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  • Jefferson Adams
    Jefferson Adams
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    Study Finds Celiac Disease in Native South American Toba People

    Celiac.com 10/21/2015 - Celiac disease has been traditionally recognized among Caucasians, with an estimated prevalence of about 1%. Latin America features a the population with European ancestry, along with native communities sharing a diverse degree of mix with European colonizers.

    Photo: CC--Beatrice MurchThe population of native Toba people comprises more than 60,000 individuals living with a clusters of villages in a forest called 'The Impenetrable' in Northeastern Argentina.

    In recent years, as a consequence of governmental food aid programs aimed at improving nutritional conditions in the community, the Toba people have undergone a drastic change in dietary habits, with wheat replacing their ancestral food sources.

    In general celiac disease can only occur in individuals with certain class II human leukocyte antigen (HLA) molecules – namely, HLA DQ2 and/or DQ8, but little information exists about the prevalence of HLA DQ2 and DQ8, and of celiac disease in native South Americans.

    The research team included Horacio Vázquez MD, María de la Paz Temprano RD, Emilia Sugai MS, Stella M Scacchi MS, Cecilia Souza MD,Daniel Cisterna MS, Edgardo Smecuol MD, María Laura Moreno MD, Gabriela Longarini MD, Roberto Mazure MD, María A Bartellini MS, Elena F Verdú MD2, Andrea González RD, Eduardo Mauriño MD, and Julio C Bai MD. They are variously affiliated with the Small Bowel Section, Department of Medicine, Hospital de Gastroenterología C Bonorino Udaondo. Buenos Aires, Argentina and the Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario.

    For their study, the research team set out to prospectively assess environmental, genetic and serological conditions associated with celiac disease among members of the Toba native population attending a multidisciplinary sanitary mission. Using an established questionnaire, an expert nutritionist determined daily gluten intake. The team then conducted gene typing for the human leuko-cyte antigen (HLA) class II alleles using DNA extracted from peripheral blood (HLA DQ2/DQ8 haplotype).

    The team then measured serum antibodies were immunoglobulin (Ig) A tissue transglutaminase (tTG) and the composite deamidated gliadin peptides/tTG Screen test. They tested positive cases for IgA endomysial antibodies.

    The team screened a total of 144 subjects, 55% of those female. Estimated average gluten consumption was 43 grams per day, ranging from 3 grams per day up to 185 grams per day. Genetic typing showed that 73 of 144 subjects had alleles associated with celiac disease; 69 of these subjects had alleles for HLA DQ8, while four had DQ2.

    Four and six subjects had antibody concentrations above the cut-off established by the authors' laboratory (>3 times the upper limit of normal) for IgA tTG and deamidated gliadin peptides/tTG screen, respectively. Four of these had concomitant positivity for both assays and endomysial anti-bodies were positive in three subjects who also presented a predispos-ing haplotype.

    The present study was the first to detect celiac disease in Native Americans. The native Toba ethnic population has very high daily gluten consumption, and a predisposing genetic background.

    This study found subjects with persistent celiac disease autoimmunity and, at least, three of them met serological criteria for celiac disease diagnosis. 

    This study invites some questions about gluten and celiac disease in the tribe. For example, does the amount of gluten in the diet of people with genetic predisposition have an impact on the likelihood of celiac disease? Given that many of these people likely had DQ2/DQ8 positivity for many generations, did the introduction of wheat into their diets trigger their celiac disease?

    Much remains to be understood about celiac disease, and studies like this can be important and insightful.

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  • About Me

    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, and science. He previously served as Health News Examiner for Examiner.com, and provided health and medical content for Sharecare.com. Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

  • Related Articles

    Jefferson Adams
    Non-classical Symptoms Common for Vast Majority with Celiac Disease
    Celiac.com 12/26/2014 - Celiac disease can have such a wide-ranging number of symptoms, ranging over so many parts of the body, that it can be hard for doctors seeking to make a diagnosis to even suspect celiac disease as an underlying cause in the first place.
    A team of researchers set out to better understand the characteristics of celiac disease by looking at the findings in a large number of celiacs diagnosed in a single referral center, and to using clear definitions of the clinical, serological and histopathological aspects of celiac disease to get a better picture of how the disease presents itself.
    The research team included Umberto Volta, Giacomo Caio, Vincenzo Stanghellini and Roberto De Giorgio of the Department of Medical and Surgical Sciences at the University of Bologna’s S. Orsola-Malpighi Hospital, in Bologna, Italy.
    For their study, their team looked at data on celiac patients admitted to S. Orsola-Malpighi Hospital from January 1998 to December 2012. They found a total of 770 patients ranging from 18 to 78 years, averaging 36 years old. A total of 599 patients were female.
    The team broke celiac disease down into three types: The first type, classical, in which patients present with malabsorption syndrome. The second type, non-classical, in which patients experience extraintestinal and/or gastrointestinal symptoms other than diarrhea. The third type, subclinical, with no visible symptoms.
    The team evaluated patient serology, duodenal histology, comorbidities, response to gluten-free diet and complications.
    A total of 610 patients (79%) showed clear physical symptoms when they were diagnosed, while 160 celiacs showed a subclinical phenotype.
    In the symptomatic group 66% of celiacs were non-classical, that is, they experienced extraintestinal and/or gastrointestinal symptoms other than diarrhea.
    Only 34% of patients in the symptomatic group showed classical malabsorption syndrome.
    The team found that just 27% of the non-classically symptomatic group complained of diarrhea, while other gastrointestinal manifestations included bloating (20%), aphthous stomatitis (18%), alternating bowel habit (15%), constipation (13%) and gastroesophageal reflux disease (12%). Extraintestinal manifestations included osteopenia/osteoporosis (52%), anemia (34%), cryptogenic hypertransaminasemia (29%) and recurrent miscarriages (12%).
    Positivity for IgA tissue transglutaminase antibodies was detected in 97%. Th steam found villous atrophy in 87%, while 13% had minor lesions consistent with potential celiac disease.
    A large proportion of patients showed autoimmune disorders, such as autoimmune thyroiditis (26.3%), dermatitis herpetiformis (4%) and diabetes mellitus type 1 (3%). Complicated celiac disease was very rare.
    This study demonstrates that the clinical profile of celiac disease has changed over time, and now features much more non-classical and subclinical phenotypes.
    Source:
    BMC Gastroenterology 2014, 14:194. doi:10.1186/s12876-014-0194-x

    Jefferson Adams
    Celiac.com 07/27/2015 - First-degree relatives of individuals with celiac disease are at increased risk for this disorder, but little is known about their risk for other autoimmune diseases.
    A research team recently set out to assess the risk of non-celiac autoimmune disease in first-degree relatives and spouses of people with celiac disease.
    The research team included Louise Emilsson, Cisca Wijmenga, Joseph A. Murray, and Jonas F. Ludvigsson. They are variously affiliated with the Primary Care Research Unit, Vårdcentralen Värmlands Nysäter, Värmland County, Sweden, the Department of Health Management and Health Economy, Institute of Health and Society, University of Oslo, Oslo, Norway, the Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands, the Division of Gastroenterology and Hepatology, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden, and with the Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    The team found individuals with celiac disease by searching computerized duodenal and jejunal biopsies, collected from 1969 through 2008, at 28 pathology departments in Sweden.
    The team found 29,096 patients with celiac disease based on biopsy reports of villous atrophy of Marsh grade 3 or higher and matched individuals with celiac disease with up to 5 of 144,522 non-celiac control patients based on sex, age, county, and calendar year.
    Through Swedish health care registries, the team identified all first-degree relatives (fathers, mothers, siblings, and offspring) and spouses of 84,648 individuals with celiac disease, and 430,942 control subjects. The team used Cox regression analysis to calculate hazard ratios (HRs) for non-celiac autoimmune disease, such as Crohn’s disease, type 1 diabetes mellitus, hypothyroidism, hyperthyroidism, psoriasis, rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus, or ulcerative colitis, within these groups.
    Cox analysis showed that during the follow-up period averaging just under 11 years, nearly 3333, or 4%, of the first-degree relatives of patients with celiac disease, and 12,860 relatives of controls (3.0%), had an autoimmune disease other than celiac disease.
    First-degree relatives of people with celiac disease had an increased risk of non-celiac autoimmune disease, compared with controls (HR, 1.28; 95% confidence interval, 1.23–1.33), as did spouses (HR, 1.20; 95% confidence interval, 1.06–1.35).
    Risk estimates for non-celiac autoimmune disease did not differ between first-degree relatives and spouses of individuals with celiac disease (interaction test: P = .11). Hazard Ratios for non-celiac autoimmune disease were highest in the first 2 years of follow-up evaluation.
    First-degree relatives and spouses of individuals with celiac disease have a significantly higher risk of non-celiac autoimmune disease.
    In addition to genetic factors, environmental factors and better awareness, testing and diagnosis might influence rates of autoimmune disorders in first-degree relatives of individuals with celiac disease.
    Source:
     Clinical Gastroenterology and Hepatology. DOI: http://dx.doi.org/10.1016/j.cgh.2015.01.026

    Jefferson Adams
    Celiac.com 08/10/2015 - The presence of specific human leukocyte antigen-DQ2 and DQ8 seems to be necessary for celiac disease development, but its usefulness for screening is still uncertain.
    A research team recently set out to conduct a systematic review and meta-analysis of the diagnostic performance of human leukocyte antigen typing tests for celiac disease screening. The research team included A. Díaz-Redondo, J. Miranda-Bautista, J. García-Lledó, J.P. Gisbert, and L. Menchén. They are variously affiliated with the Hospital General Universitario Gregorio Marañón in Madrid, Spain, and with the Instituto de Investigación Sanitaria Gregorio Marañón, Madrid, Madrid, Spain.
    The team conducted a systematic review of published studies assessing accuracy of human leukocyte antigen DQ2 and DQ8 typing for the detection of celiac disease. They searched MEDLINE and EMBASE for the period running from 1st January 2004 until 31st December 2013 and used two independent researchers to carry out selection and classification of studies, data extraction and analysis.
    The team conducted meta-analysis that combined sensitivities, specificities and likelihood ratios of HLA-DQ2 and DQ8 for the diagnosis of celiac disease and ended up with six studies that included a total of 1303 people. The results showed pooled sensitivity at 98%, with 95% confidence interval: 97-99. Overall specificity was 45% (95% confidence interval: 41-48).
    Regarding specificity, studies were heterogeneous and a the team ran a subgroup analysis according to the type of population included. Overall negative likelihood ratio was 0.05 (0.03-0.09).
    Because it offers high sensitivity and low negative likelihood ratio, the team concludes that human leukocyte antigen-DQ2/DQ8 typing makes an appropriate test for ruling out celiac disease in the general population suffering related symptoms, and even more in at risk population.
    Source:
    Rev Esp Enferm Dig. 2015 Jul;107(7):423-429.

    Jefferson Adams
    Scientists Finally Know What Causes Celiac Disease!
    Celiac.com 08/19/2015 - For the first time since it was described and named by 1st century Greek physician Aretaeus of Cappadocia, first linked to wheat in the 1940's, and specifically linked to gluten in 1952, scientists have discovered the cause of celiac disease.
    Professor Ludvig Sollid, and his team at the Centre for Immune Regulation at University of Oslo, have discovered that people with celiac disease suffer from one of two defective human leukocyte antigens (HLAs), which cause the immune system to see gluten molecules as dangerous, triggering the immune response that causes classic celiac-associated inflammation and other symptoms.
    To be true, the team was not working in the dark. They were armed with a complete map of the genes, an understanding that two types of HLA (HLA-DQ2 and HLA-DQ8) predispose a person for celiac disease, and the very crucial recent discovery by a team of German colleagues that celiac patients have antibodies for a very precise enzyme: transglutaminase 2.
    "We also found that the bits of gluten that were presented to the T-cells have some changes caused by an enzyme in the body – transglutaminase 2", says Sollid. HLAs are proteins which act as markers, binding to fragments of other proteins, and telling T-cells how to treat them.
    So it wasn't much of a stretch for Professor Sollid's team to determine that the defective HLAs bind to fragments of gluten, causing the T-cells to treat them as bacteria or viruses.
    Basically, two HLA types present gluten remnants to the T-cells, causing the T-cells to regard the gluten as dangerous, and to trigger immune reactions that cause inflammation in the intestines, and this is what causes celiac disease.
    "We think that this is huge," Sollid said. "We understand the immune cells that are activated and why they are activated."
    At present, Professor Sollid and his group are investigating how antibodies against transglutaminase are formed.
    This is a simple, but huge moment in the annals of medicine and in the annals of celiac disease. It's a discovery that will help researchers develop new approaches to treatment, and/or a cure for celiac disease in the future.
    Source:
    Med.uio.no

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    Thank you GFinDC. Question. When you say, "quick rinse", can you define what is safe for us to use when washing our fruits and veggies? I know that might sound like something I should know but I am seriously taking no chances (at least not on purpose). I've been buying organic produce because I was told I needed to. Do you find that to be true or do I need to find a new nutritionist? 😉
    Hi Wade, You areright, there are lots of little gotchas out there in the gluten-filled world.  That's why it is easier/safer to stick with whole foods at the beginning of the gluten-free diet.  The list of ingredients on an apple or an orange or a steak is usually real short.  So you can get out of the grocery store quicker by eating whole foods like those.  Plain frozen veggies or canned are usually safe too.  And fresh produce as long as you give it a quick rinse.
    Why....why would your doctor not follow the standard of care for testing celiac disease?  I think you need to think about  finding another doctor.  If you are in the US, you can “walk” into a lab and order the test and pay cash: https://labtestsonline.org/tests/celiac-disease-antibody-tests No, your result does not significantly lower your odds of getting a celiac disease diagnosis.  She ordered the LEAST commonly used test, especially since she only ordered that one alone.  I think she thinks you do not have celiac disease, but that you may have a gluten sensitivity.  But that is wrong!  There is no test for gluten sensitivity.  http://www.cureceliacdisease.org/screening/ https://www.mayocliniclabs.com/it-mmfiles/Celiac_Disease_Diagnostic_Testing_Algorithm.pdf https://celiac.org/about-celiac-disease/screening-and-diagnosis/screening/ https://www.verywellhealth.com/celiac-disease-blood-tests-562694 https://www.niddk.nih.gov/health-information/diagnostic-tests/celiac-disease-health-care-professionals I am not a doctor though.  Perhaps, you can ask her why she did not order the complete panel or at least the screening tests most often ordered for celiac disease. Know that some celiacs are asymptomatic (no symptoms) Some just have one symptom.  Some have classic symptoms.  I presented with only anemia and no GI symptoms with only a positive on the DGP IgA.    I hope this helps.  
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