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Found 13 results

  1. Hello all! I'm fairly new to this community. Although I've been reading many posts on here for a while, this is only my second posting! I am pre-diagnosis, although I am almost 100% certain that I am at least gluten sensitive. Due to time, I'll make another post later on detailing more of my symptoms and my experiences on this crazy journey. Currently on a gluten-free diet because it is not worth the suffering (cheated enough times that now just looking at a cookie makes my everything hurt). This question is more towards anybody who has a good understanding of genes, alleles, etc. I have finally coughed up the dough to get genetic testing done, and my alleles are HLA-DQ 8 and HLA-DQ 3. To my very elementary understanding, HLA-DQ 8 is one of the two HLA genes associated with the development of celiac disease. There is also some controversial and currently unreplicated data suggesting that HLA-DQ 3 is associated with gluten sensitivity. Regardless of that controversial piece, it is also my understanding that HLA-DQ 8 is a "form" of the HLA-3 allele. If HLA-DQ 8 is a form of HLA-DQ 3, what is the difference between HLA-DQ 3 and HLA-DQ 8, that I have both of them? In other words, what makes it HLA-DQ 3, instead of one of its sub-categories or forms? Not sure if the question makes sense, or if anybody knows! Thanks for any info!!
  2. Hi all! I have fatigue bloating and gas with stomach pain and sometimes diarrhea for a couple of years until I figured it might be gluten related. No matter how much I sleep I am exhausted. I have “chicken “ skin for years and feel foggy minded. I recently tested positive for the two or more Celiac genes hla dqa1 05 and DQ2.2. Also higher risk for autoimmune disorders. My mom also has gluten intolerance. Been as gluten free as possible with some relief but fatigue and sinus headaches all the time and some bloating remains. I know with celiac testing you need t eat gluten before you get tested. I’m just worried that that might trigger for me to get more sick. Does anyone else feel this way in regards to testing?
  3. Beginning a few months ago, I thought I was just gluten intolerant. Then I started to really question what was wrong with me. Since I was a baby, I had intolerance to dairy. They would make us drink milk at school, and they (the government, basically) told us it was essential to our health. Yet, I was always in the health room after lunch in pain. Everyone thought I was faking it because I didn't like being at school. It wasn't until I entered high school that I diagnosed myself as lactose intolerant. I never had those stomach aches, gas, etc. again as long as I didn't consume dairy. Since I was 20, I lost a lot of weight. My BMI is 19.0, but it was 18.2 when it first happened. To maintain my weight, I don't exercise, and I overeat. This is not how things are supposed to be! I miss working out! I don't like worrying about eating when I don't want to. I'm pale, I'm cold, I can't sleep because I get a pins-and-needles feeling all over my body, sometimes I'll lose feeling in a toe, I've been told I look unhealthy, or like a ghost, I have no energy anymore, my anxiety, anger, and other mood issues are through the roof. I developed borderline personality disorder (ironically, probably, and partially stems from the emotional neglect of my parents about my physical and mental health for all those years. Saying it's all in my head, etc. I actually cried 3 times today, first time in months. My mom doesn't believe anythings wrong with me. I stayed up all night interpreting my DNA results to try getting her to believe me. We've been fighting all day. She always tries to minimize my problems and calls me a bypochondriac). My hair is becoming finer and possibly even thinning. I was diagnosed with ADD, bipolar, and psychosis. At about 17, I developed acid reflux - lots of throat-related issues like clearing it a lot, and post-nasal drop. All of this happened at the same time, basically. About 1 year ago. I had a genetic test done. There are two haplogroups related to celiac, I have the HLA DQA1 version (the most common). There are 13 (I believe) SNPs related to celiac disease. I have 12. My cousin had a similar issue and did NRT. And she's never felt better. They didn't give her diagnoses but told her to watch her dairy intake. What are your thoughts? Is it safe to assume I have the disease? I want to be myself again, but I don't know how to do that unless I know what's causing the problem. And please please please don't tell me to see a doctor, because some of us can't afford it, nor can we afford putting another medical issue on our profile. Thank you!
  4. I was wondering if anyone has ancestors from the present-day region of Alsace, France, or near there, who had celiac disease on that side of the family? This condition and related ones (diabetes) are common in my family on this side. I have traced it up the family tree and am wondering for research purposes.
  5. Why did I call this post “Time for a Vitamin Reformation”? I see this a lot. So I wanted to write more about it. I share/write these posterboy blog post’s so that others might not have to suffer the same things’ I have. As always I hope you find it helpful to learn how/what someone else did to help their own selves in this journey/road we all walk/or have walked on as a Celiac Disease/NCGS patient. I know this post is way too long (again) as usual but I had a lot of ground to cover. So hang on if you can and will and if you have an interest in learning how I became the posterboy for Celiac and Pellagra. Learn from my mistakes! Quoting the Celiac and now Pellagra Posterboy “No man is so dumb as the man/woman who won’t learn from other people’s mistakes.” I have made too many (mistakes) to count. Take as much honey (knowledge) as you can from my mistakes so bad (lack of knowledge) health will not sting your quality of life. Is it any wonder God’s promised’ land was described as a land flowing with milk and honey? Where knowledge (truth) flows there is health of mind and body. Truth of the right diagnosis can free us from the error of a wrong diagnosis. SADLY! Few listen. But some (Pellagrins’) who have received a Celiac diagnosis co-morbid have heard (listened to) the good news that Pellagra is reversible (when it is mimicking Celiac disease in a clinical setting) and have gotten better. Don’t be the Last! Tell others! So again Why did I call this post “Time for a Vitamin Reformation”? Most people (in the US anyway if you are reading this in some other country) are aware of the Protestant Reformation but most people are not as aware of the Catholic Reformation. Where basically the Catholic’s got smart? If you will and said all these Protestant’s are writing books (fresh off the invention of Gutenberg’s printing press (the internet of their day)) and the Catholic church said let us start printing our own books about how great the Catholic church is plus some minor changes essentially stopped the reformation in it’s tracks. And today there is still 1 Billion (with a Bee Catholics in this world. (I am not against either by the way) this is only by the way of illustration. I had recently wrote a blog post about this why Supplementation wins the War but I wanted to take another stab at it again. And even though I will have only used Vitamin(s) in this post. I want it to be clear this is for Vitamins and Minerals . . . like Iron, Magnesium, Calcium etc. It is just easier to type/write colloquially to use Vitamins to stand in for both Vitamins and Minerals together. See any of my comments or Ennis_Tx’s about Magnesium taken as Magnesium Citrate or Magnesium Glycinate. And why it is easy for the Protestant’s to claim a victory of sorts (there are Protestants still right) it is a pyrrhic victory at best because according to answers.com Catholics outnumber Protestant’s 2 to 1. https://answers.yahoo.com/question/index?qid=20070213184757AAHuhGz If you don’t still don’t believe me visit some of the old Cathedral’s of Europe you guessed it nearly all of them are Catholic Cathedral’s. Back to our point about Vitamins needing a Reformation. Such is the reign of Genetics today we blame it (our Genes) for everything today. Yet new research indicates maybe less than 1/3 of cancer’s day has anything to with Genetics at all. http://www.foxnews.com/health/2015/01/02/study-concludes-that-many-cancers-caused-by-bad-luck-in-cell-division.html Why this research is old it highlights my point that lifestyle (nutrition/vitamins etc) can and do help prevent Cancer today even in this GENETIC age we live in. http://www.cbsnews.com/news/lifestyle-changes-can-prevent-40-of-cancers-study/ To quote them from cbsnews “”We didn’t expect to find that eating fruit and vegetables (VItamin rich foods my words) would prove to be so important in protecting men against cancer,” Parkin said in the statement. … “This adds to the now overwhelmingly strong evidence that our cancer risk is affected by our lifestyles,” Dr Rachel Thompson, deputy head of science for the World Cancer Research Fund, told The Guardian. “ We hope this study helps to raise awareness of the fact that cancer (sickness) is not simply a question of fate (it’s in our genes my words) and that people can make changes today that can reduce their risk of developing cancer in the future.” My point is we need to be saying. Nutrition (Vitamins’ make us healthy) and not let Genetics get all the credit these day’s this includes our GI health too! I believe. It is actually probably more true too realize/say the balance is 50/50 because stress/environment effect both our health and yes even Genes. I think of it in these terms. A Vitamin is a substance we need in a “Min”ium” amount without which we become sick. I understand completely there is a lot of confusion about this topic. I will provide you some of the sources that lead/helped me come to my conclusions. Dr Prousky’s research is what I based my conclusion’s on and helped me to realize my Celiac Disease with/where he concluded “Niacin treats digestive problems” could also be confused for Low Stomach Acid. http://www.yourhealthbase.com/database/a124b.htm This is the link to the abstract. I realized this was going to be a future post when I saw Ennis_Tx muse about this question in a previous thread. Digestion is a north south process and it begins to make much more sense when you begin to understand the stomach protects your Small Intestine and if your defense are low (low stomach acid) when it is commonly thought to be high invading proteins like lactose, soy, and gluten etc. get through. http://divinehealthfromtheinsideout.com/2012/03/digestion-101/ Try a low carb (i.e. and also gluten free) diet for about a month and see if you flare ups don’t improve I think you will find your trigger is gluten and carbs. If so this will work but you will have to come to this conclusion on your own. It took me 3 years of study to understand these things God being my help. 2 Timothy 2:7 “Consider what I say; and the Lord give thee understanding in all things” this included. If you are now taking an acid reducer/proton pump inhibitor (I can’t lie) there will be a transition period. They all have a wall effect (burning when stopped) that often lock people in to using them for years and years when they were only intended to be used for 6 weeks or less to let ulcer’s heal. Actually on the OTC kind people usually buy without a prescription. It is even less than that. Only 14 days is recommended. . . . not 14 months ++ as is so often the case for people when they begin an acid reducer. See the FDA box warning. https://www.fda.gov/drugs/drugsafety/ucm245011.htm It will take courage and conviction on your part to take a Vitamin when all you hear these days’ that the “average” person doesn’t need a Vitamin. (see link below about why all the hate for Celiac’ drug/medicine treatment?/ trials?) by Jefferson Adams which inspired my title. https://www.celiac.com/articles/24099/1/Why-All-the-Hate-for-Celiac-Disease-Drug-Treatments/Page1.html Or put another way why ‘all the hate” for Vitamins? these days” instead of “Time for a Vitamin Reformation” (though I believe it is. .. I am also convenienced) it will take another generation to realize Pellagra is now being diagnosed as Celiac disease today instead. It takes a generation to make a change unless there is Education. This posterboy blog post is about that education process/the things I have learned from studying this subject myself. Do not change any of your supplementation/medical regime unless you have consulted with a doctor. . . but I found it helped me. The ignorance of this fact that Pellagra can occur with/in/as part of a Celiac diagnosis is so strong that so much so the “average joe” won’t take a Vitamin for their health? Well an IBS/NGCS patient/ Celiac Patient is not the average patient. They are known to develop malabsorption syndromes and B Vitamins are known to help celiac patient’s why wouldn’t you at least try a B-Vitamin or B-Complex to see if could help your GI symptom’s. https://www.celiac.com/articles/21783/1/B-Vitamins-Beneficial-for-Celiacs-on-Gluten-Free-Diet/Page1.html (though this study does not include the effects of full spectrum B-complex) it would have been nice if it did. I ask again “Who’s Afraid of a B Vitamin” See my earlier posterboy blog post about this topic Or to ask it rhetorically why all the hate for Vitamins these day (reader)? Or you (reader) afraid of a Vitamin? Or have you been too (reader) taught to hate Vitamins? And it isn’t just Niacinamide by the way (which is the focus of this post) it is most B-Vitamins. See this article about how B-1 Thiamine can help reverse Kidney Damage in Type 2 Diabetes http://news.bbc.co.uk/2/hi/health/7796073.stm Entitled “Thiamine ‘reverses Kidney Damage’ in Type 2 Diabetes” As usual this research is almost 10 years old and doctor’s clinical practices have not caught on to this fact proven by research. Instead the standard reply is “you don’t need Vitamins” or at least the average person does not. People who have TD2 or Celiac disease should not be considered the average person. Let me say at this point. Why is this not on the front page of every newspaper in the US and the UK and the world. Here we have a Vitamin that reversed Kidney Damage but no one is talking about it. What is not considered or well understood that these same vitamins that can help these patients – a deficiency in these same vitamins can also cause these same symptom’s. http://glutenfreeworks.com/blog/2010/06/23/niacin-vitamin-b3-deficiency-in-celiac-disease/ Now back to Niacinamide for a few minutes. What if had a Vitamin that was known to treat GI problems? We do but clinical practice has not yet again caught up with the research. That is why Prousky’s research is so ground breaking and misunderstood because the same vitamin (commonly misunderstood) associated with these problems has been proven to help the same problems it (Vitamin B3) has been thought to cause … though not commonly (well) understood Niacin treats digestive problems. http://www.yourhealthbase.com/database/a124b.htm *****I must say at this point this is not medical advice only my experience with Niacinmaide See my previous posterboy blog post about how the average clinical delay is 17 years in implementing new research into doctor’s protocols’/treatment regimens. This clinical gap is a devastating delay. And also I want to make this disclaimer. The default (thought) here is you are not taking Niacin or any version of B-3 (in its many forms) or have either not taken it for Cholesterol management previously or are now taking it for your GI problems. If you are now taking Niacinamide/Niacin etc. this post does/is not directed at you (or other Vitamins/Minerals) for that matter . . . like Magnesium or Iron etc. Also see my posterblog post about how supplementing can help you fight a two front war. Any Vitamin or Mineral can be taken to excess . . . contributing to a worsening of your conditon.. . including Niacinamide, Iron, Calcium etc. This comment/thread is directed to those who have not yet considered supplementation previously. And with the intent you will only take this for a cycle of time. Say 4 to 6months for most people or 6 to 12 months max for the most severe forms of this disease. See this link where it explains how “up to 12 months” B-Vitamins helps improved/improves moods for those who are depressed. https://www.ncbi.nlm.nih.gov/pubmed/7477807 Reader, Do some of the research of I have listed here and if you still feel the same way. I get it. I have been on that same journey. But this is not as uncommon or unplausible as it might sound. The “House TV” show/medical drama noted this fact in their episode on Celiac Disease. Google House season 2 episode 22 on Celiac disease entilted “Forever” and you will find articles about it and probably a link to watch it. I think it would be enlightening to see how these two diseases are entangled like Siamese twins. When digestion works properly the God given burp is produced (not soda’s) but you burp like a healthy child at 6 months of age so too will an adult when they take Niacinamide (the nonflushing form of Vitamin B-3) for 6 months 2/day (especially if you are not taking PPIs currently). Your results might be different but you won’t know unless you try it. When I began my journey I was/became known as the posterboy for Celiac disease. What it has turned into unexpectedly is me being/becoming the posterboy for Pellagra too! It (Pellagra in Celiac’s) is not as rare as people think it is today especially 2ndary Pellagra caused by your original Celiac diagnosis since Vitamin absorption is frequently compromised in Celiac’s. I always have to say. **** This is not medical advice and should not be considered such. Results may vary. Always consult your doctor before making any changes to your medical regimen. But I have found (and my friends have found) if you take it (Niacinamide) like an antibiotic (UNTIL BURPING) then 95% of your GI stress will be in remission. And I don’t mean twenty minutes after you have eaten but 2+ hours later when burping has replaced burping and bloating that start’s almost as soon as you take you first bite. Or burping that occurs with drinking soda or a carbonated drink. Again I say 2 Timothy 2:7 “Consider what I say; and the Lord give thee understanding in all things” I hope this is helpful. Posterboy by the Grace of God, That is all for now until the next post. (Whenever that is) but the intent of this/theses post’s is “Too Educate” and anyone of my posterboy blog posts could help you without the need to read all my posterboy blog posts??? So I am sorry if I run a little long some times. . . but people need to know if this is the only blog post they read. . . Pellagra in Celiac’s can be successfully treated with supplementation or AKA a Vitamin Reformation (in the way we think) about GI problems according to Prousky who almost 17 years ago proved Niacinamide can help those with low stomach acid misdiagnosed. Will you listen? and take the Niacinamide Challenge taking it until you are burping 2 hours after you finish a meal. This usually takes 3 to 4 months taken it 3/day or morning and evening and (one hour before) bedtime (if it is not convenient to bring to work) works well for most people. This tends to be one 300 count bottle for most people. Though a smaller amount might work I want you to have a positive experience and thus recommend conservatively a 3 month to 4 month cycle – the amount your body can typically store in your liver – thus helping to reset your body’s stress clock (my words). This schedule works well for Magnesium as well. . . and usually it (Magnesium Citrate/Glycinate) causes restful dreaming in the first month of taking it. The power to change is in your hand for “To Educate is to Free” As always remember **** This is not medical advice and should not be considered such. Results may vary. Always consult your doctor before making any changes to your medical regimen. But I have found (and friends have found) if you take it (Niacinamide) like an antibiotic (UNTIL BURPING) then 95% of your GI stress will be in remission. It is time for a Vitamin Reformation (a change in the way we think about Vitamins – a shift in our paradigm) praise bee to God! Back to when in the 20th century they understood Vitamins make us healthy! They even gave Nobel Prizes for discovering these substances called Vitamin(s) and rightly so! If this is the case for you – you the reader also have/had developed 2ndary Pellagra due to your primary diagnosis of Celiac disease. See my earlier posterboy blog post where I talked about my experience of developing Pellagra 2ndarly to my Celiac diagnosis. All those who have ears to hear may they listen! Feel free to read all my posterboy blog post’s if this pique’s your curiosity/interest but there is only so much in a/one blog post than can be explained but it really Is not necessary or visit the website/blog in my profile where I have told the same story hundreds of time that ONE fellow sufferer like myself may/might be helped by the same wisdom, I found God being my help, when I learned Pellagra and Celiac disease are Siamese twins and separating one (supplementing one to death) will kill the other (cause the other to go into remission). Also see my posterboy blog post of how I supplemented Pellagra to death/into remission. Noted above (earlier) in this post but provided here again for easy reference. And I believe you can too! Praise bee to God! 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 (fellow sufferer) which are in any trouble, by the comfort wherewith we ourselves are comforted of God.” Posterboy by the Grace of God, 2 Timothy 2:7 “Consider what I say; and the Lord give thee understanding in all things” this included. As always it is in this spirit of truth that I share so that others like my-self might not have to suffer the same things I did.
  6. Celiac.com 01/08/2018 - Imagine gluten-free wheat. Well, actually you don't have to imagine it, because a group of scientists has used a gene-editing technique called CRISPR/Cas9 to cut selected genes from a wheat genome, and presto, gluten-free wheat is a thing. As people in numerous countries debate genetically modified crops, some countries, including France and Germany, have passed laws to prohibit their cultivation. Remember, we're not talking about hybridization here, which is based on natural selection and works by interbreeding plant strains. Researchers have used hybridization to develop strains of wheat that are low in gluten, but so far no one has made a strain that is entirely free of gluten. In this case, we're talking about genetic modification; changing the basic genetic structure of the plant. The greatest objections around GMO practices have been focused on the insertion of DNA from one species into another species, says Francisco Barro, a plant biotechnologist at the Institute for Sustainable Agriculture in Spain. To steer clear of this genetic process, Barro and his team used the gene-editing technique CRISPR/Cas9 to remove certain genes from a wheat genome. Their team focused on alpha-gliadins, gluten proteins that are thought to be the trigger for immune system reactions in people with celiac disease and gluten sensitivity. To accomplish their goal of removing the culprit gene(s), the research team used the scissorlike Cas9 protein to cut out 35 of the 45 alpha-gliadin genes. Lab tests showed that the new wheat strain reduced the immune response by 85 percent, the team reported. Far from being any kind of decisive breakthrough though, this is just one “really important step in maybe producing something that is going to be incredibly useful,” says Wendy Harwood, a crop geneticist at the John Innes Center in England. Meanwhile, Barro says his team is working on targeting more gluten-triggered genes to develop a completely safe strain of wheat for celiac patients. Source: Scientific American
  7. Celiac.com 01/01/2018 - A team of researchers recently set out to conduct a genome-wide association study (GWAS) of general cognitive ability ("g"), further enhanced by combining results with a large-scale GWAS of educational attainment. The research team included Max Lam, Joey W. Trampush, Jin Yu, Emma Knowles, Gail Davies, David C. Liewald, John M. Starr, Srdjan Djurovic, Ingrid Melle, Kjetil Sundet, Andrea Christoforou, Ivar Reinvang, Pamela DeRosse, Astri J. Lundervold, Vidar M. Steen, Thomas Espeseth, Katri Räikkönen, Elisabeth Widen, Aarno Palotie, Johan G. Eriksson, Ina Giegling, Bettina Konte, Panos Roussos, Stella Giakoumaki, Katherine E. Burdick, Antony Payton, William Ollier, Ornit Chiba-Falek, Deborah K. Attix, Anna C. Need, Elizabeth T. Cirulli, Aristotle N. Voineskos, Nikos C. Stefanis, Dimitrios Avramopoulos, Alex Hatzimanolis, Dan E. Arking, Nikolaos Smyrnis, Robert M. Bilder, Nelson A. Freimer, Tyrone D. Cannon, Edythe London, Russell A. Poldrack, Fred W. Sabb, Eliza Congdon, Emily Drabant Conley, Matthew A. Scult, Dwight Dickinson, Richard E. Straub, Gary Donohoe, Derek Morris, Aiden Corvin, Michael Gill, Ahmad R. Hariri, Daniel R. Weinberger, Neil Pendleton, Panos Bitsios, Dan Rujescu, Jari Lahti, Stephanie Le Hellard, Matthew C. Keller, Ole A. Andreassen, Ian J. Deary, David C. Glahn, Anil K. Malhotra, and Todd Lencz. They are variously associated with the dozens of research facilities listed below. Their study provided a large-scale GWAS of cognitive performance, combined with GWAS of educational attainment; 70 independent genomic loci associated with individual differences in cognition. The study found that implicated genes suggest potential treatment targets for cognitive enhancement. The team also observed genetic overlap between cognitive ability and multiple health-related phenotypes. For their genome-wide association study (GWAS) of general cognitive ability ("g"), the team evaluated 107,207 subjects. They further enhanced their data pool by combining results with a large-scale GWAS of educational attainment. They also identified 70 independent genomic loci associated with general cognitive ability. Observing the outcomes, the team saw substantial enrichment for genes triggering Mendelian disorders with an intellectual disability phenotype. Analysis of competitive pathways pointed to neurogenesis and synaptic regulation, as well as the gene targets of two pharmacologic agents: cinnarizine, a T-type calcium channel blocker, and LY97241, a potassium channel inhibitor. According to the researchers: "we observed modest, yet nominally significant, inverse correlations between cognition and autoimmune diseases such as eczema and Crohn's disease, attaining Bonferroni significance for rheumatoid arthritis (rg for MTAG results = −0.2086; p = 1.60E−08). There was also a Bonferroni-significant positive genetic correlation with celiac disease (rg for MTAG results = 0.1922; p = 0.0001)." Full analysis of both the transcriptome and epigenome showed that the implicated loci were enriched for genes expressed across all brain regions; mostly in the cerebellum. Interestingly, only genes expressed in neurons were enriched, not those expressed in oligodendrocytes or astrocytes. Lastly, the team observed genetic correlations between cognitive ability and various phenotypes, including psychiatric disorders, autoimmune disorders, longevity, and maternal age at first birth. Source: Cell.com. DOI: http://dx.doi.org/10.1016/j.celrep.2017.11.028 The research team members are variously associated with the following: Campbell Family Mental Health Institute, Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada Institute of Mental Health, Singapore, Singapore BrainWorkup, LLC, Los Angeles, CA, USA Institute for Behavioral Genetics, University of Colorado, Boulder, CO, USA Division of Psychiatry Research, Zucker Hillside Hospital, Glen Oaks, NY, USA Department of Psychiatry, Hofstra Northwell School of Medicine, Hempstead, NY, USA Center for Psychiatric Neuroscience, Feinstein Institute for Medical Research, Manhasset, NY, USA Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA Department of Genetics and Genomic Science and Institute for Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, USA Mental Illness Research, Education, and Clinical Center (VISN 2), James J. Peters VA Medical Center, Bronx, NY, USA Department of Neurology, Bryan Alzheimer's Disease Research Center and Center for Genomic and Computational Biology, Duke University Medical Center, Durham, NC, USA Department of Psychiatry and Behavioral Sciences, Division of Medical Psychology, Duke University Medical Center, Durham, NC, USA Laboratory of NeuroGenetics, Department of Psychology & Neuroscience, Duke University, Durham, NC, USA Human Longevity Inc., Durham, NC, USA Department of Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA Department of Psychology, Yale University, New Haven, CT, USA Department of Psychology, Stanford University, Palo Alto, CA, USA Clinical and Translational Neuroscience Branch, Intramural Research Program, National Institute of Mental Health, National Institute of Health, Bethesda, MD, USA Lieber Institute for Brain Development, Johns Hopkins University Medical Campus, Baltimore, MD, USA Neuroimaging, Cognition & Genomics (NICOG) Centre, School of Psychology and Discipline of Biochemistry, National University of Ireland, Galway, Ireland Neuropsychiatric Genetics Research Group, Department of Psychiatry and Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin, Ireland Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK Department of Psychology, University of Edinburgh, Edinburgh, UK Alzheimer Scotland Dementia Research Centre, University of Edinburgh, Edinburgh, UK Division of Brain Sciences, Department of Medicine, Imperial College, London, UK Centre for Epidemiology, Division of Population Health, Health Services Research & Primary Care, The University of Manchester, Manchester, UK Centre for Integrated Genomic Medical Research, Institute of Population Health, University of Manchester, Manchester, UK Division of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Salford Royal NHS Foundation Trust, Manchester, UK Department of Biological and Medical Psychology, University of Bergen, Bergen, Norway Department of Medical Genetics, Oslo University Hospital, University of Bergen, Oslo, Norway NORMENT, K.G. Jebsen Centre for Psychosis Research, University of Bergen, Bergen, Norway Dr. Einar Martens Research Group for Biological Psychiatry, Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway Department of Psychology, University of Oslo, Oslo, Norway Department of Psychology, University of Edinburgh, Edinburgh, UK Dr. Einar Martens Research Group for Biological Psychiatry, Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge, UK Department of Medical Genetics, University of Helsinki and University Central Hospital, Helsinki, Finland Department of General Practice, University of Helsinki and Helsinki University Hospital, Helsinki, Finland National Institute for Health and Welfare, Helsinki, Finland Folkhälsan Research Center, Helsinki, Finland Helsinki Collegium for Advanced Studies, University of Helsinki, Helsinki, Finland Department of Psychiatry, Martin Luther University of Halle-Wittenberg, Halle, Germany Department of Psychology, University of Crete, Crete, Greece Department of Psychiatry, National and Kapodistrian University of Athens Medical School, Eginition Hospital, Athens, Greece University Mental Health Research Institute, Athens, Greece Neurobiology Research Institute, Theodor-Theohari Cozzika Foundation, Athens, Greece Department of Psychiatry and Behavioral Sciences, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD, USA McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA 23andMe, Inc., Mountain View, CA, USA
  8. Celiac.com 10/18/2017 - Celiac disease is a chronic inflammatory disease of the small intestine mucosa due to permanent intolerance to dietary gluten. A team of researchers recently set out to clarify the role of small intestinal epithelial cells in the immunopathology of celiac disease, especially the influence of celiac disease-associated bacteria. The research team included G Pietz, R De, M Hedberg, V Sjöberg, O Sandström, O Hernell, S Hammarström, and ML Hammarström. They are variously affiliated with the Department of Clinical Microbiology, Immunology, and the Department of Clinical Sciences and Pediatrics at Umeå University, in Umeå, Sweden. The team collected duodenal biopsies from children with active celiac disease, treated celiac disease, and a group of clinical control subjects. They then purified intestinal epithelial cells, and analyzed them for gene expression changes at the mRNA and protein levels. To assess how interferon-γ, interleukin-17A, celiac disease-associated bacteria and gluten influence intestinal epithelial cells, they used two in vitro models for human intestinal epithelium, small intestinal enteroids and polarized tight monolayers. In patients with active celiac disease, intestinal epithelial cells significantly upregulated more than 25 defense-related genes, including IRF1, SPINK4, ITLN1, OAS2, CIITA, HLA-DMB, HLA-DOB, PSMB9, TAP1, BTN3A1, and CX3CL1. Of these genes, 70 percent were upregulated by interferon-γ via the IRF1 pathway. Notably, IRF1 was also upregulated by bacteria associated with celiac disease. Intestinal epithelial cells also expressed the NLRP6/8 inflammasome yielding CASP1 and biologically active interleukin-18, which induces interferon-γ in intraepithelial lymphocytes. Over-expression of IRF1 appears to be a key factor in the epithelial reaction in celiac disease. This may be inherent, but may also be due to presence of undesirable microbes that trigger or influence IRF1. From this study, the researchers conclude that activation of IRF1 and IRF1-regulated genes together, both directly and via the interleukin-18 dependent inflammasome, would greatly increase the severity of the inflammatory response, and trigger the pathological gut response that is common in active celiac disease. Could this provide a key to unlocking the mysteries of celiac disease and its associated symptoms? Source: PLoS One. 2017 Sep 21;12(9):e0185025. doi: 10.1371/journal.pone.0185025.
  9. Celiac.com 05/30/2016 - People with HLA genes have the highest risk factor for developing autoimmune disorders. The vast majority of people with celiac disease carry the HLA DQA1*05 and DQB1*02 alleles, both of which encode the DQ2.5 molecule. A research team recently set out to examine the implications for anti-gluten T cell response of the preferential expression of HLA-DQ2.5 genes associated with celiac disease with respect to non-predisposing HLA genes. The research team included L Pisapia, A Camarca, S Picascia, V Bassi, P Barba, G Del Pozzo, and C Gianfrani. They are variously affiliated with the Institute of Protein Biochemistry-CNR, the Institute of Genetics and Biophysics-CNR in Naples, Italy, and the Institute of Food Sciences-CNR in Avellino, Italy. In order to activate pathogenic CD4+ T lymphocytes, that is, to trigger active celiac disease, it is necessary for the body to form complexes between DQ2.5 and gluten peptides on antigen-presenting cells (APCs). It is widely accepted by clinicians that the DQ2.5 genes establish the different intensities of anti-gluten immunity, depending on whether they are in a heterozygous or a homozygous configuration, that is, whether both genes are activated, or only one gene is activated. The research team's recent study shows that, in celiac patients, HLA DQA1*05 and DQB1*02 gene expression is much higher than expression of non-celiac-associated genes. This, in turn, impacts protein levels and causes a comparable cell surface exposure of DQ2.5 heterodimers between DQ2.5 homozygous and heterozygous celiac patients. As a consequence, the magnitude of the anti-gluten CD4+ T cell response is strictly dependent on the antigen dose, and not on the DQ2.5 gene configuration of APCs. These findings are important, because they support the idea that the expression of DQ2.5 genes is an important risk factor in celiac disease. The preferential expression of DQ2.5 alleles observed in this study offers a new explanation of why these genes are so frequently associated with celiac disease and with other autoimmune disorders. Source: J Autoimmun. 2016 Apr 12. pii: S0896-8411(16)30029-4. doi: 10.1016/j.jaut.2016.03.016.
  10. I received my gene testing results back. I've been googling and trying to understand, but I'm lost. Would really appreciate ANY help!! HLA-DQA1 1 HLA-DQA1 3 HLA-DQB1 301 HLA-DQB1 603 It says I was negative for DQ2 and DQ8, so no celiac. Just trying to get help with these numbers since my TTG IGG came back positive for the antibodies, even after going gluten-free for almost a year, and only eating a little bit of gluten for a little while before the test. I keep seeing the B1*0301 come up in results that show interesting stuff. Is that the DQ7? At least I think that is what Wikipedia says it is? I'm trying to figure out my "type"? This stuff is losing me here! Please help! Thank you!
  11. Hi, I'm hoping someone can help me interpret my genetic tests etc from Enterolab. I am skeptical of the IGA testing as per other posts I've read on here, but I've gotten to the point where I've medically ruled out just about everything else, so I'm willing to go the long road of an experimental diet to see what happens. Basically, I've had bacterial overgrowth on and off, acid reflux, mix of C and D on and off for years without any apparent cause. Since spring, despite being on super high doses of PPis, I have persistent chest pain and nausea etc... I've had two blood tests and biopsies for celiac over the last four years, all negative. In October I had tests that showed low esophageal motility and esophagitis. A barium swallow a month later showed normal motility, but the chest pain and esophagitis continues. Medicine's not helping. Also, I have really low levels of vitamin D. However, my doctors can't seem to prove that the esophagitis is coming from acid... it remains a mystery, and I'm not sure what to do next... I know I have some susceptibility to autoimmune stuff because I have Hashimoto Disease (hypothyroidism) which was discovered last Christmas over the course of testing for various GI problems. That's under control more or less now, and so that shouldn't be affecting any of the GI stuff which is, if anything, worse than before treatment. So, anyway, other than all that, I'm an athletic 29 year old female. Here's my testing results- I'm hoping someone can tell me the liklihood of gluten sensitivity (and whether I should also try the no egg and casein thing...) Gluten/Antigenic Food Sensitivity Stool Panel Fecal Anti-gliadin IgA 69 Units (Normal Range is less than 10 Units) Fecal Anti-casein (cow’s milk) IgA 19 Units (Normal Range is less than 10 Units) Fecal Anti-ovalbumin (chicken egg) IgA 43 Units (Normal Range is less than 10 Units) Fecal Anti-soy IgA 10 Units (Normal Range is less than 10 Units) Gluten Sensitivity Gene Test HLA-DQB1 Molecular analysis, Allele 1 0202 HLA-DQB1 Molecular analysis, Allele 2 0303 Serologic equivalent: HLA-DQ 2,3 (Subtype 2,9) Thank you so much! I'm honestly getting really desperate... so much time and money and discomfort with no diagnoses... GC
  12. Celiac.com 12/12/2008 - For some time now scientists have been working to better understand the connection between celiac disease and diabetes. About 10% of children and 2% of adults with Type 1 diabetes also have celiac disease, as compared to just 1% of the general population. Moreover, celiac disease and diabetes are known to have a common genetic susceptibility locus in the HLA system, specifically, HLA class II alleles on chromosome six. The primary susceptibility genes for type-1 diabetes are HLA-DQB1 and HLA-DRB1, but they act in combination with non-immune system genes as well as environmental factors that are still undiscovered. Celiac disease also has a major susceptibility gene in the HLA system — HLA-DQB1 — as well as locations outside the HLA complex. Recently, a research team led by John Todd, Ph.D., of the University of Cambridge, set out to better understand the connection between the two diseases, and to determine if they shared any non-HLA regions. They discovered another seven regions outside of the HLA system that are tied to both celiac disease and diabetes. One of those regions is the 32-base pair insertion-deletion variant on chromosome three that leads to a non-functional CCR5 receptor on T cells. People who carry both pairs of these genes enjoy some protection against HIV infection, and its role in both celiac disease and diabetes indicates that lymphocytes are a key factor in both diseases. Carriers of these genes also face a greater risk of developing either celiac disease or diabetes, or both conditions in their lifetimes. In genome-wide association studies, eight loci outside the HLA system have been associated with celiac disease. Similarly, 15 non-HLA loci have been linked with Type 1 diabetes. Dr. Todd and colleagues genotyped single nucleotide polymorphisms (SNPs)—single letter variations in the genetic code—in the eight celiac loci and in the 15 diabetes loci. They then screened DNA samples from 9,339 control subjects, 2,560 subjects with celiac disease, and 8,064 subjects with diabetes. They also tested the diabetic children, along with both biological parents in 2,828 families. The overall statistical significance was P<1.00×10−4. At the same level of significance, three celiac disease locations—RGS1 on chromosome one, IL18RAP on chromosome two, and TAGAP on chromosome six—were also associated with Type 1 diabetes. The minor alleles of IL18RAP and TAGAP were associated with some protection from in Type 1 diabetes, but were associated with susceptibility in celiac disease. The CCR5 variant on chromosome three was newly tied to Type 1 diabetes (at P=1.81×10−8) and was also tied with celiac disease, together with PTPN2 on chromosome 18 and CTLA4 on chromosome two. Counting SH2B3 on chromosome 12, which already known to be a shared locus—the number of non-HLA areas strongly tied to both celiac disease and diabetes stands at seven. Dr. Todd and colleagues said it's possible that a common genetic background with respect to autoimmunity and inflammation—combined with disease-specific variation at HLA and non-HLA genes as well as non-genetic factors -- might lead to different clinical outcomes. It is possible that dietary exposure to gluten in the form of cereal grains might play a role in the pathogenesis of Type 1 diabetes. These findings offer support a growing scientific view that many common diseases share genetic risk factors, and indicate that celiac and diabetes may in fact have common biological causes, and that the two disorders may be more closely linked than previously understood. More research is needed to determine which shared risk factors might reveal previously unexpected biologic connections between diseases. New England Journal of Medicine 2008; 359: 2767-77, 2837-2838
  13. Gastroenterology, Oct 2003, Vol 125, No 4, p1032-41 Celiac.com 10/30/2003 – A Dutch research team has identified the specific regions of chromosome 19 that contribute to celiac disease. Despite its well-known association with human leukocyte antigen (HLA)-DQ2 and DQ8, the pathogenesis of celiac disease has remained largely unknown. The team studied 82 Dutch families who met strict diagnostic criteria which included biopsies that presented Marsh III lesions. The 216 independent celiac disease patients were compared to 216 age and sex-matched controls. As expected the study found significant linkage to the suspected HLA region, but more importantly found additional, previously unknown and significant linkages at 19p13.1 (with a peak at marker D19S899), and at 6q21-22, which is ~70 cm downstream from the HLA region in question. The researchers conclude: "Significant linkage of celiac disease to chromosome region 19p13.1 was detected in our genome-wide screen. These results were confirmed by the association of D19S899 to celiac disease in an independent case-control cohort. Furthermore, we identified a possible second celiac disease locus on chromosome region 6q21-22." The study was dedicated to the memory of Lodewijk Sandkuijl (1953-2002), who died shortly after its completion. He was an inspiration to the researchers and was a world expert on biostatistics.
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