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    Does Celiac Disease in Kids Mean Greater Psychiatric Risk?


    Jefferson Adams


    • Journal of Gluten Sensitivity Spring 2017 Issue


    Image Caption: Photo: CC--Travis Wise

    Celiac.com 05/16/2017 - A number of studies have indicated that kids with celiac disease face an increased risk for mood disorders, anxiety and behavioral disorders, ADHD, ASD, and intellectual disability. A new study by a team of researchers in Sweden puts it more precisely. They put the increased risk for psychiatric disorders in children with celiac disease at 1.4-fold over kids without celiac disease.


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    The research team assessed the risk of any type of childhood psychiatric disorders, including psychosis, mood, anxiety, and eating disorders, psychoactive substance misuse, behavioral disorder, ADHD, ASD, and intellectual disability, in children aged 18 and younger, along with their siblings. The researchers included Agnieszka Butwicka, MD, PhD, of the department of medical epidemiology and biostatistics, Karolinska Institute, Stockholm, Sweden, and colleagues.

    For each of the 10,903 children with celiac disease, the research team randomly selected 100 non-celiacs from the general population. These control subjects were then matched by gender and year and country of birth. For each of the 12,710 siblings of celiac disease subjects, the research team randomly assigned 100 healthy control siblings from the general population. These were also matched by gender, year and country of birth of both siblings. Both sets of siblings were required to be free of celiac disease to age 19.

    The researchers reviewed histological data on patients who showed villous atrophy in small intestine biopsy specimens between 1969 and 2008, and equated villous atrophy with celiac disease.

    In the main cohort study, the researchers estimated the risk for any psychiatric disease, as well as specific psychiatric disorders (ie, mood, anxiety, eating, and behavioral disorders, as well as neuropsychiatric disorders such as attention deficit hyperactivity disorder (ADHD), autistic spectrum disorders (ASD), and intellectual disability) in children with celiac disease, compared with general population controls. They used sibling analyses to assess whether underlying familiar factors could account for the associations. As a comparing factor, they compared the risk for psychiatric disorders in the siblings against the risk in siblings of the general population.

    The team conducted both univariate and multivariate analyses, adjusting for maternal/paternal age at the child's birth, maternal/paternal country of birth, level of education of highest-educated parent, and the child's gestational age, birthweight, Apgar score, and history of psychiatric disorders prior to recruitment.

    During follow-up, 7.7% of children were diagnosed with a psychiatric disorder. A positive association was found in the first univariate analysis between celiac disease and any psychiatric disorder, which remained even after the researchers adjusted for maternal/paternal age at childbirth and country of birth, parental education level, and child's gestational age, birthweight, Apgar score, and previous history of psychiatric disorders.

    The overall prevalence of psychiatric disease in the entire sample celiac disease patients was about 7% (95% CI, 6.4%-7.4%). That number remained steady in the 10 years after biopsy. However, once the researchers analyzed the findings by cohort, they found that rates of psychiatric disorders had actually increased 8-fold over that 10-year period.

    The siblings of celiac disease patients showed no increased risk for any psychiatric disorder. The study showed that psychiatric disorders "may precede a diagnosis of celiac disease in children." The research team called this finding "important." They write that their study also offers "insight into psychiatric comorbidities in childhood celiac disease over time." The study showed that children with celiac disease definitely faced an elevated risk for specific psychiatric disorders, including mood disorders (HR, 1.2; 95% CI, 1.0-1.4), anxiety disorders (HR, 1.2; 95% CI, 1.0-1.4), eating disorders (HR, 1.4; 95% CI, 1.1- 1.8), behavioral disorders (HR, 1.4; 95% CI, 1.2-1.6), ADHD (HR, 1.2; 95% CI, 1.0-1.4), ASD (HR, 1.3; 95% CI, 1.1-1.7), and intellectual disability (HR, 1.7; 95% CI, 1.4-2.1).

    Although the study showed that patients with celiac disease are more likely to have prior psychiatric disorders (OR, 1.8; 95% CI, 1.5-2.1; P

    The team notes that they have yet to determine "the mechanisms underlying the association between celiac disease and psychiatric orders." The fact that the siblings of celiac disease patients showed no increased risk of psychiatric disorders indicates that these may be an "effect of celiac disease per se rather than common genetic or within-family environmental factors," the researchers add.

    The researchers conclude that their study "underscores the importance of both mental health surveillance in children with celiac disease and a medical workup in children with psychiatric symptoms."

    This study offers yet another piece in the complex puzzle that is celiac disease. It emphasizes the need for doctors and parents to remain on the lookout for potential psychiatric issues when dealing with children who have celiac disease.

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    Last Friday, April 16, 1943, I was forced to stop my work in the laboratory in the middle of the afternoon and to go home, as I was seized by a peculiar restlessness associated with a sensation of mild dizziness.  On arriving home, I lay down and sank into a kind of drunkenness which was not unpleasant and which was characterized by extreme activity of imagination.  As I lay in a dazed condition with my eyes closed (I experienced daylight as disagreeably bright) there surged upon me an uninterrupted stream of fantastic images of extraordinary plasticity and vividness and accompanied by an intense, kaleidoscope-like play of colors.  This condition gradually passed off after about two hours. From http://www.psychedelic-library.org/hofmann.htm. Several days later Dr. Hofmann intentionally ingested 250 µg of LSD which he hypothesized would be a threshold dose.  Here is what he said about his second ingestion:
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    Jefferson Adams
    Celiac.com 05/04/2012 - Some studies have shown that people with untreated celiac disease can have higher rates of psychiatric disorders, but little study has been made to determine whether people with psychiatric disorders have higher rates of celiac disease.
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    Gastroenterology and Hepatology

    Jefferson Adams
    Celiac.com 07/21/2016 - Celiac disease is a condition that can sometimes have vague symptoms, including mental and neurological symptoms, and that can make it hard to diagnose. Sometimes, individual cases can help to shed light on the serious nature of celiac disease, as well as the importance of a gluten-free diet in treatment. Consider the case of a 37-year-old Ph.D. candidate began to suffer from mysterious delusions, details of which appear in The New England Journal of Medicine.
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    Jean Duane
    Celiac.com 08/18/2017 - In a recent issue of Journal of Gluten Sensitivity, we announced a research study/survey for adults who are 18 or older and living the "gluten-free" lifestyle in a household with other adults over 18. Click here to read the Survey Overview Article.
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    Jean Duane
    Celiac.com 01/11/2018 - Gluten-free, food allergies and celiac disease have reached the media in the form of jokes and ridicule. This is a serious development because the media influences viewer's day-today reactions to various social situations. In many ways, TV becomes a role model for social interactions. DeVault (1991) says that "an enormous body of science, literature and even humor tells us how a middle-class man and woman might 'do' family life" (p. 16). This is the fundamental reason why the media jabs about gluten-free and food allergies are so impactful. What we see on TV, we emulate in life. If 'doing gluten free' is something to be ridiculed, as with the examples below, then those of us with food allergies need to unite our voices to be heard in public forums to change this practice.
    An example of food-allergy ridicule is found in a scene in The Smurfs 2 when the unctuous "Corndog King" presents every child at a birthday party with a corn-dog. A concerned parent asks if the corn-dogs contain peanuts, and he says, "No, I would never use peanuts." Meanwhile, a little boy is shown eating the corn-dog just as the Corndog King recalls that they are fried in peanut oil. The parents rush to the little boy urging him to spit it out. Here is the snippet:
    . I think the producers thought this incident was funny. Newsflash: It isn't. This scene has been criticized on various blog sites as making light of allergies, but one criticism from a parent of a child who recently died from inadvertently eating peanuts is especially poignant. The parent said scenes like this are not funny, nor entertaining. Scenes of this nature on TV undermine the consequences of food allergies.As much as I love Frankie and Grace, the game that the siblings played in Season 3, Episode 1, called "Bud's Super Needy Girlfriend Game" is offensive. It shows them eavesdropping as Allison, Bud's girlfriend, talks about her allergies to a stranger at the art show. With each statement Allison makes, such as, "it is easier to tell you what I am not allergic to," the group takes a shot of liquor. Allison says, "and that's when I realized I have celiac disease" and the siblings laugh and take another shot. This goes on for several rounds. The siblings ridicule Allison's allergies and maladies in a very uncompassionate way, setting an example for viewers on how to respond when there is a person in the crowd who has allergies. In another episode, when Allison faints, the reaction from the siblings is, "…she always has to be the center of attention. She conjures up some kind of illness. But there's a name for it, 'Fictitious disorder.'" (For a transcript of this and similar scenes, please check out: http://thewalkingallergy.com/2017/08/grace-and-frankie-i-bet-allison-has-mcas/). These responses to Allison's physical malaise are callous and may encourage copycat behavior in real life situations.
    Humans are easily influenced, starting from infancy when they imitate their parents (McCall, Parke & Kavanaugh, 1977) and continue to be guided by what they view in the media, especially on TV. Ramasubramanian (2010) conducted a study to discover how stereotypes of laziness and criminality changed as a result of reflecting on TV depictions of racial/ethnic groups by white viewers (p. 109) and concludes that the ways these scenes influence opinions and attitudes is worrisome (p. 106), perpetuating stereotypes and prejudice. A study conducted by Tan and Kinner (1982) found that interracial children who watched a TV program showing cooperative, positive behavior, yielded "pro-social" (p. 654) social interactions, when compared with a control group. The impact of what is viewed on TV and how it translates to social (or anti-social behavior) has been validated. Humans imitate what they see. Similar to how racial stereotyping is reinforced by the media, so are people with food allergies who become the butt of jokes. The media is teaching unacceptable social norms disguised as humor.
    Disney's episode of Quitting Cold Koala (edited out after parents complained, but still on YouTube in a home-video snippet) shows the character named Stuart (who has a "five page list of dietary problems" according to his nanny) sitting at the breakfast table with other children. He is a cute little boy who wears glasses cocked awkwardly on his nose. He told the cook that he couldn't eat pancakes that contained gluten only to be attacked by other children throwing gluten-containing pancakes in his face! Here it is on:
    . Stuart reacts the way anyone would who has celiac disease. He says, "That's gluten!" and frantically tries to wipe it off his face. I agree with the person who put the video of it on YouTube. This is not "remotely funny. Depending on how sensitive Stuart is, he may have had to suffer through a reaction because of those mean kids. And though this segment was deleted from the final cut of the episode, several people captured videos of it so it remains on the Internet for anyone to see. It sets a sad, and arguably violent standard for how to treat the child that has special dietary needs. Huesmann and Taylor (2006) found that violent behavior on TV poses "a threat to public health inasmuch as it leads to an increase in real-world violence and aggression" (p. 393). Violence toward someone with food allergies, such as throwing pancakes at the person who has just declared they are sensitive to gluten is an example of how behavior seen on TV could be re-enacted in real-life.How do scenes like the three examples above translate into our everyday social interactions? Does the waiter who watches a scene on a sit-com ridiculing someone with food allergies doubt the customer the next day as she orders a gluten-free meal? Does the waiter play a derivation of the "Needy Game" seen on Frankie and Grace and have a shot of liquor in the back room with his waiter-buddies for every customer that orders a special meal? Ridicule in the media completely undermines the severity of celiac disease, and other food-related illnesses.
    I experienced a situation the may have been influenced by commercial programming recently while ordering at a restaurant. I special-ordered my salad, deliberately sitting on the end of the table and explaining to the waiter that I needed to ensure it was gluten and dairy free. I spoke quietly, but since there were only two others at the table, unfortunately the conversation stopped during ordering and the others heard me. The waiter rolled his eyes when I gave him my order, and moved on to the next person who said, "I'll take the salad 'regular' with all the fixings" in a kind of a sarcastic way that belittled my order. My dinner was spoiled because I was irked with my dinner companion, and because I was skeptical of the food I was served. This kind of slight happens all the time, and is likely because of the role models depicted on TV and other media that portrays that it is it socially acceptable to mock the person with special needs.
    It is hard to understand why food sensitivities trigger so much negativity. If someone says they have heart disease, they are taken seriously. Other autoimmune diseases such as rheumatoid arthritis, lupus, Hashimotos, and diabetes are met with seriousness, but gluten-sensitivities seem to be a charged 'trigger' reaction, that I believe has been perpetuated by the media. People ordering in a restaurant seem to be challenged by the waiter – scrutinized whether it is an 'allergy,' 'autoimmune response' or 'fad diet.' When did waiters have the prerogative to make that kind of decision? Where did this 'right' come from? I believe the media has perpetuated these attitudes.
    Nobody with special needs should endure scrutiny or ridicule. I'm frankly glad for the publicity gluten has received because it has enhanced awareness, but I am discouraged about how the media seems to think celiac disease, gluten intolerance and food allergies are a joke. Here is our call to action: When we see something offensive in the media ridiculing food allergies, we need to say something in a public forum to bring attention to this unacceptable portrayal of people with food sensitivities. Please post on social media, or on Celiac.com to create a buzz that this type of ridicule/humor is unacceptable. Perhaps by doing this, we can influence positive changes.
    And on another subject… the winners from the survey.
    A couple of months ago, a survey studying the impact of food sensitivities on adults living together offered a $25 gift card to Amazon to four lucky winners. Those are: Morgan, Angela, David and Tricia. (Winners have been notified and gift cards were sent via email.) Congratulations! And thank you for your participation in the study.
    References
    DeVault, M. L. (1991). Feeding the family: The social organization of caring as gendered work. Chicago, IL: University of Chicago Press. Huesmann, L. R., & Taylor, L. D. (2006). The role of media violence in violent behavior. Annual Rev. of Public Health (27), 393-415. McCall, R. B., Parke, R. D., Kavanaugh, R. D., Engstrom, R., Russell, J, and Wycoff, E. (1977). Imitation of live and televised models by children one to three years of age. Monographs of the Society for Research in Child Development 42(5), 1-94. Tan, A. S., Kinner, D. (1982). TV role models and anticipated social interaction. Journalism Quarterly 59(4), 654-656.

    Betty Wedman-St Louis, PhD, RD
    Celiac.com 01/31/2018 - Methylation is a biochemical reaction in the human body that requires a variety of nutrients to perform indispensable roles in neurological health, detoxification, amino acid metabolism, gene regulation and vitamin assimilation. Every person with celiac disease needs to have their methylation variants tested by their physician so they can achieve good health. How well your body can "methylate" is important to your overall health.
    Methylation pathways in the body are important in cardiovascular health, neuroprotection from dementia and Alzheimer's disease, cognition skills in the young and old, along with emotional wellness and cellular function. A simple blood test- MTHFR- which is available at all major laboratories can determine if common genetic variants require additional supplementation of B vitamins.
    The MTHFR (Methylene Tetrahydrofolate Reductase) converts folate (vitamin B9) and riboflavin (vitamin B2) into an active part of the energy production cycle. In addition, it can indicate if higher levels of Vitamin B12 are needed. Since it is a genetic factor, some clinics do not test it but every celiac needs to know what variants they have in order to optimize their nutritional needs. (Author's note: I wish I had done this testing when I first learned about it 20 years ago. It has made all the difference in the world in my health these past 8 years!)
    The role of methylation is to help enzymes in our body work efficiently. Enzymes are like switches for chemical reactions in cells and tissues. Inadequate methylation nutrients- folate (NOT folic acid), methylcobalamin - the active form of B12 (NOT cyanocobalamin- the cheap cyanide form), and vitamin B6 as pyridoxal-5-phosphate can improve anemia, sleep, energy production and detoxification of chemicals from gasoline fumes to ammonia odors and personal care fragrances.
    Research over the past twenty years has provided a wealth of knowledge about methylation. It is the responsibility of each person to know their MTHFR variants which were inherited from mom and dad. Here is a brief list of the medical conditions affected by variants in MTHFR.
    Neurological Disorders: Parkinson's, Alzheimer's, Dementia, Multiple Sclerosis, Autism Cardiovascular Disorders: Atherosclerosis, Pulmonary Embolisms, General Clotting Disorders Mental Dysfunction: Depression, Anxiety, Insomnia, ADD/ADHD, Bipolar, Addictive Behaviors, Schizophrenia Conception: Infertility, Recurrent Miscarriages Immune Function: Allergies, Chronic Viral Infection Diabetes: Retinopathy, Neuropathy, Nephropathy Increased Sensitivity: Chemicals, Drugs, Supplements Birth Defects: Congenital Heart Defects, Cleft Palette, Spinal Bifida, Down's Syndrome Cancer Thyroid Dysfunction Chronis Conditions: Pain, Fibromyalgia, Chronic Fatigue Syndrome These MTHFR variants are NOT uncommon but unfortunately few in the medical arena are educated to address dietary concerns related to them. A book MTHFR- Methylation Diet is available on my website www.betty-wedman-stlouis.com for those who need assistance understanding their profile and designing dietary plans. The Methylation Diet is a high protein diet with lots of folate rich vegetables. Thos individuals with MTHFR variants should avoid folic acid as a dietary supplement and foods enriched with it like cereals, breads, flour, etc.

  • Recent Articles

    Jefferson Adams
    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.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    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.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    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.