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Found 7 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 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.
  4. I'm still awaiting the results of my biopsy. I have Latent Autoimmune Diabetes of Adults, which is basically type 1 diabetes diagnosed as an adult. (I was 32.) I have second degree relatives with celiac, although, my mom and my sister have yet to be tested. My mom's side of the family has a variety of autoimmune issues. My tTg-IgA was weakly positive (7.5), my DGP IgA was weakly positive (26), and my EMA was positive. My GI MD said he could see some inflammation on my duodenum during my EGD. I desperately want an answer to the issues I've been having. My primary complaints have been fatigue and joint pain, so I hadn't really considered celiac, thinking my GI issues were due to exhaustion. I am thinking I may stay gluten-free regardless of the biopsy results. I've been feeling better since cutting out gluten immediately after my EGD. I also feel like my lab work, diabetes, and family history are enough to warrant caution. Any thoughts or advice on this would be greatly appreciated. Thanks!
  5. Let me introduce myself. You can call me MK. I was diagnosed with Type 1 Diabetes about 6 years ago. I found the complete life change to be a major challenge, as would anyone. I admit, I never really fully was able to, leading to many health issues and many stays in the hospital with diabetic ketoacidosis. Then, to make matters even worse, about a year and a half ago, I was tested and it was confirmed that I have Celiac’s Disease. I have yet to eliminate gluten from my diet. I have made many attempts to do it, but I fall off the band wagon every time. Now to top things off. I lost my job over the summer and found myself living out of my car. I managed to find a part time job, but that barely pays for the car itself. I have to buy food on the fly, since there is nowhere to store food and nowhere to even cook it. This, as you can imagine, limits my options to the point where I don’t even know what to do. I eat anything I can, whenever it is possible. If I eat over another person’s house, I take what I can get. It is wreaking havoc on my intestines and my digestive tract. It has become a nightmare. Recently, my mother has been letting me stay on her couch, which opens up some possibilities for me to finally start getting myself straight. Although she buys a lot of bread and gluten full products, I have been talking to her about trying to work with me and buy some better options for me. That can get expensive and neither she nor I can truly afford to do it. Everything I have seen for sale that is gluten free, such as bread, pasta, etc., is way out of our very limited budget. I need to fix this, though. I need to get healthy or I am afraid I will die. Not even exaggerating. I need some support and didn’t know where else to look. I found this place and was hoping I could maybe find some help and advice. Or even just an ear (or a set of eyes?) to turn to. Thanks in advance. MK
  6. My 9 year old daughter has had type 1 diabetes(t1d) for about two years, and was dx with Hashimoto's(hypothyroidism)earlier this year. She had an appointment with her endocrinologist last week, and had blood work done to check her thyroid levels and screen for celiac. She has no obvious symptoms, it's just done as a routine screening, since celiac is dx more often with people with t1d. Last year her ttg was 3, this year it's 154! She's having a biopsy in a week or so, and I know you can have false positives (I've heard that's more likely if you have t1d), but does anyone know how likely a false positive is? Does it matter how high her ttg is? Thanks!
  7. I'm new here, and happy to be reading all the posts. I'm in the midst of a personal storm, both physical and emotional. I lost my son four months ago... and that should explain all my symptoms, especially the emotional. Except, my symptoms look more like celiac or gluten intolerance. I should mention that I am a Type 1 (insulin dependent) Diabetic. Briefly: 5 years ago I underwent a rapid weigh loss, and severe depression. I was given an endoscopy, blood tests for gluten... all were negative. Yet, the ONLY thing that helped me climb out of that mess and eventually regain my health and normal weight were eliminating gluten and dairy. (and eggs). At that time, a stool test through Genova/Metametrix did show off-the-chart sensitivity to gliadin. So, regardless of what the testing showed, I really stuck with the gluten-free diet. I've been fine since then, except if I cheat much on the gluten... I can "feel" the old symptoms coming back. But since I didn't have "celiac", I never was 1000% gluten free. Then in early January, I got a flu. I was already emotionally distraught over my son. And I do recall being more lax with avoiding gluten. (Went to several restaurants in Los Angeles on a trip, and wound up having a French Dip sandwich, some Chinese food with coated chicken, etc.) Suddenly the weight loss and fatigue are back... 20 pounds in two months. This time, huge abdominal issues, constant burping, constipation, nausea. Everyone is alarmed... and the depression is also oppressive. I just went back to a GI doc who did an MRI (looking for pancreatitis), and he also did the blood gluten testing, which was completely negative. I do NOT have fat in my stools, so this apparently rules out most major problems (including gluten intolerance?) The thing is, to prove that I am eating (and not simply depressed), I've kept a food journal. I'm eating 2500 calories or more every day, including a ton of fat and oil. WHERE does this food go, if not down the toilet, or digested onto my body? I should be big as a house. Any thoughts or advice would be SO appreciated! I haven't been able to work or function now in a month. Blessings~
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