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Celiac.com 02/03/2023 - Multiple sclerosis is a chronic autoimmune disease of the central nervous system that affects individuals worldwide. People with multiple sclerosis often have other autoimmune diseases such as hypothyroidism, inflammatory bowel disease, rheumatoid arthritis, and diabetes, which suggests that there may be common genetic or environmental exposures between multiple sclerosis and other autoimmune diseases. Epidemiological studies have also shown that individuals with one autoimmune disease have an increased susceptibility to developing another autoimmune disease. Celiac disease is an autoimmune gluten-sensitive enteropathy that results in small intestinal lesions and malabsorption in affected individuals. Celiac disease develops based on genetic factors and mucosal immune response. Almost all individuals with celiac disease have HLA DR3-DQ2 and/or the DR4-DQ8. These HLA class II haplotypes have a strong association with multiple sclerosis. celiac disease is also associated with neurological manifestations and diseases such as ataxia, epilepsy, neuropathy, and multiple sclerosis. However, the exact relationship between celiac disease and multiple sclerosis is not well understood. In order to evaluate the prevalence of celiac disease in multiple sclerosis cases, two researchers conducted a systematic review and meta-analysis using PubMed, Scopus, EMBASE, Web of Science, and Google Scholar. The search included all relevant studies published up to October 2022. The researchers independently searched all databases and also references of included studies. They included cross-sectional studies/case, articles which had been published in the English language, and studies in which the diagnostic criteria were biopsy of the duodenum. They excluded letters to editors, case reports, and RCT studies. They found a total of 1,113 articles by literature search, and after deleting duplicates, 519 remained. Sixteen articles remained for meta-analysis. A total of 31,418 patients were evaluated and the total number of possible/confirmed cases was 124. Studies were published between 2004 and 2020, and the most published studies were from Italy. Five studies provided information regarding controls. The pooled rates of this systematic review showed that celiac disease is not common in multiple sclerosis cases. However, the study did have some limitations. There were studies that used serologic evaluation for celiac disease diagnosis which were excluded. Additionally, there were no reports from some countries, and the control groups were different; as in some studies, the control group was healthy subjects, and in others, the control group was patients with other diseases except multiple sclerosis. The study authors suggest that larger multicenter studies from numerous countries are needed to fully understand the relationship between celiac disease and multiple sclerosis. It is important to note that while the rates of celiac disease in multiple sclerosis patients may be low, patients with multiple sclerosis still suffer from a wide range of gastrointestinal manifestations such as dysphagia, constipation, and/or fecal incontinence. Dyspeptic symptoms and associated pain are also common in multiple sclerosis cases, which can negatively affect quality of life and interfere with daily activities. Because of this, it's important for doctors to be aware of the potential for these symptoms in multiple sclerosis patients, and to consider a range of possible causes. Read more in the American Journal of Gastroenterology
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Hi everyone. First time poster. A few weeks ago I would have never guessed I'd be talking about any of this. My blood and urine tests have all been positive for celiac. I had a skin biopsy that also pointed towards DH. Endoscopy was yesterday but I was essentially told I have celiac regardless of the outcome. I just turned 30 and am shocked by all of this because I dont feel that bad. My biggest symptom this whole time has been a loose stool and DH, which showed up once and never came back. No one in my family tree has celiac or any other auto immune issues. I've accepted that I have celiac and Im prepared for the dieting, but I am absolutely terrified of MS. Is it something I should expect one day? Do the majority of people with celiac develop other auto immune diseases? I went from thinking "I just have to eat a strict diet" to now thinking that's just the tip of the iceberg. Its got me in a bad place mentally. Is it likely for MS to be in m future?
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To All, I have been busy with life issues lately.....so my forum time has been reduced lately. Recently there was a popular article on Reishi Mushrooms and could it help Celiacs. Here is the link to the article for those not familiar with the article. This caused me to do some digging to see if there is something in Mushrooms that might be helping Celiac's the doctor's might of have forgotten... And after a little research I hit on NAG....it is found in the Arthritis section of most Vitamins shops... Here is three studies of it on/in either IBS or Celiac's where it (NAG) has been shown to improve Celiac's conditions as a potential therapeutic.... But for whatever reason has been forgotten. Research them yourselves and see what you think. I would love to hear what the forum thinks. Here is the three best research articles I could find on N. Acetyl Glucosamine aka NAG as studied in GI patients. https://pubmed.ncbi.nlm.nih.gov/7877884/ https://pubmed.ncbi.nlm.nih.gov/2394351/ https://pubmed.ncbi.nlm.nih.gov/11121904/ We are finding potential therapeutics that are not drugs which is exciting to me. And some that have been forgotten for 30 years. As always I hope this is helpful but it is not medical advise. Posterboy,
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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
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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.
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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,
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