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Found 22 results

  1. Celiac.com 12/14/2007 - Celiac & Addison's patients seem to be at greater risk for both diseases. People with celiac disease have a higher risk of developing Addison’s disease, and those with Addison's have a higher risk of developing celiac disease. In both cases, the numbers are far higher than for the general population at large. Doctors are advising that people with Addison's be screened for celiac disease. However, as Addison’s is still rare overall, they are holding off recommending screening of celiac patients for Addison's. Instead, they are advocating that doctors treating celiac patients maintain a heightened awareness for signs of Addison’s, and to react accordingly. This latest evidence is the result of a case history review of 15,000 people with celiac disease. The review was conducted by a team of doctors led by one Dr. Peter Elfstrom of Sweden‘s Orebro University Hospital. A number of studies have shown a link between celiac disease and Addison’s disease, but little has been done to elucidate that connection. And, while this review goes farther than most, the doctors emphasize that the data is strictly preliminary, as they have looked at a relatively small number of cases and tested patients with Addison’s for celiac disease, but not vice versa. The data show a significant connection between celiac and later development of Addison's disease, citing a hazard ratio of 11.4. The results were the same for both adults and children with celiac, and remained so even after adjustment for diabetes, and the socio-economic conditions of the patients. Patients with existing Addison's had a significantly higher risk of celiac disease, citing a hazard ratio of 8.6. The connection between celiac and Addison's was shown to exist both pre- and post-diagnosis for celiac disease. The researchers don’t feel that celiac causes Addison's disease or vice versa, but that they might have related or common genetic traits. Journal of Endocrin. Metabol. 2007: 3595-3598.
  2. Celiac.com 07/28/2016 - Celiac disease is an immune-mediated enteropathy triggered by gluten in genetically susceptible individuals. Researchers know that innate immunity plays a role in triggering celiac disease, but they don't understand the connection very well at all. Although previous in vitro work suggests that gliadin peptide p31-43 acts as an innate immune trigger, the underlying pathways are unclear and have not been explored in vivo. The research team included RE Araya, MF Gomez Castro, P Carasi, JL McCarville, J Jury, AM Mowat, EF Verdu, and FG Chirdo. They are variously affiliated with the Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP)(CONICET-UNLP), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina; the Catedra de Microbiología, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina; the Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada; the Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, Scotland, United Kingdom; and with the Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP)(CONICET-UNLP), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina. Their team observed that introduction of p31-43 into the gut of normal mice causes structural changes in the small intestinal mucosa consistent with those seen in celiac disease, including increased cell death and expression of inflammatory mediators. The effects of p31-43 were dependent on MyD88 and type I IFNs, but not Toll-like receptor 4 (TLR4), and were enhanced by co-administration of the TLR3 agonist polyinosinic:polycytidylic acid. Together, these results indicate that gliadin peptide p31-43 activates celiac-related innate immune pathways in vivo, such as IFN-dependent inflammation. These findings also suggest a common mechanism for the potential interaction between dietary gluten and viral infections in the pathogenesis of celiac disease, meaning that certain viral infections may pave the way for celiac disease to develop. Source: Am J Physiol Gastrointest Liver Physiol. 2016 Jul 1;311(1):G40-9. doi: 10.1152/ajpgi.00435.2015. Epub 2016 May 5.
  3. Celiac.com 11/07/2017 - Researchers still don't have much good data on the consequences of antibiotic use in early life and how that relates to the risk of certain autoimmune diseases. A team of researchers recently set out to test the association between early-life antibiotic use and islet or celiac disease autoimmunity in genetically at-risk children prospectively followed up for type 1 diabetes (T1D) or celiac disease. Their study is part of a larger study called The Environmental Determinants of Diabetes in the Young, or TEDDY, for short. The reasearch team enrolled HLA-genotyped newborns from Finland, Germany, Sweden, and the United States between November 20, 2004, and July 8, 2010, and analyzed data from November 20, 2004, to August 31, 2014. They also enrolled individuals from the general population, and those having a first-degree relative with T1D, with any 1 of 9 HLA genotypes associated with a risk for T1D. The team charted parental reports of the most common antibiotics, such as cephalosporins, penicillins, and macrolides, used between age 3 months and age 4 years. Islet autoimmunity and celiac disease autoimmunity were defined as being positive for islet or tissue transglutaminase autoantibodies at 2 consecutive clinic visits at least 3 months apart. The team used Cox proportional hazards regression models to assess the relationship between antibiotic use in early life before seroconversion and the development of autoimmunity, and to calculate hazard ratios and 95% CIs. The team conducted tests for islet and tissue transglutaminase autoantibodies on 8,495 children (49.0% female), and 6,558 children (48.7% female) who were enrolled in the TEDDY study, and they found that antibiotic exposure and frequency of use in early life or before seroconversion did not influence the risk of developing islet autoimmunity or celiac disease autoimmunity. Additionally, cumulative use of any antibiotic during the first 4 years of life was not tied to the appearance of any autoantibody (hazard ratio , 0.98; 95% CI, 0.95-1.01), multiple islet autoantibodies (HR, 0.99; 95% CI, 0.95-1.03), or the transglutaminase autoantibody (HR, 1.00; 95% CI, 0.98-1.02). Using any of the most common antibiotics during the first 4 years of life, in any geographic region, did not influence the later development of autoimmunity for T1D or celiac disease. Based on these results, the team concluded that doctors recommending antibiotics for young children at risk for T1D or celiac disease need not be concerned that the use will lead to islet or tissue transglutaminase autoimmunity. Source: JAMA Pediatr. Published online October 9, 2017. doi:10.1001/jamapediatrics.2017.2905 The research team included Kaisa M. Kemppainen, PhD; Kendra Vehik, PhD; Kristian F. Lynch, PhD; Helena Elding Larsson, MD, PhD; Ronald J. Canepa, BSc; Ville Simell, MSc; Sibylle Koletzko, MD, PhD; Edwin Liu, MD; Olli G. Simell, MD, PhD; Jorma Toppari, MD, PhD; Anette G. Ziegler, MD, PhD; Marian J. Rewers, MD, PhD; Åke Lernmark, PhD; William A. Hagopian, MD, PhD; Jin-Xiong She, PhD; Beena Akolkar, PhD; Desmond A. Schatz, MD; Mark A. Atkinson, PhD; Martin J. Blaser, MD; Jeffrey P. Krischer, PhD; Heikki Hyöty, MD, PhD; Daniel Agardh, MD, PhD; and Eric W. Triplett, PhD; for The Environmental Determinants of Diabetes in the Young (TEDDY) Study Group. They are variously affiliated with the Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville; the Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa; the Department of Clinical Sciences, Lund University Clinical Research Center, Skåne University Hospital, Malmö, Sweden; the MediCity Laboratory, University of Turku, Turku, Finland; the Division of Paediatric Gastroenterology and Hepatology, Dr von Hauner Children's Hospital, Ludwig Maximilian University, München, Germany; the Digestive Health Institute, Children's Hospital Colorado, Anschutz Medical Campus, University of Colorado Denver, Aurora; the Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland; the Department of Pediatrics, University of Turku, Turku University Hospital, Turku, Finland; the Department of Physiology, Institute of Biomedicine, University of Turku, Turku, Finland Institute of Diabetes Research, Helmholtz Zentrum München, München, Germany; the Klinikum Rechts der Isar, Technische Universität München, München, Germany; the Forschergruppe Diabetes e.V., Neuherberg, Germany; the Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora; the Pacific Northwest Diabetes Research Institute, Seattle, Washington; the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland; the Department of Pediatrics, College of Medicine, University of Florida, Gainesville; the Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Gainesville; the Department of Medicine and Microbiology, New York School of Medicine, New York; the Department of Virology, Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland; and with Fimlab Laboratories, Pirkanmaa Hospital District, Tampere, Finland.
  4. 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.
  5. Celiac.com 05/02/2017 - Do women who use dietary supplements during pregnancy face higher rates of celiac disease in their offspring? To answer this question a team examined the maternal use of vitamin D, n-3 fatty acids (FA) and Fe supplements during pregnancy and looked for any corresponding risk for celiac disease autoimmunity, or celiac disease, in their children. The study, known as The Environmental Determinants of Diabetes in the Young, or "TEDDY," prospectively followed from birth children with increased genetic risk. The team defines celiac disease autoimmunity as the presence of persistently positive tissue transglutaminase autoantibodies (tTGA). The TEDDY research team includes Jimin Yang, Roy N. Tamura, Carin A. Aronsson, Ulla M. Uusitalo, Åke Lernmark, Marian Rewers, William A. Hagopian, Jin-Xiong She, Jorma Toppari, Anette G. Ziegler, Beena Akolkar, Jeffrey P. Krischer, Jill M. Norris, Suvi M. Virtanen, and Daniel Agardh. For their study, the team enrolled 6,627 children with confirmed celiac disease. They confirmed celiac diagnosis either with biopsy results, and also included those with likely celiac, if they had persistently elevated levels of tTGA>100 AU. Of the 6,627 children originally enrolled, 1,136 developed celiac disease autoimmunity at a median 3·1 years of age (range 0·9–10) and 409 developed celiac disease at a median 3·9 years of age (range 1·2–11). The data showed that 66% of mothers used supplements containing vitamin D, 17% containing n-3 FA, and 94% containing iron, at 3–4 months postpartum. Over the entire pregnancy, mothers consumed an average total intake of 2,014 μg vitamin D (sd 2045 μg), 111 g n-3 FA (sd 303 g) and 8,806 mg Fe (sd 7,017 mg). After adjusting for country of residence, child's human leucocyte antigen genotype, sex, family history of celiac disease, any breast-feeding duration and household crowding, Cox's proportional hazard ratios showed no statistically significant association between the intake of vitamin D, n-3 FA or Fe, and risk for celiac disease autoimmunity or celiac disease. The use of dietary supplements during pregnancy may improve nutrition, but it is not likely to have any effect upon the risk for celiac disease in the offspring. Source: Cambridge.org The researchers in this study are variously associated with the Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL, The Diabetes and Celiac Disease Unit, Department of Clinical Sciences, Lund University, 20502 Malmö, Sweden, Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO, Pacific Northwest Diabetes Research Institute, Seattle, WA 98122, USA, the Center for Biotechnology and Genomic Medicine, Augusta University, Augusta, GA, the Department of Physiology, Institute of Biomedicine, University of Turku, Finland, the Department of Pediatrics, Turku University Hospital, 20520 Turku, Finland, the Institute of Diabetes Research, Helmholtz Zentrum München and Klinikum rechts der Isar, Technische Universität München, and Forschergruppe Diabetes e.V., 80804 Neuherberg, Germany, the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MA, the Department of Epidemiology, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO, the Unit of Nutrition, National Institute for Health and Welfare, 00300 Helsinki, Finland, the Health Sciences Center, Center for Child Health Research, University of Tampere, Tampere University Hospital, 33521 Tampere, Finland, and the The Science Center, Pirkanmaa Hospital District, 33521 Tampere, Finland.
  6. Celiac.com 10/31/2016 - Responding to observations and reports that many patients with postural tachycardia syndrome (PoTS) adopt a gluten-free diet without medical consultation, a team of researchers recently set out to evaluate the prevalence of celiac disease and self-reported gluten sensitivity in patients with PoTS, and to compare the results against data from the local population. The research team included HA Penny, I Aziz, M Ferrar, J Atkinson, N Hoggard, M Hadjivassiliou, JN West, and DS Sanders. They are variously affiliated with the Academic Department of Gastroenterology Departments of Cardiology, Radiology, and Neurology at Royal Hallamshire Hospital, and Upperthorpe Medical Centre in Sheffield, UK. For their study, the team recruited 100 patients with PoTS to complete a questionnaire that screened for gluten sensitivity, related symptoms and dietary habits. They also screened patients for celiac disease. For comparison, they calculated local celiac prevalence from a total of 1,200 control subjects (group 1) and another 400 control subjects (group 2), frequency matched for age and sex, who completed the same questionnaire. Overall, 4/100 (4%) patients with PoTS had serology and biopsy-proven coeliac disease. This was significantly higher than the local population prevalence of celiac disease (12/1200, 1%; odds ratio: 4.1, 95% confidence interval: 1.3-13.0; P=0.03). PoTS patients also had a higher prevalence of self-reported gluten sensitivity (42 vs. 19%, respectively; odds ratio: 3.1, 95% confidence interval: 2.0-5.0; P<0.0001). This is the first study to show a possible connection between gluten-related disorders and PoTS. They note that a prospective study which examines this relationship further might promote better understanding and treatment of these conditions. Source: Eur J Gastroenterol Hepatol. 2016 Sep 7.
  7. This article originally appeared in the Winter 2011 edition of Celiac.com's Journal of Gluten-Sensitivity. Celiac.com 05/16/2011 - Nearly 75% of the 24 million Americans suffering from autoimmune disease are women, according to the American Autoimmune Related Diseases Association (AARDA). Women appear to mount larger inflammatory responses than men when their immune systems are triggered, thereby increasing their risk of autoimmunity. The fact that sex hormones are involved is indicated by the fact that many autoimmune diseases fluctuate with hormonal changes such as those that occur during pregnancy, during the menstrual cycle, or when using oral contraceptives. A history of pregnancy also appears to increase the risk for autoimmune disease. The sex hormone that is commonly low in such women is Dehydroepiandrosterone (DHEA). This is a natural steroid and is produced by the adrenal glands, the reproductive organs and the brain. DHEA is used by the body to make the male and female hormones, testosterone and estrogen respectively, and is known to have anti-inflammatory effects. It has been proposed that a DHEA deficiency is a contributing factor in autoimmune diseases. Last year a study was done to look at precisely that effect. The study’s conclusions have been supported by other, similar research and I think you’ll find it quite interesting. The Journal of Clinical Endocrinology & Metabolism Vol. 94, No. 6 2044-2051(2009) published an article entitled “Low Serum Levels of Sex Steroids Are Associated with Disease Characteristics in Primary Sjogren’s Syndrome; Supplementation with Dehydroepiandrosterone Restores the Concentrations”. The authors investigated whether there was a relationship between steroid levels and the disease characteristics of Sjogren’s. They based their study on the known data that DHEA not only declines with aging but is reduced in Sjogren’s, an autoimmune disease. The study was populated by 23 post-menopausal women with primary Sjogren’s syndrome and subnormal levels of DHEA. The investigation was a controlled, double blind crossover study, conducted over a 9 month period, where DHEA was assessed by sophisticated laboratory measurements and typical symptoms of Sjogren’s such as dry mouth and eyes and salivary flow rates were similarly assessed. Results revealed a strong correlation between low DHEA and Sjogren’s symptoms. DHEA and its sex hormone metabolites (testosterone and estrogen) were found to increase with DHEA supplementation but not with the placebo. Symptoms such as dry eyes were seen to improve as estrogen levels The researchers concluded that the disease manifestations of primary Sjogren’s syndrome were associated with low sex hormone levels and the supplementation of DHEA allowed the body to transform into androgens, testosterone and estrogen, with testosterone production predominating. Please allow me to add some personal interpretation. For the most part I agree with the premise and applaud the results. The facts that autoimmune disease occurs more often in women, that women frequently have low DHEA, and that androgens have anti-inflammatory effects that can benefit autoimmune disease are all true. But should we simply give such women DHEA and call it a day? I don’t think so. I propose that we do three things: First, evaluate hormonal levels in women regularly; Second, address WHY their hormonal levels are imbalanced; And third, when supplementing with hormones such as DHEA, ensure that the delivery system is one that mimics what the body does naturally. Remember that autoimmune disease can begin many years before the first symptoms become manifest. Therefore evaluating hormonal levels in our younger women is a good idea. When I find DHEA levels that are low, my first order of business is to assess why. Frequently it is due to a phenomenon known as “pregnenelone steal” that occurs when the adrenal glands are under stress. It is a common occurrence and one of the fantastic abilities of the human body to shift from one pathway to another when under stress. The “steal” pathway diverts the body away from making sex hormones and instead it makes more “stress” hormones. So while adding some DHEA into the mix might very well help, does it make sense to find out WHY it’s being diverted away from making sex hormones? I hope so because it’s the very foundation of the medicine that we practice—functional medicine. Once you understand the root cause of the deficiency you can take steps to truly remedy it rather than simply covering it up by taking DHEA. Not to keep hitting you over the head with this concept, but supplementing with DHEA as your sole treatment misses the underlying cause since the body is designed to make adequate quantities of DHEA. A common reason for the diversion or “steal” pathway to become activated is adrenal stress from poor absorption of nutrients, unstable blood sugar and the presence of infections—all problems we see with the gluten intolerant patient! While I’m not implying that every autoimmune patient has a gluten intolerance, it certainly warrants screening all of them because of its high prevalence. As we travel down the road to optimal health through avoiding any food the body isn’t tolerating well, improving the integrity of the small intestine and normalizing adrenal function, there are certainly times when hormonal supplementation is beneficial. I don’t recommend the oral route because the first place the hormone travels is to the liver and this can be burdensome to that organ. When the body makes hormones naturally it delivers them straight to the bloodstream. In an effort to mimic that delivery system we use a buccal route (placed between cheek and gum in the mouth) that does a good job in bringing the hormone directly to the bloodstream and bypassing the liver and digestive tract. Autoimmune diseases comprise the third leading cause of death in our country and research strongly suggests that its rapid increase is due to environmental factors, especially those that weaken the small intestine. I am committed to earlier diagnosis while the disease is still remediable, as well as overall reduction of incidence through addressing digestive health. I hope you find this informative. Please share this information with those who have autoimmune disease themselves as well as in their family.
  8. Celiac.com 05/16/2016 - A number of epidemiological and clinical studies suggest a connection between inflammation and Alzheimer disease, their relationship is not well understood and may have implications for treatment and prevention strategies. A research team recently set out to figure out if a subset of genes involved with increased risk of inflammation are also associated with increased risk for Alzheimer disease. The research team included JS Yokoyama, Y Wang, AJ Schork, WK Thompson, CM Karch, C Cruchaga, LK McEvoy, A Witoelar, CH Chen, D Holland, JB Brewer, A Franke, WP Dillon, DM Wilson, P Mukherjee, CP Hess, Z Miller, LW Bonham, J Shen, GD Rabinovici, HJ Rosen, BL Miller, BT Hyman, GD Schellenberg, TH Karlsen, OA Andreassen, AM Dale, RS Desikan; and the Alzheimer’s Disease Neuroimaging Initiative. They are variously affiliated with the Departments of Neurosciences, Cognitive Sciences, Psychiatry, and Radiology at the University of California, San Diego, La Jolla, the Departments of Neurology, Radiology and Biomedical Imaging at the University of California, San Francisco, the Department of Psychiatry, Washington University, St Louis, Missouri, the Division of Mental Health and Addiction, Oslo University Hospital, the Norwegian Centre for Mental Disorders Research, Institute of Clinical Medicine, University of Oslo, the Division of Gastroenterology, and the Norwegian PSC Research Center and KG Jebsen Inflammation Research Centre, Research Institute of Internal Medicine, Division of Cancer Medicine, Surgery and Transplantation at Oslo University Hospital Rikshospitalet, Oslo, Norway, the Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany, the Department of Neurology, Massachusetts General Hospital, Boston, and the Department of Pathology and Laboratory Medicine at the University of Pennsylvania Perelman School of Medicine, Philadelphia. Using data from numerous genome-wide association studies from several clinical research centers, the team conducted a genetic epidemiology study in July 2015, in which they systematically investigated genetic overlap between Alzheimer disease (International Genomics of Alzheimer's Project stage 1) and Crohn's disease, ulcerative colitis, rheumatoid arthritis, type 1 diabetes, celiac disease, and psoriasis. The team assessed P values and odds ratios from genome-wide association studies of more than 100, 000 individuals from previous comparisons of patients vs respective control groups. They used consensus criteria to confirm diagnosis for each disorder previously made in the parent study. The main outcome was the pleiotropic (conjunction) false discovery rate P value. Follow-up for candidate variants included neuritic plaque and neurofibrillary tangle pathology; longitudinal Alzheimer's Disease Assessment Scale cognitive subscale scores as a measure of cognitive dysfunction (Alzheimer's Disease Neuroimaging Initiative); and gene expression in Alzheimer disease vs control brains (Gene Expression Omnibus data). These findings confirm genetic overlap between Alzheimer disease and immune-mediated diseases, and suggest that immune system processes influence Alzheimer disease pathogenesis and progression. For more detail, and exact data results, see JAMA Neurol. 2016 Apr 18. doi: 10.1001/jamaneurol.2016.0150.
  9. Of the many immune related disorders linked with the celiac condition, the best established connection is with Type I diabetes (mellitus). Type I diabetes occurs at a rate of about 0.5% in the general population, but at a rate estimated at 5-10% among celiacs. Normally the diabetes is diagnosed first, both because this form of diabetes tends to strike early in life and its diagnosis is certain. No connection has been found with the more common form of diabetes (mellitus= honey , from the sugar laden urine when uncontrolled), Type II which occurs at a rate of 2-2.5% in the general population. Like celiac disease, Type I diabetes is more common in those of northern European extraction. Like celiac disease, it is highly linked to the so-called HLA markers of the immune system, those marking white blood cells. Celiacs are likely to be positive for both HLA-B8 and HLA-DR3; Type Is are most linked to HLA-B8 and either HLA-DR3 or HLA-DR4. An English study about 6 months ago found that multiple genes were linked to Type I reflecting the fact that parents of a Type I are often diabetes free: the interpretation being that genes were required from both sides. The recent request for celiac siblings for a study of genetic typing intends to duplicate that one looking for celiac genes. References: Gluten Intolerance Group of North America newsletter, V. 13, Issue 2, 1987; New York Times, Sept. 13, 1994, genetics study by Dr. John Todd at Oxford, summarized by Kemp Randolph. For more information see our Related Disorders page.
  10. Celiac.com 11/04/2015 - A research team that conducted an analysis of the relationship between seronegative celiac disease and immunoglobulin deficiencies also conducted a literature search on the main medical databases, which revealed that seronegative celiac disease poses a diagnostic dilemma. The research team included F. Giorgio, M. Principi, G. Losurdo, D. Piscitelli, A. Iannone, M. Barone, A. Amoruso, E. Ierardi, and A. Di Leo. They are variously affiliated with the Section of Gastroenterology at University Hospital Policlinico, Department of Emergency and Organ Transplantation at University of Bari in Bari, Italy. They note that villous blunting, intraepithelial lymphocytes (IELs) count and gluten "challenge" are the most reliable markers in addressing seronegative celiac disease. They also note that immunohistochemistry/immunofluorescence tissue transglutaminase (tTG)-targeted mucosal immunoglobulin A (IgA) immune complexes in the intestinal mucosa of seronegative celiac disease patients may be useful. In the team's view, tTG-mRNA was similarly increased in seropositive celiac disease and suspected seronegative celiac disease, and strongly correlated with the IELs count. This increase is found even in the IELs' range of 15-25/100 enterocytes, suggesting that there may be a "grey zone" of gluten-related disorders. An immune deregulation, severely lacking B-cell differentiatio, underlies the association of seronegative celiac disease with immunoglobulin deficiencies. Therefore, celiac disease may be linked to autoimmune disorders and immune deficits, known as common variable immunodeficiency (CVID)/IgA selective deficiency. CVID is a heterogeneous group of antibody dysfunction, whose association with celiac disease revealed only by a positive response to a gluten-free diet. The research team suggests a possible familial inheritance between celiac disease and CVID. Selective IgA deficiency, commonly associated with celiac disease, accounts for IgA-tTG seronegativity. Selective IgM deficiency (sIgMD) is rare, with less than 300 documented cases, and is connected to celiac disease in 5% of cases. The team diagnosed seronegative celiac disease in a patient affected by sIgMD using the tTG-mRNA assay. One-year on a gluten-free diet restored IgM levels. This study data support a link between seronegative celiac disease and immunoglobulin deficiencies, and invites researchers to take a closer look at this connection. Source: Nutrients. 2015 Sep 8;7(9):7486-504. doi: 10.3390/nu7095350
  11. Celiac.com 04/23/2007 - The results of a recent Dutch study published in the World Journal of Gastroenterology have confirmed a connection between Hashimotos Thyroiditis and celiac disease. In the study, 104 individuals with Hashimotos Thyroiditis were tested for immunoglobulin A anti-transglutaminase (tTG) antibodies, IgA anti-endomysial antibodies (EMA) and HLA-DQ typing. Those who tested positive for any of the serological tests were given an intestinal biopsy. Sixteen patients (15%) showed positive celiac serology and five patients clear villous atrophy were diagnosed with celiac disease (4.8%; 95% CI 0.7-8.9). All five patients diagnosed with celiac disease, and 53 patients with Hashimotos thyroiditis (50%; 95% CI 43-62), showed the presence of HLA-DQ2 (and/or -DQ8). In a separate test within the study, 184 Individuals with known celiac disease were given a serological test for thyroglobulin and thyroid peroxidase Antibodies, after first being given thyroid biochemical, a thyroxine-free thyroid stimulating hormone. 39 patients (21%) showed positive thyroid serology. According to thyroid biochemistry results, ten patients showed euthyroidism (5%; 95% CI 2-9), seven showed sub-clinical hypothyroidism (3.8%; 95% CI 1.8-7.6), and 22 patients showed overt hypothyroidism, Hashimotos thyroiditis (12%; 95% CI 8-16). Furthermore, four patients with celiac disease had Graves disease (2%; 95% CI 0.8-5) and one patient had post-partum thyroiditis. The study concludes that there is a clear association between Hashimotos thyroiditis and celiac disease. Accordingly, it is recommended that patients with Hashimotos thyroiditis be screened for celiac disease and that patients with known celiac be screened for Hashimotos thyroiditis. World Journal of Gastroenterology 2007; 13(10). health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
  12. This article appeared in the Winter 2006 edition of Celiac.coms Scott-Free Newsletter. Celiac.com 07/10/2006 - Three years ago my father was diagnosed with celiac disease and I was told by my mother that it is hereditary and that I too should get screened for it. I did some research and immediately knew that I had this disease. I wouldn't admit it to anyone at the time because how on earth could I possibly live without pasta and fresh-baked bread for the rest of my life?! You should know that I have been sick for my entire life—I had colic until I was six, got ulcers when I was eight, appendicitis at 14, calcium bone spurs at 17, 19, 24 and 36, infertility at 24, gall stones at 37—just to mention a few of the conditions Ive had that were likely related to my untreated celiac disease. About six months later I decided to go see my doctor—I was in a severe state of depression, and I had lost the ability to think—much less talk. Carrying on a full conversation was nearly impossible because of my inability to speak in full sentences. I was extremely sick with a severe cold, and I had an infection or the flu at least once each month for the preceding two to three years. I told my doctor that I thought that he should test me for celiac disease. Since I weighed in at over 300 pounds he literally laughed at this idea. According to him there was absolutely no way that I could have celiac disease—because I was fat! Shortly after that my parents came to visit and tried to talk me into eating gluten-free—at least during the time that they were here. I agreed because I had to cook gluten-free for them anyway. Within three days of starting a gluten-free diet I felt like a million bucks. My depression lifted and within a month I was losing weight and my brain started working again. I have been gluten-free for three years now—not only do I feel like a million bucks, but I have lost over 100 pounds. I shudder at the idea that I was literally eating myself to death—and it was not because I didn't have any will power or that I was eating bad food—it was because my body couldnt process and absorb the food that I was eating. My personal experience, combined with my research, has left me completely convinced that celiac disease is (and will continue to be) a significant cause of obesity—and that this will continue to be the case until there is a better understanding of the disease and its relationship to obesity. What is Celiac Disease? Celiac disease is a permanent intolerance to gluten1, which is a protein found in, wheat, rye, and barley. When gluten is ingested the digestive system is unable to properly break it down, and an autoimmune response is triggered in the gut that causes the villi of the small intestine to become damaged—leading to malabsorption of crucial nutrients. There is no cure, and the only way to control it is through a 100% gluten-free diet. The disease has a vast array of symptoms, and it is rare that two people will exhibit the same ones. Some will have diarrhea while others will have constipation, and some will not have either but instead may have osteoporosis, diabetes, headaches, fatigue, autoimmune thyroid disorder or any number of other conditions and symptoms found to be associated with it. In many cases these symptoms are associated with the inability to gain weight—children with celiac disease are often small and fail to thrive 1. Nearly every source that I consulted for this paper referred to malabsorption and how most people with celiac disease lost weight or couldn't gain weight. Only a few sources even mentioned obesity—and when they did it was only in passing. As celiac disease awareness steadily increases and more research is done on it hopefully it will become apparent that many cases of obesity are also related to it. The Common Thread Autoimmune thyroid disease has recently been linked to celiac disease. Recent research has demonstrated that 3.4% of patients with autoimmune thyroid disease also have celiac disease2. The thyroid gland secretes hormones to control the body's metabolic rate3, and to accomplish this it must have iodine. When celiac disease is present along with autoimmune thyroid disorder, the body does not have the ability to absorb the iodine to produce the necessary hormones. Additionally there are many different disorders such as obesity, diabetes, allergies, weight-loss, gastrointestinal problems, etc., that can be caused by having a damaged or compromised thyroid gland3 (all of these disorders, by the way, can be related to celiac disease). It has been known for years that obesity has been linked to thyroid problems, and that the thyroid produces 5-monodeiodinase, the bodys natural method of conserving fuel during shortage," and the body "elicits the same physical reaction as famine," which can then cause the affected person to gain weight3. Another disorder commonly associated with celiac disease is malabsorption, which can also lead to malnutrition. When someone with celiac disease eats foods that contain gluten it results in damage to the surface of the small intestine and destruction of their nutrient-absorbing villi. This can lead to leaky gut and an inability for them to absorb vital nutrients from their food. By continuing to eat foods containing gluten, eventually vital organs including the brain, thyroid, liver, kidneys—essentially any organ that depends heavily on nutrients—will be starved, which will leave them susceptible to other diseases and conditions. I personally experienced brain malfunctions, gall bladder problems, and was diagnosed numerous times with an under-active thyroid. Naturally treatments for this proposed thyroid condition didnt work because their true cause had not yet been found. At one point a doctor asked me to consider the idea that my obesity was the result of my bodys attempt to cope with malnourishment4. This phenomenon is similar to yo-yo dieting, where dieters who have deprived themselves or proper nutrition for too long gain weight at faster rates than non-dieters after they resume eating normally. I always thought that I had fallen victim to yo-yo dieting, and that I had dieted myself into a permanent state of obesity. I now understand that it was because I had undiagnosed celiac disease, and my body was actually malnourished. Under normal nutritional conditions humans only absorb about 80 percent of the nutrients from the food they eat, and the rest of the nutrients pass through the body4. With celiac disease, however, the body is unable to absorb the necessary nutrients, which causes some peoples bodies to become a super-efficient machine that begins storing as much fat as possible in order to survive. This nutrient deficiency convinces the body that it is starving to death, which sends it into starvation-mode. Since humans need a certain percentage of body fat reserves to stay alive—and because it takes more work for the body to burn fats than carbohydrates—a body that is in starvation mode tends to crave carbohydrates and more efficiently convert them to fat for later use4. There has been much research that links celiac disease to diabetes. Diabetes occurs when the bodys cells are unable to absorb enough blood sugar5. Although the cause is different, the resulting malabsorption is similar to that seem in celiac disease—although in the latter the malabsorption is not just limited to sugar. The connection between diabetes and celiac disease as described by Marschilok: Both diseases have genetic and environmental origins. This means an individual is more at risk of developing either problem when a close relative also has it. On the genetic side, development of one reveals the pre-existing and larger risk that the genes for the other may be present. At least two genes and gene locations are connected with each disease. One gene for each disease is near one gene for the other on the same chromosome. Nearby genes are more likely to pass together to offspring. However, while the genes are necessary, they are not sufficient to produce the diseases. On the environmental side, researchers know gluten is needed to produce celiac disease, but they also know its not the only environmental cause. With diabetes, the environmental causes are being extensively studied for prevention and cure. Roughly ten percent of celiacs either have Type I diabetes or might develop Type II diabetes6 . An astonishing 40% of people with diabetes are also obese—even though there was not very much in the way of medical research to indicate why this is so. Diabetes is described as your cells inability to produce or absorb insulin, which leads to an excess of sugar in the blood stream7. If a person injects or produces too much insulin it will increase the level of hunger and cause obesity. I personally find this information disturbing as there are some in the medical community who still blame obesity on character flaws—I cant begin to tell you how many times I have been told: if you just didn't eat so much you wouldn't be fat. A number of overweight and obese acquaintances of mine have asked me how I managed to lose over 100 pounds and look so healthy while doing it. I explained my celiac disease diagnosis and gluten-free diet to them, and how the diet has made me not feel hungry for the first time in my life—due to the fact that I am now absorbing nutrients properly. Six of these extremely obese people have actually gone to their physicians to get tested for celiac disease—and each was met with the same skepticism as me. They persisted and finally got their doctors to perform the necessary tests—and to the surprise of all each were diagnosed with celiac disease! Immediately after going on the gluten-free diet they all experienced a decrease in hunger and massive weight-loss. For the first time they were eating only when their bodies were truly hungry, instead of eating too much due to starvation signals caused by malabsorption. This could also be part of the reason that high protein, low carbohydrate diets work so well for many people. By removing the carbohydrates from ones diet you generally remove a large portion of the gluten as well, which can cause those with celiac disease who are obese to lose weight quickly—at least for a month or so. However, on the high protein diet you are still not removing all gluten which will eventually cause them to gain the weight back—even though they are still on the diet. This was my experience with the low carbohydrate diet, and I suspect that a lot of others who are obese and have undiagnosed celiac disease had or will have the same experience. Conclusion I once had a family member literally yell at me about my weight and ask me why I was being so selfish and not thinking about my husband and daughter—they told me that I should just lose the weight. I was devastated, I truly had tried every diet on the face of the earth and each and every time I would loose 20-30 pounds quickly (regardless of the type of diet), only to gain it back (while still following the program)—sometimes as much as two fold! Since being diagnosed with celiac disease three years ago I have not only lost the weight but I have also kept it off, and each week a little bit more comes off. I am completely convinced that celiac disease does and will continue to be a common cause of obesity until the medical community—through scientific research—realizes that there is a connection. Many obese people might not be overweight if they were just properly diagnosed and treated. Certainly it is not the case that all obese people are that way because they just plain eat too much and do not have any will power. I suspect that there are better medical reasons to explain most cases of obesity, and celiac disease is just one of them. Not too long ago it was estimated that celiac disease only affected 1 in 10,000 Americans8. That figure was then revised to 1 in 5,000, and now, after much research, it is at least 1 in 133. The actual diagnosis rate, however, is only about 1 in 5,000, which is only a small fraction of those who have it. Similarly, the causes of obesity in America are not fully understood, and more research needs to be done to determine just how many cases of obesity are caused by untreated celiac disease. I believe that a significant percentage of obese people have undiagnosed celiac disease, and that celiac disease screening should be part of ordinary blood workups for all obese people. References: Adams, S. (May 2005). A Celiac Disease and Gluten-Free Resource since 1995. Retrieved May 18, 2005, from www.celiac.com. Collin, Kaukinen, Valimaki & Salmi, (2002). Endocinological Disorders and Celiac Disease, Endocrine Reviews (pp 1-38). 3. Life Extension, Thyroid Deficiency, Online reference for Health Concerns. Retrieved May 26, 2005 from www.lef.org/protocols/prtcls-txt/t-prtcl-104.html. Balley, L. (June 2004) Obesity in Developing Countries Compares to U.S. Yo-Yo Dieting. Retrieved June 16, 2005 from: http://www.eurekalert.org/pub_releases/2004-06/uom-oid060804.php. Katz H., (2005). Hope for Obesity and Diabetes. Retrieved June 19, 2005 from http://www.reporter-archive.mcgill.ca/Rep/r3112/mice.html. Marschilok, K., (1997). Diabetes and celiac Disease. Gluten-free Living. Hoover, J., (2001). Obesity Causes Diabetes–Fat Chance! Diabetes Health Magazine. Retrieved June 19, 2005 from http://www.diabeteshealth.com/read,1009,2168.html Vogren, C.L., (September 15, 2003). Awareness Can Be Best Medicine: Parents who lost son to celiac disease want to shed light on often-overlooked ailment. The Gazette. Retrieved June 19, 2005 from http://www.csaceliacs.org/CDintheNews/COSpringsGazette091503.php
  13. This article originally appeared in the Winter 2011 edition of Celiac.com's Journal of Gluten-Sensitivity. Celiac.com 08/29/2011 - Nearly 75% of the 24 million Americans suffering from autoimmune disease are women, according to the American Autoimmune Related Diseases Association (AARDA). Women appear to mount larger inflammatory responses than men when their immune systems are triggered, thereby increasing their risk of autoimmunity. The fact that sex hormones are involved is indicated by the fact that many autoimmune diseases fluctuate with hormonal changes such as those that occur during pregnancy, during the menstrual cycle, or when using oral contraceptives. A history of pregnancy also appears to increase the risk for autoimmune disease. The sex hormone that is commonly low in such women is Dehydroepiandrosterone (DHEA). This is a natural steroid and is produced by the adrenal glands, the reproductive organs and the brain. DHEA is used by the body to make the male and female hormones, testosterone and estrogen respectively, and is known to have anti-inflammatory effects. It has been proposed that a DHEA deficiency is a contributing factor in autoimmune diseases. Last year a study was done to look at precisely that effect. The study’s conclusions have been supported by other, similar research and I think you’ll find it quite interesting. The Journal of Clinical Endocrinology & Metabolism Vol. 94, No. 6 2044-2051(2009) published an article entitled “Low Serum Levels of Sex Steroids Are Associated with Disease Characteristics in Primary Sjogren’s Syndrome; Supplementation with Dehydroepiandrosterone Restores the Concentrations”. The authors investigated whether there was a relationship between steroid levels and the disease characteristics of Sjogren’s. They based their study on the known data that DHEA not only declines with aging but is reduced in Sjogren’s, an autoimmune disease. The study was populated by 23 post-menopausal women with primary Sjogren’s syndrome and subnormal levels of DHEA. The investigation was a controlled, double blind crossover study, conducted over a 9 month period, where DHEA was assessed by sophisticated laboratory measurements and typical symptoms of Sjogren’s such as dry mouth and eyes and salivary flow rates were similarly assessed. Results revealed a strong correlation between low DHEA and Sjogren’s symptoms. DHEA and its sex hormone metabolites (testosterone and estrogen) were found to increase with DHEA supplementation but not with the placebo. Symptoms such as dry eyes were seen to improve as estrogen levels The researchers concluded that the disease manifestations of primary Sjogren’s syndrome were associated with low sex hormone levels and the supplementation of DHEA allowed the body to transform into androgens, testosterone and estrogen, with testosterone production predominating. Please allow me to add some personal interpretation. For the most part I agree with the premise and applaud the results. The facts that autoimmune disease occurs more often in women, that women frequently have low DHEA, and that androgens have anti-inflammatory effects that can benefit autoimmune disease are all true. But should we simply give such women DHEA and call it a day? I don’t think so. I propose that we do three things: First, evaluate hormonal levels in women regularly; Second, address WHY their hormonal levels are imbalanced; And third, when supplementing with hormones such as DHEA, ensure that the delivery system is one that mimics what the body does naturally. Remember that autoimmune disease can begin many years before the first symptoms become manifest. Therefore evaluating hormonal levels in our younger women is a good idea. When I find DHEA levels that are low, my first order of business is to assess why. Frequently it is due to a phenomenon known as “pregnenelone steal” that occurs when the adrenal glands are under stress. It is a common occurrence and one of the fantastic abilities of the human body to shift from one pathway to another when under stress. The “steal” pathway diverts the body away from making sex hormones and instead it makes more “stress” hormones. So while adding some DHEA into the mix might very well help, does it make sense to find out WHY it’s being diverted away from making sex hormones? I hope so because it’s the very foundation of the medicine that we practice—functional medicine. Once you understand the root cause of the deficiency you can take steps to truly remedy it rather than simply covering it up by taking DHEA. Not to keep hitting you over the head with this concept, but supplementing with DHEA as your sole treatment misses the underlying cause since the body is designed to make adequate quantities of DHEA. A common reason for the diversion or “steal” pathway to become activated is adrenal stress from poor absorption of nutrients, unstable blood sugar and the presence of infections—all problems we see with the gluten intolerant patient! While I’m not implying that every autoimmune patient has a gluten intolerance, it certainly warrants screening all of them because of its high prevalence. As we travel down the road to optimal health through avoiding any food the body isn’t tolerating well, improving the integrity of the small intestine and normalizing adrenal function, there are certainly times when hormonal supplementation is beneficial. I don’t recommend the oral route because the first place the hormone travels is to the liver and this can be burdensome to that organ. When the body makes hormones naturally it delivers them straight to the bloodstream. In an effort to mimic that delivery system we use a buccal route (placed between cheek and gum in the mouth) that does a good job in bringing the hormone directly to the bloodstream and bypassing the liver and digestive tract. Autoimmune diseases comprise the third leading cause of death in our country and research strongly suggests that its rapid increase is due to environmental factors, especially those that weaken the small intestine. I am committed to earlier diagnosis while the disease is still remediable, as well as overall reduction of incidence through addressing digestive health. I hope you find this informative. Please share this information with those who have autoimmune disease themselves as well as in their family.
  14. Celiac.com 09/03/2009 - Every night thousands of people lose sleep because of a gnawing, tingling urge to move their legs, disturbing their sleep and are often causing chronic pain. These people wake feeling unrested, with aching muscles. In addition to lost sleep and discomfort, these people often suffer chronic pain. Often, these symptoms baffle both patients and primary care doctors. Little do these people and their doctors know that the pain and restlessness is due to Restless Legs Syndrome (RLS) and is likely caused by a problem with the digestive tract. RLS affects 7% to 15% of the population, especially older adults and pregnant women. RLS symptoms can have a major impact on quality of life, and the syndrome often stymies the medical community. In recent years a number of drugs have been introduced to help the symptoms of RLS, but until now the cause has remained unknown. Small intestinal bacterial overgrowth (SIBO) is a condition where abnormally large numbers of bacteria exist in the small intestine. Symptoms often include diarrhea, bloating, excess gas and abdominal pain. SIBO has strong ties to IBS, diabetes, celiac disease and Crohn’s disease. St. Louis-based Gastroenterologist Dr. Leonard Weinstock has led research that has recently established a link between RLS and SIBO. Dr. Weinstock's clinical trials have shown that treating SIBO often sends the RLS into remission. “When a patient was diagnosed with SIBO, given a course of treatment that included rifaximin, an antibiotic that is not absorbed by the bloodstream, we found that the patient showed quick, dramatic and continuing relief of RLS symptoms,” explains Weinstock. This discovery promises a new lease on life for many RLS sufferers. Weinstock discovered the association while treating a patient for Irritable Bowel Syndrome (IBS) who also suffered from RLS. Treatment of the IBS, also seemed to send the patient’s RLS into remission. This discovery led to a number of trials, all of which produced the same overall result. “While many new drugs help treat the symptoms of RLS. This research shows us the cause of the disease and in turn allows us to treat the RLS rather than just helping the symptoms,” says Weinstock. Based on a standard RLS severity scale, all Weinstock’s patients have shown substantial improvement. In the most recent trial, severity scores for 9 of 14 patients dropped an average of 65% after one course of antibiotics. After an initial lack of response, two patients received a second round of antibiotics and no longer had any symptoms. A third patient was cured after discovering that she had celiac disease and beginning on a gluten-free diet. The link between non-responsive celiac disease and SIBO has also been documented. The fact that such a link exists between SIBO and RLS, and other conditions such as celiac disease, IBS and Crohn’s disease clearly warrants further study, and should give anyone suffering from RLS some information to share with their clinician in approaching the issue. Source: http://www.pitchengine.com/specialistsingastroenterologyadvancedendoscopycenter/sending-restless-legs-syndrome-rls-into-remission/21146/
  15. Celiac.com 02/27/2012 - The relationship between celiac disease and inflammatory bowel disease has not been well documented. One study that hasn't gotten too much attention was published in 2008. To get a better idea regarding any connection, a team of researchers studied rates of celiac disease in patients with inflammatory bowel disease, along with the rates of inflammatory bowel disease in patients with celiac disease. The research team included J.S. Leeds, B.S. Höroldt, R. Sidhu, A.D. Hopper, K. Robinson, B. Toulson, L. Dixon, A.J. Lobo, M.E. McAlindon, D.P. Hurlstone, and D.S. Sanders. They are affiliated with the Gastroenterology and Liver Unit of Royal Hallamshire Hospital in Sheffield, UK. The team recruited patients from clinics specializing in inflammatory bowel disease and celiac disease, along with control subjects from the local population. They then tested subjects for Antigliadins, endomysial, tissue transglutaminase antibodies and total IgA levels. They offered duodenal biopsy to patients with positive antibodies. The team reviewed colonoscopy and biopsy data for celiac patients. In all, the team assessed 305 patients with celiac disease, 354 patients with IBD, and 601 healthy control subjects. The IBD group included 154 patients with ulcerative colitis (UC), 173 with Crohn's disease, 18 with indeterminate colitis, and nine cases of microscopic colitis. Forty-seven patients showed positive antibodies, while three patients showed villous atrophy upon biopsy. All three patients with villous atrophy showed positive anti-tissue transglutaminase antibodies, but only two tested positive for endomysial antibody (EMA). Ten celiac patients had IBD (5 UC and 5 lymphocytic colitis). Five control subjects had celiac disease, while two had IBD (1 Crohn's disease and 1 UC). Stepwise multiple logistic regression showed that only antibody positivity was a factor (p<0.0001). The results showed that people with celiac disease had IBD at rates ten times higher than the control group (odds ratio 9.98, 95% CI 2.8-45.9, p=0.0006), while patients with IBD had celiac disease at about the same rates control subjects (odds ratio 1.02, 95% CI, 0.24-4.29, p=1.0). Source: Scand J Gastroenterol. 2008;43(10):1279-80
  16. Celiac.com 03/15/2008 - For the first time, medical researchers have shown that an activation of the inflammatory response system accompanies major depression and that pro-inflammatory cytokines and lipopolysaccharide (LPS) may trigger symptoms of depression. In the face of the study results, researchers are recommending that patients with depression be screened for leaky gut using IgM and IgA panels. Researchers set out to determine the role played by increased gastrointestinal permeability coupled with an increased translocation of LPS from gram-negative bacteria in the pathophysiology of major depression (MDD). The researcher team was made up of M. Maes, M. Kubera, J.C. Leunis. The team created a study to evaluate serum levels of IgM and IgA against LPS of the gram-negative enterobacteria Hafnia Alvei, Pseudomonas Aeruginosa, Morganella Morganii, Pseudomonas Putida, Citrobacter Koseri, and Klebsielle Pneumoniae in MDD patients and normal controls. Compared to the non-depressive control groups, patients with major depression (MDD) showed significantly greater prevalences and median values for serum IgM and IgA against LPS of enterobacteria. Increased levels of IgM and IgA are associated with fatigue, autonomic and gastro-intestinal symptoms and a subjective feeling of infection. Leaky Gut a Factor in Major Depression The results demonstrate that intestinal mucosal dysfunction marked by an elevated translocation of gram-negative bacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression. Researchers are suggesting that IgM and IgA panels be used to screen people who suffer from depression for leaky gut. Neuro Endocrinol Lett. 2008 Feb;29(1):117-24.
  17. Celiac.com 04/04/2011 - Having been diagnosed with celiac disease, I know from having to follow a strict gluten-free diet that monitoring one's diet and health can be inconvenient, time-consuming, and challenging. Similarly, keeping one's blood sugar level under control for diabetics can be tough, but studies are showing how important this is, as it has been shown to prevent diabetic neuropathy, that is, nerve damage peculiar to diabetics, and its devastating effects. According to Tedd Mitchell, M.D., President of the Texas Tech University Health Sciences Center, there are two types of diabetic neuropathy, peripheral and autonomic. Peripheral neuropathy is "a degeneration of the nerves in the feet and hands," according to Dr. Mitchell, which, as it occurs "slowly but progressively," reduces sensitivity to touch while heightening sensations of pain and itching. The second type is autonomic neuropathy, which is, Dr. Mitchell says, "damage to nerves that control bodily functions, such as digestion, urination, heart rate, blood pressure, sexual function and even sweating." Some of the symptoms of this type are digestive problems, urinary problems, and reductions in blood pressure. The longer one has been diabetic, the higher one's risk for neuropathy. Thankfully, evidence supports that long-term blood sugar control can reduce this risk. It may seem like a challenge for some diabetics to control their blood sugar, but with some determination and effort, it can successfully be achieved. MedicalMoment.org, a website developed by Columbia St. Mary's, an organization of hospitals and clinics, offers various ways to get started controlling your blood sugar. First, in liaison with your health care provider, test your blood sugar and keep a record of your results and pertinent information, on a daily basis. Follow your doctor's prescribed diabetes medicine plan while eating foods low in fat, sugar, and sodium and high in fiber on a regular basis, aiming for the same caloric intake every day. It's important to get regular exercise, starting slowly if need be, such as swimming and walking. Your diet and exercise routine should be geared toward maintaining your ideal weight, which should be determined by your health care provider. You'll want to stay aware of signs of possible nerve damage such as sores that won't heal, blisters, swelling, and ulcers. MedicalMoment.org also offers several tips for keeping blood sugar under control. Low blood sugar should be treated quickly with the use of special glucose gel or tablets. Smoking, which harms the heart and the circulatory system, should be avoided. Next, learn as much as possible about your diabetic condition and treatment; knowledge is power in this case, as I know from being a celiac disease patient. Lastly, avoid stress and get support by staying connected with friends and relatives or a support group who can help you keep your blood sugar under control. It isn't unusual for me to focus some of my work as an author, researcher, and gluten-free and health advocate, on the area of diabetes; after all, according to Celiac.com, evidence is growing which supports that people with Type 1 diabetes are at high risk for celiac disease. In this research, the necessity of maintaining blood sugar is clear. With the help of your medical practitioner and other resources, you can achieve proper self-care in controlling blood sugar level and lower this risk of nerve damage. Resource: Mitchell, Dr. Tedd. "Nerve damage: One more reason to keep blood sugar under control." USA Weekend: July 9-11, 2010.
  18. Celiac.com 05/20/2010 - In Germany, a team of scientists led by Doctor Mathias Hornef of Hannover Medical School, acknowledged that people with inflammatory diseases like celiac, Crohn's and ulcerative colitis, have a different chemical mix of bacteria in their intestines. They also knew that the method in which a child is delivered can affect their bacteria mixture. It was this information that led the team of scientists to speculate if children with celiac, Crohn's or ulcerative colitis had a higher incident of cesarean births. Doctor Hornef and his colleagues studied children and adolescents with celiac, Crohn's and ulcerative colitis, as well as children with other gastrointestinal complications. They also studied a control group of children with unrelated conditions. The results clearly demonstrated that the children with the highest rate was the celiac group with 28% of them born by cesarean section. The other four groups had no more than 19% born by cesarean section. Coincidentally, the average celiac child was diagnosed earlier than the other patients used for this study. Doctor Hornef's findings were a scientific breakthrough previously undocumented by any other scientist. No link has ever been established between children with celiac disease and cesarean deliveries. The results of the study have led to much speculation in the scientific community as to why the celiac children had a higher rate of cesarean births compared to the children with the Crohn's and ulcerative colitis, being that they are all inflammatory diseases which develop in many related ways. Hornef said one explanation of the celiac C-section connection could be that celiac disease is often stimulated early in life and therefore, those newborns born with abnormal intestinal bacteria may be especially susceptible to C-section births. Other scientists unrelated to this study were very interested in the results, but didn't exclude the other possibilities that may not involve the method of birth for the babies. Director of clinical research at the Celiac Disease Center at Boston's Beth Isreal Deaconess Medical Center, Doctor Leffler, suggested that since celiac is a genetic disease, many of the children with celiac may have had mother's with undiagnosed celiac. Undiagnosed celiac disease can cause complications in the birthing process and would explain the increased number of cesarean section births among that population. Dr. Leffler sites the growing awareness of celiac disease as a possibility for more diagnosed children than mothers. He stated that the study results may actually be an indication that doctors should be testing for celiac disease in young women looking to become pregnant. Doctor Leffler further stated that early celiac diagnosis and a gluten-free diet decreases the chances of a cesarean birth, and renders mothers just as likely to be at risk for a cesarean section as the general public. Leffler added that untreated celiac disease can also effect the fetus by things like, a slower growth rate and an increased risk of premature births. Doctor Joseph Murray of the Rochester, Minnesota Mayo Clinic is a gastrointestinal doctor that specializes in celiac disease. Doctor Murray suggested initiating a study to evaluate the possible link between cesarean birth and diabetes, since diabetes is substantially related to celiac disease. Doctor Hornef adamantly emphasized that cesarean sections can be lifesaving for many babies. Furthermore, Doctor Hornef does not advocate avoiding cesarean births. He said that larger studies and more data is needed before any conclusions can be made with the connection between celiac disease and cesarean section births. Source: doi:10.1542/peds.2009-2260
  19. Celiac.com 08/16/2010 - There have been a number of studies connecting celiac disease with impairments in women's reproductive health, including such disorders as infertility, delayed puberty, amenorrhea, and early menopause. Associations between celiac disease and oligomenorrhea, hypomenorrhea, metrorrhagia, and dysmenorrhea have also been observed. In 2008, a case-controlled study in Italy was executed to determine the association between female reproductive health and celiac disease. The study evaluated 62 celiac women, and 186 healthy control patients between the ages of 15 and 49. Of the celiac women evaluated, the average age when diagnosed with celiac disease was about 24 years old. Most of the women, 69.3% exhibited a bloated stomach, 61.3% exhibited anemia, 51.6% exhibited weight loss, 40.3% exhibited diarrhea, and 17.7% exhibited vomiting as their main symptom during onset of celiac disease. 40.3% of the women evaluated claimed to have other symptoms at the time they were diagnosed for celiac disease, including menstrual cycle disorders. Of the celiac women evaluated, 47.6% reported that they noticed the onset of their menstrual cycle disorders before they noticed any other classic celiac symptoms, 28.6% noticed the onset of the menstrual symptoms after the other celiac related symptoms presented, and 19% noticed menstrual problems at the same time as other celiac symptoms. 19.4% of celiac women exhibited menstrual disorders. Exactly 50% of the celiac women tested and 50% of the controls tested had been pregnant at least once prior to entering the study. Celiac women reported 63 total pregnancies and 49 of those were brought to full term. The control group reported 203 pregnancies with 179 brought to full term. While only 11.8% of the control groups pregnancies ended in miscarriages, 22.2% of the women with celiac disease had miscarriages. Additionally, the average birth rate of the children born from the celiac mothers was lower than the birth rate of the control group babies. This study confirmed the association between celiac disease and pregnancy disorders. However, there have not been enough studies yet to determine the exact correlation between celiac disease and female related reproductive issues. It has been hypothesized that the connection might be due to the fact that celiac disease can cause malabsorbtion and therefor malnutrition in some individuals, which could possibly play a role in ovarian dysfunction. Although from this study and others, the connection between celiac disease and reproductive disorders has been demonstrated to be significant enough that women exhibiting reproductive issues are recommended to undergo celiac screenings. Source: BMC Gastroenterology 2010, 10:89
  20. Celiac.com 04/25/2011 - Research shows that celiac disease is associated with numerous gastric abnormalities. An international research team recently set out to examine the association between rates of celiac disease and Helicobacter pylori infection in an Iranian population of 250 patients. The research team included Mohammad Rostami Nejad BS1, Kamran Rostami MD PhD, Yoshio Yamaoka MD PhD, Reza Mashayekhi MD1, Mahsa Molaei MD, Hossein Dabiri PhD, David Al Dulaimi MD, Dariush Mirsattari MD, Homayoun Zojaji MD, Mohsen Norouzinia MD, and Mohammad Reza Zali MD FACG AGAF. The team members are variously affiliated with the Research Institute of Gastroenterology and Liver Disease, Shahid Beheshti University, M.C., in Tehran, Iran, the School of Medicine, University of Birmingham in the UK, the Department of Medicine-Gastroenterology, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine in Houston, Texas, and the Department of Gastroenterology, Alexandra Hospital, Redditch, UK. For the study, the team took topsides from the gastric antrum and duodenum. They assessed morphology and histology using the updated Sydney system and modified Marsh criteria, respectively. In order to simplify the assessment of gastric lesions, the team classified gastritis in both macroscopic and microscopic stages. They screened for anti-tissue transglutaminase antibody to determine the presence of celiac disease. Of the 250 patients, 232 (93%) showed histological evidence of Helicobacter pylori infection, while 24 patients (10%) showed histological abnormalities (Marsh I to IIIc). Of the 24 patients with histological abnormalities 20 (83%) showed Helicobacter pylori infection. Of the total 250 patients, 25 patients (10%) showed positive anti-tissue transglutaminase antibody screens, nine (3.6%) of whom showed microscopic and macroscopic enteritis (Marsh I to IIIc). Clinically, there was no way to distinguish the presentation of celiac disease from those cases infected with Helicobacter pylori. Histology, even in patients with positive antibody screens, was non-specific and not useful. The results also showed a high prevalence of Helicobacter pylori infection and chronic gastritis in the study group. However, neither was associated with celiac disease, but rather, matched average rates in Western population studies. Source: Archives of Iranian Medicine, March 2011
  21. Eur Psychiatry. 2004 Aug;19(5):311-4. Celiac.com 09/12/2004 - Israeli researchers conducted a study designed to determine whether or not an association exists between celiac disease and schizophrenia. Past studies have indicated that such a connection may exist. The researchers screened 50 consecutive patients over 18 years old who were diagnosed with schizophrenia and their matched controls for celiac-specific anti-endomysial IgA antibodies. All patients also completed a detailed questionnaire. There were no significant differences between the groups in gender, Body Mass Index (BMI) or country of birth, and the mean age of the study group was significantly higher than the controls. All tests for anti-endomysial antibodies in both groups were negative, and the researchers concluded that "In contrast to previous reports, we found no evidence for celiac disease in patients with chronic schizophrenia as manifested by the presence of serum IgA anti-endomysial antibodies. It is unlikely that there is an association between gluten sensitivity and schizophrenia" Celiac.com Comments on this Study: This was a relatively small study that did not include other celiac disease screening methods, such as IgG (antigliadin antibody), tTG (tissue Transglutaminase), or intestinal biopsies. A recent study has shown that only 77% of those with total and 33% of those with partial villous atrophy actually have positive blood tests for celiac disease, so many cases of celiac disease may be missed by using only blood tests to screen for it. Further, about 4% of celiacs are anti-endomysial IgA deficient, so anyone in this subclass would have been missed in the study. Given such a small number of people in the study--50--if even one celiac were missed it would greatly affect the outcome of the study. Both groups should have been given much more comprehensive celiac disease screening to ensure that no cases of celiac disease were missed. In the article by Dr. Hadjivassiliou titled Gluten Sensitivity as a Neurological Illness he says: The introduction of more celiac disease specific serological markers such as anti-endomysium and more recently transglutaminase antibodies may have helped in diagnosing celiac disease but their sensitivity as markers of other manifestations of gluten sensitivity (where the bowel is not affected) is low. This certainly reflects our experience with patients with gluten sensitivity who present with neurological dysfunction. Endomysium and transglutaminase antibodies are only positive in the majority but not in all patients who have an enteropathy. Patients with an enteropathy represent only a third of patients with neurological manifestations and gluten sensitivity. Antigliadin antibodies unlike endomysium and transglutaminase antibodies are not autoantibodies. They are antibodies against the protein responsible for gluten sensitivity. Only one third of the patients with neurological disorders associated with gluten sensitivity have villous atrophy on duodenal biopsy. Even some with biochemical markers of malabsorption such as low serum vitamin B12, low red cell folate, or vitamin D concentrations had normal conventional duodenal histology. These cases may illustrate the patchy nature of bowel involvement in coeliac disease and the inaccurate interpretation of duodenal biopsies by inexperienced histopathologists. Preliminary data based on staining of the subpopulation of T cells in the small bowel epithelium suggests that these patients have potential celiac disease. There are, however, patients where the immunological disorder is primarily directed at the nervous system with little or no damage to the gut. Our practice is to offer a gluten-free diet to these patients unless the HLA genotype is not consistent with susceptibility to gluten intolerance (that is, other than HLA DQ2, DQ8, or DQ1). All patients are followed up and any clinical response is documented.
  22. The following piece was written by Ronald Hoggan who is a teacher at Queen Elizabeth High School in Calgary, Alberta, Canada. There is much evidence linking untreated celiac disease with malignancy. I have recently been notified of publication of a report I have written on that connection, which is promised for the September, 1997 issue of Medical Hypotheses (1). In that report, I combine a review of the literature with an outline of a possible biochemical pathway whereby psychoactive peptides derived from the pepsin digests of wheat, rye and barley may down-regulate the activation of natural killer cells, the bodys first line of defense against malignancy. This is not a postulation that glutinous grains are carcinogenic. Humankind has been exposed to carcinogens throughout its ~ two million year evolution. But it is only in recent centuries that malignancy has increased exponentially, and has struck so many children and adolescents. This is clearly a counter-evolutionary trend when youngsters are afflicted, because the incidence should be decreasing over time, as these youngsters genes are being pruned from the gene pool. There is some evidence that has come to light since my aforementioned report, which will be of interest to celiacs and members of their families. M. Stanislas Tanchou, a truly visionary physician, and campaigned with Napoleon Bonaparte, presented a paper to the Paris Science Society in 1843, which was a complex statistical examination of malignancy, offering evidence of increased malignancy with increased civilization (2). One of the prime indicators of a civilizing trend was a diet that included cereal grains. The greater the consumption of these foods, the greater the incidence of malignancy (3). Dr. Chris Reading, an orthomolecular psychiatrist, in Australia, has documented the treatment of five cancer patients for depression (4). His testing for food allergies, and subsequent treatment of depression with dietary exclusion of cereal grains resulted in total remission of the cancers (which were also given conventional treatments) in all five patients he reports treating. One of these patients did die, but that was from the cancer treatment. There are also two reports in the Journal of Clinical Gastroenterology (5) Lancet (6) that I cite in my Medical Hypotheses article. These reveal a total remission of malignancy in each patient. One report then recants the original diagnosis, and identifies the correct diagnosis as lymphadenopathy. In the other report, which spurs a heated debate, the original diagnosis is supported by a resected section of malignant bowel, and there can be no doubt as to the correct diagnosis. Further, in a 1977 report, in Nutrition and Cancer (8), from Stanford University, all the children suffering from radiation and chemotherapy damage to the small bowel recovered fully from their chronic enteritis, and suffered no relapse of either the bowel obstruction or the disease. The treatment they were given was a gluten-free, dairy-free, low fat, low residue diet. In an obscure Czech journal, a report has recently indicated that one or more of the gliadins, a sub-set of proteins in gluten, may also interfere with natural killer cell activation in peripheral blood (9). They tested the levels of natural killer cell activation in normal, and in treated celiacs, and found no significant difference. BUT, after 30 minutes exposure of the celiacs blood to gliadin, there was a reduced activation of natural killer cells. For the last hundred years, billions of dollars have been spent identifying carcinogens. Most of what we encounter in our environment appears to have some measure of carcinogenic potential. Unfortunately, we have failed to reconcile that Humanity has been exposed to most of these carcinogens throughout its evolution. Conventional wisdom has pointed to the increasing levels of chemical pollution and environmental damage. And I do not doubt that these factors are contributing to the current epidemic of malignancy. What I do doubt is that segment of the population, variously reported at 20% to 30%, which has the HLA factors which predispose to celiac disease and many other autoimmune diseases, can mount an adequate immune response, with natural killer cells, against malignancy. References: Hoggan R, Considering Wheat, Rye, and Barley Proteins as Aids to Carcinogens in press Medical Hypotheses, 1997. Tanchou S, Statistics of Cancer London Lancet 1843; Aug 5, 593. Audette R, personal communication. Reading C, Meillon R, Your Family Tree Connection, Keats; New Canaan, Conn.: 1988. Wink A, et. al. Disappearance of Mesenteric Lymphadenopathy with Gluten-Free Deit in Celiac Sprue, J. Clin. Gastroenterol, 1993; 16(4): 317-319. Wright DH, et. al. Celiac disease and Lymphoma, Lancet 1991; 337:1373. Wright DH, et. al. letter Lancet 1991; 338: 318-319. Donaldson SS, Effect of Nutrition as Related to Radiation and Chemotherapy, Nutrition and Cancer, Winick ed. 1977; Wiley & Sons, NewYork, 137153. Castany M, Nguyen H, Pospisil M, Fric P, Tlaskalova-Hogenova H, Natural Killer Cell Activity in Celiac Disease: Effect of in Vitro Treatment on Effector Lymphocytes and/or Target Lymphoblastoid, Myeloid and Epithelial Cell Lines with Gliadin, Folia Microbial, 1995 (Praha) 40; 6: 615-620.
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