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Found 9 results

  1. Celiac.com 03/25/2019 - Some researchers have suspected that myelin proteins may be involved in multiple sclerosis (MS). A recent report in Science and Translational Medicine, suggests that additional non-myelin-related protein may also play a role. Researchers examined protein samples from the brains of 31 people who had died from suspected or confirmed MS. They found that T cells from 12 people reacted to the enzyme guanosine diphosphate-L-fucose synthase, or GDP-L-fucose-synthase. The enzyme usually helps to process sugars that are crucial to cell function and communication, including the function and communication of neurons. Researcher Dr Roland Martin, from the University Hospital of Zurich, Switzerland, has helped to figure out which myelin proteins and peptides come under attack in MS, and which cells and immune molecules do the attacking. Paper coauthor Mireia Sospedra, of University Hospital of Zurich, suggests that “other auto-antigens might be involved in initiating the disease." She believes that the attack on this newly identified auto-antigen triggers tissue damage that exposes other myelin proteins that are likely targets for attack. Sospedra suspects that some variations in myelin protein structure might be susceptible to immune attack, and that genetic variation in immune cells might influence the body’s response to a given infection. She suggests that the offending antigens may differ between individuals, as the structure of our molecular machinery is genetically determined. Northwestern University immunology professor Stephen Miller, who did not work on this research, but has worked with Dr. Martin in the past, suggests that there’s likely not just “one particular virus or bacteria or environmental factor that triggers MS in every patient. There are probably many things that can trigger an autoimmune reaction against a particular infection," he says. "But the more antigens we identify that can contribute to the disease, the better." Researchers have pointed out that numerous autoimmune diseases seem to cluster in certain gene sequences. Multiple gene areas seem to correlate with numerous autoimmune conditions. Prior comprehensive genetic association studies have found 90 genetic areas associated with T1DM, celiac disease, multiple sclerosis, and/or rheumatoid arthritis. Celiac disease and MS sufferers share some things in common, including a tendency to develop rosacea. Rosacea is a common inflammatory skin condition that shares the same genetic risk location as autoimmune diseases such as type 1 diabetes mellitus (T1DM) and celiac disease. The connections between multiple sclerosis and celiac disease is a common topic of discussions on many forums. Read more at: medscape.com
  2. I’ve been gluten free now for eight years. I have had two separate biopsies confirming celiac disease. I’ve had scopes since diagnosis that showed regrowth of microvilli. The diet has worked and I gained back all the weight that I lost before diagnosis. Lately, I’ve had some alarming symptoms. I’m having trouble making certain expressions with my face, I have a very hard time finding words or pronouncing words. I’ve had loss of feeling in my hands And numbness in tingling. I also get strangled very easily when I’m drinking or eating. I’m experiencing a trimmer in my right hand particularly although I’ve never had a very steady hand. The doctor checked all my vitamins etc. and put me on vitamin D months ago, but other than that everything has been fine as far as blood work. I have not changed anything. Just wondering if any of you have experience this and if you found out what caused it.
  3. Forum Members, Has anyone else seen this new research on the Epstein-Barr Virus and it possible link to various Auto-immune diseases including Celiac disease. https://medicalxpress.com/news/2018-04-epstein-barr-virus-linked-diseases.html I will quote the whole article for easy reading as it appeared on Medical Express. It is very similar to the research reported by Popular Science approx. a year that mentioned the link between a reovirus (rotavirus) and how it might trigger higher Celiac rates in Finland. I think Ennis_tx started a thread on it. Epstein-Barr virus linked to seven serious diseases April 16, 2018, Cincinnati Children's Hospital Medical Center This electron microscopic image of two Epstein Barr Virus virions (viral particles) shows round capsids—protein-encased genetic material—loosely surrounded by the membrane envelope. Credit: DOI: 10.1371/journal.pbio.0030430.g001 A far-reaching study conducted by scientists at Cincinnati Children's reports that the Epstein-Barr virus (EBV)—best known for causing mononucleosis—also increases the risks for some people of developing seven other major diseases. Those diseases are: systemic lupus erythematosus (SLE), multiple sclerosis (MS), rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), inflammatory bowel disease (IBD), celiac disease, and type 1 diabetes. Combined, these seven diseases affect nearly 8 million people in the U.S. Study results published April 12 in the journal Nature Genetics. The project was led by three scientists: John Harley, MD, PhD, Director of the Center for Autoimmune Genomics and Etiology (CAGE) at Cincinnati Children's and a faculty member of the Cincinnati VA Medical Center; Leah Kottyan, PhD, an immunobiology expert with CAGE; and Matthew Weirauch, PhD, a computational biologist with the center. Critical contributions were provided by Xiaoting Chen, PhD, and Mario Pujato, PhD, both also in CAGE. The study shows that a protein produced by the Epstein-Barr virus, called EBNA2, binds to multiple locations along the human genome that are associated with these seven diseases. Overall, the study sheds new light on how environmental factors, such as viral or bacterial infections, poor diet, pollution or other hazardous exposures, can interact with the human genetic blueprint and have disease-influencing consequences. "Now, using genomic methods that were not available 10 years ago, it appears that components made by the virus interact with human DNA in the places where the genetic risk of disease is increased," Harley says. "And not just for lupus, but all these other diseases, too." The full impact of this study could take years to explore. Here are some of the initial implications: New concern about the 'kissing disease' EBV is a strikingly common virus. In the US and other developed nations, more than 90 percent of the population becomes infected by age 20. In less-developed nations, 90 percent of people become infected by age 2. Once infected, the virus remains in people for their entire lives. Mononucleosis, which causes weeks of extreme fatigue, is the most common illness caused by EBV. Mono was nicknamed the "kissing disease" years ago because the virus spreads primarily via contact with saliva. Over the years, scientists have linked EBV to a few other rare conditions, including certain cancers of the lymphatic system. Harley, who has devoted much of his career to studying lupus, found possible connections between lupus and EBV years ago. That work includes proposing mechanisms that the immune system uses in response to the virus that lead to lupus, and showing that children with lupus almost always are infected with EBV. Today's study adds weight to those lupus findings and adds six more well-known diseases to the list. "This discovery is probably fundamental enough that it will spur many other scientists around the world to reconsider this virus in these disorders," Harley says. "As a consequence, and assuming that others can replicate our findings, that could lead to therapies, ways of prevention, and ways of anticipating disease that don't now exist."So far, no vaccine exists that will prevent EBV infection. "I think we've come up with a really strong rationale for encouraging people to come up with more of an effort," Kottyan says. "Some EBV vaccines are under development. I think this study might well encourage them to push forward faster and with rededicated effort." How EBV hijacks our immune system When viral and bacterial infections strike, our bodies respond by commanding B cells within our immune systems to crank out antibodies to battle the invaders. However, when EBV infections occur, something unusual happens. The EBV virus invades the B cells themselves, re-programs them, and takes over control of their functions. The Cincinnati Children's research team has discovered a new clue about how the virus does this, a process that involves tiny proteins called transcription factors. Our bodies have about 1,600 known transcription factors at work within our genome. Each cell uses a subset of these to become what they are and to respond to their environment. These proteins constantly move along the strands of our DNA, turning specific genes on and off to make sure cells function as expected. Credit: Cincinnati Children's However, when the transcription factors change what they do, the normal functions of the cell can also change, and that can lead to disease. The Cincinnati Children's team suspects that the EBNA2 transcription factor from EBV is helping change how infected B cells operate, and how the body responds to those infected cells. The new paper shows that seven seemingly unrelated disease states actually share a common set of abnormal transcription factors, each affected by the EBNA2 protein from the Epstein-Barr virus. When these EBNA2-related clusters of transcription factors attach themselves to one portion of the genetic code, the risk of lupus appears to rise. When those same transcription factors land on another part of the code, the risk of multiple sclerosis appears to rise. And so on. "Normally, we think of the transcription factors that regulate human gene expression as being human," Kottyan says. "But in this case, when this virus infects cells, the virus makes its own transcription factors, and those sit on the human genome at lupus risk variants (and at the variants for other diseases) and that's what we suspect is increasing risk for the disease." New leads emerge for improving treatment It remains unclear how many cases of the seven diseases listed in the study can be traced to prior EBV infection. More genomic analyses involving many more patients with these diseases will be required to make reliable estimates. "The impact of the virus is likely to vary across the diseases," Harley says. "In lupus and MS, for example, the virus could account for a large percentage of those cases. We do not have a sense of the proportion in which the virus could be important in the other EBNA2-associated diseases." However, the breakthrough identification of specific transcription factors connected to EBV infections opens new lines of study that could accelerate efforts to find cures. "This same cast of characters is a villain in multiple immune-related diseases," Weirauch says. "They're playing that role through different ways, and doing it at different places in your genome, but it's the same sinister characters. So if we could develop therapies to stop them from doing this, then it would help multiple diseases." A number of compounds—some experimental, some approved as medications for other conditions—already are known to be capable of blocking some of the high-risk transcription factors listed in the paper, Weirauch says. Teams at Cincinnati Children's have begun deeper studies of some of these compounds. Findings go far, far beyond EBV While the EBV-related findings involved more than 60 human proteins linked to seven diseases, the Cincinnati Children's research team already has taken a huge next step. They applied the same analytic techniques to tease out connections between all 1,600 known transcription factors and the known gene variants associated with more than 200 diseases. The results of that massive cross-analysis also appear in today's study. Intriguing associations were documented involving 94 conditions. "Our study has uncovered potential leads for many other diseases, including breast cancer," Harley says. "We cannot possibly follow up on all of these, but we are hoping that other scientists will." After devoting decades of research to hunting down the causes of lupus, Harley says this study represents the most important discovery of his career. "I've been a co-author in almost 500 papers. This one is more important than all of the rest put together. It is a capstone to a career in medical research," he says. Software behind discoveries to be made public Detecting and tracking the activities of these transcription factors took years of work involving dozens of laboratory and computational experts. The project required gathering massive sets of genetic data, then analyzing every genetic change affecting the activity of the virus. Doing this required creating two new algorithms, called RELI and MARIO, which were developed at Cincinnati Children's by Weirauch and colleagues. Both software tools and a related website will be made publicly available. "We are going to great lengths to not only make the computer code available, but all of the data and all of the results," Weirauch says. "We think it's an interesting approach that could have implications for many diseases, so we're contacting experts on the various diseases and sharing the results and seeing if they want to collaborate to follow up on them." Explore further: Study: Epstein Barr virus protects against autoimmune disease More information: John B. Harley et al, Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity, Nature Genetics (2018). DOI: 10.1038/s41588-018-0102-3 Journal reference: Nature Genetics Provided by: Cincinnati Children's Hospital Medical Center It is me again. What do you think have they found the trigger for Celiac disease. We know stress is common before a Celiac disease diagnosis and having Mono would definitely qualify for stress. Has one one else thought stress was their trigger? And why I was tested for Mononucleosis in the fifth grade I don't think it was the cause of my Celiac disease since I always had GI problems as a kid but in cause you have had Mono/EBV it might be something worth being aware of. I have had herpe simplex which is a similar disease that causes mouth sores often and my sores (ulcers) virtually went away when I started my gluten free diet. . . . later keep in check by taking the amino acid Lysine. Though who knows it (EBV/Mono) might of made it worse. Maybe I was only NCGS at the time and this could/might of pushed into the Celiac territory? (this would make great article on celiac.com by the way) if the admin thinks it is something worth reporting on. Here is a great overview on EBV/Mono "Kissing Disease" if you have ever wanted to know/wondered what it is and if you have ever had it. http://archive.boston.com/news/health/articles/2008/10/06/why_is_there_no_vaccine_against_infectious_mononucleosis/ *****This is is not medical advice but I hope it is helpful. 2 Corinthians (KJV) 1:3,4 3) “Blessed be God, even the Father of our Lord Jesus Christ, the Father of mercies, and the God of all comfort; 4) who comforteth us in all our tribulation, that we may be able to comfort them which are in any trouble, by the comfort wherewith we ourselves are comforted of God.” 2 Timothy 2: 7 “Consider what I say; and the Lord give thee understanding in all things” this included. Posterboy by the grace of God,
  4. Hello I am asking for my husband seeing as how I'm the one who tends to him ha ha! Has anyone had trouble getting diagnosed with gluten issues ? My husband's doctor seems to think he could have MS or gluten issues wondering if anyone is in the same boat.
  5. Hi Everyone, I am new to these boards. I have been reading though and the information posted by others has been very helpful. Thank you to all of you but especially to Ravenwoodglass. Five years ago, one of my sons was diagnosed with type 1 diabetes. While he was in the hospital, he was screened for celiac, and the blood tests came back positive. He ended up with a celiac diagnosis too, and it became apparent he could produce more of his own insulin when adhering strictly to the gluten-free diet. He experienced a prolonged t1d "honeymoon" which did not end until he had been in college for a year. While away at school he has had many more gluten accidents which I am sure was a contributing factor to his now need for more injected insulin. One funny detail is the medical doctors insisted that my son would need less insulin when glutened (as food won't be absorbed properly for a little while afterwards). But for my son, it was always the opposite. During his t1d "honeymoon period" he still made much insulin -- his honeymoon lasted an unprecedented three years (as compared to typical, six months for a newly diagnosed t1d patient). My son's basal insulin need would at least double after a glutening. It would take days for his body's own residual insulin production to return to normal. (I haven't bothered to explain what a t1d honeymoon period is, as it probably is of no interest to people who do not have t1d in their family -- and those who do have it in the family likely know what the honeymoon is -- hope that's ok). In 2011 I did a gluten challenge and had great difficulty with it. I had gone gluten free a year earlier to see what the challenges were, so as to help my son with his diet. Three weeks into the gluten-free diet I had noticed great improvements in how I felt. On the challenge, I could not consume more than a tiny amount of gluten (half a saltine) - I would then have severe dizziness and watery D. Foolishly, I continued with the challenge, going on an off gluten that month (going off when I had to drive the next day). The dizziness was far too severe to allow me to drive, and the D kept me near a bathroom. My antibodies had tested negative (not surprising as I had been gluten-free for the year before being tested). My endoscopy was negative for celiac, and I was pronounced non-celiac, and just presumed gluten sensitive by my reaction to gluten (the dizziness and D). Long story short - the four years since then have been bad news. I had the endoscopy in Aug 2011and started to recover from it, but then started getting worse again in Oct 2011. It took me about 15 months to figure out I had become more sensitive to CC. I stopped eating diner fried eggs (for example) and the persistent D went away. But neurological problems continued getting worse. Next thing I was getting worked up for possible MS, and had abnormal brain and cervical spine MRIs. But oddly, I was presenting with a relapsing remitting pattern in terms of symptoms, while the images looked more like PPMS -- few lesions, but in very bad locations. Lesions to cervical spine, brainstem, cerebellum. Also, my vitamin levels were dropping, especially B12 and zinc. Actually, the drop in B12 happened earlier (around the time the damage to spinal cord was detected). More recently I was diagnosed as deficient in zinc. The detection of the zinc deficiency is helpful as I had also developed new immune system problems - low lymphocyte counts, low celiac disease cell counts -- I was tested for HIV eighteen months ago (when immune cell counts became abnormal and I was getting repeated shingles, odd for someone my age). I was HIV negative (no surprise there). So it seems zinc deficiency interferes with production of immune system blood cells. I am hoping the white blood cells will normalize with zinc supplementation. Of course it took forever to discover the zinc deficiency, since I have "no risk factors" for it -- since I was officially deemed celiac disease negative with my negative endoscopy (which I should add was done properly, according to all accepted rules, by a top expert in celiac disease). I had a neurologist who did not bother with spinal tap, and actually tried to conceal from me some of the abnormal findings (I think he thought it was untreatable PPMS and I was better off not knowing, and he might have figured my neuro abnormalities were still mild enough he could get away with delaying the "bad news"). But I was having horrible flares and finally consulted a different neuro, who did the spinal tap. NEGATIVE for o-bands, negative for increased igg index 0-- and slightly LOW rather than high spinal fluid protein level. I also recently discovered there were already periventricular white matter hyperintensities on a brain MRI done in 2003. These were not mentioned in the radiology report from 2003 (ridiculous). I have none of the typical "Dawson's fingers" that one sees with MS. Mine are smaller and milder. (That too would be consistent with PPMS, less damage visible on brain MRI -- unless, it isn't MS at all, which might be suggested by the spinal tap done a month ago which was negative for all signs of MS). So given the chronology and the fact I took ill especially immediately following the gluten challenge, and because I realized I am very sensitive to CC (cross contamination) -- about three weeks ago I tightened up the gluten-free diet, eliminating all grains (as I have heard grains, even gluten-free ones, can have miniscule contamination with gluten). I am doing so much better. No dizzy spells since eliminating all grains and other processed foods! I have lots of damage, numbness in legs, feet, and especially toes, and some in hands and on my face (inside my mouth too, and I have had swallowing problems). I have some hearing loss too which I think is a result of damage near the acoustic nerve, in my cerebellum. I lost my acoustic reflexes (more evidence of "dings" in brainstem). But I will stick to my new, very strict diet, and will see how it goes. Since going on the very clean diet (for presumed super sensitivity to gluten),I have had some new mild pain in formerly totally numb toes. I seem to be regaining some more sensation on my face. And I have had no vertigo, and no light headeness! I have never had a positive blood test for TTG or anything like that, but two of my three sons tested positive (DGP IGG, TTG). I did an enterolab test for gliadin, and the value actually tripled between the time I was on the gluten challenge (in 2011) and summer of 2013, when I was already showing significant signs and symptoms of MS. In 2013 I had been on a gluten-free diet since my gluten challenge ended in summer 2011, but the Enterolab report commented that there likely were hidden sources of gluten in my diet as I was still producing the gliadin antibodies and the level was so much higher. I can't be certain the cleaner diet is responsible for me feeling better these last 3 weeks -- since my symptoms have had a waxing and waning quality. However, I am going to give it a serious trial, and for at least the next year I will not do anything that could be risky, in terms of diet (I will continue to avoid processed food and grains). I appreciate all the helpful advice posted on this site. Any advice directed my way would be most welcome. I will keep you posted on my progress. Thanks again to everyone who has posted helpful info in the past. Cheers, Hannah
  6. Hi, im back again with another theory. I wrote last week how i started a gluten free diet and after about a month started to slur my words. It got quite bad, tongue swelled up and i was finding it hard to form sentences. I went to a and e, then did a brain scan. I was sent for MRI told i probably have MS. I havent spoke to a neurologist yet, just waiting for an appointment. Im trying to find alternatives to this diagnosis and it seems a coincidence this happened when i changed my diet. I have been reading about b12 brain lesions. I realised that first month of the diet i probably hadnt eaten anything with b12 in it. Im vegetarian and wasnt eating gluten free bread etc. After reading about b12, i starting taking some. My speech came back after about 2 or 3 days of taking b12. I have all the symptoms of b12 deficiency as i have cfs. I also found this interesting article on fingernails http://www.health-boundaries-bite.com/Fingernails.html My are the exact same, ridged with blue skin underneath. Anyway what i wanted to ask is do you think my B12 levels could have dropped much further in my first gluten-free month and caused speech problems and be the possible cause of the brain lesions? This might be a stupid question-could i have had b12 in my blood before gluten-free diet but i wasnt able to absorb it properly, then i stop gluten and i suddenly absorb the b12 i have in my blood. Then i dont eat any b12 for a month causing a huge drop. Am i being mad? Thanks for any help Leis
  7. Hi! I'm new to these forums (though I've lurked the last couple years), and I'm hoping you might have some advice, insight, or experiences to share with me. My husband was "diagnosed" with celiac disease in late 2009. His blood tests were ordered by our family practitioner and they came back positive. We were referred to a local GI doc. The GI told my husband that it was fine to continue the gluten-free diet prior to the endoscopy (we now know that is not the case). The doc also took only 1 or 2 samples of the small intestine. The endoscopy came back negative. Our family practitioner told us she was certain my husband had it, and she was willing to refer us to a GI doctor in a local large city, but since we already had a $1000 bill from a procedure that was done incorrectly, and it was obvious the gluten-free diet was working, we declined. Since then, my husband has maintained a strict gluten-free diet with no "cheating." He recently began having some neurological symptoms, mostly intermittent numbness/tingling in his arms and numbness and pain in his legs (especially the left). We've found a new GI and we're also seeing a neurologist. Thus far, the neurologist had ordered a brain/spine MRI, which came back negative. Blood levels of B12 are normal (though he does have low Vitamin D levels). The neuro is scheduling him for an EMG. He wanted to know if our new GI was going to confirm the celiac diagnosis, because celiac can be a cause of nerve damage. We had discussed the possibility with our GI. He ran a celiac panel, which came back negative, as was expected since my husband consumes no gluten whatsoever. If he was to do an endoscopy, he'd have to do a gluten challenge, and I have reservations. Nerve damage is nerve damage---the gluten-free diet isn't solving the numbness issues, so do we really need a diagnosis in terms of how we'll treat the nerve problems? My husband will get really sick---I don't know if it's worth affecting his job performance (he's at a new job and there's no paid time off for him, plus he's in the running to move up pretty quickly), let alone the fact that we have three small children...I'm just wondering if having that official diagnosis is worth the path to get there, considering it doesn't really change anything that we'll be doing. Anyway, it feels like we're hanging in limbo with no answers and it's frustrating. We're trying to figure out what's causing these nerve issues but we have no answers thus far. Also, if somehow it is celiac-related, obviously my husband is following his diet, so it doesn't look like there's much promise of the diet fixing the nerve issues. If you have any experience, please share! I don't even know how to continue this post because that's how up-in-the-air we are right now.
  8. I am making this post on behalf of my girlfriend. She is currently being run through a variety of tests to determine if she has MS. Bloodwork, MRI, spinal tap. She has had a hard time not eating gluten products, and has it in spurts. She has been diagnosed with celiac disease since she was 17, suspected at 13, and is now 21. So she has continued eating gluten products since her diagnosis. Her symptoms include: Constant numbness in her limbs, with attacks of severe numbness and loss of control. Difficulty Walking/legs giving out. Difficulty with balance. Active brain lesions in her white matter and spine. Some vitamin deficiences, but we do not know the specifics. She has had a spinal tap performed, but the results have not come back yet. I have done some research and I have found that celiac disease can cause white matter lesions and spinal lesions, and all or most of these symptoms. I have not been able to find if celiac disease will cause a positive result for oligoclonal bands or antibodies in the CSF. I am very worried that her neurologist will continue to diagnose her disorder as MS, when her celiac disease (and ultimately malnourisment) has been presenting MS-like symptoms. She has told her neurologist that she had celiac disease, and the doctor had basically no reaction. Can anyone provide any useful information or has had any similar situations where they were on a path to MS diagnosis, had lesions and everything... but it was ultimately a misdiagnosis? As of right now she is on a gluten-free diet, and I am hoping that her symptoms cease. She has said that they have in the past. However the lesions may always be there, which her neurologist may not understand can also be caused by celiac disease.
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