Paoli A, Rubini A, Volek JS, Grimaldi KA. Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. Eur J Clin Nutr. 2013 Aug;67(8):789-96

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    Guest Suzanne

    Posted

    The author of this article has insight , but fails to mention the mutation on chromosome 1 called MTHFR, which is likely probable here. Also the features you have from teen years, are possibly indicative of EDS (larger eyes, smaller nose- a bit pinched and small mouth. Do you have joint hyper mobility? What is your B12 level? We have gone down the road, so I'm sharing. Celiac is also on the Steroidogenic Pathways (as something gone wrong) that methylation can turn "off" if improved. Poor methylation happens with the MTHFR mutation and there are two variants to test that seem the most common and bothersome in the system. 23 and Me genetic testing was a one stop shop for us and we learned a lot and solved bigger parts of a three year puzzle for my daughter.

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    I have Celiac disease, but I also have to avoid Nightshades. Three potato chips and my brain starts to react. Potato starch is frequently used in a lot of gluten free products. If you or anyone you know is having brain related issues please have them try eliminating Nightshades. Potatoes, peppers, and tomatoes are all Nightshades. It does make a huge difference.

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    I happen to have kidney damage secondary to coeliac, (my daughter has joint damage secondary to coeliac.) I do wonder, if, having made gluten antibodies that also attack my kidneys - the presence of my kidneys is enough to keep the antibody load up. i.e., You would no longer need a further trigger with gluten. If correct, this would account for other tissue damage to keep going, once it has been triggered.

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    Guest Frances L. Garcia, MD

    Posted

    I think we have a lot to learn yet about Celiac Disease. I have developed spasmodic non-kinesigenic dyskinesia, a movement disorder and I have adhered to a strict gluten-free diet for the past 15 years, but spent 20 trying to get a diagnosis. . Did not know about night shades and I love all three. rnInterestingly, one gene for the dyskinesia actually overlaps the Celiac gene. This is something to look into. There is a thing in genetics called epigenetics, where DNA anywhere in your genome affects the expression of other genes. This includes "junk DNA". Maybe this is a mechanism for the diversity of non-GI symptoms we are discovering related to Celiac.

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    Conversely, I would be most reluctant to accept the interdiction of meats, organic or otherwise. On the other hand, growth promotion using low doses of anti-biotics can result in delivering anti-biotic resistant microbes. Poultry, hogs, and cattle are all high risk meats. Further, grains, especially gluten grains and corn, combine to form the mainstay of feeds used to fatten these animals and birds for market, where weight is the determining factor in the price paid for these meats.
    Bredesen also pointed, quite rightly, to the small number of subjects as a weakness in his study. However, when 9 of their 10 subjects achieved such remarkable results, especially in the context of the common belief that dementia, at any stage, is irreversible, this study certainly suggests that exploring dementias as a group of metabolic illnesses is a potentially fruitful path.
    This is a perspective that is enjoying considerable support from a variety of sources. Many researchers have, for the past decade or so, thought of many dementias as type 3 diabetes, with a growing body of support for this perspective amassing in the peer reviewed literature (41). More recently, chronic sleep deprivation has been similarly implicated in several ways. The first is specific to Alzheimer's disease, where beta amyloid deposits or plaques characterize this ailment. New research has shown that during sleep, brain tissues shrink, while the fluids that surround the brain permeate these tissues and inter-cellular structures, assimilating amyloid, which is a group of protein fragments (peptides) that are waste products of daytime brain cell activities (42). Because there is no lymphatic system in the brain, it has long been believed that the brain did not dispose of its waste products. However, another field of brain research has shown that conduits of these fluids form surrounding the blood vessels, carrying waste products into the bloodstream and, ultimately, out of the brain for disposal (42). Since average nightly sleep duration has shortened from nine hours to seven hours, given the above research findings, this reduction in sleep decreases our nightly capacity to remove waste amyloid and other detritus, leading to the formation and growth of amyloid deposits, which characterize at least one form of dementia.
    This same culture-wide sleep deprivation also induces memory disturbances and memory losses. It does so by a circuitous route. Throughout the day, each of us encodes memories through our hippocampus, a small region of the brain that is also involved in spatial navigation and contributes, with other parts of the lymbic system, to the regulation of many body functions. During sleep, the day's memories are thought to be processed and integrated with prior knowledge, emotions, and impressions in the neo-cortex. Some researchers are now postulating that this integration process is what results in our dreams (43-45). Regardless of whether it is the author of our dreams, Dr. Robert Stickgold and colleagues have shown that sleep helps us to consolidate the day's learning experiences, thus improving our memory retention. He has also shown that inadequate sleep compromises learning (43). The net result is that we not only need sleep to permit the brain to clean out the day's wastes, we also need it to form and preserve learning.
    Although Bredesen made no mention of it, there is another complicating factor here. Statin drugs are aimed at reducing cholesterol. However, they have also been shown to induce memory problems. One friend of mine was prescribed a statin drug, and he stopped being able to recognize me. After discontinuing this medication, he told me that I looked familiar, but he couldn't even guess at my name or where he knew me from. He waves hello to me from across the street, but doesn't cross it to visit anymore. And that seems to be where the recovery of his memory is stalled. It is with heart-rending sadness that I occasionally see him in passing. I say hello. But if he doesn't notice me waving or hear me shouting, there isn't even an exchange of greetings. He seems happy enough. So perhaps the loss is mostly mine. But I don't imagine that he would willingly have chosen this "new" world of his.
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    15. Vincent A, Crino PB. Systemic and neurologic autoimmune disorders associated with seizures or epilepsy. Epilepsia. 2011 May;52 Suppl 3:12-7.
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    18. Currie S, Hadjivassiliou M, Clark MJ, Sanders DS, Wilkinson ID, Griffiths PD, Hoggard N. Should we be 'nervous' about coeliac disease? Brain abnormalities in patients with coeliac disease referred for neurological opinion. J Neurol Neurosurg Psychiatry. 2012 Dec;83(12):1216-21.
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    21. Caio G, De Giorgio R, Venturi A, Giancola F, Latorre R, Boschetti E, Serra M, Ruggeri E, Volta U. Clinical and immunological relevance of anti-neuronal antibodies in celiac disease with neurological manifestations. Gastroenterol Hepatol Bed Bench. 2015 Spring;8(2):146-52.
    22. Finsterer J, Leutmezer F. Celiac disease with cerebral and peripheral nerve involvement mimicking multiple sclerosis. J Med Life. 2014 Sep 15;7(3):440-4. Epub 2014 Sep 25.
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    28. Porcelli B, Verdino V, Bossini L, Terzuoli L, Fagiolini A. Celiac and non-celiac gluten sensitivity: a review on the association with schizophrenia and mood disorders. Auto Immun Highlights. 2014 Oct 16;5(2):55-61.
    29. De Santis A, Addolorato G, Romito A, Caputo S, Giordano A, Gambassi G, Taranto C, Manna R, Gasbarrini G. Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3.
    30. Blair A. Wheat-free diet gives food for thought. The Times (UK) June 12, 2004 http://www.timesonline.co.uk/tol/news/uk/article444290.ece
    31. Zingone F, Siniscalchi M, Capone P, Tortora R, Andreozzi P, Capone E, Ciacci C. The quality of sleep in patients with coeliac disease. Aliment Pharmacol Ther. 2010 Oct;32(8):1031-6.
    32. Brown KJ, Jewells V, Herfarth H, Castillo M. White matter lesions suggestive of amyotrophic lateral sclerosis attributed to celiac disease. AJNR Am J Neuroradiol. 2010 May;31(5):880-1.
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    35. Hadjivassiliou M, Rao DG, Grìnewald RA, Aeschlimann DP, Sarrigiannis PG, Hoggard N, Aeschlimann P, Mooney PD, Sanders DS. Neurological Dysfunction in Coeliac Disease and Non-Coeliac Gluten Sensitivity. Am J Gastroenterol. 2016 Feb 2.
    36. Hadjivassiliou M, Duker AP, Sanders DS. Gluten-related neurologic dysfunction. Handb Clin Neurol. 2014;120:607-19.
    37. Hadjivassiliou M, Rao DG, Wharton SB, Sanders DS, Grünewald RA, Davies-Jones AG. Sensory ganglionopathy due to gluten sensitivity. Neurology. 2010 Sep 14;75(11):1003-8.
    38. Hu WT, Murray JA, Greenaway MC, Parisi JE, Josephs KA. Cognitive impairment and celiac disease. Arch Neurol. 2006 Oct;63(10):1440-6.
    39. de la Monte SM. Brain insulin resistance and deficiency as therapeutic targets in Alzheimer's disease. Curr Alzheimer Res. 2012 Jan;9(1):35-66
    40. de la Monte SM, Tong M. Brain metabolic dysfunction at the core of Alzheimer's disease. Biochem Pharmacol. 2014 Apr 15;88(4):548-59.
    41. de la Monte SM. Type 3 diabetes is sporadic Alzheimer's disease: mini-review. Eur Neuropsychopharmacol. 2014 Dec;24(12):1954-60.
    42. Nedergaard M, Goldman SA. Brain Drain. Scientific American. 2016 March; p. 44-49.
    43. Stickgold R. Parsing the role of sleep in memory processing. Curr Opin Neurobiol. 2013 Oct;23(5):847-53.
    44. Stickgold R. Early to bed: how sleep benefits children's memory. Trends Cogn Sci. 2013 Jun;17(6):261-2
    45. Stickgold R, Walker MP. Sleep-dependent memory triage: evolving generalization through selective processing. Nat Neurosci. 2013 Feb;16(2):139-45.
    46. Taheri S, Lin L, Austin D, Young T, Mignot E (2004) Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Med 1(3): e62. Sleep deprivation raises ghrelin & lowers leptin production.

    Jefferson Adams
    Celiac.com 04/13/2017 - A team of researchers recently set out to determine whether hospital admission for autoimmune disease is associated with an elevated risk of future admission for dementia.
    The research team included Clare J Wotton, and Michael J Goldacre, both affiliated with the Unit of Health-Care Epidemiology, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
    The pair set up their retrospective, record-linkage cohort study using national hospital care and mortality administrative data from 1999–2012. From that patient data, they assembled a study group of people admitted to hospital with a range of autoimmune diseases, along with a control group, and followed forward in time to see if how many patients eventually developed dementia.
    Data revealed a total of 1,833,827 people admitted to hospital with an autoimmune disease. The number of patients for each autoimmune disease group ranged from 1,019 patients in the Goodpasture's syndrome group, to 316,043 people in the rheumatoid arthritis group.
    The researchers found that the rate ratio for dementia after admission for an autoimmune disease, compared with the control cohort, was 1.20 (95% CI 1.19 to 1.21). For patients whose dementia type was specified, the rate ratio ranged from 1.04 to 1.08 for Alzheimer's disease, and 1.26 to 1.31 for vascular dementia.
    Of the 25 autoimmune diseases studied, 18 showed significant positive associations with dementia, 14 of which were statistically significant. Significant associations include Addison's disease (1.48, 1.34 to 1.64), multiple sclerosis (1.97, 1.88 to 2.07), psoriasis (1.29, 1.25 to 1.34) and systemic lupus erythematosus (1.46, 1.32 to 1.61).
    The connections with vascular dementia may be one aspect of a wider connection between autoimmune diseases and vascular damage. Though findings were significant, effect sizes were small. Researchers advise clinicians to note the possibility of dementia in patients with autoimmune disease.
    The researchers are calling for further studies to assess their findings and to explore possible ways to reduce any increased risk.
    Source:
    BMJ

    Jefferson Adams
    Celiac.com 06/12/2017 - Previously, Transcranial Magnetic Stimulation in de novo celiac disease patients has signaled an imbalance in the excitability of cortical facilitatory and inhibitory circuits.
    Researchers have reported that, after about of 16 months on a gluten-free diet, patients experience a global increase of cortical excitability, which suggests some kind of compensation for disease progression, likely mediated by glutamate.
    To better assess these finding, a team of researchers recently conducted cross-sectional evaluation of the changes in cortical excitability to TMS after a much longer gluten-free diet.
    The research team included M. Pennisi, G. Lanza, M. Cantone, R. Ricceri, R. Ferri, C.C. D’Agate, G. Pennisi, V. Di Lazzaro, and R. Bella. They are variously affiliated with the Spinal Unit, Emergency Hospital "Cannizzaro", Catania, Italy, the Department of Neurology IC, I.R.C.C.S. "Oasi Maria SS.", Troina, Enna, Italy, the Department of Medical and Surgical Sciences and Advanced Technologies, Section of Neurosciences, University of Catania, Catania, Italy, the Gastroenterology and Endoscopy Unit, University of Catania, Catania, Italy, the Department "Specialità Medico-Chirurgiche,” University of Catania, Catania, Italy, and the Institute of Neurology, Campus Bio-Medico University, Rome, Italy.
    For their study, the team enrolled twenty patients who had followed an adequate gluten-free diet for about 8.35 years, on average. They then compared the results with twenty de novo patients, and twenty more healthy controls. The team measured Transcranial Magnetic Stimulation, recorded from the first dorsal interosseous muscle of the dominant hand, as follows: resting motor threshold, cortical silent period, motor evoked potentials, central motor conduction time, mean short-latency intracortical inhibition and intracortical facilitation.
    De novo patients showed a shorter cortical silent period, while responses for gluten-free diet participants were similar to controls. Regardless of diet, all celiac patients showed a significantly smaller amplitude of motor response than did control subjects,
    Again, without regard to diet, all celiac patients showed a statistically significant decrease of mean short-latency intracortical inhibition and enhancement of intracortical facilitation with respect to controls.
    The team also observed that gluten-free celiac patients showed more intracortical facilitation compared to non-gluten-free patients. Neurological examination and celiac disease-related antibodies were both negative.
    This study showed that a gluten-free diet helps to mitigate the electrocortical changes associated with celiac disease. Even so, in many patients, an intracortical synaptic dysfunction, mostly involving excitatory and inhibitory interneurons within the motor cortex, may persist.
    The calls for further investigation into the clinical significance of subtle neurophysiological changes in celiac disease.
    Source:
    PLoS One. 2017 May 10;12(5):e0177560. doi: 10.1371/journal.pone.0177560. eCollection 2017.

    Dr. Rodney Ford M.D.
    Celiac.com 07/27/2017 - It was five years ago when I launched the concept of "gluten is bad for us all!"
    Yes, you read that right - bad for you, bad for me, and bad for everyone else! This implies that the whole world should avoid gluten.
    This is a bold and an unrealistic statement to make. However, I thought that there was enough evidence about the harm of gluten for us to demand massive changes to everyone's diet, our farming practices and food manufacturing industry. Eventually, this could substantially improve the health of our Nations. However the practicalities of such a change would be very difficult overcome. Especially with the economic forces of Big-Pharma, Big-Agriculture and Big-Government.
    I was not alone in thinking this. Many other medical/health professionals had also reached this conclusion with the growing research evidence of gluten-related diseases. Five years ago the top 15 celiac-doctors acknowledged that gluten-related-illness was a common problem that needed much better diagnostic tests. In their landmark paper "Spectrum of gluten-related disorders: consensus on new nomenclature and classification." http://www.biomedcentral.com/1741-7015/10/13, they concluded: "all individuals, even those with a low degree of risk, are susceptible to some form of gluten reaction during their life span."
    This publication was later expanded into a book. The description of this book is: "A Clinical Guide to Gluten-Related Disorders provides primary health care providers the succinct material they need to immediately evaluate and support their patients. Gluten-related disorders have a wide presentation, and this text covers the recognition, evaluation, and multi-disciplinary approach to the management of disease. Readers will benefit from the general overview of gluten intolerance and from the common sense approach to developing treatment and dietary plans. Clinical vignettes offer clinicians real-life scenarios to help put the disease and its treatment in context for their patients."
    I predicted, that in another generation, gluten will be rejected by most reputable food processing companies. This will be a difficult concept for many people to accept because wheat products are currently the very foundation of our diet. After 10,000 years of eating gluten grains it comes as a huge shock that our staple food has been demonstrated as harmful.
    Over the last five years I continue to see children and families made very unwell by eating gluten grains. It is also likely that that gluten may not be the sole culprit, as there are other wheat proteins that are toxic to humans. However, a gluten-free diet will eliminate these other wheat proteins.
    I have just seen Caleb who is 10 years old and was referred to me three months ago because of generalised intermittent abdominal pains. These pains come and go, but trouble him on most days of the week. These pains sometimes Bring him to tears, and on occasions he has presented to the emergency department at the hospital with severe abdominal pain. The usual investigations did not show up any specific abnormality, and his scans and x-rays for all within normal limits, other than showing that he had some constipation.
    He had also been suffering from sore throats and gastric reflux has been implicated, for which he was prescribed Omeprazole.
    In addition, he was not putting on much weight.
    My concluding remarks about him were "It is possible he is gluten intolerant. This could explain all of his symptoms (abdominal pain, constipation, gastric reflux, and tiredness). His mother has irritable bowel and has previously benefited from a gluten-free diet. I recommend that Caleb go on a three month trial of a gluten-free diet. His parents will let me know of his progress in three months time."
    Well, I've just seen him again following his three-month gluten-free trial. Mum said "what a difference! He now has regular bowel motions without the need for Macrogol, he no longer has abdominal pain and his reflux has disappeared and he is no longer needing Omeprazole. In addition he is growing again. With gluten infringements he gets a sore tummy, sore throat with some reflux and constipation again."
    It has taken Caleb a while to get into the swing of things. He still will eat gluten foods if he has the opportunity! He has to pay the consequences with his symptoms. He is also growing again. I am thrilled with his progress. He needs to stay gluten-free for the long haul. He needs to be as close to gluten zero as possible. He is lucky that both of his parents have joined him on his gluten-free diet. His mother is a lot better and has lost substantial weight, his dad also feels a lot more healthy on a gluten-free diet.
    Caleb is just one of millions of children who are currently suffering from guilty related diseases, but un-diagnosed and un-recognized.
    Yes, it was five years ago when I launched the concept of "gluten is bad for us all!" I have not change my opinion. Indeed, I am more confident about what I have written about the harm that gluten has caused throughout the world. I looked the 8 following questions. I wonder what your opinion might be:
    1. Why pick on Gluten?
    10 decades of Celiac; 10 years of Gluten Syndrome; 10 months of ZERO gluten.
    2. Why is gluten so bad for us all?
    Cannot digest it; gut leaky; toxic proteins.
    3. Why are there so many sick people?
    "Nobody knows what's wrong with me." Old technology for modern disease.
    4. How much illness can be attributed to gluten?
    The catalogue of gluten-illness. Health burden of gluten.
    5. Can gluten really damaged brains and nerves and minds?
    Brain symptoms, nerve damage, mental disorders.
    6. What other illnesses might be linked to gluten?
    Auto-immune diseases.
    7. Should we really change what we eat?
    Diet - not Drugs. The alternative grains. Health-giving foods.
    8. How can we feed 7 billion people
    Is bad food better than no food?
    Dr Ford's book is available as an e-book:
    Gluten: ZERO Global (http://www.glutenZEROglobal.com)
    Gluten is bad for us all – the evidence for a gluten free planet.
    Warning: go gluten free now before it is too late.
    Written in the spirit of cooperation and knowledge sharing.

    Jefferson Adams
    Celiac.com 11/22/2017 - A team of physicians recently reported on the case of a 3-year-old Albanian girl who presented at their clinic with carpal spasms and hand paresthesia. The physicians include Atifete Ramosaj-Morina; A. Keka-Sylaj; V. Hasbahta; A. Baloku-Zejnullahu; M. Azemi; and R. Zunec.
    A physical exam showed the girl to be in good physical condition, with a body weight of 10.5 kg (10 percentile). She was suffering from carpal spasms and paresthesias of her extremities. Positive Chvostek and Trousseau signs
    indicated neuromuscular irritability.
    Blood tests showed severe hypocalcemia with a total serum calcium of 1.2 mmol/L (normal range 2.12 to 2.55 mmol/L), ionized calcium of 0.87 (normal range 1.11 to 1.30 mmol/L), and 24-hour urine calcium excretion of 9.16 mmol (normal range female
    The team screened the girl for celiac disease with antigliadin immunoglobulin A, anti-tissue transglutaminase, and anti-endomysial immunoglobulin A antibodies. All tests were positive. The girl underwent a duodenal biopsy, which showed lymphocyte infiltration, crypt hyperplasia, and villous atrophy compatible with celiac disease grade IIIb according to the Marsh classification.
    Following her celiac diagnosis, the team conducted human leukocyte antigen typing, which provided a definite diagnosis of celiac disease. She was started on a gluten-free diet. Apparently, the girl did not follow a gluten-free diet, which caused a recurrence of carpal spasms. At 7 years of age, the girl showed signs of delayed psychophysical development.
    Although hypocalcemia is not uncommon in people with celiac disease, it is rare for hypocalcemic carpal spasm to be the first manifestation of the disease. Because of this, the doctors urge other physicians to consider the possibility of celiac disease in patients with repeated carpal spasms that seem to resist easy treatment.
    They indicate that celiac disease should be considered even in the absence of gastrointestinal symptoms, since hypocalcemia and carpal spasm may appear as the first symptoms of celiac disease, even in young children.
    Source:
    J Med Case Reports. 2017;11(252)

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    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.

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023