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Found 69 results

  1. Celiac.com 10/29/2018 - Researchers Emma L. Smith with UCB Pharma Ltd., Slough, United Kingdom, and Mark Peakman from the Department of Immunobiology, King’s College London, London, United Kingdom recently set out to catalog clinical advances in peptide immunotherapy for Type 1 diabetes. Autoimmune and allergic diseases occur when a person’s body has an incorrect immune response to an antigen from the person’s own body, or to an innocuous antigen from outside the body. This triggers a pathogenic T-cell response which causes damage to certain tissues and organs. In Type 1 diabetes, this process results in the destruction of the insulin-secreting β cells, which leads to permanent need for recombinant insulin to make up for the loss. The best way to restore immune homeostasis and prevent further tissue damage is to reduce or cease the pathogenic T-cell response by using antigen-specific peptide immunotherapy. Smith and Peakman found that recent clinical advances with peptide therapy approaches in both Type 1 diabetes and other diseases are beginning to show encouraging results. New treatments that target peptides specific to certain cell types are also moving from the development stages into clinical use. Drug developers still face numerous hurdles in reaching full clinical use, including determining optimal dose and dosing frequency, but peptide immunotherapy for Type 1 diabetes is clearly becoming a very active field of drug development. Read their full report: Front Immunol. 2018; 9: 392.Published online 2018 Feb 28. doi:  10.3389/fimmu.2018.00392PMCID: PMC5836708PMID: 29541078
  2. Celiac.com 10/22/2018 - A team of researchers recently set out to determine if there is any association between prenatal gluten exposure and offspring risk of type 1 diabetes in humans. The research team first designed a national prospective cohort study using the national health information registries in Denmark. They looked at data on pregnant Danish women enrolled into the Danish National Birth Cohort, between January 1996 and October 2002, and assessed maternal gluten intake, based on maternal consumption of gluten containing foods, as reported in a 360 item food frequency questionnaire at week 25 of pregnancy. The team gathered information on type 1 diabetes occurrence in the participants’ children, from 1 January 1996 to 31 May 2016 by linking to the Danish Registry of Childhood and Adolescent Diabetes. Overall, their study included data on 101,042 pregnancies in 91,745 women, of whom 70,188 filled out the food frequency questionnaire. Once they corrected the figures to account for multiple pregnancies, pregnancies ending in abortions, stillbirths, lack of information regarding the pregnancy, and pregnancies with implausibly high or low energy intake, they included 67,565 pregnancies and 63,529 women. Gluten intake averaged 13.0 grams per day, ranging from under 7 grams per day to more than 20 grams per day. There were 247 children with type 1 diabetes among the group, for an incidence rate of 0.37%, with an average follow-up of 15.6 years. Risk of type 1 diabetes in offspring increased proportionally with maternal gluten intake during pregnancy per 10 grams per day increase of gluten. Compared to women with the lowest gluten intake of under 7 grams per day, those with the highest gluten intake who consumed 20 or more grams a day had double the risk for type 1 diabetes development in their children. These numbers indicate that high gluten intake by mothers during pregnancy may increase the risk of their children developing type 1 diabetes. However, the team is calling for further study to confirm the findings, preferably in an intervention setting. Read more in BMJ 2018;362:k3547. doi: https://doi.org/10.1136/bmj.k3547 The research team included Julie C Antvorskov, assistant professor, Thorhallur I Halldorsson, professor in food science and nutrition, Knud Josefsen, senior researcher, Jannet Svensson, associate professor5, Charlotta Granström, statistician, Bart O Roep, professor, Trine H Olesen, research assistant, Laufey Hrolfsdottir, director, Karsten Buschard, professor, and Sjudur F Olsen, adjunct professor of nutrition. They are variously affiliated with the Bartholin Institute, Rigshospitalet in Copenhagen, Denmark; the Centre for Foetal Programming, Department of Epidemiology Research, Statens Serum Institute, Copenhagen, Denmark; the Unit for Nutrition Research, Landspitali University Hospital, Reykjavik, Iceland; the Faculty of Food Science and Nutrition, University of Iceland, Reykjavik, Iceland; the Copenhagen Diabetes Research Center (CPH-DIRECT), Department of Children and Adolescents, Copenhagen University Hospital Herlev, Herlev, Denmark; the Department of Diabetes Immunology, Diabetes and Metabolism Research Institute at the Beckman Diabetes Research Institute, City of Hope, Duarte, CA, USA; the Departments of Immunohematology and Blood Transfusion, Leiden University Medical Centre, Leiden, Netherlands; the Department of Education, Science, and Quality, Akureyri Hospital, Akureyri, Iceland; and the Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
  3. Celiac.com 10/19/2018 - Work to develop a vaccine for celiac disease could soon lead to a vaccine for diabetes. After successful phase 1 studies of Nexvax2, their peptide-based therapeutic vaccine for celiac disease, ImmusanT has seen a significant investment from venture philanthropy organization JDRF T1D. ImmusanT's peptide therapy program for celiac disease may provide lessons for a similar therapeutic treatment for Type 1 diabetes. The investment will support ImmusanT as it attempts to develop a vaccine to prevent Type 1 diabetes, based on the early success of its peptide immunotherapy program for celiac disease, the two entities announced in a press release. ImmusanT’s celiac peptide therapy program works by identifying antigens that trigger an inflammatory responses in people with autoimmune diseases. Once identified, the peptide therapy is used to neutralize the autoimmune response. This celiac disease program goes back to 1998, when Anderson first began his efforts to find and identify the peptides. The findings were published in 2010, and the company was founded shortly afterward by Leslie Williams, BS, RN, MBA, director, president and CEO of ImmusanT. From there, ImmusanT conducted five phase 1 trials for its celiac therapy. Those trials have proven very promising, and the latest investment into a similar drug for diabetes is proof of that promise. In the case of celiac disease, the drug works by “targeting T cells in patients. Those T cells that are engaged as peptides are distributed throughout the body after the injection, and we see evidence that the T cells are being activated about 2 hours later,” Robert Anderson, BMedSc, MB, ChB, PhD, FRACP, chief scientific officer for ImmusanT, told Endocrine Today. “We found that if we gradually increase the dose in patients building up to a maintenance dose level, they become non-reactive to those peptides.” With much of the early research targeted towards demonstrating the drug’s safety, and getting the right dose and dose regimen, the development of a version targeted at diabetes, says Anderson, “should be more streamlined due to the lessons learned during the celiac disease program. That’s partly because the team knows “a lot more going into Type 1 diabetes about how peptide therapy works and how to optimize it than we did when we started celiac disease, where it was a blank slate.” This is really exciting news. A vaccine for celiac disease is exciting, to be sure, but a viable vaccine for diabetes would be a major development in disease prevention. Stay tuned for more news as the story develops. Read more at Healio.com
  4. I am a adolescent female and I have celiac disease. I get all the typical celiac symptoms but over the last couple of days I have developed strange symptoms I have never had before. I feel Extremely. Thirsty all the time even if I drink water, I am urinating constantly but it dosent hurt. I have a new pain in my upper,upper abdomen and I feel faint occaisonally and I am getting leg cramps but I have no idea whether the cramps are related to diabetes or not. We went to the doctor and the doctor did a urine sample on me to test for sugar in my urine but she said she couldnt detect any. Anyway she booked me in for a blood test to make sure. What I am wondering is if anyone was diagnosed with diabetes type 1 but had a negative urine test? Or if they have heard of anyone like this?. I have also posted a question similair on a diabetes forum but I wanted to see if anyone knew about it from a celiac point of view because I was wondering if something to do with celiac caused the urine test to be negative though I havent researched it yet .Please can you help? Thanks in advance
  5. hi all! i was wondering if there were any super low gi grains like barley (which has a gi of 28 or something). I need to find something because i have problems with blood sugar, but obviously cant have barley with celiac. I know that there are vegetables with a low gi but i need something with comparable calories (~350/cup) and id have to eat a 5 kg of carrots to get that lol! any ideas?
  6. Hello all. I've been living with celiac for about 4 years now. I'm a type 1 diabetic and as mentioned have celiac. I have not followed the diet, never really feeling the effects until the past year. I'e always been in decent shape, but realized I was losing weight in such a way that I look malnutritioned. After trying my best to push weights, and do pushups, I realized I am the weakest I've ever been. I'm 22 and feel like I have the strength of a 14 year old. Is this the end? I want to dedicate my self to the diet, but feel like at this point there is no use.
  7. A new study was released this week. Although not a true scientific study, the results are promising for Type 1 diabetics and in my personal opinion, Type 2, as well. I am sharing this because Type 1 has a strong affiliation with celiac disease. Of course, more studies are needed. Unfortunately, as you all know, food treatment for an illness is not well funded as there is little money to be made (e.g. pharmacutical companies). I have Type 2 diabetes (thin and athletic) and have managed to avoid insulin or drugs on a low carb diet for the past four years. Managed meaning, maintaining near or normal blood sugars. Personally, perhaps all of us should focus on a lower carb diet with fewer non-processed foods. It may slow down our obesity crisis and all the health issues that typically follow. https://www.nytimes.com/2018/05/07/well/live/low-carb-diet-type-1-diabetes.html Google more. Do not trust just my word. Keep advocating for your health!
  8. Celiac.com 05/03/2018 - Time to spring into action and take control of your celiac disease and dermatitis herpetiformis! This means I have to "Scare you Silly" about not fully conforming to the gluten-free diet. Anemia, tiredness, and vitamin deficiency will continue to dog you if your gluten-free diet is non-compliant. You know those "just can't resist" items in your diet, the ones where the ingredient list does not actually say it is gluten-free, which may leave you open to cross-contamination that is common in the food industry? There is an estimated three million Americans with celiac disease, yet the vast majority still remain undiagnosed. The prevalence of celiac disease in Canada and the United States is growing, not diminishing! The high prevalence of celiac disease is also found in individuals with other disorders such as Type 1 diabetes, autoimmune thyroid disease and Down Syndrome. The prevalence of celiac disease in Type 1 diabetes around the world is 3 – 16%. According to Shelley Case, Author of Gluten-Free Diet: A Comprehensive Resource Guide: "Studies by Columbia University in New York and the Canadian Celiac Association revealed that adults suffer from the disease for an average of 10 - 12 years before being correctly diagnosed." The rare, but wise, physician who has diagnosed celiac disease correctly also sends the patient to be checked for diabetes and thyroid disease. Do you know what Gluten Ataxia is? Ataxia is a symptom in many conditions that affect the nervous system. Ataxia causes clumsiness or loss of balance and coordination that is not due to muscle weakness. Ataxia symptoms can be worrisome, and more so if you have been cheating on your celiac diet. Symptoms may vary but can include: Trouble using fingers, hands, arms and/or/legs Trouble speaking Trouble moving eyes Poor coordination and/or balance Tingling in extremities Gait problems Damage to the cerebellum (the part of the brain that controls coordination). Gluten ataxia is a rare immune-mediated disease in which the body's immune system attacks the nervous system as a reaction to the ingestion of gluten. It is a rare condition, but it can be related to celiac disease as well as non-celiac gluten sensitivity. Those with gluten ataxia often do not always have digestive issues or other symptoms. A strict gluten-free diet usually improves symptoms for those with gluten ataxia. Early diagnosis and treatment through the gluten-free diet can help stop progression and further cerebellum damage. People who have dermatitis herpetiformis know only too well what that gluten-containing doughnut or tart can do to their bodies. The DH sores are so itchy, and well, just sore, that prior to my first diagnosis I thought I had head lice and self-treated myself it on three separate occasions! Though DH is a miserable disorder to have, and the sores appear in the same places time and time again leaving scars, it at least leads to a faster diagnosis once a dermatologist sees the itchy sores, which often appear in bunches on your scalp, upper arms, shoulders and shins. While other people are watching television you are itching at sores in your head, picking off scabs, and in general feeling very miserable until the DH sores eventually heal. A biopsy of one of the lesions by that dermatologist can show dermatitis herpetiformis, but sometimes only after two or even three biopsies. The IgA deposits remain under the skin and that is why the DH sores keep coming back to the same place in your body. They are still there, and just come to the surface when you ingest gluten. Some with DH have to remain on dapsone for the rest of their lives. I have been on dapsone for over 30 years, even though I attempted on several occasions to stop taking it. To me it is a wonder drug, but one that I have to be careful not to abuse, because dapsone can cause anemia, and something similar to anorexia because when you ingest it regularly you do not feel hungry, and thus lose weight. To heavy people this may seem like the perfect weight loss program. Believe me, it isn't. It can also cause Methemaglobinemia which, when ingesting will prevent your arteries from functioning as an oxygen carrier and can seriously affect your body so that oxygenated blood does not reach your starved blood cells. You either carry a SAT Machine to measure the oxygen levels in your blood, or go to the Emergency Department where they can check your saturation levels. If below 90 they will admit you, run a battery of tests, and you may be put into a side room somewhere to get an infusion of Methane Blue to flush out your blood system, and you may need to have a blood transfusion. If you are away on holidays this can be a very serious condition where you are unaware you have Methemaglobinemia, except for a feeling of being out of breath, and NEED to get to hospital as soon as possible so your SAT levels can be monitored. Scaring you straight means not cheating day after day and then hoping a few dapsone will improve the condition. It won't—if you have passed the safe guideline of one pill daily. It is not simply a matter of taking dapsone in a 5 - 4- 3 - 2 - 1 as I was advised to do by an internist when I was first diagnosed with dermatitis herpetiformis. Ingestion over five days will no longer help you, and to my chagrin, can cause the condition to worsen. It is a serious condition; you can actually die from lack of oxygen in your blood! These few descriptions do not cover the fall out (of your hair) and the scarring of the sores on your legs and upper arms the Prednisone that they want to give you can cause a "roid rage" similar to what weight lifters have when they purposely ingest Prednisone to build up their muscles and become extremely irritable because of the Prednisone. ONE helpful clear lotion that I have to buy across the border in the U.S.A. is Scalpacin or Renewal, the latter being the generic name for Salicylic Acid (3%) which lessens the intense itching when applied directly to the sores (not to be ingested!). It says only 3% Salicylic Acid and I will confess that when I first "latched" onto this amazing "scalp itch and Dandruff relief liquid" I often applied twice daily to all the sores in my scalp and on my body. Did you know that approximately 3% of the general population in the U.S.A., according to Dr. Peter Green, have celiac disease? Once a patient develops one autoimmune condition the odds of developing another are greatly increased. Autoimmune disorders run in families, and different diseases may affect different parts of the body. A friend of our grandson was diagnosed as having celiac disease simply because she went to her doctor with complaints of a stomach ache. The doctor could have easily asked her if she had exams coming up, sent her for a blood test to rule out an appendicitis and left it at that, but he was a wise doctor who asked more questions and ordered the celiac blood tests. When that cameback positive he actually followed it up with a biopsy of the jejunum. She, as a teenager, was positive for celiac disease, but that doctor could have easily not ventured past the stomach ache at that first visit and gone no further with his investigations. Fortunately, vigilance paid off this time. He was thorough enough to refer her to a dietitian, but you know, she still cheats! I believe the reason she cheats is because she does not suffer from any of the symptoms of celiac disease right now, and does not have dermatitis herpetiformis. Amazing how vigilant you become with your diet when you break out in painful sores over 25% of your body, and experience diarrhea, stomach aches, nausea and vomiting! We never got into the other diseases she could possibly get from cheating on the gluten-free diet. Sjogren's Disease, Turner Syndrome, Type 1 diabetes, Williams Syndrome, Juvenile idiopathic arthritis, lactose intolerance, migraines, peripheral neuropathy, liver disease, are but a few of the disorders that can be connected to celiac disease. Have you ever looked up the symptomatology of these autoimmune diseases? Time you did! Did you know that there is a Celiac Disease Center at Columbia University which is one of the leading authorities for unexplained infertility issues, and that the prevalence of celiac disease in women with unexplained fertility is higher than the general population? Celiac disease may also be asymptomatic, meaning you show no symptoms at all. This is one of the reasons why it may be difficult for some people and their doctors to connect the dots between celiac disease and unexplained fertility. I worked with obstetrician/gynecologists for years and never found one that, when doing the laboratory testing, included a test for celiac disease, yet it is common knowledge now that a celiac disease screening should definitely be part of the work-up that is done for infertility issues. People of reproductive age spend an enormous amount of money, time and energy trying to become pregnant and carrying the baby to term. There are more women depressed because they cannot conceive or those that cannot bring a baby to term. Several studies over the past ten years have found a link between celiac disease, infertility and spontaneous abortion. It is not known yet whether the nutritional issues (malabsorption) that occurs with untreated celiac disease is the cause of the reproductive issues, or if the immune system may be to blame. Many doctors define infertility as the inability to get pregnant after one year of unprotected sex. In women, fertility difficulties often result from a problem with ovulation, while in men, infertility usually occurs because the man does not produce enough sperm or produces abnormal sperm. Note that undiagnosed or untreated celiac disease can lead to a host of seemingly unrelated problems, including osteoporosis, depression, and anemia. Medical researchers “along with some observant obstetrician/gynecologists are realizing that undiagnosed celiac disease may also be a cause of otherwise unexplained infertility in both men and women." A study undertaken in England, which has one of the world's largest celiac populations, indicates that fertility often returns after you start the gluten-free diet. There are many causes for infertility, but up to 30 percent of couples who are infertile will be told that no specific reason for their infertility can be found. When this happens a diagnosis of unexplained infertility is given. In recent years, awareness of celiac disease has increased. You may not be able to quote "Celiac Disease is a chronic autoimmune disorder", but it is a good sentence to spread around to those who ask you, "Do you follow the gluten-free diet because it is trendy or you want to lose weight"? As awareness for celiac disease has increased, some researchers have started looking at a possible like between celiac disease and unexplained infertility. Some of the known causes are: Low sperm count, - sperm with mobility or motility issues Enlarged veins in the scrotum called varicocele. Klinefelter syndrome, a genetic disorder. Although Klinefelter syndrome carries with it the risk testicular cancer, autoimmune diseases have been associated with this disorder, which is a chromosomal disorder. KS might increase the risk of some autoimmune diseases. It has been suggested that some autoimmune diseases may be more common in people with Klinefelter syndrome than in others, but the evidence so far is sparse. A research paper out of Oxford, England entitled "Associations between Klinefelter's Syndrome and Autoimmune Diseases” came to the conclusion that those with Klinefelter syndrome have increased risk of some autoimmune diseases. If you have the test for celiac disease, at least the blood test, and if your partner has the ultrasound done for it you can go into the obstetricians office with a list of questions, including family history, research you have undertaken yourself. I have seen so much heartache while nursing, watching a couple lose their baby prior to delivery, and those than cannot conceive but cannot afford invitro- fertilization. The damage that undiagnosed or untreated celiac disease can result in ongoing gastrointestinal symptoms such as vomiting, chronic diarrhea, stomach pain, and cramps. A number of these symptoms may also affect the reproductive system of women, for example: Delayed onset of menstruation Irregular periods No periods at all, known as amenorrhea Chronic pelvic pain And yes, endometriosis (where part or parts of the uterine lining attaches itself to the uterus and begins to grow) needs to be mentioned here. Many women who have this painful disease have been told that their only way of ridding themselves of this very painful disorder is to get a total hysterectomy. This is not always the case. There are now medications to help rid the uterus of endometriosis. Many obstetricians will perform a laparoscopy to determine the extent of the endometriosis, endeavour to lyse the adhesions from the wall of the uterus. Often this is all that is needed to ensure an introduction from the egg to the sperm and conception takes place. Other, more difficult cases can be referred to an infertility specialist, but be prepared for large costs. Many infertility specialists will tell you that if you can obtain a pregnancy while still struggling with endometriosis it often alleviates the problem. Did you know that men with celiac disease may have gonadal dysfunction, which could complicate fertility issues? (That was a big learning surprise for me!) This ultrasound test can be ordered by your family physician, a gonadal ultrasound to rule out a cystocele. Finding out that your husband has a cystocele is not Earth shattering—it involves a small corrective surgery. Did you know that Semen issues (specifically sperm morphology) found in men with celiac disease improved after following a gluten-free diet? Few studies have been conducted on celiac disease and male infertility. There is also a lack of scientific information and research studies on the potential link between non-celiac gluten sensitivity (NCGS), also commonly referred to as "gluten intolerance" and infertility. While research needs to be done, those with non-celiac gluten sensitivity are thought to possibly be at an increased risk of reproductive issues. However, the connection between NCGS and infertility is not yet known or proven. One case review did suggest that a strict gluten-free diet may improve fertility for those with NCGS. According to Healthline experts do not fully understand the effects of celiac disease on the reproductive system. The effects may be caused by malabsorption of nutrients, the impact it has on the immune system, or another currently unexplained reason. Some studies have noticed a link in untreated celiac disease in the mother and recurrent miscarriage, pre-term birth, and low birth weight. In a meta analysis that looked at studies on infertility and celiac disease, researchers noted that women with infertility were over three times more likely to have celiac disease than the control group. You have to admit that is a large number, and what upsets me is the fact that numerous obstetrician/gynecologists do not automatically send this part of the women's population for celiac disease screening. Yet women with unexplained infertility, were six times more likely to have celiac disease than women in the control group. Despite these studies, not all experts in the field are convinced about the connection. They state that more research is needed. BUT wouldn't you want to know that there is strong evidence that infertility and celiac disease are connected, and at least make your own decision with regards to getting tested? The tests undertaken by people with infertility are difficult to endure, are not only embarrassing but invasive. If celiac disease or gluten sensitivity runs in your family, or you suspect you have celiac disease, make a list of your symptoms. You'll want to discuss your concerns with your doctor and ask to be screened for celiac disease. A Reproductive Endocrinologist is who you would be referred to here in Canada, but you may have another title in the United States. If you are vigilante about eliminating gluten from your diet, you will stop the damage celiac disease is doing to your body. This may include lessening or eliminating the impact it may be having on your reproductive system. Sources: https://www.ncbi.nim.nih.gov/pubmed/25564410 Celiac Disease A Hidden Epidemic, Dr. Peter H.R. Green American College of Obstetricians and Gynecologists (ACOG) Resource Center: http://www.acog.org American Society for Reproductive Medicine: http://www.asrm.org Reproductive Changes Associated with Celiac Disease: https://www.ncbi.nim.nih.gov/pmc/articles/PMC3001971/ Healthline https://www.ncbi.nml.nih.gov/pmc/articles/PMC4600520/
  9. 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,
  10. Celiac.com 02/28/2018 - In an effort to discover more genes that trigger type 1 diabetes, a team of researchers recently conducted a large, prospective study of children at risk for type 1 diabetes. The end goal is to reveal more targets for treating or even preventing the disease. The research team included A Sharma, X Liu, D Hadley, W Hagopian, WM Chen, S Onengut-Gumuscu, C Törn, AK Steck, BI Frohnert, M Rewers, AG Ziegler, Å Lernmark, J Toppari, JP Krischer, B Akolkar, SS Rich, JX She; and TEDDY Study Group. The team identified six new chromosomal regions in young people who have already developed type 1 diabetes, or who have started making antibodies against their insulin-producing cells, often a step toward full-blown diabetes that requires lifelong insulin therapy. Their analysis of 5,806 individuals, which is published in the Journal of Autoimmunity, also confirms three regions already associated with one of those related conditions. The team observed two top autoantibodies. The first, called IAA, acts directly against insulin. The second, called GADA, acts against the enzyme glutamate decarboxylase, which regulates the insulin-producing beta cells in the pancreas. According to Dr. She, about 90 percent of patients with type 1 diabetes start with one of the autoantibodies, and many patients eventually end up with both. The second autoantibody may surface in a few days or even years later. They began this study with 176,586 SNPs, or single nucleotide polymorphisms. Nucleotides are basic building blocks of our genetic information. According to Sharma, the SNPs evaluated by TEDDY scientists were already linked with other autoimmune conditions like rheumatoid arthritis or celiac disease, but not type 1 diabetes. The researchers figured out which of these SNPs are different in TEDDY participants with type 1 diabetes versus those with Islet cell autoantibodies versus those with neither. Previous research has shown that the genes associated with IA and actual type 1 diabetes can differ. Dr. She says that even though clinicians regard Islet cell autoantibodies (IA) as a red flag for type 1 diabetes, not every child with IA goes on to develop diabetes, though multiple autoantibodies definitely increase that risk. The team notes that it is possible that the genes that promote IA development may differ from those that lead to full-blown disease progression. She says that this is the first study of gene identification for any disease to use this sort of longitudinal information. She add that this and other studies by the TEDDY research group help to clarify the search for important non-HLA genes by adding the "time to disease" perspective. Source: J Autoimmun. 2018 Jan 5. pii: S0896-8411(17)30739-4. doi: 10.1016/j.jaut.2017.12.008. The researchers are variously affiliated with the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA; Division of Biostatistics and Data Science, Department of Population Health Sciences, Medical College of Georgia, Augusta University, Augusta, GA, US; the Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL, USA; the Division of Population Health Sciences and Education, St George's University of London, London, United Kingdom; the Pacific Northwest Research Institute, Seattle, WA, USA; the Center for Public Health Genomics, University of Virginia, Charlottesville, VA, USA; the Department of Clinical Sciences, Lund University/CRC, Malmö, Sweden; the Barbara Davis Center for Childhood Diabetes, University of Colorado, Denver, Aurora, CO, USA; the Institute of Diabetes Research, Helmholtz Zentrum München, Munich-Neuherberg, Germany; Klinikum rechts der Isar, Technische Universität München, Munich-Neuherberg, Germany; Forschergruppe Diabetes e.V., Munich-Neuherberg, Germany; the Department of Pediatrics, Turku University Hospital, Turku, Finland; the National Institutes of Diabetes and Digestive and Kidney Disorders, National Institutes of Health, Bethesda, MD, USA; and the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA.
  11. Celiac.com 06/26/2013 - Do people with type 1 diabetes (T1D) and celiac disease die younger than people with T1D who do not have celiac disease? Do celiac patients without T1D live longer than those with T1D? Currently, not much is known about how celiac disease might influence mortality rates in people with T1D. A team of researchers recently set out to examine rates of death in patients with both T1D and celiac disease. The researchers include K. Mollazadegan, D.S. Sanders, J. Ludvigsson, and J.F. Ludvigsson. The are variously affiliated with the Clinical Epidemiology Unit of the Department of Medicine, Solna, Karolinska Institutet, and with St. Erik Eye Hospital, Karolinska Institutet in Stockholm, Sweden. The research team set out to examine mortality in patients with both type 1 diabetes (T1D) and celiac disease. For their study, the team used biopsy reports to identify all people diagnosed with celiac disease between 1969 and 2008, within all 28 pathology departments in Sweden. They defined T1D as a diagnosis of diabetes recorded in the Swedish National Patient Register between 1964 and 2009 in individuals aged ≤30 years. Their follow-up showed 960 patients with both T1D and celiac disease. For each individual with T1D and celiac disease, they selected up to five subjects with T1D alone (no celiac disease) as a reference group of 4608 individuals. They then matched all reference individuals for sex, age and calendar period of diagnosis. The team used stratified Cox regression analysis with celiac disease as a time-dependent covariate to estimate the risk of death in patients with both T1D and celiac disease compared to those with T1D alone. The results showed that celiac disease was not a risk factor for death in patients with T1D in the first 5 years after celiac disease diagnosis [hazard ratio (hazard ratio) 0.87, 95% confidence interval (CI) 0.43-1.73]. However, with the passage of time, that reality changed, and mortality risk rose in direct relation to follow-up time (5 to In the end, for people with T1D, having a celiac disease diagnosis for at least 15 years was associated with a 2.80 times greater risk of death (95% CI 1.28-6.12). Source: J Intern Med. 2013 May 23. doi: 10.1111/joim.12092.
  12. I was diagnosed with Celiac October of 2015. I was very unhappy when I received the initial diagnosis and spent a few months angry and frustrated as I adjusted to a gluten-free diet. I managed to change my diet and my attitude as I slowly became thankful that I had a disease that could be treated by just avoiding gluten. Fast forward to this week, I was diagnosed with Diabetes* (they think it's Type 2, but we're still testing to see if it's Type 1 or Type 2 or a hybrid) and I feel like I'm right back where I was when I first received my Celiac diagnosis in 2015, but worse, because now there's a whole universe of foods I have to be careful with (in addition to having to take medication with gross side effects, change my physical activity, and test my blood glucose levels). Many of the gluten-free substitutes I relied upon are now unacceptable (because of their high carb content) and items that used to be completely safe (fruit, vegetables) now have to be monitored and recorded. I'm frustrated and sad and feel like I'm back at square one. My initial internet searches for Celiac Diabetics haven't turned up much in terms of community. When I was first diagnosed with Celiac, these message boards were really helpful. I'm hoping to find other people who have the co-diagnoses and to learn how they coped and what recipes and products they rely on. *I received an initial Diabetes Type 2 diagnosis (based off one in-range A1C, which is not the standard for diagnosis, but the doctor had erred on the side of an early diagnosis to get me into the diabetes management classes) when I was diagnosed Celiac, but my A1Cs went back into normal range once I went on a gluten-free diet, so the diagnosis was rescinded (with the thinking that the insulin resistance was attributed to the cortisol and adrenaline of a gluten-eating Celiac).
  13. Celiac.com 10/27/2017 - It has long been understood that two autoimmune diseases, celiac disease and type 1 diabetes are related. They share common genes and the incidence of celiac disease is higher among type 1 diabetics. There have been some anecdotal reports regarding children diagnosed with type 1 diabetes who were put on a gluten-free diet soon after their diagnosis and for a period of two years or more didn't require any insulin. The thought was that the gluten-free diet effectively halted the progression of the diabetes, at least for the duration of the study. Studies of mice have shown that despite utilizing a genetic strain of mice that were strongly in-bred to increase the risk of type 1 diabetes, 2/3 of them did not do so when a drug was administered to prevent leaky gut. This study was performed by Dr. Alessio Fasano at the University of Maryland Celiac Research Center. Dr. Fasano is one of the world's acclaimed researchers in the area of celiac disease and gluten sensitivity. Leaky gut is associated with the initiation and continuation of autoimmune disease and Dr. Fasano's work with these genetically predisposed mice shed a great deal of light on the power of an undamaged gut lining to effectively forestall development of a genetic condition, in this case type 1 diabetes. A recent study out of Immunology, dated August 22, 2012, is titled "Dietary gluten alters the balance of proinflammatory and anti-inflammatory cytokines in T cells of BALB/c mice". The title is a mouthful but here is what the researchers out of Denmark found: Their initial premise was based on the idea, as I mentioned above, that dietary modifications, specifically a gluten-free diet, could reduce the risk of developing type 1 diabetes. The question they posed was, "How did this occur?" They discovered that wheat gluten induced the production of pro-inflammatory chemicals called cytokines that would damage the intestinal lining and immune tissues of the small intestine. More importantly, a gluten-free diet didn't just neutralize the negative effects just mentioned, but it actually caused the production of anti-inflammatory chemicals that would provide protection for the immune system and gut. So, while gluten is a known bad guy, a gluten-free diet doesn't just take the negative away, it actually induces a positive, healing response. Clinically we frequently see this with patients. As soon as we meet a patient with any history of autoimmune disease, we quickly test them for celiac disease and gluten sensitivity via lab tests and a 30 day elimination diet. If we discover any negative immune reaction to gluten, we begin a strict gluten-free diet. Happily, we often see stabilization, if not reversal, of their autoimmune disease. We support the gluten-free diet with our other protocols for normalizing gut permeability (healing a leaky gut) and strengthening the immune system. Taken together this program yields excellent results. If you know anyone suffering from an autoimmune disease, please show them this article. Gluten could be a component in furthering their disease and a gluten-free diet could be a positive influence in their journey to improved health. I hope this was helpful. Please feel free to contact me should you have any questions. And if your health is not at the level you would like, I can also offer you a free health analysis. Call us at 408-761-3900. Our destination clinic treats patients from across the country and internationally and we would be delighted to help you. To your good health.
  14. So, where to begin... I was officially diagnosed with Celiac Disease about 2.5 years ago and have been trying to fully heal since then. I knew prior that I had celiac disease but didn't know how serious being gluten free needed to be if you have it. My intestines got so damaged that I had no energy (needed about 12 hours of sleep a day when I normally would sleep 8) and could barely function. I ended up having to quit my job because of how much time I had missed (had used all FMLA, vacation, etc) and spent about 5-6 months recovering till I had enough energy to work a 32 hour/week job but even then was calling out because of gluten exposure. The biggest problem for me has been Rx medication. Food has been hardly an issue at all, at least in comparison. I currently take 2 types of prescriptions and have had problems with both over the past 2.5 years; Hypothyroid medication (T3/T4) & SSRI for depression/energy. I used to go between Paxil and Cymbalta. I would be on one for about 9 months, switch to the other, and repeat (because of the immune system's "short term memory"). I've had a lot of trouble with generic brands and more recently have been using only name brands because they are the only ones now that are listed as Gluten Free on glutenfreedrugs.com, but, now I seem to be having problems with them as well. My doctor has told me that I'm very sensitive to gluten (I think she said I've ranged from an 8-12?). I'm not sure what scale she was referring to, but I know I'm very sensitive based on how my body's reacted to the smallest amount of gluten. When I ingest gluten, my body seems to react by my gallbladder producing a lot more bile (this is most noticeable about 8 hours after I consume gluten), which causes me to have severe diarrhea for about a week (it's basically all liquid). I take my Rx medications everyday, so it's non-stop diarrhea, which makes it hard to stay hydrated. The more water I drink, the more I just end up ****ing it out. I've been taking Benadryl at night because I heard it can help with upset stomach for people with celiac disease. Before I started taking the Benadryl at night I was waking up after about 6 hours of sleeping with extreme stomach pain (too much bile in my stomach?) and having to rush to the bathroom, and would be in there for about an hour. I'm very in tune to knowing when I'm getting gluten exposure for 2 reasons: 1) the slightest amount will cause my stool to get softer and I can smell a difference when I go to the bathroom (my guess is it's from the bile, which has a strong odor), and 2) the amount of long acting insulin required for me per day is less depending on how damaged my small intestines are (I have type 1 Diabetes). I started taking Cymbalta 60 mg about 2 weeks ago and notice severe gluten exposure. I was on it for about 5 days and stopped taking it for a day to see if the symptoms lessened and I couldn't see a difference from only a day. I tried to stop taking it for 2 days but the withdrawl symptoms were too severe (intense sadness/hopelessness, strong suicidal thoughts, etc) and I don't even remember if the gluten exposure symptoms lessened because I could barely function mentally. I'm pretty sure that's where the gluten is coming from because it was the biggest change at the time. I had actually switched from a generic Cymbalta (duloxetine by Mylan) slightly early from my 9 month usual switch because I was having gluten symptoms (at the time, glutenfreedrugs.com listed it on their list but soon changed it to "now questionable"). I'm currently trying Zoloft (been on it for about 3 days now) and the gluten symptoms seem to be slightly less but I won't know for at least another few days. Plus, I don't know if it's actually going to work for me (depression wise). I was going between Paxil & Cymbalta for about 15 years and they were working for me very well (as far as depression) up until recently (because of gluten). I know I've tried Celexa, Lexipro, & Wellbutrin in the past and cannot take them because they either make things worse or the negative side effects outweigh the benefits. I may have tried another type or two of SSRI but it's been so long that I can't remember for sure. I'm making this post to try and get some advice, or even just words of encouragement, on any generic Rx versions of Cymbalta (and Paxil as well, but I won't be taking it for a while so it's less relevant at this point) that people have recently had success with. I've searched online & this site but haven't been able to find anything recent about these medications (most of the posts I've found are from many years ago). I'm scared. Scared of all the times I want to kill myself in any given day because of not taking an SSRI to try and reduce the gluten exposure. Scared that things will get as bad as they've gotten before and I will have to quit my job again. Scared to cry because I'll become even more dehydrated and may not be able to keep fluid in me because of my body is currently not being able to absorb water the way I need it to. The past 3 years have been really tough and I don't really know where to turn at this point. Sorry if this post isn't the most organised. I'm currently an emotional wreck while typing this and at least trying to get out all the important info. Here is a list of new things I've been eating in case someone reads this and sees something they've had problems with that might (also?) be causing gluten issues: Schär Gluten Free Artisan Baker Multigrain Bread (to try and soak up some of the bile, but with constant gluten exposure this doesn't help much) Ensure Original Nutrition Shake (says Gluten Free on it) Pedialyte Advanced Care+ Benadryl
  15. Celiac.com 07/05/2017 - Numerous researchers have documented a connection between celiac disease and type 1 diabetes. One team of researchers recently set out to examine international differences in celiac disease rates and clinical characteristics of youth with coexisting type 1 diabetes and celiac disease compared with type 1 diabetes only. The research team included Maria E. Craig, Nicole Prinz, Claire T. Boyle, Fiona M. Campbell, Timothy W. Jones, Sabine E. Hofer, Jill H.Simmons, Naomi Holman, Elaine Tham, Elke Fröhlich-Reiterer, Stephanie DuBose, Helen Thornton, Bruce King, David M. Maahs, Reinhard W. Holl and Justin T. Warner. To analyze the relationship between outcomes, including HbA1c, height-standard deviation score [sDS], overweight/obesity, and type 1 diabetes with celiac disease versus type 1 diabetes alone, adjusting for sex, age, and diabetes duration, the team created multivariable linear and logistic regression models. The analysis included 52,721 people under 18 years of age with a clinic visit between April 2013 and March 2014. The team used the following data sources: the Prospective Diabetes Follow-up registry (Germany/Austria); the T1D Exchange Clinic Network (T1DX) (U.S.); the National Paediatric Diabetes Audit (U.K. [England/Wales]); and the Australasian Diabetes Data Network (ADDN) (Australia). The researchers found biopsy-confirmed celiac disease in 1,835 young people, or 3.5%. These patients were diagnosed on average at age 8.1 years, with a range of 5.3 to 11.2 years. Most young people (37%) with diabetes upon celiac disease diagnosis had it for less than one year. Eighteen percent with diabetes had it for 1-2 years at celiac diagnosis, 23% had diabetes between 3 and 5 years at celiac diagnosis, while 17% had diabetes for more than 5 years at celiac diagnosis. Celiac disease rates ranged from 1.9% in the T1DX to 7.7% in the ADDN and were higher in girls than boys (4.3% vs. 2.7%, P < 0.001). Children with coexisting celiac disease were diagnosed with diabetes at 5.4 years on average, compared with those with type 1 diabetes only, who were diagnosed at 7.0 years of age, on average. Also, fewer children with both conditions were non-white, 15 vs. 18%. Height-SDS was lower in those with celiac disease (0.36 vs. 0.48) and fewer were overweight/obese (34 vs. 37%, adjusted P < 0.001), whereas average HbA1c values were comparable: 8.3 ± 1.5% (67 ± 17 mmol/mol) versus 8.4 ± 1.6% (68 ± 17 mmol/mol). This study clearly documented that celiac disease is not uncommon in young people with type 1 diabetes. Differences in disease rates may be due to variations in screening and diagnostic practices, and/or risk levels. Although the groups showed similar glycemic control, the research team encourages close monitoring of growth and nutrition in this population, due to the lower height-SDS. Source: Diabetes Care 2017 May; dc162508. The researchers in this study are variously affiliated with the Children’s Hospital at Westmead, Sydney, New South Wales, Australia; University of New South Wales, Sydney, New South Wales, Australia; Charles Perkins Centre Westmead, University of Sydney, Sydney, New South Wales, Australia; Institute of Epidemiology and Medical Biometry, University of Ulm, Ulm, Germany; German Center for Diabetes Research, Munich-Neuherberg, Germany; Jaeb Center for Health Research, Tampa, FL; Leeds Children’s Hospital, Leeds, U.K.; The University of Western Australia, Perth, Western Australia, Australia; Telethon Kids Institute, Perth, Australia; Department of Pediatrics, Medical University of Innsbruck, Innsbruck, Austria; Vanderbilt University Medical Center, Nashville, TN; Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, U.K.; Women’s and Children’s Hospital, Adelaide, South Australia, Australia; Department of Pediatrics, Medical University of Graz, Graz, Austria; St. Helens and Knowsley Teaching Hospitals NHS Trust, St. Helens, U.K.; John Hunter Children’s Hospital, Hunter Medical Research Institute, University of Newcastle, Callaghan, New South Wales, Australia; Lucile Salter Packard Children's Hospital Stanford, Stanford University Medical Center, Palo Alto, CA; and the Children's Hospital for Wales, Cardiff, U.K.
  16. Celiac.com 04/18/2017 - Even though gluten-free diets are more popular than ever, researchers still don't have much good data on gluten intake and long-term health. A team of researchers recently set out to assess three large cohort studies, the Nurses' Health Study (NHS, n=69,276), the NHSII (n=88,610), and the Health Professionals Follow-Up Study (HPFS, n=41,908), and to estimate gluten intake using a validated food-frequency questionnaire collected every 2-4 years. The research team included Geng Zong, of the Harvard T.H. Chan School of Public Health, Boston, MA; Benjamin Lebwohl, Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY; Frank Hu, Laura Sampson, Lauren Dougherty, Walter Willett, Andrew Chan, and Qi Sun, of the Harvard T.H. Chan School of Public Health in Boston, MA. The team defined incidental Type 2 diabetes as physician diagnosed diabetes, and confirmed with supplementary information. Their results showed that average gluten intake, give or take standard deviation, was 5.83±2.23, 6.77±2.50, and 7.06±2.76 grams/day in NHS, NHSII, and HPFS, respectively. That gluten intake cam, mainly from carbohydrate sources, especially refined grains, starch, and cereal fiber (Spearman correlation coefficients > 0.6). The team confirmed 15,947 Type 2 diabetes cases over 4.24 million years of follow-up time. In all three groups, the team observed an inverse connection between gluten consumption and Type 2 diabetes risk. The multivariate adjustment (table), and hazard ratio (HR, 95% confidence intervals [95%CI]) comparing extreme quintiles were 0.80 (0.76, 0.84; P<0.001). The connection dissipated slightly after adjusting for cereal fiber (HR [95%CI]= 0.87 [0.81, 0.93]), but not for other carbohydrate components. For study participants under 65 years of age, and without major chronic diseases, changes in gluten intake were not associated with weight gain in multivariate adjusted model. Overall, the 4-year weight change (95%CI) was 0.08 (-0.06, 0.22; P=0.25) in NHS, -0.05 (-0.18, 0.08; P=0.43) in NHSII, and 0.36 (-0.24, 0.96; P=0.24) HPFS for each 5 grams increase in gluten intake. These findings suggest that gluten intake likely doesn't cause or promote Type 2 diabetes or excess weight gain. Reducing dietary gluten is unlikely to help prevent Type 2 diabetes, and may actually reduce consumption of cereal fiber or whole grains that help to lower overall diabetes risk. Source: AHA EPI
  17. Hey guys. So I was newly diagnosed with Celiac last month and was recommended to this site by my doctor for your helpful guidance to those struggling with this diagnosis. I just had some questions about some concerning symptoms that I have been having that will not go away. Any help would be greatly appreciated. I am a 23 year old very active male. I have been gluten free for over a month now eating a very strict diet. I have had extremely fatigued muscles with shaking in the hands. Its noticeable anytime I try to do something that involves fine motor skills. Also I have been very exhausted with extreme hunger cravings, especially sugary item (Despite eating a high protein, veggie diet and eating more frequently than I have in the past). The shaking concerns me and I had my resting glucose levels and resting thyroid levels tested with negative results. I am at a loss at what is causing this and it is pretty scary at times. Anyone have similar symptoms that won't subside or have any idea of what is causing it? I also had my B vitamin levels checked along with calcium and they both came back normal. The shakiness is visible slightly and was brushed off by my physician. I just want to feel at least half way normal again as my social life and schoolwork have taken major hits due to feeling sickly.
  18. Celiac.com 02/22/2017 - Type 1 diabetes mellitus (T1DM) and celiac disease (celiac disease) are autoimmune diseases that share similar genetic patterns. T1DM treatment is based on diet, physical activity and insulin therapy, whereas celiac disease treatment is based on a gluten-free diet. A research team recently set out to evaluate the quality of life (QoL) of individuals with the association of T1DM and celiac disease, to characterize their nutritional status and to compare it with those with only one disease and to healthier control subjects. The research team included JG Nunes-Silva, VS Nunes, RP Schwartz, S1 Mlss Trecco, D Evazian, ML Correa-Giannella, M Nery, and MS Queiroz. The are variously affiliated with the Nutrition and Dietetics Division, Central Institute of Clinics Hospital, the Lipids Laboratory (LIM-10), Endocrinology and Metabolism Division of Hospital das Clinicas, Faculty of Medical Sciences, the Radiology Institute of Clinics Hospital, the Cellular and Molecular Endocrinology Laboratory (LIM-18), and the Endocrinology Division, Internal Medicine Department, all at the University of São Paulo Medical School, São Paulo, Brazil. The researchers evaluated sixty patients controlled by sex, age and body mass index (BMI). Patients were further divided into the following groups based on previous diagnosis: DMCD group (T1DM and celiac disease); DM group (T1DM); celiac disease group (celiac disease); or HC (healthy control subjects). They used the SF-36 questionnaire to assess psychological well-being, and compared the results with glycemic control, presence of complications related to diabetes, and adhesion to gluten-free diet (GFD). Using BMI, waist circumference, bio-impedance, general laboratory tests and whole-body densitometry, they determined nutritional status and body mass composition. Both the DMCD and DM groups had similar times of diagnosis, but the duration of celiac disease was significantly higher in the celiac disease group compared with DMCD. The SF-36 analysis revealed statistically significant differences between DM and HC groups in two domains: general health (P=0.042) and energy/vitality (P=0.012). QoL was also correlated with compliance to a GFD, and scores were similar in both groups: DMCD and celiac disease. Forty percent of individuals in the celiac disease group had visceral fat area above 100 cm2, compared with just 20% in the other groups. So, are people with both Type 1 diabetes and celiac disease automatically doomed to worse health? It seems not. To be sure, they are generally less healthy than control subjects, but the study found that the DMCD group had similar scores to DM, celiac disease and HC on QoL, as well as on their nutritional status and bone metabolism. The researchers conclude from this that the association of T1DM and celiac disease did not deteriorate the health status of the individuals with both Type 1 diabetes and celiac disease. So, it seems that having both Type 1 diabetes and celiac disease dose not automatically mean having worse health, nutrition and well-being. Source: Nutr Diabetes. 2017 Jan 9;7(1):e239. doi: 10.1038/nutd.2016.43.
  19. Celiac.com 02/01/2017 - More and more evidence shows a connection between gut inflammation and type 1 diabetes (T1D). A team of researchers recently set out to assess gut inflammatory profiles and microbiota in patients with T1D, and to compare them with healthy controls (CTRL) and with celiac disease patients as gut inflammatory disease controls. The research team included Silvia Pellegrini, Valeria Sordi, Andrea Mario Bolla, Diego Saita Roberto Ferrarese, Filippo Canducci, Massimo Clementi, Francesca Invernizzi, Alberto Mariani, Riccardo Bonfanti, Graziano Barera, Pier Alberto Testoni, Claudio Doglioni, Emanuele Bosi, and Lorenzo Piemonti. They are affiliated with the Diabetes Research Institute at the IRCCS San Raffaele Scientific Institute in Milan, Italy. The team evaluated inflammatory status and microbiome composition in biopsies of the duodenal mucosa from 19 patients with T1D, 19 with celiac disease, and 16 healthy control subjects, recruited at San Raffaele Scientific Institute, in Milan, Italy, between 2009 and 2015. They assessed inflammation by gene expression study and immunohistochemistry and used 16S rRNA gene sequencing to analyze microbiome composition. Compared to CTRL and celiac disease patients, the team found an increased expression of CCL13, CCL19, CCL22, CCR2, COX2, IL4R, CD68, PTX3, TNFα and VEGFA genes in T1D patients. The immunohistochemical analysis confirmed T1D specific inflammatory status was mainly marked by increased monocyte/macrophage lineage infiltration, compared to healthy and celiac disease control tissues. The T1D duodenal mucosal microbiome also proved to be different from the control groups. This was mainly marked by increased Firmicutes, and Firmicutes/Bacteroidetes ratio and a reduction in Proteobacteria and Bacteroidetes. The expression of genes specific for T1D inflammation was associated with the excess of specific bacteria in duodenum. This study shows that patients with T1D show specific abnormalities in gut inflammation and microbiota. Greater knowledge of the complex pathogenesis of T1D will likely provide new directions for therapies targeting the gut. Look for more studies in this area in the near future, as scientists look to nail down specific treatments to prevent gut inflammation. Source: The Journal of Clinical Endocrinology & Metabolism. DOI: https://doi.org/10.1210/jc.2016-3222
  20. Celiac.com 01/24/2017 - Diabetes is a condition in which blood glucose rises high enough to cause: damage to blood vessel walls, neurological injury, vision loss, and a host of other maladies. Most currently recognized cases of diabetes fall into one of two categories which are identified as type 1 and type 2 diabetes. While these two types of diabetes share many symptoms, the underlying causes are, in most cases, quite distinct, although there is also some overlap which will be explored shortly. There are also cases of gestational diabetes and some researchers are now suggesting that type 3 diabetes may be yet another entity that causes accelerating cell death in the brain, resulting dementia (1) but these latter two types of this condition are not included in the current discussion. All but one of these forms of diabetes involves cellular resistance to the action of insulin, although there is some gray area between type 1 and type 2 diabetes. Type 1 diabetes is the result of an autoimmune attack on a specific group of pancreatic cells called islets of Langerhans. These are the cells that produce insulin, a hormone that moves glucose out of the bloodstream and into various cells. About 14% of type 2 diabetics are also thought to experience a late-onset, slowly developing damage to pancreatic islet cells, which results in reduced insulin production in combination with their insulin resistance(2). This may be caused by autoimmunity, similar to type 1 diabetes, or it may be damage induced by other factors. Nonetheless, while type 2 diabetes can often be controlled either during weight loss or by reduced carbohydrate consumption alone, type 1 diabetes is not typically viewed as a condition that can be remedied by a change in eating habits. Yet there are some hints in the literature suggesting that dietary interventions may be therapeutically useful, especially if begun early enough in the disease process. Researchers Amanda MacFarlane and Fraser Scott report that there are several environmental factors, including specific foods, as well as viral, bacterial, and chemical agents that have been hypothesized to incite an autoimmune attack on the islet cells (2). They also report that about half of the animals that develop type 1 diabetes are mounting an immune response to wheat, which may also be involved in the attack on the insulin producing cells of the pancreas by either or both of two pathways they outline (2, 3). These hypothesized biological processes are identified as molecular mimicry or bystander activation and cell death. While these authors favor bystander activation, either or both of these pathways may lead to an autoimmune attack on pancreatic islet cells. Regardless of the specific biological route, type 1 diabetes can be induced in a significant portion of genetically susceptible rats and mice, simply by feeding them a diet dominated by wheat gluten. Further, the severity of their disease varies directly with the proportion of wheat gluten in the diet (2). These investigators go on to say that "These similarities between coeliac disease in humans and diabetes in BB rats, NOD mice and type 1 diabetic patients are consistent with the idea that wheat is involved in diabetes pathogenesis, possibly by inducing a subclinical, gut inflammation in many individuals that develop this form of diabetes" (2). They go on to report that: "Our data suggest that dietary modulation has effects at two (or more) levels: At the target cells before classic insulitis, changing the growth pattern of insulin-producing cells, enhancing islet mass and changing metabolism and insulin reserves . Dampening an ongoing inflammatory condition in the gut." (2) Scott's work (4, 5) along with investigations conducted by several groups of his colleagues (6-10) indicate that significant numbers of diabetes patients show immune reactions to the prolamins which are storage proteins in wheat, rye, and barley. Further, investigators have long understood that there is significant overlap between celiac disease and type 1 diabetes, with estimates ranging between 5% and 12% in each disease group (2, 11). MacFarlane and Scott point out that 33% to 40% of patients with type 1 diabetes show transglutaminase autoantibodies which are similar to those found in celiac patients but usually at lower levels (2). Low concordance rates in monozygotic (identical) twins also suggest that environmental factors play a large role in causing type 1 diabetes (2). Again, the most compelling evidence indicates that dietary consumption of wheat gluten and similar prolamins is an important factor in the autoimmune attack that destroys the pancreatic capacity to produce insulin, in genetically susceptible individuals. Indirect support for this perspective is offered by animal research published in July of 2011. It shows that gamma-Aminobutryic acid (GABA) supplements not only inhibit the autoimmune attack on islet cells, GABA also incites regeneration of insulin producing cells (12). GABA is a non-toxic substance that is produced by the beta cells of the pancreas (13). It plays an inhibitory role throughout the nervous system which may be significant when taken in conjunction with Rodney Ford's identification of gluten as the agent which, directly and indirectly, induces neurological damage in those with celiac disease and those with non-celiac gluten sensitivity. One pathway Ford identifies is gluten-induced neuronal excitation leading to cellular self-destruction. In light of Ford's hypothesis, the inhibitory role of GABA on neuronal tissues, both at and near synapses, offers an inviting new window for envisioning the process that incites, and therefore may reverse, type 1 diabetes. Clearly there is considerable cause to suspect gluten grain consumption as an important factor in the onset and perpetuation of many cases of type 1 diabetes. While genetically coded HLA markers predispose to the disease, and a number of other environmental factors may play a role in its pathogenesis, prolamins from wheat and its close relatives are clearly a frequent and important contributor to this life-long condition in which exogenous insulin (injection with hypodermic needles) is necessary for maintaining optimal health (12) while living with this malady. However, given the insights offered by the above, the following case history may offer insights that might otherwise incite only scepticism. MacFarlane and Scott suggest the following: "One approach to achieving this [prevention] is to understand and modify the environmental factors that induce disease or equip those at risk with better means of avoiding or handling these agents"(2). Case Study: On January 18, 2008, three year old K and her anxious mother were taken to a hospital emergency department in Gilbert, AZ, where the attending physician concluded that the child had experienced a febrile seizure of about 5 minutes' duration. At examination, she had a 102.5 degree temperature. In addition to fevers, K complained of abdominal pain and showed abdominal bloating. During this examination of K, she vomited. Laboratory tests showed elevated glucose (133 mg/dl) and an elevated white blood cell count (19,000). Tylenol was used to bring K's temperature down and she was discharged with instructions for the parents to administer more Tylenol as needed, and to follow up with her regular health care provider within two days. By February 29, K experienced more fevers, ranging between 101 and 104, intermittently over 24 hours. Every four hours, when the effects of the previous dose of Tylenol wore off, the fever would, again, spike to 103-104. K was taken to see her regular physician the following day and urinalysis revealed ketone bodies. K and her parents were then sent to the emergency department of Banner Children's Hospital. At the hospital, testing showed elevated urinary ketone bodies in the Large category, and blood showed elevated glucose at 193 mg/dL. Type 1 diabetes was diagnosed and K was admitted to hospital where she stayed for four days. Her condition was stabilized with ½ unit of Novalog and 4 units of Lantus. Meanwhile parents were educated about type 1 diabetes, insulin measurement and injection. They were taught to inject 1 unit of insulin for every 20 grams of carbohydrates consumed (20:1 ratio). K's parents repeatedly wondered, in the presence of the diagnosing endocrinologist, just how much insulin K was producing and how many carbohydrates a thirty pound child needed to be healthy? * K's father has a history of joint pain when consuming gluten grains. K was still experiencing abdominal bloating and because of the overlap between type 1 diabetes and celiac disease (2) serum IgA antibody tests were undertaken and both transglutaminase and gliadin antibody tests were negative. However, the parents observed that variations in the types of food K ate seemed to have a greater impact on blood glucose than a specific food's putative sugar content. In keeping with their observations that different foods, despite their equal sugar content, produced different blood glucose results, the father's history of joint pain when eating gluten, K's abdominal bloating, and the widely documented connection between gluten grains and type 1 diabetes, these foods and several others were eliminated from her diet. K's parents were quickly able to adjust the insulin therapy to a 40:1 ratio while K typically maintained a blood glucose range of between 80 and 95 mg/dl, which is well within the reference range for a healthy, non-diabetic person. In fact, this is a far narrower range than is prescribed by the American Diabetes Association which is 70-120 mg/dl for diabetic patients. K's family continued to target and achieve the 80-95 mg/dl range. After a few months of lower than normal blood sugars, still on insulin therapy, with the carbohydrate ratio now 40/1, the parents sought permission from the endocrinologist to take K off insulin completely, on the condition that her blood sugar continued within the normal range of 85-95 mg/dl. This was monitored on a daily basis. The first 24 hours were a success and another day was granted. After six months of following a strict and intense food therapy diet for K, the family started reintroducing foods. Some foods were reintroduced without a rise in blood sugar. She was also able to eat a larger amount of carbohydrate each meal with the same blood sugar control. Clearly, the pancreas was producing increasing quantities of insulin. On August 21, 2008, six months into this intensive and individualized food therapy, the patient's blood test results indicated a regeneration of the pancreas and a complete reversal of her type 1 diabetes. Her A1C was 4.8, well within the normal range for a non-diabetic person. Today, more than three years later, the patient is still insulin free and is using food therapy alone to maintain healthy and normal glucose control. Signs of pancreatic inflammation were also absent. Each of these findings echo MacFarlane and Scott on the issue of dietary intervention in animal studies. The intensive food therapy has now been replaced with a maintenance program. The variety of foods the patient can eat is vast. However, grain and casein continue to be avoided. It appears that, in this case, these foods may have contributed to K's Type 1 diabetes. It may also be that the underlying cause of the fever K experienced early in this process was a factor in the onset of her type 1diabetes, and the transient nature of this fever, and its cause, may be at the root of her recovery from this ailment. Nonetheless, given the many converging research findings indicting grains and dairy proteins, along with K's suggestive signs and symptoms, and her father's reactions to gluten, continued avoidance of these foods seems a more likely explanation. Thoughtful readers may also wonder just how much insulin K was producing, at the time of her diagnosis, and just how many carbohydrates a thirty pound child needs to be healthy? It may be that GABA supplements and other chemical miracles will be unnecessary for large numbers of children who suffer from type 1 diabetes. Perhaps early diagnosis and permanent dietary adjustments will be what is needed to facilitate complete recovery for many, perhaps most, children afflicted by this insidious condition. Perhaps this case history will provide the necessary impetus to encourage undertaking controlled studies of dietary factors early in the disease process of type 1 diabetes. * While there are no carbohydrates that are essential to good health, there are essential amino acids and essential fats. Sources: de la Monte SM, Wands JR. Alzheimer's disease is type 3 diabetes-evidence reviewed. J Diabetes Sci Technol. 2008 Nov;2(6):1101-13. http://www.medicine.uottawa.ca/Students/MD/BlockOrientation/assets/documents/e_inf_week05.pdf http://www.elements4health.com/type-1-diabetes-patients-have-immune-response-to-wheat-proteins.html Scott FW, Sarwar G, Cloutier HE. Diabetogenicity of various protein sources in the diet of the diabetes-prone BB rat. Adv Exp Med Biol 1988; 246: 277–85. Scott F. Dietary initiators and modifiers of BB rat diabetes. In:Shafrir E, Renold AE, eds. Frontiers in Diabetes Research:Lessons from Animal Diabetes. London: Libbey, 1988: 34–9. Hoorfar J, Buschard K, Dagnaes-Hansen F. Prophylactic nutritional modification of the incidence of diabetes in autoimmune non-obese diabetic (NOD) mice. Br J Nutr 1993; 69: 597–607. Funda DP, Kaas A, Bock T, Tlaskalova-Hogenov H, Buschard K. Gluten-free diet prevents diabetes in NOD mice. Diabetes Metab Res Rev 1999; 15: 323–7. Bao F, Yu L, Babu S et al. One third of HLA DQ2 homozygous patients with type 1 diabetes express celiac disease-associated transglutaminase autoantibodies. J Autoimmun 1999; 13:143–8. Lampasona V, Bonfanti R, Bazzigaluppi E et al. Antibodies to tissue transglutaminase C in type I diabetes. Diabetologia 1999; 42: 1195–8. Pocecco M, Ventura A. Coeliac disease and insulin-dependent diabetes mellitus: a causal association? Acta Paediatr 1995; 84: 1432–3. Hansen D, Brock-Jacobsen B, Lund E, Bjørn C, Hansen LP, Nielsen C, Fenger C, Lillevang ST, Husby S. Clinical Benefit of a Gluten-Free Diet in Type 1 Diabetic Children With Screening-Detected Celiac Disease A population-based screening study with 2 years' follow-up Diabetes Care 29:2452-2456, 2006 Soltani N, Qiu H, Aleksic M, Glinka Y, Zhao F, Liu R, Li Y, Zhang N, Chakrabarti R, Ng T, Jin T, Zhang H, Lu WY, Feng ZP, Prud'homme GJ, Wang Q. GABA exerts protective and regenerative effects on islet beta cells and reverses diabetes.Proc Natl Acad Sci U S A. 2011 Jul 12;108(28):11692-7. Epub 2011 Jun 27. Bouzane B, Postmedia News June 28, 2011 Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
  21. Celiac.com 10/13/2016 - Researchers don't currently know much about rates of celiac disease autoimmunity or tissue transglutaminase autoantibodies (TGA) in patients with type 1 diabetes (T1D) and autoimmune thyroid disease (AITD) in the Chinese population. A team of researchers recently set out to assess rate of celiac disease autoimmunity amongst patients with T1D and AITD in the Chinese population. The research team included Zhiyuan Zhao, Jing Zou, Lingling Zhao, Yan Cheng, Hanqing Cai, Mo Li, Edwin Liu, Liping Yu, and Yu Liu. The study included 178 patients with type 1 diabetes, along with 119 with AITD where 36 had both T1D and AITD, classified as autoimmune polyglandular syndrome type 3 variant (APS3v). The study also included 145 patients with type 2 diabetes (T2D), 97 patients with non-autoimmune thyroid disease (NAITD), and 102 healthy control subjects. The team used radioimmunoassay to measure serum islet autoantibodies, thyroid autoantibodies and TGA. They found TGA positivity in 22% of patients with either type 1 diabetes or AITD, much higher than the 3.4% seen in T2D patients (p< 0.0001) the 3.1% seen in NAITD patients (P < 0.0001) or the 1% seen in healthy controls (1%; p<0.0001). Thirty-six percent of patients with APS3v who had both T1D and AITD positive for TGA, significantly higher than patients with T1D alone (p = 0.040) or with AITD alone (p = 0.017). At diagnosis, T1D and AITD showed overlap frequencies of 20% and 30%, respectively. Chinese population with existing T1D and/or AITD shows high rates of TGA positivity, which are even higher in people with both diseases. The study team recommends routine TGA screening in patients with T1D or AITD will help to identify celiac disease autoimmunity early on, and will yield better clinical patient care. Source: Plos.org
  22. Celiac.com 08/10/2016 - Low HDL cholesterol (HDL-C) concentrations have long been tied to increased cardiovascular risk. People with type 1 diabetes (T1D) who presented complications (1) and people with untreated celiac disease also have low HDL-C levels. People with both TID and celiac disease might face a sharper lipid abnormalities and a more aggressive the atherosclerotic process. Can a gluten-free diet reverse that process? A team of researchers recently set out to examine the effects of a gluten-free diet lipid on profiles of patients with Type 1 diabetes. They study was conducted on behalf of the for the Diabetes Study Group of the Italian Society of Pediatric Endocrinology and Diabetology (ISPED). The research team included Silvana Salardi, Giulio Maltoni, Stefano Zucchini, Dario Iafusco, Santino Confetto, Angela Zanfardino, Sonia Toni, Barbara Piccini, Maximiliano Zioutas, Marco Marigliano, Vittoria Cauvin, Roberto Franceschi, Ivana Rabbone, Barbara Predieri, Riccardo Schiaffini, Alessandro Salvatoni, Petra Reinstadler, Giulia Berioli,Valentino Cherubini and Giuseppe d'Annunzio. They are variously affiliated with the Department of Pediatrics, S. Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy, the Department of Pediatrics, Second University of Naples, Naples, Italy, the Meyer Children's Hospital, University of Florence, Florence, Italy, the Regional Center for Pediatric Diabetes, Clinical Nutrition & Obesity, Department of Life & Reproduction Sciences, University of Verona, Verona, Italy, the Pediatric Unit, S. Chiara Hospital, Trento, Italy, the Department of Pediatrics, University of Turin, Turin, Italy, the Department of Medical and Surgical Sciences for Mothers, Children and Adults, University of Modena and Reggio Emilia, Modena, Italy, the Endocrinology and Diabetes Palidoro Unit at the University Department of Pediatric Medicine, Bambino Gesu Children's Hospital, IRCCS, Rome, Italy, the Pediatric Clinic, Insubria University, Varese, Italy, the Department of Pediatrics, Regional Hospital, Bolzano, Italy, the Department of Gynaecological, Obstetric and Paediatric Sciences at the University of Perugia in Perugia, Italy, the Division of Paediatric Diabetes in Children and Adolescents, Maternal-Infantile Department, Salesi Hospital, Ancona, Italy, and with the Department of Pediatrics, IRCCS Gaslini Children's Hospital at the University of Genova in Genova, Italy. From 13 centers within the Italian Society of Pediatric Endocrinology and Diabetology (ISPED), the team collected data on a large number of children with both T1D and concurrent biopsy-proven celiac disease. They collected data at the time they initiated a gluten-free diet, and again after 1 year of a gluten-free diet. They verified gluten-free status using serum tests for celiac disease-related antibodies. They enrolled 201 children with T1D diagnosed at age of 5.8 +/- 3.8 years, and celiac disease diagnosed at age of 7.5 +/- 4.5 years. To compensate for any metabolic derangement at diabetes onset, they included only cases in which celiac disease diagnosis was made at least 3 months after that of T1D. As a control group, they used 224 patients with T1D only, matched by age, sex, diabetes duration, and HbA1c. Before subjects began a gluten-free diet, the team found that HDL-C values were significantly lower in children with celiac disease and T1D than in the control group, with the greatest decrease found in younger children aged, 6 years. Subjects with HDL-C values below pediatric percentile cutoffs for sex and age were younger than those with normal values (6.2 +/- 4.4 vs. 8.6 +/- 4.3 years, P , 0.0001) and also had lower HbA1c (7.5 +/- 0.8 vs. 8.0 +/- 1.5%, P , 0.005). After a gluten-free diet the average values of HDL-C in the total study population rose sharply to 60.9 +/- 13.7, compared with 51.3 +/- 13.6 mg/dL (P , 0.0001), and returned to normal. The percentage of subjects with HDL-C values lower than pediatric percentile cut points fell significantly (P , 0.0001) from 42 to 16%. Subjects with complete adherence to gluten-free diet showed the most significant improvement of HDL-C, and subjects with partial adherence showed a lower, but significant, improvement of HDL-C. These results dovetail with other data from the past few years, but more clearly indicated the reduction in HDL-C at diagnosis, and the better recovery with a gluten-free diet. The researchers view the reduction HDL-C either as a proxy marker for intestinal inflammation, or as the result of a change in the intestinal secretion of apolipoprotein AI (5), the major HDL structural protein. This change is seen most sharply in the youngest children, who probably suffer more severely, as indicated by signs of malabsorption, e.g., lower HDL-C and HbA1c levels. Children with T1D and untreated celiac disease, especially young children, typically show an unfavorable lipid profile, i.e., low HDL-C values. Following a gluten-free diet normalizes HDL-C levels, with the greatest benefits can be seen in individuals who follow the diet strictly, and in the youngest individuals. Because of the possibility of increased risk of cardiovascular disease, a strict gluten-free diet is mandatory in these children. Source: Diabetes Care. DOI: 10.2337/dc16-0717
  23. Celiac.com 07/13/2016 - A really interesting study about gluten-free diets in mice just popped up over at the medical journal Diabetes, that has implications for both diabetes and celiac disease. The study found that a maternal gluten-free diet reduces inflammation and diabetes rates in the offspring of non-obese diabetic mice. The study was conducted by a research team that included Camilla H.F. Hansen, Åukasz Krych, Karsten Buschard, Stine B. Metzdorff, Christine Nellemann, Lars H. Hansen, Dennis S. Nielsen, Hanne Frøkiær, Søren Skov, and Axel K. Hansen. They are variously affiliated with the Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg, Denmark, the Department of Food Science, Faculty of Science, University of Copenhagen, Frederiksberg, the Bartholin Institute, Rigshospitalet, Copenhagen, Denmark, the Division of Toxicology and Risk Assessment, National Food Institute, Technical University of Denmark, Søborg, Denmark, and the Department of Biology, Faculty of Science, University of Copenhagen in Copenhagen, Denmark. Researchers have known for some time that early life interventions in the intestinal conditions have been shown to influence diabetes rates in mice. For example, a gluten-free diet in known to decrease type 1 diabetes incidence. Their team hypothesized that a gluten-free diet for pregnant mice only during pregnancy and lactation period would protect offspring mice against development of diabetes. The team fed pregnant non-obese diabetic (NOD) mice either a gluten-free or a standard diet, until all mice pups were weaned to standard diet. The early gluten-free mice showed significantly lower rates of diabetes and insulitis. Gut microbiota analysis by 16S rRNA gene sequencing showed significantly increased Akkermansia, Proteobacteria, and TM7 between both mothers and their offspring in the gluten-free diet group. Moreover, the gluten-free offspring showed increased pancreatic FoxP3 regulatory T cells, along with an increase in M2 macrophage gene markers and tight junction-related genes in the gut, coupled with lower intestinal gene expression of pro-inflammatory cytokines. Higher numbers of T cells in the pancreas expressing the mucosal integrin α4β7 suggests that the mechanism involve increased trafficking of gut-primed immune cells to the pancreas. This study supports the conclusion that a gluten-free diet during fetal and early postnatal life reduces development of diabetes. This may be due to changes in gut microbiota and better inflammatory and immunological conditions in the gut and pancreas. So, could it be that human mothers who eat a gluten-free diet through weening can impart the same kind of protection against diabetes? Clearly more studies need to be done until we can know for sure, but following a gluten-free diet while pregnant probably wouldn’t cause any harm to the mother or the baby. Source: Diabetes 2014 Apr; DB_131612.
  24. Of the many immune related disorders linked with the celiac condition, the best established connection is with Type I diabetes (mellitus). Type I diabetes occurs at a rate of about 0.5% in the general population, but at a rate estimated at 5-10% among celiacs. Normally the diabetes is diagnosed first, both because this form of diabetes tends to strike early in life and its diagnosis is certain. No connection has been found with the more common form of diabetes (mellitus= honey , from the sugar laden urine when uncontrolled), Type II which occurs at a rate of 2-2.5% in the general population. Like celiac disease, Type I diabetes is more common in those of northern European extraction. Like celiac disease, it is highly linked to the so-called HLA markers of the immune system, those marking white blood cells. Celiacs are likely to be positive for both HLA-B8 and HLA-DR3; Type Is are most linked to HLA-B8 and either HLA-DR3 or HLA-DR4. An English study about 6 months ago found that multiple genes were linked to Type I reflecting the fact that parents of a Type I are often diabetes free: the interpretation being that genes were required from both sides. The recent request for celiac siblings for a study of genetic typing intends to duplicate that one looking for celiac genes. References: Gluten Intolerance Group of North America newsletter, V. 13, Issue 2, 1987; New York Times, Sept. 13, 1994, genetics study by Dr. John Todd at Oxford, summarized by Kemp Randolph. For more information see our Related Disorders page.
  25. Celiac.com 04/18/2016 - Some studies have shown dietary gluten has been proven to play a role in both celiac disease and type 1 diabetes (T1D), and others have suggested as much, but stopped short of actual proof. A team of researchers recently set out to assess the role of gluten in celiac disease and Type 1 diabetes. The research team included G Serena, S Camhi, C Sturgeon, S Yan S, and A Fasano. They are variously affiliated with the Graduate Program in Life Sciences at the University of Maryland School of Medicine in Baltimore, Maryland and with the Center for Celiac Research, Mucosal Immunology and Biology Research Center at Massachusetts General Hospital and Division of Pediatric Gastroenterology and Nutrition, Massachusetts General Hospital for Children in Boston. Some studies have shown dietary gluten has been proven to play a role in both celiac disease and type 1 diabetes (T1D), and others have suggested a the same. In celiac disease, gluten is the know autoimmune trigger. When the trigger is removed by the patient following a gluten-free diet, that autoimmune process stops, the gut heals, and the patient's serological markers for celiac disease usually return to normal. However, for T1D, researchers have not been able to find a causative agent, something like gluten in celiac disease. Nevertheless, researchers continue to debate the role of dietary gluten in development of T1D, and the potentially beneficial effect of removing gluten from the diet of patients with T1D. In a recent review, their team discusses the comorbid occurrence of celiac disease and T1D and explore current evidences for the specific role of gluten in both conditions, specifically focusing on current evidence on the effect of gluten on the immune system and the gut microbiota. Read more in Nutrients.
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