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Found 6 results

  1. Celiac.com 09/28/2017 - Celiac Disease is a global disease and affects almost 0.7% of the world's population. In India, researchers estimate that celiac disease affects about six to eight million Indians. Rates in the north India community are 1 in 100. In a bid to discuss and explore the best ways to address the challenges faced by patients with celiac disease and the way forward, the 17th International Celiac Disease Symposium (ICDS 2017) was held for the first time in Asia from the 8th to the 10th of September 2017. ICDS offers a platform for researchers, gastroenterologists, clinical scientists, nutritionists, and other relevant industry leaders from across the globe to gather and address common challenges faced by patients living with celiac disease. Highlights of this event included keynote lectures, theme-based symposia, and debates as also sessions reflecting joint interests and needs of scientists, clinicians, nutritionists, and patients. In addition to discussions of treatment and management of celiac disease, ICDS 2017 also addressed ways to increase awareness among health care professionals and the general public about the disease, The conference also offered presentations on team-based management of patients with celiac disease, proper counseling and supervision of patients, training of dietitians in the management of celiac patients, industrial production of reliable and affordable gluten-free food, and food labeling for gluten contents. The symposium was organized by the All India Institute of Medical Sciences (AIIMS) in association with the Indian Society of Gastroenterology (ISG), International Society for the Study of Celiac Disease (ISSCD), and the Asia-Pacific Association of Gastroenterology (APAGE). Read more at biotechin.asia
  2. Celiac.com 03/25/2015 - In what may prove to be a remarkable step in understanding human diseases, a team of scientists affiliated with Northeastern University has found a way to connect diseases based on their shared molecular interactions. A paper by the Northeastern team appears in the journal Science. The paper details their creation of a mathematical tool to analyze the map of the molecular interactions within cells, called the human interactome, and the discovery that over-lapping disease modules, or "neighborhoods" of disease-associated proteins, can give rise to some very unexpected relationships between diseases. Increasing amounts of research, says Albert-László Barabási, are making it very clear that "human diseases can be interpreted only in the context of the intricate molecular network between the cell’s components." Barabási is Robert Gray Dodge Professor of Network Science and University Distinguished Professor and director of Northeastern’s Center for Complex Network Research. The Northeastern researchers are based in the Center for Complex Network Research. The team comprises Barabási, Menche, postdoctoral researcher Maskim Kitsak, research assistant professor Amitabh Sharma, and graduate physics student Susan Dina Ghiassian, PhD’15. For their study, the Northeastern team analyzed 299 diseases that had at least 20 associated genes. They found that 226 of the diseases had their own specific "neighborhood" within the interactome. They noticed that diseases within the same neighborhood had more in common in terms of molecular functions or symptoms, while diseases that were far away from each other within the interactome had very little in common in terms of molecular functions or symptoms. Among their findings, they noted that asthma, and celiac disease are localized in overlapping neighborhoods, which suggests shared molecular roots, even though they have very different pathobiologies. This is the first study to show that the available network maps offer enough coverage and accuracy to provide valuable information about the molecular origins of disease-disease relationships, says Jörg Menche, a postodoctoral researcher and one of the authors on the paper. This is a very interesting and potentially promising discovery that may pave the way for a much deeper understanding of relationships between celiac and numerous other diseases. Stay tuned for more news. Source: Northeasternnews.edu
  3. Celiac.com 05/30/2012 - From what we understand about celiac disease, both genetic and environmental factors play a part in its development: eople with certain genetic dispositions are more likely to develop it, but studies of twins at high risk of developing celiac disease have shown that in 25% of cases, only one of the twins will develop the disease. This indicates an environmental effect, and with more research it might be possible to discover what these environmental factors are so that parents with celiac disease can take steps to prevent their children from developing the disease themselves. Breast-feeding has already demonstrated some protective effect on infants at risk of developing celiac disease, but it is still unclear how the modulation of intestinal bacteria affects the formation of the disease. Understanding the role various strains of intestinal bacteria play in the intestine could be the key to understanding why breast-feeding helps prevent celiac disease, and perhaps why celiac disease develops at all. In the present study, 75 newborns with at least one first degree relative with celiac disease were broken into breast-feeding, formula-feeding groups, high (7-28%) and low (less than 1%) genetic risk groups, then tested at 7 days, 1 month and 4 months for prevalence and diversity of intestinal bacteria. Infants at high risk of developing celiac disease had more Bacteroides vulgatus, regardless of feeding methods while infants at low risk of developing celiac disease had more Bacteroides ovatus, Bacteroides plebeius and Bacteroides uniformis. Formula-fed infants had more Bacteroides intestinalis, Bacteroides caccae and Bacteroides plebeius, though prevalence depended on the testing stage. The most striking finding of the experiment seems to indicate that both low genetic risk of celiac disease development and breast-feeding are positively correlated with the prevalence of Bacteroides uniformis in the intestines. This might explain why breast-feeding can help protect against development of the disease, by introducing more Bacteroides uniformis into the infant's intestinal bacteria community. The implications of this research are still unclear, but a follow-up study on these infants is intended. Further research may explain how the prevalence of these bacteria in the intestine actually affects the development of celiac disease in infants. Source: http://www.ncbi.nlm.nih.gov/pubmed/21642397
  4. This article appeared in the Summer 2006 edition of Celiac.coms Scott-Free Newsletter. Celiac.com 08/31/2006 - All of us have patterns of proteins on the surface of our white blood cells. These proteins are known as human leukocyte antigens (HLA), one of which is DQ. Celiac disease and non-celiac gluten sensitivity (NCGS), and several autoimmune conditions occur more frequently with certain HLA DQ types. DQ gene testing is performed by analyzing cells from a blood sample or from a Q-tip swab of the mouth. HLA types have a naming system that can be confusing even to scientists and physicians but here is my explanation of the testing, the results, and what they may mean to you and your family. Each of us has two copies of HLA DQ. Because there are 9 serotypes of DQ we are all DQx/DQx where x is a number between 1 & 9. For example, I am DQ2/DQ7. I received the DQ2 from one of my parents and the DQ7 from the other. Because we get one DQ type from each of our parents and give one to each of our children it is easy to to see how the DQ genes pass through a family. This is important because two DQ types, DQ2 and DQ8, are estimated to be present in over 98% of all people who have celiac disease, the most severe form of gluten sensitivity. Rarely, true celiac disease or dermatitis herpetiformis, the skin disease equivalent of celiac, have been reported to occur in people who do not have DQ2 and/or DQ8. However, according to unpublished data from Dr. Ken Fine of Enterolab, the other six types, except DQ4, are associated with risk for elevated stool antibodies to gliadin, the toxic fraction of gluten, and/or tissue transglutaminase (tTG) an enzyme. Both of these antibodies are usually elevated in the blood of individuals with celiac disease though they may be normal in the blood of individuals who are gluten sensitive and have a normal small intestine biopsy but respond favorably to a gluten-free diet. Fine has publicly reported that elevated stool antibodies to gliadin and/or tTG have been detected in all of the untreated celiacs tested in his lab and 60% of non-celiacs who have symptoms consistent with gluten sensitivity but in none of the controls tested including cow manure. Follow up surveys of those individuals with elevated stool antibodies who initiated a gluten-free diet compared with those with elevated antibodies who did not reportedly showed significantly improved quality of life and improved symptoms in the gluten-free group. He also reported DQ2 and DQ8 positive individuals have had, as a rule, the highest elevations of stool gliadin antibody followed by those who are DQ7 positive. Only those who are doubly positive for DQ4 have not been found to have significantly elevated antibodies to indicated gluten sensitivity. This is consistent with the differences in prevalence rates of celiac disease seen in various parts of the world since DQ4 is not generally found in Caucasians of Northern European ancestry where celiac incidence is highest but in those from Asia or Southern Africa where there is a very low incidence of celiac disease and gluten intolerance. DQ2 & DQ8, the two major types present in 90-99% of people who have celiac disease, are present in approximately 35-45% of people in the U.S., especially those of Caucasian race of Northern European ancestry, with highest risk of celiac disease but the prevalence in U.S. of celiac disease is 1%. Though a prevalence of 1 in 100 is very common and much higher than had been believed for years, only a fraction of the genetically at risk are confirmed to have celiac disease by abnormal blood tests and small intestine biopsies. However, the number of people who report a positive response to gluten-free diet is much higher. The stool antibody tests results would support this and the concept of a spectrum of gluten sensitivity that is much broader and in need of better diagnostic definitions. I am an example of someone who is DQ2/DQ7 who has normal blood tests for celiac disease but abnormal stool antibody tests and symptoms that responded to gluten-free diet. The strict criteria for diagnosing celiac disease, which is abnormal blood tests and a characteristic small intestine biopsy showing classic damage from gluten, is much narrower than what is being seen clinically. It is becoming obvious to many of us who have personal and professional medical experience with gluten intolerance and celiac disease that the problem of gluten sensitivity is much greater and extends beyond the high risk celiac genes DQ2 and DQ8. Traditionally it is reported and believed by many that if you are DQ2 and DQ8 negative you are unlikely to have celiac disease or ever develop it, though this cannot be said with 100% certainty especially since there are documented cases of celiac disease and the skin equivalent of celiac disease, known as dermatitis herpetiformis (DH) in individuals who are DQ2 and DQ8 negative. Therefore, knowing your DQ specific serotype pattern may be helpful for several reasons. For example, if you have more than one copy of DQ2 or DQ8, you carry two of the major genes. For example, if you are DQ2/DQ2, DQ2/DQ8, or DQ8/DQ8, a term Scott Adams of www.celiac.com has dubbed a "super celiac" you may be at much higher risk for celiac disease and have more severe gluten sensitivity. Certainly if you are DQ2 and/or DQ8 positive you are at increased risk for celiac disease. After a single copy of DQ2 or DQ8, it appears that DQ7/DQ7 might be next highest risk. Dr. Fine has also noted some other associations of the DQ patterns with microscopic or collagenous colitis, neurologic manifestations of gluten sensitivity and dermatitis herpetiformis, which has been one of the gluten sensitive conditions noted to be, at times, occurring in DQ2, DQ8 negative individuals. Why some people get celiac Disease or become gluten sensitive is not well understood but certain factors are believed to include onset of puberty, pregnancy, stress, trauma or injury, surgery, viral or bacterial infections including those of the gut, medication induced gut injury or toxicity e.g. non-steroidal anti-inflammatory medications such as aspirin, ibuprofen, etc., immune suppression or autoimmune diseases especially since several of those factors are associated with onset or unmasking of gluten sensitivity in someone who is at risk or not manifesting any recognizable symptoms. There is also well known group of individuals who are termed "latent" celiacs. They are at high risk because they have close relatives who have celiac disease with whom they share one or more of the celiac genes DQ2 and/or DQ8 though they usually have few or no symptoms but sometimes have abnormal blood tests and/or biopsies indicating possible or definite celiac disease. Others have negative blood tests and normal biopsies but symptoms that respond to a gluten-free diet. The severity of the sensitivity to gluten appears to be related to the DQ type, family history (highest risk is in the non affected identical twin of a celiac), pre-existing intestinal injury, degree of exposure to gluten (how frequent and large a gluten load an individual is exposed to), and immune status. Once initiated, gluten sensitivity tends to be life long. True celiac disease requires life-long complete gluten avoidance to reduce the increased risk of serious complications of undiagnosed and untreated celiac such as severe malabsorption, cancers, especially of the GI tract and lymphoma, other autoimmune diseases and premature death due to these complications. Again, DQ testing can be done with cells from blood or by a swab of the inside of the mouth but not all labs test for or report the full DQ typing but only the presence or absence of DQ2 and DQ8. The lab that performs DQ testing is usually determined by an individual insurance company on the basis of contracts with specific commercial labs. However, if your insurance contracts with Quest Labs or the Laboratory at Bonfils (Denver, CO) full DQ can be done if ordered and authorized by the insurance company. For those willing to pay out of pocket, Bonfils performs full DQ testing for Enterolab (www.enterolab.com) on a sample obtained by a Q tip swab of the mouth. Since it is painless and non-invasive it is well tolerated especially by young children. Also because the testing can be ordered without a physician and the sample obtained in their home using a kit obtained from Enterolab it is convenient. The kit is returned by overnight delivery by to Enterolab who forwards the test onto Bonfils. The cost is $149 for the genetic testing alone and has to be paid for in advance by credit card or money order and is generally not reimbursed by insurance. Enterolab also provides the stool testing for gliadin and tissue transglutaminase antibodies to determine if gluten sensitivity is evident. The gliadin antibody alone is $99 or the full panel includes genetic typing, stool testing for gluten and cows milk protein antibodies, and a test for evidence of malabsorption is $349. Again, the advantages of full DQ testing is determining if someone has more than one copy of DQ2 or DQ8 or carry both and therefore have a higher risk for celiac disease or more severe gluten intolerance. If you are DQ2 or DQ8 negative then your risk of celiac disease is low, though not non-existent. If you are not DQ4/DQ4 then you do have risk for gluten sensitivity. If you determine all DQ types within enough family members you can piece together a very accurate history of the origin of celiac and gluten sensitivity within a family and make some very accurate predictions of risk to other family members. Though the lay public and many clinicians are finding the genetic tests helpful, many, including most physicians, do not understand the genetics of gluten sensitivity. We are awaiting Dr. Fines published data on the significance of stool antibody tests and their association to the other DQ types as his lab is the only lab offering the stool antibody tests in the U.S. Other celiac researchers in U.S. have failed to reproduce his assay but scattered reports in the literature are appearing including a recent article in the British Medical Journal indicating stool antibody testing is feasible, non-invasive, and using their protocol, highly specific but not sensitive for celiac disease in children. (Editors note: When present, these antibodies indicate celiac disease. However, they are not present in many cases of celiac disease.) In the meantime, many patients are faced with the uncertainty and added cost of full DQ testing and stool testing due to the failure of traditional blood tests, small bowel biopsies, and the presence or absence of DQ2 and DQ8 to diagnose or exclude gluten sensitivity. Physicians unfamiliar with this testing are increasingly presented with the results and confused or skeptical pending published reports. The medical community continues to lack a consensus regarding the definitions of non-celiac gluten sensitivity and what tests justify recommendations for gluten-free diet. It is clear that gluten sensitivity, by any criteria, is much more common than ever thought and a hidden epidemic exists. Dr. Scot Lewey is a physician who is specialty trained and board certified in the field of gastroenterology (diseases of the digestive system) who practices his specialty in Colorado. He is the physician advisor to the local celiac Sprue support group and is a published author and researcher who is developing a web based educational program for people suffering from food intolerances, www.thefooddoc.com Article Source: EzineArticles.com
  5. Celiac.com 04/04/2011 - Having been diagnosed with celiac disease, I know from having to follow a strict gluten-free diet that monitoring one's diet and health can be inconvenient, time-consuming, and challenging. Similarly, keeping one's blood sugar level under control for diabetics can be tough, but studies are showing how important this is, as it has been shown to prevent diabetic neuropathy, that is, nerve damage peculiar to diabetics, and its devastating effects. According to Tedd Mitchell, M.D., President of the Texas Tech University Health Sciences Center, there are two types of diabetic neuropathy, peripheral and autonomic. Peripheral neuropathy is "a degeneration of the nerves in the feet and hands," according to Dr. Mitchell, which, as it occurs "slowly but progressively," reduces sensitivity to touch while heightening sensations of pain and itching. The second type is autonomic neuropathy, which is, Dr. Mitchell says, "damage to nerves that control bodily functions, such as digestion, urination, heart rate, blood pressure, sexual function and even sweating." Some of the symptoms of this type are digestive problems, urinary problems, and reductions in blood pressure. The longer one has been diabetic, the higher one's risk for neuropathy. Thankfully, evidence supports that long-term blood sugar control can reduce this risk. It may seem like a challenge for some diabetics to control their blood sugar, but with some determination and effort, it can successfully be achieved. MedicalMoment.org, a website developed by Columbia St. Mary's, an organization of hospitals and clinics, offers various ways to get started controlling your blood sugar. First, in liaison with your health care provider, test your blood sugar and keep a record of your results and pertinent information, on a daily basis. Follow your doctor's prescribed diabetes medicine plan while eating foods low in fat, sugar, and sodium and high in fiber on a regular basis, aiming for the same caloric intake every day. It's important to get regular exercise, starting slowly if need be, such as swimming and walking. Your diet and exercise routine should be geared toward maintaining your ideal weight, which should be determined by your health care provider. You'll want to stay aware of signs of possible nerve damage such as sores that won't heal, blisters, swelling, and ulcers. MedicalMoment.org also offers several tips for keeping blood sugar under control. Low blood sugar should be treated quickly with the use of special glucose gel or tablets. Smoking, which harms the heart and the circulatory system, should be avoided. Next, learn as much as possible about your diabetic condition and treatment; knowledge is power in this case, as I know from being a celiac disease patient. Lastly, avoid stress and get support by staying connected with friends and relatives or a support group who can help you keep your blood sugar under control. It isn't unusual for me to focus some of my work as an author, researcher, and gluten-free and health advocate, on the area of diabetes; after all, according to Celiac.com, evidence is growing which supports that people with Type 1 diabetes are at high risk for celiac disease. In this research, the necessity of maintaining blood sugar is clear. With the help of your medical practitioner and other resources, you can achieve proper self-care in controlling blood sugar level and lower this risk of nerve damage. Resource: Mitchell, Dr. Tedd. "Nerve damage: One more reason to keep blood sugar under control." USA Weekend: July 9-11, 2010.
  6. Celiac.com 04/10/2009 - According to the latest findings by a Norwegian research team, the inner workings of a particular enzymatic reaction is helping scientists figure out how celiac disease develops. In the latest issue of the Journal of Proteome Research, doctors Siri Dørum, Burkhard Fleckenstein, and associates at Norway’s University of Oslo and Rikshospitalet University Hospital describe how they used a quantitative MS method to chart a significant association between the amount of deamidation and the rate at which various epitopes are recognized by T cells of people with celiac disease. The team set out to determine whether the rate of TG2 deamidation correlates with T cell recognition of gluten peptide epitopes. Celiac disease is a common digestive disorder, in which people suffer from an adverse reaction to gliadin proteins in the gluten of wheat, barley, and rye. When people with celiac disease eat gluten, an adverse immune reaction occurs, in which the intestinal villi, the finger-like projections that line the small intestine and serve to absorb nutrients, suffer damage and eventually flatten and disappear. Currently, the only treatment is the adoption of a gluten-free diet that eliminates exposure to the proteins that trigger the immune response. In most cases, the gluten-free diet heals the intestinal damage. So, how does gluten exposure cause this adverse immune system reaction? Much of this process remains a mystery, but there appears to be a strong genetic component. It is known that most people with celiac disease display the human leukocyte antigen (HLA) molecules DQ2 or DQ8, which function as receptors on antigen-presenting cells. The standard method of measuring deamidation is to tie the transglutaminase activity to a secondary enzymatic reaction, which gives off ammonium. But this method is not direct, and if there are multiple peptides in a mixture, which may be highly complex, one can only assess the total production of ammonium. By contrast, the MS method allows the detection of changes on each peptide, and allows the locations of those modifications to be pinpointed within each peptide. The team achieved their results by measuring the centroid masses of the peptides’ isotopic envelopes before TG2 treatment, and comparing the results to the values obtained after TG2 treatment. Depending on the sequence context, the glutamine residues were shown to influence the extent of residual deamidation by TG2. Additionally, they team revealed that peptide length also plays a key role in the process—the longer the given gliadin peptide, the more likely it is to have deamidated glutamines. The team examined an array of gluten peptides with known epitopes, both individually and in mixture, to assess the degree of deamidation. A 33-mer, shorter α-gliadin peptides, and one peptide from γ-gliadin all showed rapid deamidation. The rest of the peptides showed only partial deamidation, even after a long period of incubation. They observed that the frequency of the T cell response in celiac disease patients seems to be tied to the rate of peptide deamidation. T cells from nearly every patient recognized the 33-mer and the α-gliadin peptide, which also served as good TG2 substrates. In comparison, the glutamines of most γ-gliadin peptides were deamidated less often and were recognized less frequently by patient T cells. However, one γ-gliadin peptide showed itself to be an exception. The γ-II epitope functions as an excellent substrate for TG2, but is poorly recognized by T cells. Another factor may be proteolytic stability, as it is understood that the γ-II epitope is part of a gluten fragment that is less stable than the 33-mer. By analyzing gluten peptides using MS, researchers were able to figure out whether the rate of glutamine deamidation by TG2 impacts the recognition of these peptides by the immune systems of those with celiac disease. J. Proteome Res., 2009, 8 (4), pp 1748–1755
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