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    Scott Adams
    Arch Dis Child 2004;89:871-876. Celiac.com 07/12/2005 – Australian researchers have determined that a gluten-free diet in children with Type 1 diabetes mellitus and celiac disease can improve both growth and diabetes control. In the study 21 children (mean age 7.5 years) with both conditions went on a gluten-free diet for 12 months, and their growth and insulin dosages were carefully measured and compared with that of two matched diabetic, non-celiac controls. The group on a gluten-free diet showed significant increases in weight and body mass index compared with the control group, although an increase in height found in the study was not found to be significant. At the time of diagnosis insulin dosages for the celiac disease group were less than that of the control group, but became similar to the controls once a gluten-free diet was started—although the increase in insulin dosage had no effect on HbA1c levels.
    The researchers conclude: “Identification and dietary treatment of celiac disease in children with diabetes improved growth and influenced diabetic control. Evaluation of the outcome of treatment of celiac disease in diabetics should include assessments of gluten intake.” Obviously all children (and everyone) with celiac disease should be on a gluten-free diet, but what is noteworthy about this study is that a connection was found between insulin levels, diabetes control, and the gluten-free diet.

    Jefferson Adams
    Celiac.com 09/24/2009 - Could a reduced level of antibodies against infectious agents indicate a protective role for such infections in T1DM development in susceptible individuals? Recent research points in that direction. Type 1 diabetes mellitus (T1DM) is an autoimmune disease with intricate and poorly understood associations between genetic and environmental factors.
    A joint Israeli-Colombian research team recently set out to examine the connections between anti-infectious antibodies and autoimmune-associated autoantibodies in patients with Type I diabetes mellitus and their close family members. Among other things, their findings confirmed a strong association between celiac disease and Type 1 diabetes mellitus.
    The research team was made up of Ilan Krause, Juan Manuel Anaya, Abigail Fraser, Ori Barzilai, Maya Ram, Verónica Abad, Alvaro Arango, Jorge García, and Yehuda Shoenfeld. The team compared levels of antibodies to numerous infectious agents and of autoimmune-associated antibodies between Colombian T1DM patients, their close family members and healthy control subjects.
    T1DM patients showed substantially reduced levels of antibodies against several infectious agents, including: cytomegalovirus (P= 0.001); Epstein-Barr virus (P= 0.02); Helicobacter pylori (P= 0.01); and Toxoplasma (P= 0.001).
    T1DM patients showed markedly elevated levels of IgG-anti-gliadin antibodies (P= 0.001) and IgG-antitissue transglutaminase antibodies (P= 0.03), and a marginal connection with anti-centromere antibodies (P= 0.06).
    T1DM patients also showed a reduced level of antibodies against infectious agents that may be associated with their younger ages, but could also indicate a protective role for such infections in T1DM development in susceptible individuals.
    The results reinforce the connection between T1DM and celiac disease, though the
    possible connection with the anti-centromere antibody requires a deeper examination.
    Studies like this are important to help build a record of all of the points of contact between these associated conditions so we can begin to understand the intricate web that ties these conditions together, and inch toward the deeper causes that lie at the heart of the mystery of celiac disease, diabetes, and so many other auto-immune/inflammatory disorders.
    Source:
    Annals of the New York Academy of Sciences - Volume 1173 Issue Contemporary Challenges in Autoimmunity, Pages 633 - 639


    Jefferson Adams
    Celiac.com 07/22/2011 - Many reports indicate a hypercoagulative state in diabetes mellitus as result of endothelial damage. Numerous researchers have reported a strong association between type 1 diabetes mellitus (DM1) and celiac disease.
    Clinical data indicate that vascular dysfunction can result from a cascade of biochemical events triggered by a metabolic malfunction. The net result changes the cells that line the interior surface of the blood vessels; from a surface called a thrombo-resistant surface to one called a thrombo-genic surface.
    A research team recently set out to determine whether celiac disease in a group of DM1 patients is connected with a different expression of certain hemostatic factors, and with a different manifestation and/or progression of microvascular complications of DM1, as compared to patients with diabetes alone.
    For the study, the team enrolled ninety-four adult patients with DM1, who they then screened for celiac disease. They found anti-endomysial antibodies (EMA) in 13 of 94 DM1 patients (13.8%). The team then confirmed celiac disease diagnosis by histology and organ culture.
    The mean age and duration of DM1 of patients also affected by celiac disease were similar to those patients with diabetes alone, but the groups showed very different parameters for metabolic control and hemo-coagulation. In DM1 patients with celiac disease those parameters include:

    Signiï¬cantly lower concentrations of glycosylated hemoglobin (HbA1c) (P.05), cholesterol (P.001), triglycerides (P.001), factor VII antigen (FVII:ag) (P.005), factor VII coagulant activity (FVII:c) (P.05), and prothrombin degradation fragments (F1+2) (P.001). Higher values of activated C protein (APC) (.001).
    DM1 patients with celiac disease showed no retinal abnormalities and no signs of renal damage.The results suggest a potential protective role of celiac disease in the pro-thrombotic state of DM1.
    Source:

    Acta Diabetol. DOI 10.1007/s00592-011-0301-1

    Jefferson Adams
    Celiac.com 08/20/2012 - People with Type 1 Diabetes (T1D) suffer from celiac disease at rates ranging from 4.4 to 11.1%, compared with rates of 0.5% for the general population.
    The reason for this connection is due at least in part to the fact that the HLA genotypes DR3-DQ2 and DR4-DQ8 are strongly associated with T1D, while DR3-DQ2 is associated with celiac disease.
    To get a better sense of the issue, a research team recently assessed celiac disease in type 1 diabetes mellitus.
    The research team included Maria Erminia Camarca, Enza Mozzillo, Rosa Nugnes, Eugenio Zito, Mariateresa Falco, Valentina Fattorusso, Sara Mobilia, Pietro Buono, Giuliana Valerio, Riccardo Troncone, and Adriana Franzese.
    The are variously affiliated with the Department of Paediatrics, "Federico II" University, the School of Movement Sciences (DiSIST) at Parthenope University, and the Department of Cellular and Molecular Pathology "L. Califano", "Federico II" University, all in Naples, Italy.
    People with T1D rarely show classical severe symptoms of celiac disease. Usually, they have few or mild symptoms of celiac disease, or show no symptoms at all (silent celiac disease).
    In fact for T1D patients, diagnosis of celiac disease is usually done by blood screening.
    The effects of gluten-free diet (GFD) on the growth and T1D metabolic control in celiac disease/T1D patient are controversial.
    There is some debate about whether gluten-free foods have a higher glycemic index compared with to gluten-containing foods; and also about whether gluten-free foods might be be lower in fiber and higher in fat.
    Adherence to a gluten-free diet by children with celiac disease-T1D has generally been reported at below 50%, compared with about 73% for those with celiac disease alone. Failure to follow a gluten-free diet is even more common among asymptomatic patients.
    The more severe problems of gluten-free diet adherence usually occur during adolescence when non-compliant subjects report the lowest quality of life.
    The researchers suggest providing psychological and educational support for these patients.
    Source:
    Ital J Pediatr. 2012; 38: 10. doi: 10.1186/1824-7288-38-10

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    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