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Found 41 results

  1. Celiac.com 06/13/2012 - In general, doctors and researchers know a good deal about how celiac disease works, and they are finding out more all the time. However, they know very little about non-celiac gluten sensitivity (NCGS). In an effort to learn more about non-celiac gluten sensitivity, a team of researchers recently carried out a study to measure the presence of somatization, personality traits, anxiety, depression, and health-related quality of life in NCGS individuals, and to compare the results with celiac disease patients and healthy control subjects. They also compared the response to gluten challenge between patients with non-celiac gluten sensitivity and those with celiac disease. The research team included M. Brottveit, P.O. Vandvik, S. Wojniusz, A. Løvik, K.E. Lundin, and B. Boye, of the Department of Gastroenterology at Oslo University Hospital, Ullevål in Oslo, Norway. In all, the team looked at 22 patients with celiac disease and 31 HLA-DQ2+ NCGS patients without celiac disease. All patients were following a gluten-free diet. Over a three day period, the team challenged 17 of the celiac disease patients with orally ingested gluten. They then recorded the symptoms reported by those patients. They did the same with a group of 40 healthy control subjects. The team then had both patients and healthy control subjects complete questionnaires regarding anxiety, depression, neuroticism and lie, hostility and aggression, alexithymia and health locus of control, physical complaints, and health-related quality of life. Interestingly, patients with non-celiac gluten sensitivity reported more abdominal (p = 0.01) and non-abdominal (p < 0.01) symptoms after the gluten challenge than patients with celiac disease. The increase in symptoms in non-celiac gluten sensitivity patients was not related to personality. However, the two groups both reported similar responses regarding personality traits, level of somatization, quality of life, anxiety, and depressive symptoms. Responses for both groups were about the same as for healthy controls. The results showed that patients with non-celiac gluten sensitivity did not show any tendencies toward general somatization, as both celiac disease patients and those with non-celiac gluten sensitivity showed low somatization levels. Source: Scand J Gastroenterol. 2012 Apr 23.
  2. Celiac.com 09/26/2018 - Non-celiac gluten sensitivity (NCGS) is a clinical syndrome marked by both intestinal and extra-intestinal symptoms that respond to the elimination of gluten-containing food and the adoption of a gluten-free diet. A team of researchers recently set out to review the diagnostic challenges surrounding non-celiac gluten sensitivity, and to summarize recent advances in research and provide a brief overview of the history of the condition for the benefit of professionals working in gastroenterology. The research team included Giovanni Casella, Vincenzo Villanacci, Camillo Di Bella, Gabrio Bassotti, Justine Bold, and Kamran Rostami. They are variously affiliated with General Practioner National Health Italy; the Institute of Pathology Spedali Civili Brescia Italy; the Pathology Department, Carate Brianza Hospital, ASST-Vimercate (Monza Brianza), Italy; the Gastroenterology and Hepatology Section of the Department of Medicine at the University of Perugia School of Medicine in Perugia, Italy; the Department of Gastroenterology Milton Keynes University Hospital, Milton Keynes, UK; and with Allied Health and Social Sciences, University of Worcester, UK. The researchers searched academic databases such as PubMed and Google Scholar using key words like ”non-celiac gluten sensitivity,” “gluten related disorders,” and the studies outlined in reference page were selected and analyzed. Clinical opinion generally holds that NCGS is best diagnosed by ruling out celiac disease and wheat allergy. Currently there is no blood test that can pinpoint NCGS. The underlying causes of symptoms in NCGS patients is poorly understood. However, there have been a few recent insights. Professional estimates of NCGS rates currently vary between 0.6 and 6%. Gastrointestinal symptoms of NCGS overlap slightly with those of irritable bowel syndrome. Researchers are currently investigating the histologic characteristics of NCGS, which range from normal histology to slightly elevated rates of T lymphocytes in the superficial epithelium of villi. Positive response to gluten free diet for up to 6 weeks, followed by a recurrence of symptoms after a gluten challenge, is still the best confirmation of NCGS. The Salerno expert criteria may help to accurately diagnose NCGS, especially in research settings, but isn’t particularly useful for diagnosis in clinical practice. Source: Gastroenterol Hepatol Bed Bench 2018;11(3):197-202).
  3. Celiac.com 01/16/2018 - More and more, people are adopting a gluten-free diet due to perceived health and weight-loss benefits. A team of researchers recently set out to ask people with celiac disease and non-celiac gluten sensitivity about their views on the health effects of gluten, and safety of vaccines and gluten-free food products. The research team included Loren G. Rabinowitz, Haley M. Zylberberg, Alan Levinovitz, Melissa S. Stockwell, Peter H. R. Green, and Benjamin Lebwohl. They are variously affiliated with the Department of Medicine, Celiac Disease Center, Columbia University College of Physicians and Surgeons New York USA; the Department of Philosophy and Religion James Madison University Harrisonburg USA, the Department of Pediatrics Columbia University College of Physicians and Surgeons New York USA, the Department of Population and Family Health, Mailman School of Public Health, Columbia University New York USA, the Department of Epidemiology, Mailman School of Public Health, Columbia University New York USA, and the Celiac Disease Center at Columbia University New York USA. Their team conducted an online survey of celiac and non-celiac gluten sensitivity patients from a celiac disease center e-mail list. They used univariate and multivariate analysis to compare responses from the two groups. The overall response rate was 27%, with 217 non-celiac gluten sensitivity responses, and 1,291 celiac disease responses. Subjects with non-celiac gluten sensitivity were more likely than those with celiac disease to disagree with the statement that "vaccines are safe for people with celiac disease." In all, 41.3% of respondents with non-celiac gluten sensitivity said vaccines are safe for celiacs, while just 26.4% of celiac patients said so. Celiac patients were slightly more likely to decline vaccination when offered, at about 31%, compared with just over 24% of gluten-sensitive respondents. After adjusting for age and gender, non-celiac gluten sensitivity subjects were more likely than celiac disease subjects to avoid genetically modified (GMO) foods, eat only organic products, believe that the FDA is not a reliable source of information, and believe a gluten-free diet will improve energy and concentration. People with non-celiac gluten sensitivity were more likely than those with celiac disease to have doubts about vaccine safety and to believe in the value of non-GMO and organic foods. The team's findings suggest that there might not be enough easily accessible information on gluten and its inclusion in food and drugs, and that may reinforce incorrect beliefs that are contrary to good public health. Source: Springer.com.
  4. Celiac.com 03/05/2018 - While people with non-celiac gluten sensitivity (NCGS) have neither celiac disease nor wheat allergy (WA), they often do have intestinal and extra-intestinal symptoms that are related to gluten consumption. Using a double-blind placebo-controlled (DBPC) gluten challenge with crossover, a team of researchers recently set out to conduct the first assessment of NCGS rates in children with chronic, gluten-associated gastrointestinal symptoms. The research team included R Francavilla MD, PhD, F Cristofori MD, L Verzillo MD, A Gentile MD, S Castellaneta MD, C Polloni MD, V Giorgio MD, E Verduci MD, PhD, E D'Angelo MD, S Dellatte MD & F Indrio MD. They are variously affiliated with the Department of Pediatrics, San Paolo Hospital, Bari Italy; the Department of Pediatrics, Santa Maria del Carmine Hospital, Rovereto TN, Italy; the Department of Pediatrics, Catholic University, Rome, Italy; the Department of Pediatrics, University of Milan, S. Paolo Hospital, Milan, Italy; the Department of Pediatrics, Santa Maria Incoronata dell’Olmo Hospital; Cava dei Tirreni SA, Italy; the Tandoi Group Factory, Corato, Italy; and the Interdisciplinary Department of Medicine-Pediatric Section, University of Bari, Bari, Italy. Their team looked at 1,114 children with chronic gastrointestinal symptoms, but no celiac disease and WA. For children showing a positive connection between symptoms and gluten ingestion, the team offered a four-stage diagnostic challenge that included: run-in, open gluten-free diet (GFD) and DBPC crossover gluten challenge. Patients randomly received gluten (10 g/daily) and placebo (rice starch) for 2 weeks each, separated by a washout week. The gluten challenge was considered positive when accompanied by a minimum 30% decrease of global visual analogue scale between gluten and placebo. Out of 1,114 children, 96.7% showed no correlation with gluten ingestion. Thirty-six children were eligible for the diagnostic challenge. After the run-in and open GFD, 28 patients underwent gluten challenge. Eleven of these children tested positive (39.2%). This is the first such study to demonstrate the need for a DBPC for diagnosing NCGS in children, since the diagnosis is ruled out in more than sixty-percent of cases. Source: The American Journal of Gastroenterology. doi:10.1038/ajg.2017.483
  5. Celiac.com 11/20/2017 - People who do not have celiac disease, but who have celiac-like symptoms that improve on a gluten-free diet are prime candidates for a condition called non-celiac gluten sensitivity (NCGS). Researchers don't know much about the condition. There are no biomarkers, so they can't just do a blood test. People with this condition often experience celiac-like symptoms. Many of people with non-celiac gluten sensitivity see their symptoms improve on a gluten-free diet. However, these people may also have puzzling sensitivities to other foods that just don't seem to add up. Interestingly, foods with gluten often contain fructans, a type of fermentable oligo-, di-, monosaccharides and polyols (FODMAPs). Fructan is one such compound. Could fructan be the culprit? A team of researchers recently set out to investigate the effect of gluten and fructans separately in individuals with self-reported gluten sensitivity. The research team includes Gry I. Skodje, Vikas K. Sarna, Ingunn H. Minelle, Kjersti L. Rolfsen, Jane G. Muir, Peter R. Gibson, Marit B. Veierød, Christine Henriksen, Knut E.A. Lundin. They are variously affiliated with the Division of Cancer Medicine, Oslo University Hospital, Rikshospitalet, 0424 Oslo, Norway; the K. G. Jebsen Celiac Disease Research Centre, University of Oslo, Norway; the Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Norway; the Department of Gastroenterology, Monash University and Alfred Hospital, Melbourne, Victoria, Australia; the Department of Immunology and Transfusion Medicine, Oslo University Hospital, 0424 Oslo, Norway; and the Centre for Immune Regulation, University of Oslo, 0424 Oslo, Norway. For their double-blind crossover challenge, the team enrolled 59 individuals without celiac disease, but who followed a self-driven gluten-free diet. The team conducted the study at Oslo University Hospital in Norway from October 2014 through May 2016. The team randomly assigned study subjects to groups. For 7 days, each group ate muesli bars containing either 5.7 grams of gluten, 2.1 grams fructans, or a placebo. Subjects then underwent a washout period that lasted until the symptoms caused by the previous challenge were resolved. Washout period was a minimum of 7 days. After the washout period, participants crossed over into a different group, until they completed all 3 challenges. To measure symptoms, the team used the gastrointestinal symptom rating scale irritable bowel syndrome (GSRS-IBS) version. They used a linear mixed model for analysis. In this study of individuals with self-reported non-celiac gluten sensitivity, researchers found that fructans induced symptoms of irritable bowel syndrome, as measured by the gastrointestinal symptom rating scale. Clinicaltrials.gov no: NCT02464150 See the article below for more information, including study results. Source: Gastrojournal.org DOI: http://dx.doi.org/10.1053/j.gastro.2017.10.040
  6. Celiac.com 08/23/2017 - A team of researchers recently set out to assess how many patients with a diagnosis of non-celiac wheat sensitivity (NCWS) still experienced symptoms of wheat sensitivity after an average follow-up time of 99 months. The research team included Antonio Carroccio, Alberto D’Alcamo, Giuseppe Iacono, Maurizio Soresi, Rosario Iacobucci, Andrea Arini, Girolamo Geraci, Francesca Fayer, Francesca Cavataio, Francesco La Blasca, Ada M. Florena, and Pasquale Mansueto. Using data collected from 200 participants from a previous study of non-celiac wheat sensitivity, performed between July and December 2016 in Italy, the team found that 148 of these individuals still followed a strict wheat-free diet. In total, 175 patients (88%) said that they had fewer symptoms after a diagnosis of non-celiac wheat sensitivity and general improvement. Of the 148 patients who adhered strictly to a gluten-free diet, 145 (98%) had reduced symptoms, compared with 30 of 52 patients who did not adhere to a gluten-free diet (58%) (P < .0001). Of the 22 patients who repeated the double-blind, placebo-controlled challenge, 20 reacted to wheat. The numbers and percentages of the 148 non-celiac wheat sensitivity patients on a strict wheat-free diet who reported that the following symptoms recurred after occasional and accidental wheat consumption: Lack of well-being 135 (91%); Tiredness 102 (69%); Foggy mind 68 (46%); Menstrual alterations 54 (36%); Anemia 46 (31%); Weight increase 45 (30%); Joint/muscle pain 35 (24%); Headache 31 (21%); Weight loss 30 (20%); Anxiety 18 (12%); Skin rash 16 (11%); Recurrent cystitis 12 (8%); Depression 10 (7%). From these numbers, the team concludes that non-celiac wheat sensitivity is a persistent condition. Clinicaltrials.gov registration number: NCT02823522. Source: Gastroenterology. DOI: http://dx.doi.org/10.1053/j.gastro.2017.03.034
  7. Celiac.com 10/12/2015 - There's been a good deal of attention devoted to gluten sensitivity in people without celiac disease, but researchers still don't know much about potential risks associated with the condition. A research team recently looked at the prevalence of autoimmune diseases among patients with non-celiac wheat sensitivity (NCWS), and investigated whether they carry antinuclear antibodies (ANA). The research team included A. Carroccio, A. D'Alcamo, F. Cavataio, M. Soresi, A. Seidita, C. Sciumè, G. Geraci, G. Iacono, and P. Mansueto. They are variously affiliated with the DiBiMIS University of Palermo, Palermo, Italy; the department of Internal Medicine at Giovanni Paolo II Hospital in Sciacca, Italy; the DiBiMIS University of Palermo, in Palermo, Italy; the department of Pediatric Gastroenterology in ARNAS Di Cristina Hospital, Palermo, Italy; and the Surgery Department at the University of Palermo in Palermo, Italy. The research team conducted a retrospective study of 131 patients diagnosed with NCWS, 121 of whom were female. The average patient age was 29.1 years, and the study was conducted at 2 hospitals in Italy from January 2001 through June 2011. The team also collected data from 151 patients with celiac disease or irritable bowel syndrome, who served as control subjects. They reviewed patient medical records to identify those with autoimmune diseases. They then conducted a prospective study of 42 patients, 38 of whom were female, with an average age of 34 years, who had been diagnosed with NCWS from July 2011 through March 2014 at 3 hospitals in Italy. For the prospective study, one hundred age- and sex-matched subjects with celiac disease or IBS served as control subjects. The team collected serum samples from all subjects and measured ANA levels using immunofluorescence analysis. Participants completed a questionnaire and the team reviewed patient medical records to identify those with autoimmune diseases. In the retrospective analysis, about 30% of patients with either NCWS or celiac disease developed autoimmune diseases; mainly Hashimoto's thyroiditis, of which there were 29 cases. Compare this with about 4% of IBS who developed an autoimmune disease (P < .001). In the prospective study, 24% of patients with NCWS, 20% of patients with celiac disease, and 2% of patients with IBS developed autoimmune diseases (P < .001). In the retrospective study, serum samples tested positive for ANA in 46% of subjects with NCWS (median titer, 1:80), 24% of subjects with celiac disease (P < .001), and just 2% of subjects IBS (P < .001). In the prospective study, serum samples were positive for ANA in 28% of subjects with NCWS, 7.5% of subjects with celiac disease (P = .02), and 6% of subjects with IBS (P = .005 vs patients with NCWS). From these results, they conclude that positive ANA results are associated with the presence of the HLA DQ2/DQ8 haplotypes (P < .001). Source: Gastroenterology. 2015 Sep;149(3):596-603.e1. doi: 10.1053/j.gastro.2015.05.040.
  8. Celiac.com 07/24/2017 - Are many non-celiac gluten-free eaters actually treating unkown medical conditions? Is the gluten-free movement less a fad than we imagine? Currently, about 3 million Americans follow a gluten-free diet, even though they do not have celiac disease. Known colloquially as "PWAGs," people without celiac disease avoiding gluten. These folks are often painted as fad dieters, or hypochondriacs, or both. Call them what you will, their ranks are growing. According to a study in the journal Mayo Clinic Proceedings, the number of PWAGs tripled from 2009 to 2014, while the number of celiac cases stayed flat. A new study from the Mayo Clinic supports these conclusions. The study derived from data gathered in the National Health and Nutrition Examination Survey, as well as serological tests. There is also a growing body of data that support the existence of non-celiac gluten sensitivities, though the evidence is not conclusive. Moreover, researchers really don't have any idea how many non-celiacs on a gluten-free diet may have legitimate reactions to gluten. The phenomenon has emerged in the past five years in medical literature. For a long time, researchers just assumed that only people with celiac disease would eat a gluten-free diet. About a decade ago, when research into celiac disease and gluten-free dieting began in earnest, says Joseph Murray, a celiac researcher at the Mayo Clinic and an author of the new research, researchers "didn't think to ask why people avoid gluten. When we designed this study 10 years ago, no one avoided gluten without a celiac diagnosis." The latest research by Murray and his colleagues showed that the total number of celiac cases leveled off in the last few years, while more non-celiacs began to avoid gluten for different reasons. Researchers still aren't sure what's driving the trend, and whether it will continue. Part of the increase is doubtless to growing awareness of gluten sensitivity. However, Benjamin Lebwohl, the director of clinical research at Columbia University's Celiac Disease Center, estimates that more than half of the 3.1 million PWAGs noted in this latest study have legitimate gluten sensitivity. "An increasing number of people say that gluten makes them sick, and we don't have a good sense why that is yet," Lebwohl said. "There is a large placebo effect — but this is over and above that." Non-celiac patients with gluten sensitivity often complain of symptoms similar to those of celiacs, such as intestinal problems, fatigue, stomachaches and mental fogginess. And while researchers don't know the reason, clinical studies have shown that these symptoms are often relieved by eliminating dietary gluten. One theory that is gaining some credence is that these people may be sensitive to other irritants, such as FODMAPS, a class of carbohydrates shown to cause gastrointestinal symptoms found in wheat, milk, onions and cheese. Look for more studies into this topic, as researchers seek to nail down answers about celiac disease and gluten-sensitivity, and similar symptoms in non-celiacs. Meantime, the number of people who suspect they have non-celiac gluten sensitivity, and who seek improvement in their symptoms by eliminating gluten from their diets, continues to grow. Source: DailyTribune.com
  9. Celiac.com 09/23/2015 - Wheat products are a key component of human diets worldwide. Despite the many beneficial aspects of consuming wheat products, it is also a trigger for several diseases such as celiac disease, wheat allergy, and non-celiac gluten sensitivity (NCGS). A team of researchers recently set out to examine the relationship between celiac disease, non-celiac gluten sensitivity and irritable bowel syndrome. The research team included M El-Salhy, JG Hatlebakk, OH Gilja, and T. Hausken. They are variously affiliated with the Section for Gastroenterology, Department of Medicine, Stord Hospital, Stord, Norway, the Section for Neuroendocrine Gastroenterology, Division of Gastroenterology, Department of Clinical Medicine, University of Bergen, Bergen, Norway, the National Centre for Functional Gastrointestinal Disorders, Department of Medicine, and the National Centre for Ultrasound in Gastroenterology, Department of Medicine, Haukeland University Hospital, Bergen, Norway. Celiac disease and irritable bowel syndrome (IBS) patients have similar gastrointestinal symptoms, which can result in celiac disease patients being misdiagnosed as having IBS. Therefore, celiac disease should be excluded in IBS patients. A considerable proportion of celiac disease patients suffer from IBS symptoms despite adherence to a gluten-free diet (GFD). The inflammation caused by gluten intake may not completely subside in some celiac disease patients. It is not clear that gluten triggers symptoms in NCGS, but there is compelling evidence that carbohydrates in wheat such as fructans and galactans do. Based on their results, the team feels that it is likely that NCGS patients are a group of self-diagnosed IBS patients who self-treat using a gluten-free diet. Source: Nutr J. 2015 Sep 7;14(1):92. doi: 10.1186/s12937-015-0080-6.
  10. Celiac.com 09/12/2016 - Wheat gluten and related proteins can trigger an autoimmune enteropathy, known as celiac disease, in people with genetic susceptibility. However, some people experience a range of gluten reaction symptoms, but without the classic blood or gut markers for celiac disease. The etiology and mechanism of these symptoms are unknown, and so far, researchers have found no biomarkers to explain the issue. A research team recently set out to determine if sensitivity to wheat in the absence of celiac disease is associated with systemic immune activation that may be linked to some type of enteropathy. The research team included Melanie Uhde, Mary Ajamian, Giacomo Caio, Roberto De Giorgio, Alyssa Indart, Peter H Green, Elizabeth C Verna, Umberto Volta, and Armin Alaedini. They are variously affiliated with the Celiac Disease Center and the Department of Medicine at Columbia University Medical Center, New York, New York, USA, Departments of Medical and Surgical Sciences and Digestive System, Centro di Ricerca Biomedica Applicata (C.R.B.A.), University of Bologna, St. Orsola-Malpighi Hospital, Bologna, Italy, and the Institute of Human Nutrition at Columbia University Medical Center, New York, New York, USA. The study included a group of healthy control subjects, patients with clinical celiac disease, and patients who reported symptoms after wheat consumption, but in whom doctors had ruled out celiac disease and wheat allergy. The team analyzed test samples for markers of intestinal cell damage and systemic immune response to microbial components. Patients with wheat sensitivity showed sharply increased serum levels of soluble CD14 and lipopolysaccharide (LPS)-binding protein, as well as antibody reactivity to bacterial LPS and flagellin. Circulating levels of fatty acid-binding protein 2 (FABP2), a marker of intestinal epithelial cell damage, were much higher in the affected individuals, and correlated with the immune responses to microbial products. Patients with wheat sensitivity who observed a gluten-free diet saw levels of FABP2 and immune activation markers move rapidly toward normal. These findings show a state of systemic immune activation, coupled with a compromised intestinal epithelium, that triggers gastrointestinal symptoms in certain individuals who have wheat sensitivity, but don't have celiac disease. Source: Gut. doi:10.1136/gutjnl-2016-311964
  11. Celiac.com 07/18/2016 - Researchers still don't have a very good understanding about what triggers non-celiac wheat sensitivity. To get a better idea, a team of researchers recently set out to examine the inflammatory response in the rectal mucosa of patients with well-defined non-celiac wheat sensitivity. Specifically, they wanted to look at type 1 innate lymphoid cells in the rectal mucosa of those patients. The research team included Diana Di Liberto, Pasquale Mansueto, Alberto D'Alcamo, Marianna Lo Pizzo, Elena Lo Presti1, Girolamo Geraci, Francesca Fayer, Giuliana Guggino, Giuseppe Iacono, Francesco Dieli, and Antonio Carroccio. They are variously affiliated with the Central Laboratory of Advanced Diagnosis and Biomedical Research (CLADIBIOR), University of Palermo, Palermo, Italy, the Dipartimento di Biopatologia e Biotecnologie Mediche (DIBIMED), University of Palermo, Palermo, Italy, the Dipartimento Biomedico di Medicina Interna e Specialistica (DIBIMIS), University of Palermo, Palermo, Italy, the Surgery Department at the University of Palermo in Palermo, Italy, and with the Pediatric Gastroenterology, ARNAS Di Cristina Hospital, Palermo, Italy 6Internal Medicine, Giovanni Paolo II Hospital, Sciacca (ASP Agrigento), Palermo, Italy. For their study, the team included 22 patients with irritable bowel syndrome (IBS)-like clinical presentation, diagnosed with non-celiac wheat sensitivity by double-blind placebo-controlled challenge. As control subjects, they used eight IBS patients who were not improving on wheat-free diet. Two weeks after each of the subjects consumed 80 grams of wheat daily as part of an oral challenge, the researchers isolated cells from rectal biopsies and thoroughly characterized them using fluorescence-activated cell sorting analysis for intracellular cytokines and surface markers. Analysis of the rectal biopsies of wheat-challenged non-celiac wheat sensitivity patients showed that a significant mucosal CD45+ infiltrate consisted of CD3+ and CD3− lymphocytes, with the latter spontaneously producing more interferon (IFN)-γ than IBS controls. About 30% of IFN-γ-producing CD45+ cells were T-bet+, CD56−, NKP44−, and CD117−, defining them as a type-1 innate lymphoid cells (ILC1). IFN-γ-producing ILC1 cells significantly decreased in 10 patients analyzed 2 weeks after they resumed a wheat-free diet. This study shows that IFN-γ-producing ILC1 cells infiltrate rectal mucosa, promoting the lymphoid cell population, which gives rise to non-celiac wheat sensitivity. Source: Clinical and Translational Gastroenterology, 2016 doi:10.1038/ctg.2016.35
  12. Celiac.com 06/13/2016 - Researchers Umberto Volta, Giacomo Caio, and Roberto De Giorgio, of the Department of Medical and Surgical Sciences at the University of Bologna in Bologna, Italy, recently submitted a letter to the medical journal Gastroenterology. In their letter, the researchers respond to a recent paper, published by Carroccio et al, reporting on the prevalence of autoimmunity (as identified by positivity of antinuclear antibodies [ANA] and associated autoimmune disorders) in non-celiac wheat sensitivity (NCWS) compared with celiac disease and irritable bowel syndrome (IBS). They note that the study results, based on retrospective and prospective data, showed that the prevalence of ANA in NCWS was significantly higher than in celiac disease and IBS (46% in NCWS vs 24% in celiac disease and 2% in IBS, retrospectively; and 28% in NCWS vs 7.5% in celiac disease and 6% in IBS, prospectively). They note also that both retrospective and prospective analysis show autoimmune disorders (mainly autoimmune thyroiditis) in a slightly higher proportion in NCWS (29% vs 24%) than celiac disease (21% vs 20%). Meanwhile, both NCWS and celiac patients showed substantially higher rates of autoimmune disorders than IBS. In both both retrospective and prospective data, ANA showed a strong relation to HLA-DQ2 and -DQ8 in NCWS, whereas these autoantibodies were associated with autoimmune disorders only in the prospective arm. The team found these results from the Carroccio study to be scientific interesting because NCWS, more than better known autoimmune disorders, such as celiac disease, shows a surprisingly high autoimmune profile. They note that celiac disease is a well-established autoimmune condition often marked by different types of autoantibodies and associated autoimmune disorders. Such autoimmune features have not been seen so far in NCWS and the odds of these patients developing autoimmune dysfunction remains unknown. The team's data showed that only 14% of 486 patients with NCWS had an associated autoimmune disorder including thyroiditis, psoriasis, Graves disease, type 1 diabetes mellitus, and atrophic gastritis. In contrast, about 30% of 770 celiac patients showed the same autoimmune manifestations. These findings are in line with previously published data. They point out that another interesting aspect that came out of Carroccio study is the very high rate of ANA in their cohort of NCWS versus celiac disease and IBS patients. The team notes that their own experience shows ANA to be higher in celiac disease than NCWS and IBS (49% vs 37% vs 6%), which indicates a substantial autoimmune profile in celiac disease, compared with the two other conditions. They also note that evidence showing patients with NCWS to have higher rates of ANA compared with IBS is in line with the results presented by Carroccio et al. They conclude their letter by stating that consistent evidence supports a major role of adaptive immunity in celiac disease more than NCWS, and this peculiarity is reflected by a predominant occurrence of autoimmune disorders and autoantibodies (eg, ANA). However, the challenging data shown by Carroccio et al provide the basis to understand whether NCWS, like celiac disease, show a wide array of autoimmune expressions mediated by adaptive mechanisms. They call for further studies to better understand what they term the "intriguing relationship between autoimmunity and NCWS." Source: Gastroenterology. 2016 Jan;150(1):282. doi: 10.1053/j.gastro.2015.08.058. Epub 2015 Nov 23.
  13. Celiac.com 05/08/2015 - While it's true that all people with celiac disease are intolerant to gluten, not all people who are intolerant to gluten have celiac disease. Several studies have confirmed the existence of non-celiac gluten sensitivity (NCGS), a hypersensitivity or form of gluten intolerance that causes numerous symptoms similar to those of celiac disease. There are several key differences between celiac disease and NCGS. NCGS is distinguished from celiac disease by the following factors: No Hereditary Link Unlike celiac disease, NCGS is not hereditary, and shows no genetic component. No Connection with Celiac-related Disorders Unlike celiac disease, NCGS is so far not associated with malabsorption, nutritional deficiencies, or a higher risk of autoimmune disorders or intestinal malignancies. No Immumological or Serological Markers Researchers have, as yet, identified no immunologic mechanisms or serologic markers for NCGS. That means that, unlike with celiac disease, there are no telltale screening tests that can point to NCGS. Absence of Celiac Disease or Wheat Allergy Doctors diagnose NCGS only by excluding both celiac disease, and an IgE-mediated allergy to wheat, and by the continued presence of adverse symptoms associated with gluten consumption. Diagnosing celiac disease can be challenging. Misdiagnosis is common, and final and accurate diagnosis can take years and visits to numerous doctors. Because of these key differences, non-celiac gluten sensitivity is often even more slippery and difficult to confirm than celiac disease, itself. How about you? Do you or someone you know have celiac disease or NCGS? Share your story in our comments section below. Source: US Pharmacist. 2014;39(12):44-48.
  14. Celiac.com 02/08/2016 - When doctors talk about non-celiac gluten sensitivity (NCGS), they are usually talking about people who have gastrointestinal symptoms without enteropathy, and for whom a gluten-free diet (GFD) provides some relief of symptoms. However, doctors don't currently know very much about the pathophysiology of NCGS, its connection to neurological manifestations, or if it is in any way different from the manifestations seen in patients celiac disease. To address this issue, a team of researchers recently set out to take a closer look at the clinical and immunological characteristics of patients presenting with neurological manifestations with celiac disease and those with NCGS. The research team included Marios Hadjivassiliou, Dasappaiah G Rao, Richard A Grìnewald, Daniel P Aeschlimann, Ptolemaios G Sarrigiannis, Nigel Hoggard, Pascale Aeschlimann, Peter D Mooney and David S Sanders. The team compared clinical, neurophysiological, and imaging data from celiac disease patients and NCGS patients who presented with neurological dysfunction, and who had regular assessment and follow up over a 20-year period. The study included 562 out of total 700 patients. The team excluded patients who had no bowel biopsy to confirm celiac disease, no HLA type available, and/or failed to adhere to GFD. All patients presented with neurological dysfunction and had circulating anti-gliadin antibodies. The most common neurological problems were cerebellar ataxia, peripheral neuropathy, and encephalopathy. Out of 562 patients, 228 (41%) had evidence of enteropathy (Group 1, celiac disease) and 334 (59%) did not (Group 2, NCGS). There was a greater proportion of patients with encephalopathy in Group 1 and with a greater proportion of neuropathy in Group 2. The severity of ataxia was about the same between the two groups. Patients in Group 1 showed more severe neuropathy. Patients from both groups responded well to a gluten-free diet. Anti-tissue transglutaminase (TG2) antibodies were found in 91% of patients in Group 1 and in 29% of patients in Group 2. Researchers saw no difference between those patients in Group 2 with HLA-DQ2/DQ8 and those without, or between those with positive TG2 compared to those with negative TG2 antibodies. Both groups showed similar serological positivity for TG6 antibodies, at 67% and 60%, respectively. The results of this study show that patients with celiac disease and NCGS have similar neurological manifestations, which respond well to a gluten-free diet. This suggests that the two conditions share common pathophysiological mechanisms. Source: The American Journal of Gastroenterology , (2 February 2016). doi:10.1038/ajg.2015.434
  15. Celiac.com 01/13/2016 - Researchers are zeroing in on markers for gluten sensitivity in people who don't have celiac disease. So far, there's been scant proof of what causes gluten sensitivity in people who don't have celiac disease. It's been difficult to even pin down the existence of a condition that can be tested and diagnosed. The results of a recent study may change that. The study, from Giovanni Barbara and his team at the University of Bologna, Italy, suggests that inflammation in gluten-sensitive individuals may result from high levels of a molecule called zonulin. Zonulin has been linked to inflammation, and people with celiac disease have been shown to have high levels of zonulin when consuming wheat protein. Symptoms include abdominal pain, bloating, alternating diarrhea or constipation. And there can be other symptoms, including "brain fog," headache, fatigue and joint and muscle pain. Barbara's study found that zonulin levels in gluten-sensitive individuals almost matched those of celiacs. The researchers stress the preliminary nature of the results, but note that this information could lead to testing methods for detecting gluten sensitivity in people who don't have celiac disease. According to gastroenterologist Alessio Fasano of Massachusetts General Hospital in Boston, about 6 percent of the global population may be sensitive to gluten, so any breakthrough in identifying and testing for non-celiac gluten sensitivity could impact tens of millions of people worldwide. Stay tuned for more on zonulin and it's role in non-celiac gluten sensitivity. Source: NPR.ORG
  16. Celiac.com 11/30/2015 - A new study by researchers in Italy shows that only a minority of patients who meet clinical criteria for non-celiac gluten sensitivity actually show symptoms when exposed to gluten in a controlled gluten challenge. Why is that? Researchers haven't had much good information on whether symptoms in people who meet clinical diagnostic criteria for non-celiac gluten sensitivity (NCGS) are specifically triggered by gluten. To provide better information, a team of researchers recently set out to assess gluten sensitivity in patients diagnosed with NCGS. The research team includes B. Zanini; R. Basché; A. Ferraresi; C. Ricci; F. Lanzarotto; M. Marullo; V. Villanacci; A. Hidalgo; and A. Lanzini. They are variously affiliated with Department of Gastroenterology, and the Department of Pathology at the University and Spedali Civili of Brescia, Brescia, Italy, and the Department of Food, Environmental and Nutritional Sciences at the University of Milan, Milan, Italy. For their in a double-blind challenge study, their team looked at 31 females and 4 males without celiac disease, who were following a gluten-free diet (GFD). Participants were randomly broken into groups that received either gluten-containing flour or gluten-free flour for 10 days, followed by a 2-week washout period, followed by a switch in gluten-free/non-gluten-free diets. The main outcome measure was the test subjects' ability to identify which flour contained gluten. Secondary outcome measures were based upon Gastrointestinal Symptoms Rating Scale (GSRS) scores. Only 12 participants (34%) classified as having NCGS correctly pointed out the gluten-containing flour. These participants showed much higher average GSRS dimension scores following gluten challenge compared to baseline. The team measured scores for: pain, 1.7 ± 0.8 vs. 2.6 ± 1.0; reflux, 1.6 ± 0.5 vs. 2.2 ± 0.9; indigestion, 1.9 ± 0.7 vs. 3.2 ± 1.1; diarrhea, 1.6 ± 0.7 vs. 2.9 ± 1.5 and constipation, 1.9 ± 0.9 vs. 2.9 ± 1.3. Seventeen participants, nearly half, erroneously considered the gluten-free flour to contain gluten. Their average GSRS dimension scores were significantly higher following gluten-free flour challenge compared to baseline. The scores were: pain, 1.6 ± 0.9 vs. 3.0 ± 0.9; reflux, 1.4 ± 0.5 vs. 2.3 ± 1.1; indigestion, 2.0 ± 1.1 vs. 3.7 ± 1.1; diarrhea, 1.6 ± 0.7 vs. 3.0 ± 1.2 and constipation, 1.6 ± 0.9 vs. 2.6 ± 1.3. The other six participants (17%) were unable to distinguish between the flours. Based on this study, only about one in three patients with clinical non-celiac gluten sensitivity showed an adverse reaction to gluten. Clearly, more needs to be done to determine the exact nature of non-celiac gluten-sensitivity, and to determine what, if anything, may be driving these adverse reactions that can be triggered by non-gluten containing foods. Source: Aliment Pharmacol Ther. 2015;42(8):968-976.
  17. Celiac.com 11/25/2015 - People with Non-Celiac Gluten Sensitivity (NCGS) suffer intestinal and non-intestinal symptoms when they consume gluten-containing food, but they do not have either celiac disease or wheat allergy. Because there is currently no known NCGS biomarker, it is important to develop reliable standard procedures to confirm NCGS diagnosis. A recent scientific paper examines expert recommendations on how the diagnostic protocol should be performed for the confirmation of NCGS. The researchers contributing to the paper include Carlo Catassi, Luca Elli, Bruno Bonaz, Gerd Bouma, Antonio Carroccio, Gemma Castillejo, Christophe Cellier, Fernanda Cristofori, Laura de Magistris, Jernej Dolinsek, Walburga Dieterich, Ruggiero Francavilla, Marios Hadjivassiliou, Wolfgang Holtmeier, Ute Körner, Dan A. Leffler, Knut E. A. Lundin, Giuseppe Mazzarella, Chris J. Mulder, Nicoletta Pellegrini, Kamran Rostami, David Sanders, Gry Irene Skodje, Detlef Schuppan, Reiner Ullrich, Umberto Volta, Marianne Williams, Victor F. Zevallos, Yurdagül Zopf, and Alessio Fasano. They are variously affiliated with 26 research institutions worldwide. They have come up with a series of recommendations known as the Salerno Experts' Criteria. Under that criteria, a comprehensive diagnosis should measure the patient's clinical response to the gluten-free diet (GFD) and assess the effect of a gluten challenge after a period of treatment with the GFD. Such an evaluation uses a self-administered instrument that relies on a modified version of the Gastrointestinal Symptom Rating Scale. In this way, the patient identifies one to three main symptoms that are quantified on a rating scale ranging from 1 to 10. Patients then follow a double-blind placebo-controlled gluten challenge by ingesting 8 grams of gluten per day for a one-week challenge followed by a one-week washout of strict GFD, and then moving to the second one-week challenge. The gluten-challenge should contain cooked, homogeneously distributed gluten. A variation of at least 30% of one to three main symptoms between the gluten and the placebo challenge should be seen to differentiate between a positive and a negative result. These guidelines are designed to help the clinician to reach a firm and positive diagnosis of NCGS and facilitate the comparisons of different studies. Source: Am J Gastroenterol. 2015 Sep 29. doi: 10.1038/ajg.2015.296.
  18. Celiac.com 11/11/2015 - If you ask me, it doesn't seem that far-fetched that some people who do not have celiac disease could still have adverse reactions to gluten. However, actually proving that scientifically continues to be challenging. Take the case of the research team that recently conducted a double-blind, placebo-controlled, cross-over, gluten-challenge trial of patients with suspected non-celiac gluten sensitivity. The team wanted to try to get an idea of the number of self-diagnosed patients with non-celiac gluten sensitivity. The team enrolled 53 women and 8 men referred to two Italian centers between October 2012 and November 2013 for suspected non-celiac gluten sensitivity. The subjects were randomly assigned to receive 4.375-g gluten or rice starch per day via gastro-soluble capsules for 1 week after a 1-week run-in period, and followed by a 1-week washout period and cross-over to the other group. The team chose rice starch as the placebo because it is "the most readily absorbable of the complex carbohydrates, and thus less fermentable, in the intestinal tract." They used a daily questionnaire to chart any changes in overall symptom scores, and conducted analysis with a per-protocol approach. A total of 59 patients completed the trial, while two withdrew due to "intolerable symptoms." Overall, one week of gluten consumption increased overall symptom severity compared with one week of placebo (P = .034), including abdominal bloating (P = .04), abdominal pain (P = .047), foggy mind (P = .019), depression (P = .02) and aphthous stomatitis (P = .025). Perplexingly, the team found that "most patients showed approximately equal degrees of overall symptoms with either gluten or placebo, although overall symptoms were worsened significantly by gluten in comparison with placebo." Got that? Significant numbers of the subjects reacted to the placebo. The short conclusion is that these results "do not represent crucial evidence in favor of the existence of this new syndrome." However, and it's a big however, the results aren't quite as clear as they might appear. In an accompanying editorial, Benjamin Lebwohl, MD, from the Celiac Disease Center at Columbia University, and Daniel A. Leffler, MD, MS, from Beth Israel Deaconess Medical Center write: The "overall positive result was driven by a minority of patients, whereas the rest had no (or at most a modest) worsening compared with placebo." They add that: "These findings can be a Rorschach test of sorts, in which the viewer draws interpretations that are based on his or her prior beliefs about NCGS. … It is therefore not surprising that this trial, like its predecessors, seems only to contribute to the uncertainty about NCGS." So, basically, there's no clear word on the existence or non-existence of non-celiac gluten sensitivity, or on the number of people who might suffer from it. Stay tuned for more studies, and more information as researchers attempt to sort it all out. Source: CGHJournal.org
  19. Celiac.com 03/23/2015 - There's been a bit of ping-ponging going on about the status of non-celiac gluten sensitivity as a valid medical condition. Studies have yielded conflicting results, with some supporting, and others negating, the existence of non-celiac gluten-sensitivity. So what's the deal? Does non-celiac gluten sensitivity exist, or not? Researchers and clinicians continue to debate whether people without celiac disease or wheat allergy who consume gluten can experience intestinal and extra-intestinal symptoms attributable to non-celiac gluten sensitivity (NCGS). Taking the latest stab at the problem, a team of researchers recently conducted a randomized, double-blind, placebo-controlled, cross-over trial to determine the effects of administration of low doses of gluten to subjects with suspected NCGS. The research team included A. Di Sabatino, U. Volta, C. Salvatore, P. Biancheri, G. Caio, R. De Giorgio, M. Di Stefano, and G. R. Corazza. They are variously affiliated with the First Department of Internal Medicine at St Matteo Hospital Foundation at the University of Pavia in Pavia, Italy, and with the Department of Medical and Surgical Sciences at St Orsola-Malpighi Hospital at the University of Bologna in Bologna, Italy. For their study, the team enrolled 61 adults without celiac disease or wheat allergy, but who believe that eating gluten-containing food to be causing of their intestinal and extra-intestinal symptoms. The team randomly assigned participants to groups that received either 4.375 g/day gluten or rice starch (placebo) for 1 week, each via gastro-soluble capsules. Study subjects spend one week on a gluten-free diet, and then switched groups. The primary outcome was the change in overall (intestinal and extra-intestinal) symptoms, determined by established scoring systems, between gluten and placebo intake. A secondary outcome was the change in individual symptom scores between gluten vs placebo. Per-protocol analysis of data from the 59 patients who completed the trial shows that intake of gluten significantly increased overall symptoms compared with placebo (P=.034). Among the intestinal symptoms, abdominal bloating (P=.040) and pain (P=.047) were significantly more severe when subjects received gluten than placebo. Among the extra-intestinal symptoms, foggy mind (P=.019), depression (P=.020), and aphthous stomatitis (P=.025) were also worse when subjects received gluten than placebo. In this cross-over trial, subjects with suspected NCGS saw significantly more severe symptoms during 1 week of intake of small amounts of gluten, compared with placebo. So, at least for now, the NGCS ball seems to be back in the court that considers it a valid medical condition. Source: Clin Gastroenterol Hepatol. 2015 Feb 19. pii: S1542-3565(15)00153-6. doi: 10.1016/j.cgh.2015.01.029. Clinical trial no: ISRCTN72857280.
  20. Celiac.com 06/11/2015 - Non-celiac gluten sensitivity (NCGS) is a somewhat controversial emerging disorder. There is no current medical consensus regarding its criteria, and study data have been inconclusive. Many alternative health practitioners recommend gluten-free diets for people who claim to be sensitive to gluten, but do not have celiac disease. Despite numerous reports of people without celiac disease experiencing celiac-like symptoms when eating gluten, there are currently no clear diagnostic guidelines for NCGS. NCGS is still diagnosed by excluding celiac disease, and finding no reliable celiac biomarkers. A team of researchers recently set out to evaluate the prevalence, diagnostic exclusion of celiac disease and the efficacy of a gluten-free diet (GFD) for NCGS patients. The research team included J. Molina-Infante; S. Santolaria; D. S. Sanders; and F. Fernández-Bañares. They are variously affiliated with the Department of Gastroenterology, Hospital San Pedro de Alcantara, Caceres, Spain, the Department of Gastroenterology, Hospital San Jorge, Huesca, Spain, the Department of Gastroenterology, Royal Hallamshire Hospital, Sheffield Teaching Hospitals, Sheffield, UK, the Department of Gastroenterology, Hospital Universitario Mutua Terrassa, Barcelona, Spain, and with CIBERehd, Barcelona, Spain. Their team conducted a PubMed search through December 2014. They defined NCGS as self-reported gluten intolerance, negative celiac serology and absence of villous atrophy. They also included studies evaluating the impact of a GFD on patients with irritable bowel syndrome (IBS). They found that rates of NCGS (0.5–13%) varied considerably. Seventeen studies met the inclusion criteria for NCGS. The studies included 1561 patients, 26 of whom were children. HLA haplotypes could not be linked to histology, either by normal or lymphocytic enteritis (LE)] in 1,123 NCGS patients. Nearly half (44%) of NCGS patients tested positive for HLADQ2/DQ8 haplotypes. Using advanced diagnostic techniques that combine LE and HLADQ2/DQ8 haplotypes, the team reclassified 39 (20%) of 189 NCGS cases as celiac disease. They found a higher than expected family history of celiac disease and autoimmune disorders in NCGS patients. For HLADQ2 positive diarrhea-predominant IBS patients, a GFD resulted in variable, but significantly improved stool frequency. Rates of NCGS are extremely variable. A subset of NCGS patients might actually be part of what many researchers refer to as celiac disease "light." The long term benefit of a gluten-free diet for NCGS patients is currently unclear, but certainly the diet, if well-balanced, would not cause any issues. The researchers do note that HLADQ2 positive diarrhea-type IBS patients might gain symptom improvement from a gluten-free diet. Clearly more studies are needed to determine if NCGS is a bona fide medical condition, as many suspect. Until then, there is very little treatment available from medical practitioners, and many people with self-diagnosed NCGS will doubtless be left to self-treatment. For many, this will include avoiding gluten. Do you, a loved one, or someone you know have gluten-sensitivity without celiac disease? Share your thoughts and comments below. Source: Aliment Pharmacol Ther. 2015;41(9):807-820.
  21. Celiac.com 06/04/2015 - Some researchers feel that people who self report non-celiac gluten sensitivity (SR-NCGS) and also follow a gluten-free diet might actually fall within the spectrum of irritable bowel (IBS). Interestingly, recent reports suggest that large numbers of people with inflammatory bowel disease (IBD) also follow a gluten-free diet. A research team recently assessed the relationship between IBD and self-reported non-celiac gluten sensitivity (SR-NCGS). The team included I.Aziz, F. Branchi, K. Pearson, J. Priest, and D.S. Sanders. They are variously affiliated with the Department of Gastroenterology, Royal Hallamshire Hospital, Sheffield Teaching Hospitals, Sheffield, United Kingdom; and the Gastroenterology and Endoscopy Unit in the Department of Pathophysiology and Transplantation at the Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Department of Pathophysiology and Transplant, Università degli Studi di Milano in Milan, Italy. To screen for SR-NCGS and the use of a GFD, they used a cross-sectional questionnaire in 4 groups: ulcerative colitis (n = 75), Crohn's disease (n = 70), IBS (n = 59), and dyspeptic controls (n = 109). They also looked at diagnostic outcomes for IBD in 200 patients presenting with SR-NCGS. A total of 25 out of 59 patients with IBS (42.4%), and 40 out of 145 patients (27.6%) with IBD reported SR-NCGS. That number was just 19 of 109 for dyspeptic control subjects (17.4%). As far a gluten-free diet, currently, 11.9% of patients with IBS, and 6.2% of those with IBD are following a gluten-free diet, as compared with just 0.9% for dyspeptic controls; P = 0.02. For the purposes of of this study, the team made no differences between ulcerative colitis and Crohn's disease. However, 40.9% of Crohn's disease patients with SR-NCGS suffered from stricturing disease, compared with 18.9% for Chrohn's patients without SR-NCGS; (P = 0.046). Crohn's disease patients with SR-NCGS showed higher overall scores on the Crohn's Disease Activity Index (228.1 versus 133.3, P = 0.002) than those without SR-NCGS. The team analyzed 200 cases presenting with SR-NCGS, and found that 197 of them, or 98.5% were most likely diet-related IBS. However, 3 of the SR-NCGS patients (1.5%) actually had IBD, with all of the associated alarm symptoms, and/or abnormal blood parameters. The results show that SR-NCGS is not exclusive to IBS, but is also seen in some patients with IBD, which is a more severe, more debilitating condition. The team is calling for randomized studies to further delineate the nature of this relationship and clarify whether a gluten-free is appropriate for certain IBD patients. Source: Inflamm Bowel Dis. 2015 Apr;21(4):847-53. doi: 10.1097/MIB.0000000000000335.
  22. Celiac.com 05/01/2015 - In his article titled "Against the Grain," published in the November 3, 2014 issue of The New Yorker, Michael Specter likens the Gluten and Allergen Free Expo to "a travelling medicine show" in the first paragraph (1). Just in case a reader was half asleep and missed the bias embodied in that phrase, Specter ends the same first paragraph with: "There was even gluten-free dog food." It's hard to miss the harsh, cynical tone, and it is a shame that he usurped the name of Melissa Diane Smith's informative book to title his invective. What, we must wonder, is the source of his bias? He does offer some detailed explanations of the bond between glutenin and gliadin, and how carbon dioxide from the fermentation process is trapped as bread and other pastry rises, making light, fluffy bread and pastry. He has done some detailed, even impressive investigation into cooking with gluten. However, he also asserts that wheat-breeding practices haven't induced any changes that might explain the increased incidence of celiac disease since World War II. He then goes on to say: "But something strange is clearly going on. For reasons that remain largely unexplained, the incidence of celiac disease has increased more than fourfold in the past sixty years." Mr. Specter acknowledges that celiac disease is on the rise and, according to Specter, there have not been any major changes to the genetics of wheat that might explain this increase. This perspective appeared in a very prestigious, highly regarded publication—The New Yorker. Many people will believe these claims just because of where they were published. And here is the problem I have with that. Mr. Specter has the genetic information all wrong: Norman Borlaug was awarded a plethora of honors for his work in developing more than 6,000 new wheat hybrids, which included several strains of disease resistant, semi-dwarf wheat that increased per-acre yields by seven to ten fold, thereby leading to wheat independence in a number of third world nations. For these scientific accomplishments he was awarded the Nobel Peace Prize, the Presidential Medal of Freedom, and a Congressional Gold Medal. Several books have been written about Dr. Borlaug and his achievements, and several foreign governments, science academies, and institutions have bestowed him with awards, honorary degrees and memberships. Borlaug has even had streets, university wings, and assorted other places and artifacts named after him and has even been mentioned in popular television shows. He has been called the father of the "green revolution" and has enjoyed very widespread recognition for having been instrumental in saving many millions of lives through increasing the world's food supply in the form of wheat. It is my belief that this venerable and compassionate man of science deserved every honor that was bestowed on him (2). However, I also think that it besmirches Dr. Borlaug's memory when Specter dismisses all those genetic changes to wheat as a possible factor in "the growing number of cases" of celiac disease based on the statement by Dr. Donald Kasarda that he was unable to find "evidence that a change in wheat-breeding practices might have led to an increase in the incidence of celiac disease". One person's failure to find evidence for something does not prove the absence of that phenomenon. Mr. Specter also quotes Dr. Joseph Murray, the very popular and famous (at least in the gluten sensitive community) gastroenterologist at the Mayo Clinic, as an expert in wheat genetics, and quotes Dr. Murray as asserting that wheat genetics haven't changed much over the past fifty years. I'm skeptical that Dr. Murray would profess expertise in the realm of cereal grain genetics. Regardless of whether this is Mr. Specter's construct, or Dr. Murray did actually make this claim to expertise in wheat genetics and the assertion that little has changed in wheat genetics since World War II, the statement is at least incorrect when it comes to wheat genetics. The conundrum Mr. Specter has created by ignoring Dr. Borlaug's work sets up an article in which he attacks what he calls "gluten anxiety". He says that "nearly twenty million people contend that they regularly experience distress after eating products that contain gluten." The implication is clear. Mr. Specter would have us believe that these people are confused about changes to how they feel, and/or whether those changes resulted from switching to a gluten-free diet—apparently all twenty million of them are so confused that they now need Mr. Specter to lead them out of the darkness of their own self-delusion, and begin to appreciate that wheat, in its present genetic form, has been consumed for at least 10,000 years and it's "a staple food that has sustained humanity for thousands of years". I'd like to point out that the Levant, where wheat was first grown, was not host to all of humanity at that, or any other time. Many humans, after leaving Africa about 85,000 years ago, evolved in a variety of environmental niches where gluten grains have not been available until quite recently. And there are many genetic variations of wheat. Which ones, I wonder, is Mr. Specter saying have been with us for so long? Contrary to his assertions, it is this variability that serves as one of the greatest barriers to the development of genetic strains of wheat that are "safe" for consumption by people with celiac disease. Dr. Sachin Rustgi, one of the scientists who is trying to develop such a safe wheat also said that: "Different celiac patients are sensitive to different 'gluten' proteins (prolamins). If one feeds peripheral blood cells sampled from a patient or a small group of patients (from a specific geographical location) with gluten proteins derived from a wheat genotype, it is expected either to see a reaction (monitored by the production of interferon gamma) or no apparent effect. But in the latter case it does not mean that the wheat genotype is non-toxic to all celiac patients" (3). Since different proteins or protein fractions (peptides) are recognized by different celiac patients' immune systems, there is an enormous number of peptides and proteins that are potentially toxic to at least some people with celiac disease. Extrapolating from that point, people with non celiac gluten sensitivity may well be reacting to any of the proteins or derivative peptides from any of the multitudinous variants of wheat. Mr. Specter also makes the claim that: "Humans have been eating wheat, and the gluten in it, for at least ten thousand years." Yet the geneticist, Dr. Martin Richards, and his colleagues report that about three quarters of Europeans are descendants of hunter-gatherers, rather than the early farmers from the Levant (4). So a large majority of people of European descent have not been eating cereal grains for more than 10,000 years. Just how long they have been consuming them depends on where they lived in Europe, which may explain the variability in the frequency of celiac disease across Europe. It is worthy of note that incidence of celiac disease is particularly increased in Scandanavia, Scotland, and Ireland, where climate and topography combined to make cereal grain cultivation more difficult. Thus, one might reasonably interpret this to suggest that these populations experienced limited past exposure to these grains. It is only with modern transportation systems, combined with the abundant excesses of wheat made possible by the work of Dr. Norman Borlaug and many others, in addition to the erroneous belief that wheat is a healthy food, that we now have almost worldwide over-consumption of gluten grains. Increased consumption has led to the increased frequency of celiac disease in these relatively grain-naive populations. Much of the rest of the world's populations have only recently begun to eat these grains. Even in the lowlands of England, where grain cultivation is relatively easy and successful, these grains have only been there for the about the last 5,000 years. Worldwide exposure to these grains varies somewhere between several thousands of years to less than 100 years. And what data supports the notion that even 10,000 years is sufficient time for humans to make the complex adaptation to eating them? Dr. Marlene Zuk has implicitly made such a claim, through reporting on much more rapid adaptations to adult consumption of dairy products (5). However, since we are mammals, and are almost universally able to consume human milk as infants, the adaptation required for the digestion of lactose into adulthood is, comparatively speaking, quite minor. Still, more than two thirds of the world's populations are unable to do so. Mr. Specter's resistance to recognizing gluten as a dietary hazard appears to be rooted in bias, rather than a thoughtful examination of the relevant data. It also appears that Mr. Specter either failed to learn, or failed to mention, that humans do not have the necessary complement of digestive enzymes needed to break some of the bonds between amino acids in the storage proteins of gluten grains, so we can fully digest them (6). Surely, if we were fully adapted to eating them, we should be able to digest these proteins. Nonetheless, Mr. Specter repeatedly disparages and dismisses the disease entity of non-celiac gluten sensitivity, and goes on to say: "The most obvious question is also the most difficult to answer: How could gluten, present in a staple food that has sustained humanity for thousands of years, have suddenly become so threatening?" Of course, this question is only difficult to answer if one ignores the many genetic manipulations of gluten grains and a substantial body of medical research into a variety of human ailments. For instance, Dr. Curtis Dohan and his colleagues were the first to publish a report on the connection between some cases of schizophrenia and gluten grains titled "Relapsed schizophrenics: more rapid improvement on a milk- and cereal-free diet" in 1969 (7). This research was conducted in a locked psychiatric ward. Similarly, seven years later, Singh and Kay followed with publication of an affirming research report that, using a different study design, identified wheat as a pathogenic factor in some cases of schizophrenia (8). This work was also conducted in a locked ward where total control of the patients' food intake could be controlled. Further, neither of these reports asserted a connection between celiac disease and schizophrenia. Over the following two decades, several reports, based on sloppy, poorly designed research, were published in the medical literature, and the notion that gluten grains could be a factor in schizophrenia was quickly forgotten. Mr. Specter would have been pleased with these latter reports. Another critic of Dr. Dohan's work, Dr. Donald Kasarda, a cereal scientist at the USDA, was quite happy to make statements such as: "Dohan wasn't much of a scientist" (9). Yet it was this same individual, Don Kasarda, whose name appeared as one of the authors of a report that asserted that a subset of schizophrenic patients mount a novel immune reaction against gluten (10). Dr. Dohan and his colleagues discovered a disease process, and an effective treatment for it, forty years ahead of the group that Dr. Kasarda worked with. Yet the earlier work was unscientific—until the publication of the work led by Dr. Samaroo, with contributions from Dr. Kasarda. Did Dr. Dohan suddenly become competent? Or is there another, more reasonable explanation? I don't understand the contradictions here. I'm also struggling to understand Mr. Specter's quoting Dr. Kasarda in his attack on non celiac gluten sensitivity. After all, Dr. Kasarda was one of the authors who published the report of non celiac gluten sensitivity in a subset of schizophrenic patients. On another front, Dr. Marios Hadjivassiliou and colleagues have been reporting, over the last twenty years, on celiac disease and non-celiac gluten sensitivity in connection with a variety of neurological diseases. These include depression, cerebral palsy, neurological dysfunction, alcohol induced cerebellar degeneration that results in gluten sensitivity, ataxia, ganglionopathy, a gluten induced condition that mimicks amyotrophic lateral sclerosis, inflammatory myopathy, chorea, headaches, balance disturbances, and neuromuscular disorders. They have also reported that antibodies against one of the protein families in gluten are found in the brain (IgG class anti-gliadin antibodies) and they also attack brain tissues (11). Others have reported connections between gluten and seizure disorders in non-celiac gluten sensitivity (12), and cerebral calcifications with seizures (13). Further, several forms of gluten induced brain damage have been reported in the context of celiac disease, which suggests a similar dynamic for those with non-celiac gluten sensitivity and brain damage. Gluten induced brain disorders include headache/migraine, attention-deficit/hyperactivity disorder, epileptic seizures, mental retardation, cerebellar ataxia and behavior disorders (14) in the context of celiac disease. Any and all of these may also suggest a similar dynamic for those with NCGS. I have worked with learning disabled students who have shown remarkable recoveries on a gluten-free diet, similar to those described by Alexandra Blair, in her 2003 Times article about dyslexic children who improved enormously on a gluten-free diet (15). Unfortunately, these data were not published in the peer reviewed literature, so they are unlikely to persuade researchers to investigate this matter further. Nonetheless, given the data on gluten's impact on neurological and brain tissues, it does seem very possible that many learning disabilities are, at least partly, the result of non-celiac gluten sensitivity, and that they may benefit from gluten avoidance. Time and space limitations prevent me from exploring the research that identifies the psychoactive properties of protein fractions in wheat, first identified by Christine Zioudrou et al, in her 1979 publication (16), or the Hudson and colleagues' report in 1976 showing that a single subgroup of gluten proteins, called gliadins, are toxic to any of a wide variety of human cells (17). Yet Mr. Specter, calling it "gluten anxiety" would have us dismiss all of this and much, much, more peer reviewed research that identifies gluten as toxic to many people who do not have celiac disease. It has never been clear to me why people such as Mr. Specter are quite willing to attack new ideas and discoveries that others have made on their quest for improved health. The attackers seem to want to mock those of us who have found an answer for ourselves. He interviewed several people, whom he quoted in his article, who were just convinced that they felt better when avoiding gluten. Mr. Specter derides those gluten sensitive individuals who were generous enough with their time to allow him to interview them, apparently at the Gluten Free Expo he attended, then compared with "a travelling medicine show". It is difficult to tell whether Mr. Specter was making news or reporting it when he interviewed these people. Please recall the fall issue of the Journal of Gluten Sensitivity, in which I explored the flaws of the research by Dr. Biesiekierski and colleagues in Australia (18). Mr. Specter cites Professor Gibson, one of the authors of the same study, as one of his sources for discrediting the notion of non-celiac gluten sensitivity. Mr. Specter goes on to present himself as having a superior insight into the issue of non-celiac gluten sensitivity, attacking Dr. William Davis, cardiologist and author of the popular book, Wheat Belly (19), and Dr. David Perlmutter, a neurologist and author of the similarly popular book, Grain Brain (20). Are we to ignore the now thousands of researchers whose peer reviewed reports are now characterizing non-celiac gluten sensitivity as a disease entity? And should we ignore the scores of popular books asserting the same thing? Or should we ignore Mr. Specter and the flawed research from Australia? I know what I'm going to do. Sources: Specter M. Against the Grain. The New Yorker. Nov 3, 2014. http://en.wikipedia.org/wiki/Norman_Borlaug Adams S. Discussion with Assistant Research Professor Sachin Rustgi on the genetic modification of wheat to make it safe for celiacs. Journal of Gluten Sensitivity. 2014; 13(2): L11-14. Richards M, Macaulay V, Hickey1 E, Vega1 E, Sykes B, Guida V, Rengo C, Sellitto D, Cruciani F, Kivisild T, Villems R, Thomas M, Rychkov S, Rychkov O, Rychkov Y, Gölge M, Dimitro D, Hill E, Bradley D, Romano V, Calì F, Vona G, Demaine S, Papiha S, Triantaphyllidis C, Stefanescu G, Hatina J, Belledi M, Di Rienzo A, Novelletto A, Oppenheim A. Tracing European Founder Lineages in the Near Eastern mtDNA Pool. American Journal of Human Genetics, 2000; 67; 5: 1251–1276. Zuk M. Paleofantasy. Norton, NY: 2013. Kagnoff M. Diagnosing Celiac Disease. CSA/USA, Seattle, WA., Oct. 3-5, 1997. Dohan F, Grassberger J, Lowell F, Johnson H, Arbegast A. "Relapsed schizophrenics: more rapid improvement on a milk- and cereal-free diet" British Journalof Psychiatry. 1969; 115: 595-596. Singh M & Kay S.: 1976, "Wheat gluten as a Pathogenic factor in Schizophrenia" Science. 1976: 191; 401-402. Kasarda, D. private communication. Samaroo D, Dickerson F, Kasarda DD, Green PH, Briani C, Yolken RH, Alaedini A. Novel immune response to gluten in individuals with schizophrenia. Schizophr Res. 2010, May;118(1-3):248-55. Hadjivassiliou M1, Mäki M, Sanders DS, Williamson CA, Grünewald RA, Woodroofe NM, Korponay-Szabó IR.Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia.Neurology. 2006 Feb 14;66(3):373-7. Bruni O, Dosi C, Luchetti A, Della Corte M, Riccioni A, Battaglia D, Ferri R. An unusual case of drug-resistant epilepsy in a child with non-celiac gluten sensitivity.Seizure. 2014 Sep;23(8):674-6. Calvani M Jr1, Parisi P, Guaitolini C, Parisi G, Paolone G.Latent coeliac disease in a child with epilepsy, cerebral calcifications, drug-induced systemic lupus erythematosus and intestinal folic acid malabsorption associated with impairment of folic acid transport across the blood-brain barrier.Eur J Pediatr. 2001 May;160(5):288-92. Diaconu G, Burlea M, Grigore I, Anton DT, Trandafir LM Celiac disease with neurologic manifestations in children. Rev Med Chir Soc Med Nat Iasi. 2013 Jan-Mar;117(1):88-94.) Blair A. Wheat-free diet gives food for thought. The Times. (of London) June 12, 2004. Zioudrou C, Streaty RA, Klee WA. Opioid peptides derived from food proteins. The exorphins. J Biol Chem. 1979 Apr 10;254(7):2446-9. Hudson, D., Purdham, D., Cornell, H., Rolles, C. Non-specific cytotoxicity of wheat gliadin towards cultured human cells. The Lancet February 14, 1976. 339-341. Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology. 2013 Aug;145(2):320-8.e1-3. Davis W. Wheat Belly. Rodale Inc. NY, 2011. Perlmutter D. Grain Brain. Little, Brown & co. NY, 2013.
  23. Celiac.com 12/15/2014 - Non-celiac gluten sensitivity (NCGS), aka `wheat sensitivity’ (NCWS), is currently included in the spectrum of gluten-related disorders. Many people with celiac disease suffer from low bone mass density, but there has been no good data on low bone mass density in people with NCWS. A team of researchers recently set out to determine rates of low bone mass density in NCWS patients and to search for correlations with other clinical characteristics. The researchers included Antonio Carroccio, Maurizio Soresi, Alberto D'Alcamo, Carmelo Sciumè, Giuseppe Iacono, Girolamo Geraci, Ignazio Brusca, Aurelio Seidita, Floriana Adragna, Miriam Carta and Pasquale Mansueto. For their prospective observation study, the team assessed 75 NCWS patients (63 women; median age 36 years) with irritable bowel syndrome (IBS)-like symptoms, along with control groups of 65 patients with IBS and 50 with celiac disease. The team recruited patients from two Internal Medicine Departments. The diagnoses of NCWS were established using an elimination diet and double-blind placebo controlled wheat challenge. The team determined bone mass density in all subjects using Dual Energy X-Ray Absorptiometry (DXA), in addition to assessing all subjects for duodenal histology, HLA DQ typing, body mass index, and daily calcium intake. The double-blind placebo controlled wheat challenge revealed that 30 of the 75 NCWS patients suffered sensitivity to multiple foods. Osteopenia and osteoporosis frequency increased from IBS to NCWS and to celiac disease (P <0.0001). Thirty-five of the patients with NCWS (46.6%) showed osteopenia or osteoporosis. Low bone mass density was related to low body mass index and multiple food sensitivity. Levels of daily dietary calcium intake were significantly lower in NCWS patients than in control subjects with IBS. The study showed that patients with NCWS suffered from higher rates of bone mass loss; which correlated with low body mass index, and was more frequent in NCWS patients who showed sensitivity to multiple foods. The team also found that patients with NCWS generally had a low daily intake of dietary calcium. Source: BMC Medicine 2014, 12:230. doi:10.1186/s12916-014-0230-2
  24. Celiac.com 09/23/2013 - Patients with non-celiac gluten sensitivity (NCGS) do not have celiac disease, but see an improvement in symptoms when they adopt gluten-free diets. A team of researchers recently investigated the specific effects of gluten after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates (fermentable, oligo-, di-, monosaccharides, and polyols [FODMAPs]) in patients with suspected NCGS. The research team included Jessica R. Biesiekierski, Simone L. Peters, Evan D. Newnham, Ourania Rosella, Jane G. Muir, and Peter R. Gibson. The team performed a double-blind cross-over trial of 37 subjects (aged 24−61 y, 6 men) with NCGS and irritable bowel syndrome (based on Rome III criteria), but not celiac disease. They assigned study participants randomly to groups given a 2-week diet of reduced FODMAPs, and were then placed on high-gluten (16 g gluten/d), low-gluten (2 g gluten/d and 14 g whey protein/d), or control (16 g whey protein/d) diets for 1 week, followed by a washout period of at least 2 weeks. The researchers then evaluated serum and fecal markers of intestinal inflammation/injury and immune activation, and indices of fatigue. The team then crossed twenty-two participants over to groups receiving gluten (16 g/d), whey (16 g/d), or control (no additional protein) diets for 3 days, using visual analogue scales to evaluate symptoms. They found that gastrointestinal symptoms consistently and significantly improved for all patients during reduced FODMAP intake, but significantly worsened to a similar degree when their diets included gluten or whey protein. The team saw gluten-specific effects in just 8% of study subjects. They saw no diet-specific changes in any biomarker. During the 3-day re-challenge, participants’ symptoms increased by similar levels among groups. Gluten-specific gastrointestinal effects were not reproduced. An order effect was observed. A placebo-controlled, cross-over re-challenge study showed no evidence of specific or dose-dependent effects of gluten in patients with NCGS placed diets low in FODMAPs. Source: Gastroenterology, Volume 145, Issue 2, Pages 320-328.e3, August 2013. More info on the FODMAP diet from Stanford Univerisity.
  25. Celiac.com 08/25/2014 - Numerous people without celiac disease claim to suffer from celiac-like gastrointestinal symptoms when they consume wheat, rye or barley products, and claim that avoiding these products makes them feel better. However, even though many people make this claim, this is largely a self-reported condition. Some data have supported the idea of gluten sensitivity, but the most recent and more complete data seem to indicate that the real culprit might not be gluten, but fermentable, poorly absorbed short-chain carbohydrates known as FODMAPs. In fact the same researcher whose early data supported the idea of non-celiac gluten sensitivity also headed the follow-up study that showed no effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. In this third study, that researcher, Peter Gibson at Monash University in Canada set out to assess patients who believe they have NCGS. The study team included Jessica R. Biesiekierski, PhD, RN; Evan D. Newnham, MD, FRACP; Susan J. Shepherd, PhD, APD; Jane G. Muir, PhD, APD; and Peter R. Gibson, MD, FRACP. They are variously affiliated with the Department of Gastroenterology, Eastern Health Clinical School, and the Department of Gastroenterology, Central Clinical School at Monash University, The Alfred Hospital in Melbourne, Australia, and with the Translational Research Center for Gastrointestinal Disorders, Herestraat in Leuven, Belgium. The team put out advertisements calling for adults who believed they had non-celiac gluten sensitivity (NCGS) and were willing to participate in a clinical trial. Respondents were asked to complete a questionnaire about symptoms, diet, and celiac investigation. They received 248 responses, and completed surveys on a total of 147 people. There were 17 men and 130 women, averaging 43.5 years of age. The team eliminated seventy-two percent of the respondents for inadequate exclusion of celiac disease (62%), uncontrolled symptoms despite gluten restriction (24%), and not following a GFD (27%), alone or in combination. A full 15% of respondents had received no testing or examination for celiac disease. Gluten avoidance was self-initiated in nearly half of respondents; while it was prescribed by alternative health professionals in 21%, by dietitians in 19%, and by general practitioners in 16%. Of 75 respondents who had received duodenal biopsies, nearly one-third had no gluten intake, or inadequate gluten intake, at the time of endoscopy. Inadequate celiac investigation was most common if gluten-avoidance was self-initiated (69%), alternative health professionals (70%), general practitioners (46%), or dietitians (43%). A total of 40 respondents fulfilled criteria for NCGS. Those folks showed excellent knowledge of and adherence to a gluten-free diet. However, a full 65% of those who met criteria for NCGS showed intolerance to other foods. Just over 1 in 4 respondents self-reporting as NCGS fulfill criteria for its diagnosis, while gluten-avoidance without adequate exclusion of celiac disease is common. In 75% of respondents, symptoms are poorly controlled despite gluten avoidance. These results also stress the importance of testing for other food sensitivities, and of celiac screening and evaluation for those people claiming non-celiac gluten-sensitivity. Clearly, more study needs to be done to determine if non-celiac gluten sensitivity exists, or if there are other possible causes for the symptoms. Sources: Nutr Clin Pract August 2014 vol. 29 no. 4 504-509 doi: 10.1177/0884533614529163 Gastroenterology. 2013 Aug;145(2):320-8.e1-3. doi: 10.1053/j.gastro.2013.04.051. The team put out advertisements calling for adults who believed they had non-celiac gluten sensitivity (NCGS) and were willing to participate in a clinical trial. Respondents were asked to complete a questionnaire about symptoms, diet, and celiac investigation. They received 248 responses, and completed surveys on a total of 147 people. There were 17 men and 130 women, averaging 43.5 years of age.
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