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    Celiac Disease Vaccine Trials Slated for 2009


    Jefferson Adams

    Celiac.com 12/18/2008 - Celiac disease is a life-long autoimmune disease. When people with celiac disease consume the gluten proteins found in wheat, rye and barley they damage the lining of the gut, which prevents normal digestion and absorption of food.


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    There is currently no cure for the celiac disease. The only treatment is life-long adherence to a strict gluten-free diet. If a gluten-free diet is not followed, the disease can ultimately lead to ill health and life-threatening conditions including malnutrition, osteoporosis, bowel cancer, and may cause infertility problems.

    The charity group Coeliac UK, recently hosted a conference at the Royal Society of Arts in central London where, among the latest findings in celiac disease research, they announced progress on the development of a possible vaccine for the condition.

    Dr. Bob Anderson of the Autoimmunity and Transplantation Division of Australia’s Walter and Eliza Hall Institute has led a research team that has isolated the toxic elements of gluten, paving the way for a possible vaccine that will suppress or prevent gluten toxicity. The research indicates that the toxic, autoimmune response in celiac patients exposed to wheat is triggered by just few dominant peptides in the gluten protein. This small number of offending peptides makes it exponentially easier for researchers to develop a vaccine.

    Dr. Anderson is a joint founder and CEO of Nexpep, an Australian company that is actively working to develop a vaccine to treat celiac disease. Dr. Anderson’s team has created a peptide-based therapeutic vaccine to treat the main problem T-cell epitopes of gluten. The vaccine has the potential to treat at about 80% of people with celiac disease and having the appropriate genetic background. Similar to traditional desensitization therapy for allergies, the peptide-based vaccines are given in multiple small doses over a course of injections in an effort to create immune tolerance not only to the selected gluten fragments, but also lower the toxicity of related toxic gluten molecules.

    Nexpep is currently raising capital for a clinical trial program for a peptide-based therapeutic vaccine and intends to commence a Phase 1 clinical trial in the first half of 2009.

    Reference:
    http://www.medicalnewstoday.com/articles/131745.php

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    Guest Michelle Witham

    Posted

    Being New Year's Day - our only wish is that a cure will be found for Celiac Disease and with this promising vaccine it gives us hope again for our 9 year old grandson who was diagnosed with both Diabetes type 1 and Celiac at age of 3...keep up the good work and Happy New Year!

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    Guest Patty Cook

    Posted

    Excellent news, I hope this vaccine works! I would try it.

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    Guest Hilda T Brower

    Posted

    Thank you so much for bringing the latest international research news to those of us who have gluten intolerance. I suspect it is more up-to-date than what the vast majority of gastroenterologists read.

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    Guest Eugene Brogan

    Posted

    This article was very interesting.

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    Guest Eugene Brogan

    Posted

    This article was very interesting.

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    Guest Kristina Quinn

    Posted

    It finally gives me hope! My two very young children who have both Celiac disease and Type 1 Diabetes, may actually get to live a somewhat normal life like other kids. It brings tears to my eyes!!

    THANK YOU !!!!!

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    Guest Mayank Agarwal

    Posted

    This news gives hope to many celiac patients. Thanks for updating the latest developments.

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    Guest Heather

    Posted

    I am hopeful this vaccine works! What wonderful news it would be for us Celiacs!

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    Guest Misty Cleeton

    Posted

    This is an excellent idea. It would be great to have my daughter be able to eat "normal" food without getting sick! Keep up the research!

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    Guest Joanne

    Posted

    Most interesting! What appropriate "genetic background" would make one eligible for this proposed vaccine?

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    Guest Roberta Wall

    Posted

    Sounds almost too good to be true! Let's keep our fingers crossed that it works. Sign me up!

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    Guest Amy Thielen

    Posted

    It would be a blessing that this vaccine would help those with Celiac. My 4 year old daughter was diagnosed at 3 years and 4 months old. She only weighed 21 lbs. and was only 33 inches tall. She is doing great with the acceptance part of having Celiac Disease, but it still breaks her heart when she sees other children in her preschool having snacks that she at one time could eat. I have another daughter who will be 3 next week, but does not have Celiac. This vaccine would be a miracle. As a mom, it breaks my heart to see her tears when she talks about her preschool friends.

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    Guest Roxanne Barco

    Posted

    The only thing you left out was how to get involved in this trial...I would love to participate if they need volunteers!

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    Guest Audrey Elderkin

    Posted

    The possibility of a vaccine is the first ray of hope I have had since being diagnosed in 2003. My son and great-niece also are celiacs. I would be willing to participate in a study on the vaccine.

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    Guest gail zamberlin

    Posted

    I am very hopeful as we have a 19 year old son that does not stay on his diet at all, he's very thin and as parents we are very concerned.

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    Guest Gloria Brown

    Posted

    My experience of Celiac is not as an allergy, but an inability to metabolize gluten from genetically not producing the required enzymes to do so. Compromising of the autoimmune system has seemed more related to the malnutrition which results from this.

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    Guest Cheri Young

    Posted

    This is good news. I have had celiac for six years but anyone with Celiac would agree, six years is six years too long as this is a difficult way to live. So, I really hope for a 'cure' soon.

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    Guest Noelle

    Posted

    Very interesting however my GI did not know anything about it and asked for a copy of the article and I haven't heard from anyone yet even though I replied to the email and signed up for the research.

    Thank you

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  • Related Articles

    Dr. Ron Hoggan, Ed.D.
    This article originally appeared in the Autumn 2002 edition of Celiac.coms Scott-Free newsletter.
    Copyright © 2002 Scott Adams. All rights reserved worldwide.
    Five years ago I became concerned about weakness in my bones after a couple of surprising fractures. At one point, I broke a rib while shingling a storage-shed roof. I leaned across the peak of the roofs ridge to pick up a shingle. I never expected such light pressure to cause a problem, however, I felt a sudden, sharp pain, and heard an odd sound. This, along with a couple of less dramatic, but similar injuries, caused me enough concern to begin looking into the question of celiac disease and bone strength.
    My explorations taught me that calcium absorption probably is not our main problem. People with celiac disease seem to be able to absorb adequate calcium1, but the primary problem appears to come from excreting too much of it, thus causing us to lose more calcium than we are absorbing. I also learned that research shows little or no benefit from calcium supplementation for celiac patients, while magnesium supplementation alone results in significant improvements2. The explanation for this may be that some of the antibodies caused by active celiac disease attack the parathyroid gland3. This organ is an important player in regulating calcium metabolism. Magnesium is necessary for the body to repair the parathyroid and to maintain its continued good function.
    Being convinced by this research, I began to take magnesium supplements without any calcium. I found that I had to be careful. Too much had me visiting the washroom frequently, and I was afraid that too little would fail to provide me the benefits I was seeking.
    At the same time, I also requested a bone density test. I wanted objective information that would allow me to evaluate the progress I hoped to make. The first test was conducted in March of 1997. The results (called "T scores") are reported based on comparison with the density of bones found in young adults. For instance, a score of 0 indicates that the bone density is about the same as would be found in an average young adult. A score in the minus range indicates a bone that has less mineral and more pores than is found in the same young adult. Thus, a score of –1.0 to –2.5 indicates mild mineral losses, while a score of –2.5 or lower indicates osteoporosis.
    My test results were not as bad as I had feared. The mineral density in my lower back was normal for my age, at –0.23. However, my upper leg, where it fits into my hip, was reported as –2.02, and my forearm was slightly stronger than that of a normal young adult at +0.19.
    As I saw it, there were only two causes for concern. First, at the tender age of 50, my hips were very close to osteoporotic, and certainly at a substantially increased risk of fracture. Such fractures can be very serious. Secondly, since only three skeletal areas had been tested for mineral density—and since there was such a wide range of density reported for each of these areas, it seemed impossible to estimate the density of the rest of the bones in my body.
    About three years after my first bone density test, some Calgary-based research made me suspect that the amount of vitamin D supplements I was taking might be too low4. I increased my intake to 1,000 IU daily.
    By the fall of 2001, I began to wonder if I was being foolish by avoiding calcium supplements based on the reports I had read. I therefore began to supplement 350 mg of calcium each day.
    In July of 2002, I underwent a second bone scan. They did not test my forearm, but the other two areas appear to have improved substantially. The T score for my lower back was now at + 0.06, and the T score for my hip had improved to –0.72.
    I realize that what I am reporting is just one persons experience. It is what the medical professionals call "anecdotal," and does not usually carry much weight. However, my experience does support the only published research of the impact of mineral supplements on bone density in celiac patients that I can find. Based on my own experience, and the relevant research, I am now convinced that magnesium is the most important supplement to consider in the context of celiac disease. I was thrilled to read my latest bone density report. Vitamin D may also be an important factor, but limitations of time and space force me to leave this topic for another day.

    References:
    Marsh MN. Bone disease and gluten sensitivity: time to act, to treat, and to prevent. Am J Gastroenterol. 1994 Dec;89(12):2105-7. Rude RK, Olerich M. Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. Osteoporos Int. 1996;6(6):453-61. Kumar V, Valeski JE, Wortsman J. Celiac disease and hypoparathyroidism: cross-reaction of endomysial antibodies with parathyroid tissue. Clin Diagn Lab Immunol. 1996 Mar;3(2):143-6. Embry AF, Snowdon LR, Vieth R. Vitamin D and seasonal fluctuations of gadolinium-enhancing magnetic resonance imaging lesions in multiple sclerosis. Ann Neurol. 2000 Aug;48(2):271-2. Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His new book "Dangerous Grains" is available at Celiac.com.

    Amy Leger
    Celiac.com 12/12/2008 - The tales of diagnois for celiac disease are almost alwaysdramatic: Some people go for years dealing with aches and pains and thinkingthat this is just the way their body was built. I remember feeling that way when my one-year-old was so crabby—walkingaround with her big old “Buddha” belly. Recently, I requested the top threesymptoms from adult and child celiacs to put together a survey of the topsymptoms on my blog. I didn’t ask forthe diagnosis stories, but people offered some insight into the trials andtribulations of getting diagnosed with celiac disease—and eventually leadinga new and healthier life!
    It took a major virus, three doctors, x-rays, blood tests toget to Emma’s diagnosis.One doctor toldme “kids throw up” (once every nine days? Really?), a second opinionrecommended Milicon for her “gassy” tummy. Luckily, it all ended the way it should have, with a diagnosis of celiacdisease that only took about 5 months—which is relatively little compared tosome of the stories you’re about to hear.
    One woman wrote me describing her daughter’s symptoms whenshe was diagnosed at age 15, but then she wrote back about the subsequentdiagnoses of her sister and mother.Jeanwas diagnosed at age 70 but she and her family tell me her severe scoliosis atage 12 was a symptom! Can you believebeing misdiagnosed for 58 years?Jean evenhad to be put in a back cast for a time.
    Jean’s daughter, Vicky was diagnosed with Crohn’s disease atthe age of 12—which included 3 major surgeries! Her celiac disease diagnosis didn’t comeuntil the age of 51. By then major damagehad been done to her body with the onsets of several health issues:rheumatoid and osteo arthritis, thyroiddisease, severe osteoporosis (both hips have been replaced ...one twice)and severe scoliosis. It turns out: three generations of women in the samefamily all started showing their symptoms in those early teen years.
    Kim wrote me and said she was diagnosedat 39 years old when she was hospitalized with stomach pain, vomiting anddiarrhea.But she added at the end ofher note, “ probably shouldhave gotten tested at [age] 11 when I had the same severe cramping that put mein the hospital.” The bright spot inthis story is that her eventual celiac diagnosis, led to the quicker diagnosisof her 5-year-old daughter who was just beginning her symptoms of low weightand anemia.
    Another contributorsaid her 14-year-old son was diagnosed with celiac two years ago, but has alsohad a kidney issue for the last 9 years.But since he has been eating gluten free…his kidneys have also gottenbetter, last report was the best since before he was brought in at age 5!! Now I wonder which really came first?”It does make you wonder.
    But there are somesuccess stories:
    One mom mentionedher son’s quick diagnosis. “[it] started with diarrhea. Thought it was a stomach bug.” Then it moved to constipation and two weekslater things still weren’t right.Thentheir doctor put two and two together, “[An]amazing pediatrician said ‘This sounds like Celiac’ and ran the bloodtests. Andrew was only ‘sick’ about 1 month before diagnosis,” shesaid. However looking back on it all, hehad a big belly and slow to grow.
    Others talked about having celiac disease and not even feeling sick.

    “I onlyfound out about the anemia through a blood test done as part of a completephysical; my general health to that point was excellent, including runningmarathons,” Danny wrote. “The only reason [my 3-year-old daughter]was diagnosed was her yearly blood draw came back positive so we had thebiopsy,” said Monica, a mom of two celiac children. Anna’s dad, Tom, was diagnosed in his 40s aftera family-round of blood testing. He isasymptomatic. The last two pointsshow how important it is to take part in preventative measures, by gettingregular blood testing done for first-degree family members. The National Institute of Diabetes, Digestiveand Kidney Diseases says, “…because celiac disease is hereditary, familymembers of a person with the disease may wish to be tested. Four to 12 percentof an affected person’s first-degree relatives will also have the disease.”
    The stories ofdiagnosing celiac disease may leave many of us angry, frustrated, and possiblygrateful—all at the same time. The missed diagnoses and misdiagnoses of those who have thisdisease presents a roller-coasterride of emotions. I hope this articlehelps you in knowing many others have gone through it and are likely goingthrough it as we speak.We just need tomake sure we’re spreading the word and getting as much awareness out there aspossible to help others in similar situations.

    Miranda Jade
    Celiac.com 02/08/2012 - Having finally being diagnosed with celiac disease myself, I enjoy writing about this autoimmune disease in my gluten-free advocacy work with my mom, Tina Turbin. However, there is a whole other segment of the population who, rather than having celiac disease, have a food sensitivity to gluten. In fact, according to The Food Intolerance Consumer, gluten-sensitive people make up 15% of Americans, whereas celiac disease is currently estimated to exist in 1% of the population. Clearly, in view of its prevalence in the U.S., gluten sensitivity needs to be addressed, but as it turns out, research is showing that an early diagnosis of gluten sensitivity is particularly crucial in preventing celiac disease and other serious health conditions from developing among the gluten-sensitive population.
    According to the website of the ALCAT Food and Chemical Sensitivity/Intolerance Test, food sensitivity "induces chronic activation of the innate immune system and gives rise to inflammatory process," and this inflammation "has been linked to countless chronic conditions, including: digestive disorders, migraines, obesity, chronic fatigue, ADD, aching joints, skin disorders, arthritis and many more.' Perhaps you're wondering how a food sensitivity is different from a food allergy. According to ALCAT, food allergies encompass reactions to food that activate the immune system to produce large amounts of histamine, which leads anaphylaxis, a condition that can be deadly, causing swelling in the throat and esophagus so that one can't access air from the lungs or other reactions such as hives and rashes.
    According to Kenneth Fine, MD, in a transcript of a talk he gave to the Greater Louisville Celiac Sprue Support Group, as published by Celiac.com, the immune system reaction that gluten sensitivity causes starts in the intestine because this is where gluten is found after being digested in foods. When this reaction causes damage to the absorptive finger-like projections that line the small intestine called villi, known as villous atrophy, celiac disease is said to exist. However, says Dr. Fine, "Although the small intestine is always the portal of the immune response to dietary gluten, it is not always affected in a way that results in villous atrophy." In fact, he says that most gluten-sensitive people don't have this symptom of celiac disease and are therefore not celiac.
    Despite this fact, the testing that has been commonly administered in order to diagnose gluten sensitivity have yielded positive results only when damage to the villi was noted, a fact which can have devastating health consequences for gluten-sensitive people without such damage, who are likely to continue ingesting gluten. According to Dr. Fine, "This can result in significant immune and nutritional consequences, many of which are irreversible even after treatment with a gluten-free diet." The list of disorders and health conditions that can manifest is long, including, Dr. Fine says, "loss of hormone secretion by glands (hypothyroidism, diabetes, pancreatic insufficiency, etc), osteoporosis, short stature, cognitive impairment, and other inflammatory bowel, liver, and skin diseases, among others." That's why he stresses early diagnosis for gluten sensitivity.
    Dr. Fine seeks to change current testing methods and clear up misconceptions that prevent early diagnosis from being made. One of the misconceptions he discusses is the reliability of specific blood testing for not only antigliadin antibodies but also autoimmune antiendomysial or anti-tissue transglutaminase antibody. He says that "a negative test does not mean you do not have the problem. This is the biggest pitfall of all because the only thing a very specific test, like blood testing for celiac disease, can do is 'rule in' the disease; it cannot 'rule it out.'" This means that people with advanced or long-term celiac disease will show positive results. In fact, when the villi were only partly damaged, only 30% of celiac individuals being tested had positive results.
    Detecting gluten sensitivity early in individuals can have major health benefits, preventing not only the development of celiac disease (that is, villous atrophy, according to Dr. Fine), but a wide array of autoimmune diseases and conditions such as osteoporosis, malnutrition, infertility, certain mental disorders, and even some forms of cancer. I myself was diagnosed in my early 20's after being in and out of hospitals and incorrect diagnoses. Additionally, the treatment for gluten-sensitive individuals diagnosed early would be simple-a gluten-free diet-which should result in improvement in symptoms. With the medical community enlightened by Dr. Fine's research, we can look forward to better testing and earlier diagnosis of the gluten-sensitivity community and their resultant health benefits.
    Resources:

    TheGlutenSyndrome.net The Food Intolerance Consumer: Gluten Intolerance and Celiac Disease Gluten Free Help
    ALCAT: What is Food Sensitivity?
    Early Diagnosis of Gluten Sensitivity: Before the Villi are Gone by By Kenneth Fine, M.D.

    Jefferson Adams
    Celiac.com 01/16/2015 - Most people with celiac disease suffer from classic symptoms like weight-loss and diarrhea before diagnosis, right? Wrong. In fact, the most common medical issues for people with celiac disease might really surprise you.
    A team of researchers who recently looked at data on 770 celiac patients admitted to S. Orsola-Malpighi Hospital from January 1998 to December 2012, found that even though 80% of people with celiac disease have symptoms other than diarrhea, only 1 in 3 people with celiac disease shows classical malabsorption symptoms.
    Notably, two out of three people with celiac disease show non-classical symptoms. The majority of people have non-gastrointestinal symptoms. In fact, the top ten medical complaints of people with celiac disease are:
    Osteopenia/Osteoporosis—a full 52% of patients with celiac disease suffer from osteopenia/osteoporosis. Anemia—about one in three celiacs (34%) suffer from anemia. Cryptogenic hypertransaminasemia—nearly one-third (29%) of people with celiac disease, have what is called cryptogenic hypertransaminasemia. Diarrhea is, in fact, a common gastrointestinal symptom of celiac disease, but believe it or not, only 27% of people with symptomatic celiac disease experienced diarrhea. Bloating—20% of celiacs complained of bloating prior to diagnosis. Aphthous stomatitis—18% of people with symptomatic celiac disease had canker sores as one of their symptoms. Alternating bowel habit—15% of celiacs with symptoms have alternating bowel habit Constipation—13% of celiacs have constipation as a symptom. Gastroesophageal reflux disease—About 12% of people with celiac disease suffer from gastroesophageal reflux disease. Recurrent miscarriages—just over one in ten (12%) people with celiac disease experience recurrent miscarriages

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    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
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    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
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    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics

    Jefferson Adams
    Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
    A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.
    For their study, the team collected urine samples from 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIPs and an LFT reader. 
    They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage.
    The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
    Source:
    Gut. 2017 Feb;66(2):250-257.  doi: 10.1136/gutjnl-2015-310148.