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Found 9 results

  1. Celiac.com 10/27/2017 - It has long been understood that two autoimmune diseases, celiac disease and type 1 diabetes are related. They share common genes and the incidence of celiac disease is higher among type 1 diabetics. There have been some anecdotal reports regarding children diagnosed with type 1 diabetes who were put on a gluten-free diet soon after their diagnosis and for a period of two years or more didn't require any insulin. The thought was that the gluten-free diet effectively halted the progression of the diabetes, at least for the duration of the study. Studies of mice have shown that despite utilizing a genetic strain of mice that were strongly in-bred to increase the risk of type 1 diabetes, 2/3 of them did not do so when a drug was administered to prevent leaky gut. This study was performed by Dr. Alessio Fasano at the University of Maryland Celiac Research Center. Dr. Fasano is one of the world's acclaimed researchers in the area of celiac disease and gluten sensitivity. Leaky gut is associated with the initiation and continuation of autoimmune disease and Dr. Fasano's work with these genetically predisposed mice shed a great deal of light on the power of an undamaged gut lining to effectively forestall development of a genetic condition, in this case type 1 diabetes. A recent study out of Immunology, dated August 22, 2012, is titled "Dietary gluten alters the balance of proinflammatory and anti-inflammatory cytokines in T cells of BALB/c mice". The title is a mouthful but here is what the researchers out of Denmark found: Their initial premise was based on the idea, as I mentioned above, that dietary modifications, specifically a gluten-free diet, could reduce the risk of developing type 1 diabetes. The question they posed was, "How did this occur?" They discovered that wheat gluten induced the production of pro-inflammatory chemicals called cytokines that would damage the intestinal lining and immune tissues of the small intestine. More importantly, a gluten-free diet didn't just neutralize the negative effects just mentioned, but it actually caused the production of anti-inflammatory chemicals that would provide protection for the immune system and gut. So, while gluten is a known bad guy, a gluten-free diet doesn't just take the negative away, it actually induces a positive, healing response. Clinically we frequently see this with patients. As soon as we meet a patient with any history of autoimmune disease, we quickly test them for celiac disease and gluten sensitivity via lab tests and a 30 day elimination diet. If we discover any negative immune reaction to gluten, we begin a strict gluten-free diet. Happily, we often see stabilization, if not reversal, of their autoimmune disease. We support the gluten-free diet with our other protocols for normalizing gut permeability (healing a leaky gut) and strengthening the immune system. Taken together this program yields excellent results. If you know anyone suffering from an autoimmune disease, please show them this article. Gluten could be a component in furthering their disease and a gluten-free diet could be a positive influence in their journey to improved health. I hope this was helpful. Please feel free to contact me should you have any questions. And if your health is not at the level you would like, I can also offer you a free health analysis. Call us at 408-761-3900. Our destination clinic treats patients from across the country and internationally and we would be delighted to help you. To your good health.
  2. Celiac.com 11/21/2016 - Even early on, strange inconsistencies caused Dan and Davina Dixon to wonder about her daughter, Rebecca. With dark hair and olive skin, Rebecca looked visibly different from her fair-complected parents. She looked different enough to wonder, as a child, if was adopted, if Dan and Davina were really her biological parents, as they assured her they were. Later, in her twenties, Rebecca developed celiac disease, which usually runs in families, even though no one else in their extended family suffered from it. Most of this was merely fodder for curiosity, until the day Davina saw a Facebook post that mentioned how rare it is for parents with blue eyes to have a child with brown eyes. Wondering about Rebecca's brown eyes, Davina went to the family doctor, who suggested a blood test. That's when the real mystery began: The blood test revealed that Rebecca's dad, Dan, was not, in fact, her biological father. There was absolutely no doubt. Dan's blood type was AB, while Rebecca's was O-Positive. That makes it impossible for Dan to be her father. A paternity test followed, and confirmed the blood results. There was simply no chance that Dan was Rebecca's biological father. Naturally, the Dixons began to search for answers. As reported by Kidspot, Rebecca was raised believing that Dan and Davina were her biological parents. The couple had tried for years to conceive a child. Unsuccessful, they turned to Dr. Norman Barwin, a gynecologist and fertility expert known by many as Canada's "baby god." The couple wondered whether there could have been some sort of mix-up in Barwin's office. Eventually, they noticed Rebecca bore a striking resemblance to Dr. Barwin, himself. Soon after that, as CTV News reported, a woman conceived at the same clinic learned that she was genetically related to Barwin. A DNA test confirmed that Rebecca and the woman were half-sisters, and their father was Dr. Barwin. Apparently, Barwin's role as a sperm donor to his own medical practice was kept secret from both sets of parents. The Dixon family is now suing Dr. Barwin for negligence and breach of trust. The lawsuit requests that Barwin turn over a DNA sample, to determine if any other children conceived at his clinic are his offspring, and to notify them accordingly. Read more at: Kidspot.com CTV News IJR.com
  3. Celiac.com 10/03/2016 - It's hard for researchers to figure out the exact rate of celiac disease, in part because the disease so often presents a range of atypical symptoms. Most people with celiac disease suffer from classic gastrointestinal symptoms, but many patients may also be asymptomatic or have extra intestinal symptoms. A team of researchers recently set out to assess celiac disease rates in patients with epilepsy, align with determining the effect of a gluten-free diet on seizure control in these patients. The research team included Homayoon Bashiri, Darioush Afshari, Nosrat Babaei, and Mohammad R. Ghadami. They are variously affiliated with the Department of Internal Medicine, and the Sleep Disorders Research Center at Kermanshah University of Medical Sciences in Kermanshah, Iran. For their study, the team assessed patients with epilepsy in Imam Reza and Farabi Hospitals, Kermanshah, Iran. The team first screened patients screened based on results of immunoglobulin A antiendomysial (IgA) antibodies. In patients with positive screens for IgA antibodies, the team took 2–3 endoscopic small bowel biopsies from the distal duodenum to confirm celiac-related changes. People with celiac disease received a gluten-free diet for 5 months, during which time the researchers regularly recorded patient seizure activity. Of the 113 patients with epilepsy, the team diagnosed seven patients (6%) with celiac disease. After 5 months of instituting a gluten-free diet, 6 patients had their seizures completely under control, and were able to discontinue anti-epileptic drugs. In one patient, dosage of anticonvulsant drugs was cut in half, seizures were also controlled. These results showed that about 6% of epileptic patients were positive for celiac disease, and that these patients see significant improvement in seizure control on a gluten-free diet. Source: Adv Clin Exp Med 2016, 25, 4, 751–754
  4. Celiac.com 05/05/2016 - Frustrated by the process of tracking gluten-free expenses in hopes of using the Canadian government's tax credit, which entitles people with celiac disease to claim the incremental costs, accountant Justin Gravelle has released an app called Celitax, designed to help people with celiac disease easily track their everyday gluten-free purchases. In Canada, people who are gluten-intolerant, and can provide the government with proof, such as a medical diagnosis of celiac disease, are entitled to the incremental cost difference between gluten-free and non-gluten free products. However, tracking those expenses over the year can be messy and frustrating. Enter Celitax. The app is currently available for iPhones, with an Android version to follow. The app digitizes receipts and stores them inside the app, allowing users to review or download them at any time and calculate their gluten-free tax credit in one click. A user simply takes a photo of their receipt, which is stored in the app for safe keeping. Next, they input their gluten-free purchases into self-created custom categories based on their purchasing habits. The Canadian government hasn't set average prices for non-gluten-free foods, Gravelle says, so users have to input an estimate themselves so the app can calculate their tax credit. Still, sounds a lot better than digging through a pile of paper receipts at the end of the year to document your gluten-free expenses. Would something like this be useful for you? Source: thestar.com
  5. Celiac.com 04/26/2016 - Vice President Dan Quayle famously stated: "what a waste it is to lose one's mind, or not to have a mind is being very wasteful, how true that is," when speaking to people involved in the United Negro College Fund (1). While it is entertaining to read and ponder, this statement evokes some ideas I have about senility, which is increasing, along with many other modern diseases, at a frightening speed. The prospect of losing my mind, my memory, my sense of connection with friends and loved-ones, and even my sense of identity and personal hygiene is a frightening spectre. Can you separate your memories and experiences, along with what you think and feel, from who you are? I can't. I'm not sure I would want to be able to do so. My identity is tied to my memories, experiences, and how I responded and continue to respond to them. I remember looking at my son's tiny hands and feet when we first brought him home from the hospital. My daughter, born prematurely, had even smaller digits. They seemed impossibly tiny yet they were all perfectly formed and quite beautiful. It seemed miraculous to me. It still does. I can't imagine anything that I'd be willing to accept in exchange for those memories. Neither would I willingly surrender my memory of the joy I felt at my first convocation or my first car. Yet those lost memories form the prison in which many people already find themselves. It appears that many more will follow. One segment of this problem, the epidemic of Alzheimer's disease (AD), already effects 5.4 million Americans and 30 million people throughout the world (2). Parkinson's disease, which is a neurological ailment that, in its later stages is often accompanied by dementia, is a similar ailment that is rapidly increasing both in absolute numbers and as a percentage of the population (3). Vascular dementia is yet another condition in which brain mass and mental acuity wane with advancing years (4). Perhaps this trend is partly due to the large number of aging baby boomers from the World War II era. But the relevant research suggests otherwise. Although we may be living longer and that may contribute to a small part of the growth of these devastating ailments, the biggest contributors appear to be lifestyle choices that include low daily activity levels, consumption of highly glycemic and inflammation-promoting refined carbohydrates and grain products, inadequate sleep duration, and exposure to toxic substances. As most students of celiac disease have long been aware, there is a powerful and potentially devastating component of brain and neurological damage associated with this ailment as a result of gluten grain consumption. In addition to the behavioral changes identified by Gibbons in 1889 (5), attention deficits identified by Reichelt (6), Neiderhofer (7, 8), and others (9 - 11), subsequent reports have connected increased incidence of seizure disorders(12-17), reductions of brain size (17 -20), a variety of neurological movement disorders (21 -23), a range of mood disorders (24, 25), and several psychiatric ailments (26, 27) including schizophrenia (28, 29), and signs of learning disabilities have been reported to improve quite dramatically and quickly on a gluten-free diet (30). Sleep disorders are also common among people with celiac disease (31). With emerging research into non-celiac gluten sensitivity over the last two decades, we have also begun to see evidence of similar connections between gluten consumption and most of these neurological/brain ailments. This added dimension of non celiac gluten sensitivity and its impact on human neurological health, were previously obscure and, in the case of amyotrophic lateral sclerosis (ALS) (26, 32), was thought to be rapidly deadly and incurable (33). Most recently, Bredesen reported that the gluten-free diet, or a low grain diet, forms one significant part of their multi-modal protocol for reversing several dementias among a small group of those who experienced recent symptom onset, including Alzheimer's disease, objectively identified disruptions in memory function or subjective, self-reported symptoms of dementia (2). Of the ten subjects studied in this latter investigation, nine showed substantial recovery in the form of symptom reversal along with either a return to work or improved performance at work (2). Harnessing the gluten-free diet makes sense, of course, because of the many neurological dimensions of gluten's harmful impact on human neurological tissues. Over the last 20 years, Dr. Marios Hadjivassiliou and colleagues, at the University of Sheffield and the Royal Hallamshire Hospital, have been reporting a wide range of neurological ailments in association with elevated anti-gliadin antibodies ( both with and without celiac disease) afflicting a large portion of their patients with neurological diseases of unknown origin (34 -37). Further, Dr. Joe Murray and colleagues have also reported on a group of thirteen patients experiencing moderate cognitive decline, three of whom experienced stabilized or improved cognitive function on a gluten-free diet alone (38). However, the protocol reported by Bredesen is aimed at correcting a greater number and broader spectrum of converging metabolic processes that are shaped, in large part, by our modern lifestyle, and are increasingly thought to be at the root of the current epidemic of dementias, including Alzheimer's disease (2). Gluten is only an important part of the overall picture. Dr. Suzanne de la Monte and colleagues have also identified a dynamic which they call type 3 diabetes at work in the brains of many patients with Alzheimer's disease (39). Insulin resistance, in the brain and elsewhere, is also a multi-factorial condition (40) which mostly involves disrupted metabolic processes, either through depletion of insulin production or, more likely, increased cellular resistance to insulin's movement of glucose into the cell. Dr. Dale Bredesen has argued that "in the past decade alone, hundreds of clinical trials have been conducted for AD, at an aggregate cost of billions of dollars, without success. This has led some to question whether the approach taken to drug development for AD is an optimal one" (2) This is the rationale that underlies his enormously broad therapeutic approach employed in his protocol. Please consider each of the following facets of Bredesen's therapeutic protocol: 1. Serum testing was conducted and subsequent supplement recommendations were made, aimed at improving vitamin, mineral, amino acid, and herb supplements to achieve optimal values. All of the foregoing is aimed at harnessing their putative anti-oxidant function, supporting various facets of metabolism, and making use of their reported anti-inflammatory properties. Chelation therapy was also used to correct heavy metal (mercury, lead, cadmium) toxicity. Non-farmed fish, vegetables, and fruits were emphasized, while meat consumption was either discouraged or patients were encouraged to eat only organic and free range meat. 2. Patients were given their choice of several low glycemic, low inflammatory, low grain diets. By this description, such a diet would exclude or severely limit gluten consumption. 3. Patients were encouraged to engage daily in strategies, including meditation and listening to music, toward reducing their stress levels, which would reduce their cortisol production. Cortisol is a hormone that triggers increased release of glucose into the bloodstream, suppresses the immune system, and inhibits bone formation. In addition to excluding or treating sleep apnea, patients were prescribed melatonin at 0.5 mg daily, toward achieving at least eight hours of sleep each night, thereby reducing production of hunger-inducing ghrelin hormones in the stomach and increasing hunger-suppressing leptin hormones which are produced in the fat cells. Each carries its message to the brain. Reductions in cortisol and ghrelin secretion in combination with increasing leptin production would have a net effect of reducing inflammation while aiding weight loss and reducing blood glucose levels to normal fasting levels and targeting reduction of hemoglobin A1c levels to below 5.5, further reducing inflammation. Optimum levels of thyroid hormones, along with progesterone and pregnenolone were also pursued, along with reductions of free homocysteine to below 7 mg/L by prescription of vitamin B6, B12, and folic acid supplements, to reduce vascular damage and blockage that can be caused by elevated free homocysteine levels. Twice daily dietary supplementation with medium chain triglycerides (MCTs) also provides strategy for altering hormone production aimed at improved cognitive function. In humans, medium chain fatty acids resist storage. They must either be converted to ketone bodies in the liver, or rapidly utilized for energy. Because MCTs can induce the liver to increase ketone production, it provides an alternative energy source for many of the brain's cells, without requiring insulin to usher these ketones into the cells, as glucose does. In essence, adequate ketone production provides an alternative fuel both for many brain and other cells throughout the body. The liver mostly produces the ketone called beta-hydroxybutyrate. This acts not only as a fuel source, but is also a powerful anti-oxidant that does not require insulin to enter the cell, unlike vitamin C, which does require insulin to enter cells. 4. To further promote these values and other facets of wellness arising out of regular activity, patients were asked to exercise for 30 to 60 minutes per day, 4 to 6 days each week. Each and all of the above have been reported somewhere in the literature as valid and valuable as part of reversing dementias, which Bredesen's list of citations supports (2). However, while significant improvements in the dementia symptoms of nine of the ten subjects does argue for the validity of this protocol, wholesale acceptance of all of the concepts here would fail to narrow our focus on those factors that are most likely to contribute to causing the vast majority of the various dementias that are contributing to the emerging epidemic. Bredesen also acknowledges that study participants were encouraged to follow as many instructions as they could. They were not asked or expected to be fully compliant with the instructions they were given. Nonetheless, I would probably err on the side of caution, by implementing as many of these strategies as possible, were I dealing with a loved-one who struggled with dementia. 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. Sources: 1. https://en.wikiquote.org/wiki/Dan_Quayle 2. Bredesen DE. Reversal of cognitive decline: a novel therapeutic program. Aging (Albany NY). 2014 Sep;6(9):707-17. 3. Moustafa AA, Chakravarthy S, Phillips JR, Crouse JJ, Gupta A, Frank MJ, Hall JM, Jahanshahi M. Interrelations between cognitive dysfunction and motor symptoms of Parkinson's disease: behavioral and neural studies. Rev Neurosci. 2016 Mar 16. 4. Dey AK, Stamenova V, Turner G, Black SE, Levine B. Pathoconnectomics of cognitive impairment in small vessel disease: A systematic review. Alzheimers Dement. 2016 Feb 25. 5. Gibbons, R. (1889). The Coeliac Affection in Children. Edinburgh Medical Journal. xxxv(iv), 321-330. 6. Ziegler, A., Nødland, M., Tveiten, D. and Reichelt, K.L. (2016) The AD/HD Syndrome as a Group of Biological Disorders. Open Journal of Pediatrics, 6, 22-28. http://dx.doi.org/10.4236/ojped.2016.61005 7. Niederhofer H. Association of attention-deficit/hyperactivity disorder and celiac disease: a brief report. Prim Care Companion CNS Disord. 2011;13(3). pii 8. Niederhofer H, Pittschieler K. A preliminary investigation of ADHD symptoms in persons with celiac disease. J Atten Disord. 2006 Nov;10(2):200-4. 9. Zelnik N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2004 Jun;113(6):1672-6. 10. Welch E, Ghaderi A, Swenne I. A comparison of clinical characteristics between adolescent males and females with eating disorders. BMC Psychiatry. 2015 Mar 11;15:45. 11. KozÅ‚owska ZE. [Evaluation of mental status of children with malabsorption syndrome after long-term treatment with gluten-free diet (preliminary report)]. Psychiatr Pol. 1991 Mar-Apr;25(2):130-4. Polish. (based on amateur translation) 12. Parisi P, Principessa L, Ferretti A, D'Onofrio D, Del Giudice E, Pacchiarotti C, Villa MP. 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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. 19. Ryan AM, Ryan J, Wan-Ahmed M, Hardiman O, Farrell MA, McNamara B, Sweeney BJ. Vacuolar leucoencephalopathy and pulvinar sign in association with coeliac disease. BMJ Case Rep. 2009;2009. pii: bcr08.2008.0650. 20. Kieslich M, Errázuriz G, Posselt HG, Moeller-Hartmann W, Zanella F, Boehles H. Brain white-matter lesions in celiac disease: a prospective study of 75 diet-treated patients. Pediatrics. 2001 Aug;108(2):E21. 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. 23. McKeon A, Lennon VA, Pittock SJ, Kryzer TJ, Murray J. The neurologic significance of celiac disease biomarkers. Neurology. 2014 Nov 11;83(20):1789-96. 24. Zingone F, Swift GL, Card TR, Sanders DS, Ludvigsson JF, Bai JC. Psychological morbidity of celiac disease: A review of the literature. United European Gastroenterol J. 2015 Apr;3(2):136-45. 25. Carta MG, Conti A, Lecca F, Sancassiani F, Cossu G, Carruxi R, Boccone A, Cadoni M, Pisanu A, Francesca Moro M, Demelia L. The Burden of Depressive and Bipolar Disorders in Celiac Disease. Clin Pract Epidemiol Ment Health. 2015 Dec 31;11:180-5. 26. Catassi C. Gluten Sensitivity. Ann Nutr Metab. 2015;67 Suppl 2:16-26. 27. Lionetti E, Leonardi S, Franzonello C, Mancardi M, Ruggieri M, Catassi C. Gluten Psychosis: Confirmation of a New Clinical Entity. Nutrients. 2015 Jul 8;7(7):5532-9 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. 33. Hoggan R. 34. 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. 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.
  6. Celiac.com 02/12/2015 - Gwyneth Paltrow is making gluten-free celebrity news again for helping her longtime stylist go gluten-free and drop some major weight. David Babaii is one of Hollywood's top hair stylists. In addition to Paltrow, his celebrity roster includes Kate Hudson, Scarlett Johansson, Christina Aguilera and Uma Thurman, among others. After working with Paltrow for about 10 years, the man Vogue-crowned the "king of curls" had ballooned to 285 pounds with a 44-inch waist. At just five feet five inches tall, he became compelled to lose weight. In a recent exclusive with Marc Malkin in eonline, Babaii opens up about how Paltrow and Equinox trainer Will Castillo helped him lose 135 pounds in just four months. Babaii says that Paltrow was very supportive, non-judgmental, and encouraging of his efforts. When Babaii asked Paltrow about gluten, he says she advised him not to do anything drastic, and to take it slowly. And, armed with determination and with Paltrow's support and encouragement, Babaii began his transformation in earnest. Of course, being a personal of Gwyneth Paltrow has its perks. In Babaii's case, whenever he was hungry or in need of support, he could "email her any time of the day and if she wasn't sleeping, she'd reply right away," he told Malkin. "She would say, 'Try this. I think you'll like it. It's not boring.'"
  7. Celiac.com 01/19/2015 - A team of researchers set out to determine what factors might influence dissemination of a new and validated commercial Point-of-Care Test (POCT) for celiac disease, in the Mediterranean area, when used in settings where it was designed to be administered, especially in countries with poor resources. The research team included S. Costa, L. Astarita, M. Ben-Hariz, G. Currò, J. Dolinsek, A. Kansu, G. Magazzu, S. Marvaso, D. Micetic-Turku, S. Pellegrino, G. Primavera, P. Rossi, A. Smarrazzo, F. Tucci, C. Arcidiaco, and L. Greco. For their study, the team relied on family pediatricians in Italy, and nurses and pediatricians in Slovenia and Turkey, to look for celiac disease in 3,559 children aged 1-14 years, 1,480 (ages 14-23 years) and 771 (1-18 years) asymptomatic subjects, respectively. This was done at pediatrician offices, schools and university primary care centers The team used a new POCT that detects IgA-tissue antitransglutaminase antibodies and IgA deficiency in a finger-tip blood drop. Subjects with positive screens and those suspected of having celiac disease were referred to a Celiac Centre to confirm the diagnosis. The team then estimated POCT Positive Predictive Value (PPV) at tertiary care (with Negative Predictive Value) and in primary care settings, and POCT and celiac disease rates per thousand in primary care. At tertiary care setting, PPV of the POCT and 95% CI were 89.5 (81.3-94.3) and 90 (56-98.5) with Negative Predictive Value 98.5 (94.2-99.6) and 98.7% (92-99.8) in children and adults, respectively. In primary care settings of different countries where POCT was performed by a different number of personnel, PPV ranged from 16 to 33%, and the celiac disease rates per thousand ranged from 4.77 to 1.3, while and POCT rates ranged from 31.18 to 2.59, respectively. This study shows that interpretation of POCT results by different personnel may influence the performance of POC, but that use of POCT is an urgent priority for diagnosing celiac disease among people of countries with limited resources, such as rural populations and school children. Source: BMC Gastroenterol. 2014 Dec 18;14(1):219.
  8. Celiac.com 04/25/2013 - Anyone who has ever struggled with a gluten-free diet can likely identify with tennis star Novak Djokovic. The wold's top tennis player has struggled to faithfully remain 100% gluten-free, and has turned to his mom for a bit of help. Still, the wold's top tennis player has struggled to faithfully remain 100% gluten-free, and admits being tempted by the Balkan foods on which he grew up. In an effort to reap the benefits of a strict gluten-free diet, Djokovic has turned to help from his mom. He says his mother’s home cooking has helped him stick to the dietary plan. “I eat mostly at home, my mom cooks special food,” says Djokovic, whose father owned a pizza restaurant, and who grew up in a culture which features plenty of red meat, dumpling and sweet desserts. Djokovic has worked to avoid these and other gluten-rich foods over the past few seasons as he has risen to the top of the tennis rankings. “It’s hard, because in our country there is a certain kind of mentality towards the food. That is not very encouraging for gluten-free diet.” With mom's help, however, Djokovic is finding out just how delicious gluten-free food can be. “For me it’s absolutely normal now to have that food, and back home I love mom’s kitchen. That’s the most time spent eating there.” For now, join us in saluting Novak Djokovic and his mother in their battle to keep him gluten free, and stay tuned to learn more about Djokovic's efforts to harness his diet to improve his success on the tennis court.
  9. This article originally appeared in the Autumn 2002 edition of Celiac.coms Scott-Free newsletter. Copyright © 2002 Scott Adams. All rights reserved worldwide. Five years ago I became concerned about weakness in my bones after a couple of surprising fractures. At one point, I broke a rib while shingling a storage-shed roof. I leaned across the peak of the roofs ridge to pick up a shingle. I never expected such light pressure to cause a problem, however, I felt a sudden, sharp pain, and heard an odd sound. This, along with a couple of less dramatic, but similar injuries, caused me enough concern to begin looking into the question of celiac disease and bone strength. My explorations taught me that calcium absorption probably is not our main problem. People with celiac disease seem to be able to absorb adequate calcium1, but the primary problem appears to come from excreting too much of it, thus causing us to lose more calcium than we are absorbing. I also learned that research shows little or no benefit from calcium supplementation for celiac patients, while magnesium supplementation alone results in significant improvements2. The explanation for this may be that some of the antibodies caused by active celiac disease attack the parathyroid gland3. This organ is an important player in regulating calcium metabolism. Magnesium is necessary for the body to repair the parathyroid and to maintain its continued good function. Being convinced by this research, I began to take magnesium supplements without any calcium. I found that I had to be careful. Too much had me visiting the washroom frequently, and I was afraid that too little would fail to provide me the benefits I was seeking. At the same time, I also requested a bone density test. I wanted objective information that would allow me to evaluate the progress I hoped to make. The first test was conducted in March of 1997. The results (called "T scores") are reported based on comparison with the density of bones found in young adults. For instance, a score of 0 indicates that the bone density is about the same as would be found in an average young adult. A score in the minus range indicates a bone that has less mineral and more pores than is found in the same young adult. Thus, a score of –1.0 to –2.5 indicates mild mineral losses, while a score of –2.5 or lower indicates osteoporosis. My test results were not as bad as I had feared. The mineral density in my lower back was normal for my age, at –0.23. However, my upper leg, where it fits into my hip, was reported as –2.02, and my forearm was slightly stronger than that of a normal young adult at +0.19. As I saw it, there were only two causes for concern. First, at the tender age of 50, my hips were very close to osteoporotic, and certainly at a substantially increased risk of fracture. Such fractures can be very serious. Secondly, since only three skeletal areas had been tested for mineral density—and since there was such a wide range of density reported for each of these areas, it seemed impossible to estimate the density of the rest of the bones in my body. About three years after my first bone density test, some Calgary-based research made me suspect that the amount of vitamin D supplements I was taking might be too low4. I increased my intake to 1,000 IU daily. By the fall of 2001, I began to wonder if I was being foolish by avoiding calcium supplements based on the reports I had read. I therefore began to supplement 350 mg of calcium each day. In July of 2002, I underwent a second bone scan. They did not test my forearm, but the other two areas appear to have improved substantially. The T score for my lower back was now at + 0.06, and the T score for my hip had improved to –0.72. I realize that what I am reporting is just one persons experience. It is what the medical professionals call "anecdotal," and does not usually carry much weight. However, my experience does support the only published research of the impact of mineral supplements on bone density in celiac patients that I can find. Based on my own experience, and the relevant research, I am now convinced that magnesium is the most important supplement to consider in the context of celiac disease. I was thrilled to read my latest bone density report. Vitamin D may also be an important factor, but limitations of time and space force me to leave this topic for another day. References: Marsh MN. Bone disease and gluten sensitivity: time to act, to treat, and to prevent. Am J Gastroenterol. 1994 Dec;89(12):2105-7. Rude RK, Olerich M. Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. Osteoporos Int. 1996;6(6):453-61. Kumar V, Valeski JE, Wortsman J. Celiac disease and hypoparathyroidism: cross-reaction of endomysial antibodies with parathyroid tissue. Clin Diagn Lab Immunol. 1996 Mar;3(2):143-6. Embry AF, Snowdon LR, Vieth R. Vitamin D and seasonal fluctuations of gadolinium-enhancing magnetic resonance imaging lesions in multiple sclerosis. Ann Neurol. 2000 Aug;48(2):271-2. Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His new book "Dangerous Grains" is available at Celiac.com.
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