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    PREVENTCD's Celiac Prevention Strategy for New Mothers


    Gryphon Myers
    Image Caption: Photo: CC--Rich Moffitt

    Celiac.com 11/07/2012 - When it comes to whether or not mothers with celiac disease should breastfeed their children, there has been a fair amount of conflicting information in circulation. Some studies have found that breastfeeding renders a protective role when combined with a 'windowed' introduction of gluten, but others have shown no such protective effect. Furthermore, some researchers question the longevity of the protection offered. An international project called PREVENTCD seeks to boil down current information from a number of studies, in order to produce a primary prevention strategy for infants at risk of developing celiac disease.


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    Photo: CC--Rich MoffittThe PREVENTCD project aims to answer the following questions:

    1. Breastfeeding (BF) and celiac disease (Does any BF reduce the risk of developing celiac disease in early childhood? Is there a difference between any or exclusive BF in regard to risk reduction? Is the duration of BF related to the risk of developing celiac disease?).
    2. BF at the time of gluten introduction and celiac disease (Is gluten consumption while being breastfed important for risk reduction?).
    3. Timing of gluten introduction (Is age of gluten introduction important to the risk of developing celiac disease?).
    4. Amount of gluten at weaning (and later) and celiac disease (Is the amount of gluten ingested an independent risk factor for the development of celiac disease in early childhood? Is there a threshold level of gluten consumption for developing celiac disease in early childhood?).
    5. Does the administration of microbial supplements (probiotics) and/or substrates (prebiotics) has an effect on the risk of celiac disease?

    For this report, a collection of studies (preference given to randomized controlled trials) involving infants at risk of developing celiac disease and breastfeeding practices were examined independently by a number of researchers. Inclusion criteria were applied independently and quality of each study's data was examined using the Cochrane Collaboration's tool for assessing bias risk. Meta-analysis was planned, but outcomes and definitions were inconsistent.

    29 studies were initially identified. Of those, 12 studies were included in the analysis. Collating the data from each, the questions were answered as follows:

    Effect of Breastfeeding on Celiac Disease: Some studies show a protective effect of breastfeeding children at risk of developing celiac disease, but some show no effect and no studies show a long-term preventative effect. Thus, the main controversy surrounding breastfeeding celiac children is whether it has a significant long-term effect. This should not be interpreted as evidence that suggests breastfeeding does not render long-term protection, but rather that no studies have adequately addressed the question yet (partially due to methodological challenges). Studies showing protective effect have postulated that the protection offered by breastfeeding is the result of introducing cytokines, as well as IgA antibodies, lactoferrin and other enzymes (as well as small amounts of gluten) that contribute to passive immunity by reducing the number of infections in the gut. Data from the studies also suggests that longer breastfeeding periods have a more pronounced effect on celiac disease risk. However, there was no evidence to suggest that 'pure' breastfed children were at any less risk than those both breastfed and formula fed.

    Effect of Breastfeeding at Time of Gluten Introduction on Celiac Disease: Data from five case-control studies suggests that breastfeeding at the time of gluten introduction is associated with lower risk of celiac disease compared to formula feeding. The quality of the data is questionable, as most feeding patterns were gathered retrospectively. Again, it is also unclear whether the protective effect merely 'postpones' celiac disease. One study also showed no effect of breastfeeding at the time of gluten introduction on celiac disease autoimmunity (effect on biopsy-proven celiac disease is unknown).

    Timing of Gluten Introduction: While the role of age at time of gluten introduction in determining celiac disease risk is unclear, data from observational studies suggests that early and late introduction of celiac disease may increase risk of celiac disease. Early is defined as before 3 months, while late is defined as later than 7 months. One randomized controlled trial showed that gluten introduction after 12 months might be beneficial, but sample size and unclear risk of bias make this finding inconclusive.

    Effect of Amount of Gluten at Weaning (and Later) on Celiac Disease: One study documented that introducing gluten in large amounts versus small or medium amounts increased celiac disease risk. This echoes old data collected during Sweden's 1980s celiac disease epidemic, but it is unclear whether this is a dose-response effect or a threshold effect. However, a recent study proposes a quantitative model for a HLA-DQ2 gene dose effect in the development of celiac disease.

    Administratioin of Probiotics and/or Prebiotics: There have been no studies examining the effect of probiotics and prebiotics on celiac disease risk in infants, but it is reasonable to assume that manipulating gut microbiotia in early stages of life could affect celiac disease risk. Future studies should investigate this possibility.

    In conclusion, there are still a lot of holes in the data, but what we know thus far tells us that:

    1. Breastfeeding seems to offer some form of protective effect (whether long or short term) on celiac disease risk in infants. Longer breastfeeding periods seem to offer more protection, but some formula feeding doesn't appear to affect celiac disease risk.
    2. Gluten should be introduced in small quantities between 4 and 7 months.
    3. Gluten should only be introduced while/if the infant is breastfeeding.

    The committee on Nutrition of the European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) believes that this strategy map will not only decrease rates of celiac disease, but type 1 diabetes, mellitus and wheat allergy as well.

    Most of these recommendations have been in place for a while and there is a lot of room for more data, but in the meantime, this is probably the safest strategy for feeding infants who are at risk of developing celiac disease.

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    Quite interesting. In my own experience, breastfeeding did not prevent celiac disease in my sons. However, I do believe it helped them from being sicker. Despite very positive blood work and biopsy (my sons were 4 and 2 at diagnosis), both had minimal symptoms. In addition to breastfeeding until 20 and nearly 24 months respectively, I also gave my sons probiotics and vitamins. While I will never know, I do feel this kept them healthier despite the damage. How long that would have remained true is questionable.

     

    I have had two more children since my sons' diagnosis and we have treated food differently. Both girls were breastfed. The oldest is three, started gluten at one year, and so far has shown no problems. The other is 10 months, still breastfeeding, and barely eats any table food. She seems to have issues with food in general. No gluten has been introduced yet with all the trouble she has with simple, supposedly low allergenic foods.

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    Why is the baby sucking the top of a bottle of Australan wine? I know this wine and the kangaroo is very obvious. What does this have to do with the story?

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    Guest gryphon

    Posted

    Why is the baby sucking the top of a bottle of Australan wine? I know this wine and the kangaroo is very obvious. What does this have to do with the story?

    You can only put so many stock images of babies being breastfed or cradled by their mothers before you are tempted to put something a little more... interesting. It's just a cute, silly picture.

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  • Related Articles

    Scott Adams
    by Marshall Chrostowski of Gluten Biotech Watch
    Question: What is biotechnology?
    Short Answer: Biotechnology is a set of scientific tools and principles designed to alter living material at the molecular-genetic level by recombining DNA fragments of genes to create organisms with altered, predictable properties. Organisms that receive genetic material from an unrelated organism are said to be transgenic and are referred to as genetically modified organisms (gmos).
    Question: Is food grown from gmos safe to eat? Short Answer: The answer has several parts.
    Scientists cannot yet assure us that gm food is totally safe to eat because such foodstuffs have not been tested using scientifically acceptable procedures over sufficient time. Caution is recommended because of theoretical issues related to creation of novel large proteins and associated biochemicals that are often associated with food allergenicities. Potential problems may arise from the introduction of exotic genes from viruses and bacteria not commonly part of the human diet, especially those genes producing toxins against crop pests and diseases. The potential adverse effects of synergy between gmos and traditional foods and medicines must be carefully considered by anyone with allergies and autoimmune issues. The Precautionary Principle should apply in relation to these gmos because it should be the responsibility of the biotechnological industry to demonstrate safety to humans and the environment prior to public acceptance and distribution. Question: Should a sufferer of food intolerances be concerned with the genetic modification of other foodstuffs?
    Short Answer: Scientific studies are confirming unforeseen increases in the allergenicity of some gm foods and some instances of reduced food values in altered crops. Most media reports, however, are anecdotal and should not be accepted as proof. Just remember that children are most susceptible to increased allergens. So, be forewarned.
    Question: Should folks with food intolerances and compromised immune systems be concerned about other trends in food production?
    Short Answer: Current research is directed at introducing genetic materials into conventional crops to produce pharmaceuticals and industrial components. Of more immediate concern are the numerous environmental estrogens (called endocrine disrupters) let loose on the population in the form of pesticides and other industrial products. Gmo research and development employs additional estrogens as regulators of transgenic changes. So there is the potential danger of estrogen overload on children in pre puberty.
    Action #l: Demand responsible labeling of food and medicines as GLUTEN FREE, not only processed food but also materials added post-harvest to "fresh" food.
    Action #2: Demand that genetically modified organisms and products be withdrawn from circulation and a rigorous, scientific evaluation of these materials be completed before any possible reintroduction.
    Action #3: In the interim demand immediate labeling as GMO FREE of all gmo products to allow the consumer to make informed choices.
    Action #4: Demand from your local markets the opportunity to buy certified organic food, and that markets list what fruit and vegetables have been treated with waxes, fungicides and other post-harvest protective materials.
    Action #5: Demand from the medical establishment greater awareness of and responsiveness to celiac and related diseases and syndromes and more aggressive research and development projects aimed at alleviating acute and chronic suffering by our impacted population.
     

    Wendy Cohan
    Celiac.com 02/09/2011 - A new group focused on supporting children with celiac disease and non-celiac gluten intolerance will hold its first meeting this month, on February 19th, in Portland, Oregon. G.I.F.T.S. - Gluten Intolerant Families Teamwork & Support (www.gifts-pdx.org) will meet every other month, on the third Saturday, from 2:00 to 4:00 p.m. in the home of group moderator Wendy Cohan, RN.
    Meeting in a home environment will reduce costs for membership, but also offer the opportunity to hold cooking demonstrations, cupcake decorating contests, and a summer cook-out, all of which are planned for 2011. Each meeting will feature a speaker, with subjects alternating between short health discussions and more kid-friendly holiday themes and cooking and baking with children. Our first speaker will be Krista Anderson-Ross, ND, who will give a short talk on the important topic of "Nutritional Deficits in Children with Celiac Disease", and how best to address them.
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    We have a small advisory committee of health professionals and parents of children with celiac disease, but you are welcome to bring your ideas to the table, literally. We plan to hold social gatherings and restaurant outings in addition to regular meetings. For more information, see the website, or email us: info@gifts-pdx.org.

    Dr. Ron Hoggan, Ed.D.
    Below is Ron Hoggan's reply the editor of the Montreal Gazette regarding the article: "Is gluten really something that most people should avoid?"
    Dear Health Editor:
    Mr. Dunning represents corn as a choice for bread-making prior to the advent of wheat, rye, and barley cultivation. However, the evidence suggests that corn was not yet available 10 to 15 thousand years ago when wheat, the earliest of these three grains, was first cultivated so it wasn’t available more than 20 thousand years ago when wild barley was first exploited ( 1 ). The evidence also indicates that corn was not available in the Near East, where wheat was first cultivated, as corn was a New World food developed by Mesoamerican indigenous peoples ( 2 ) half a world away.  In short, corn was not a discarded option for bread making when and where gluten grains were first cultivated.
    Perhaps Mr. Dunning should be forgiven such a relatively minor mistake. After all, he is a journalist, not a cereal scientist. However, as he is identified, in the article in question, as a science writer and a critical analyst, that should set the bar a little higher. Surely we may expect him to conduct basic research in an area by at least glancing at some of the peer reviewed reports on this topic. The one time he does this, he harkens to a report on autism as a tool for arguing against the connection between ADHD and gluten*.  For instance, he decries the adoption of a gluten free diet by those without celiac disease, gluten induced neuropathy, or wheat allergy.  Yet more than 90% of those with celiac disease currently go undiagnosed in the USA (3) and the average delay between onset of symptoms and diagnosis is 11 years (4). Here in Canada, we have very long delays before most of us can get to see a gastroenterologist, so our delays to diagnosis may be even longer.  This suggests that our rates of diagnosis are even lower than those of the USA. Perhaps Mr. Dunning’s querulous rhetoric could be more constructively directed at these long delays and the alarming rates of under-diagnosis of celiac disease. 
    In the interim, it seems very sensible for those with undiagnosed celiac disease to follow a gluten free diet and experience the improved health and quality of life which Mr. Dunning admits are available to these individuals through a gluten free diet.  This is an issue that might be revisited when our health care system is providing a timely diagnosis to at least a majority of cases of celiac disease.
    Recent research has also shown that those with non-celiac gluten sensitivity, which afflicts about 12% of the general population ( 5), experience even higher rates of morbidity and early mortality than those with celiac disease (6 ). Yet this group is either entirely ignored in Mr. Dunning’s  article, or, more likely, it is the unstated focus of his attack.
    Mr. Dunning also seems to be unaware that humans lack the full compliment of enzymes necessary for full digestion of gluten proteins thus making many of the constituent amino acids beyond our ability to metabolize when he states that gluten is “a protein that your body uses.” He further asserts that there is no good reason to avoid gluten if one does not have one of the three conditions he lists. Yet my own work suggests that the morphine-like opioids derived from gluten grains may be a contributing factor in several types of malignancy ( 7).    
    I was pleased to read that Mr. Dunning had at least glanced at data on gluten sensitive idiopathic neuropathy, but chagrined to read his speculation regarding the prevalence of this condition. I have devoted many years to the study of gluten’s impact on human health and have yet to read any work suggesting its prevalence. Perhaps Mr. Dunning could at least hint at his source when making such contentious claims.
    Nonetheless, there is clear evidence that a majority of those who experience gluten sensitive idiopathic neuropathy (5) do so in the presence of non-celiac gluten sensitivity, an autoimmune dynamic. Closer to home, our own Scott Frazer has demonstrated that consumption of gluten proteins is a potent force behind the development of many cases of type 1 diabetes (8). Reports of the causal connection between gluten consumption and autoimmune disease abound in the peer reviewed literature and are too numerous to warrant citing.
    Mr. Dunning also asserts “there is no evidence that incidence of disease increased worldwide once wheat became a staple.”  The field of Archaeology differs dramatically with Mr. Dunning’s claim. In general, it is quite well established that pre-agricultural, hunter-gatherers were much taller and had stronger bones than their descendants who adopted agriculture (9). For instance, a common finding in the skeletal remains of early farmers is a condition of porotic hyperostosis (10).
    Mr. Dunning also seems to be unaware that fats, per gram, provide more than twice the energy available in either carbohydrates or proteins and this ignores the added weight of indigestible fibre. The increased caloric density of fats is a principle that most students learn in high school Biology classes. Yet Mr. Dunning asserts that bread was a source of high energy and light weight.
    While science requires scepticism and criticism to function, polemic rhetoric based on personal bias generates more heat than light.  Mr. Dunning’s report is rife with errors and emotion. Publication of such dogma does little to enhance either the Gazette’s or Mr. Dunning’s credibility. Newspapers are given considerable credence as many readers, myself included, assume that journalists are exercising due diligence in checking their facts prior to publication of these reports. It is only when I read an article such as this one, that is deeply flawed and falls within my area of expertise, that my faith in journalists and the media is undermined.  
    *note: The only report I could find that fits the meagre description provided by Mr. Dunning is one that involved 15 children who were studied over a 12 week period (11). If this is, indeed, the study Mr. Dunning referred to, it hardly provides conclusive evidence of anything beyond the obvious need for more comprehensive study in this area. His use of these data as a springboard for his absolutist claims seems highly questionable, to say the least.
    Sincerely,
    Ron Hoggan, Ed. D.
    Royal Roads University, Continuing Studies
    co-author: Dangerous Grains ISBN: 978158333-129-3 www.dangerousgrains.com
    editor: Journal of Gluten Sensitivity www.celiac.com     
    editor/co-author: Cereal Killers  http://tiny.cc/s7neg
    Sources:
    http://en.wikipedia.org/wiki/Wheat http://en.wikipedia.org/wiki/Maize     Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago S, Elitsur Y, Green PH, Guandalini S, Hill ID, Pietzak M, Ventura A, Thorpe M, Kryszak D, Fornaroli F, Wasserman SS, Murray JA, Horvath K. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study. Arch Intern Med. 2003 Feb 10;163(3):286-92 Green PHR, Stavropoulos SN, Panagi SG, Goldstein SL, Mcmahon DJ, Absan H, Neugut AI. Am J Gastroenterol. 2001 Jan;96(1):126-31 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. Anderson LA, McMillan SA, Watson RG, Monaghan P, Gavin AT, Fox C, Murray LJ. Malignancy and mortality in a population-based cohort of patients with celiac disease or "gluten sensitivity". World J Gastroenterol. 2007 Jan 7;13(1):146-51. Hoggan R. Considering wheat, rye, and barley proteins as aids to carcinogens. Med Hypotheses. 1997 Sep;49(3):285-8. http://www.ohri.ca/profiles/scott.asp Lutz W. [The carbohydrate theory]. Wien Med Wochenschr. 1994;144(16):387-92. Wright L, Chew F, Porotic Hyperostosis and Paleoepidemiology: A Forensic Perspective on Anemia among the Ancient Maya. Am Anthro. 1998 Dec; 100: 924-939. Elder JH, Shankar M, Shuster J, Theriaque D, Burns S, Sherrill L.    The gluten-free, casein-free diet in autism: results of a preliminary double blind clinical trial. J Autism Dev Disord. 2006 Apr;36(3):413-20.

    Jefferson Adams
    Celiac.com 07/04/2014 - Celiac disease can be a factor in many cases of unexplained infertility in women. The recent case in Orlando, Florida of a woman named Vicky Crust, serves to drive home that fact, and to illustrate the potential benefits of a gluten-free diet in such cases.
    Crust suffered for years from abdominal pain, constipation, weight loss and a skin rash that overtook her nose, mouth and legs. Now, in spite of all these symptoms, Crust married, and began trying to start a family with her husband. She conceived twice, but was unable to carry full term. She couldn’t figure it out, and neither could doctors. Doctor after doctor failed to diagnose her celiac disease, and her symptoms grew worse as she progressed into her twenties.
    In 2010, Crust was diagnosed with celiac disease and her doctors at the Mayo Clinic believed that because she was otherwise healthy, she could have a successful pregnancy if she adopted a gluten-free lifestyle. Now, to be fair to Crust’s earlier doctors, celiac disease can be hard to spot. "Not everybody has symptoms. Not everybody may have the rash, the diarrhea, just overall weakness and other manifestations of celiac disease," says Dr. Christine Greves, an OB-GYN at Winnie Palmer in Orlando.
    After her diagnosis, Crust embraced a gluten-free diet, and that paid off nicely for her. Her rash healed, her stomach pains disappeared, and, most delightfully of all, she became pregnant. "My life is great now. I couldn't conceive before and now I am six months pregnant," she said. Obviously, celiac disease will not be a factor in every case of unexplained fertility, and a great deal more work needs to be done.
    However, Crust’s story is by no means rare, and is perhaps emblematic of the effects of celiac disease and the importance of getting a proper diagnosis, and adopting a gluten-free diet once diagnosed.
    Do you know anyone with a similar story?
    This story was first reported by WESH in Orlando, Florida.

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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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    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
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    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.