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    High Levels of Oxidative DNA Damage in Children with Celiac Disease


    Jefferson Adams
    High Levels of Oxidative DNA Damage in Children with Celiac Disease
    Image Caption: New study on DNA damage and celiac disease

    Celiac.com 09/20/2010 - People with celiac disease face increased risk of cancer and a large amount of circumstantial evidence suggests that oxidatively damaged DNA may be used to help predict future cancer development in celiac patients.

    To evaluate that hypothesis, a research team set out to assess and describe oxidative stress and oxidative DNA damage in celiac disease patients.

    Anna Szaflarska-PopÅ‚awska, Agnieszka Siomek, MieczysÅ‚awa Czerwionka-Szaflarska, Daniel Gackowski, RafaÅ‚ Różalski, Jolanta Guz, Anna Szpila, Ewelina Zarakowska and Ryszard OliÅ„ski comprised the research team. They are associated with the college of medicine at Nicolaus Copernicus University, in Bydgoszcz, Poland.

    They found that children with celiac disease have higher than normal levels of the oxidative DNA damage biomarkers urinary 8-oxodG and 8-oxoGua, regardless of following a gluten-free diet.

    To measure urinary excretion of 8-oxodG and 8-oxoGua, and levels of oxidative DNA damage in the leukocytes, as well as the level of antioxidant vitamins, the team used high-performance liquid chromatography (HPLC) and HPLC/gas chromatography with isotope dilution mass detection.

    They observed parameters for DNA damage in a group of children with untreated celiac disease, in a group of children with celiac disease following a strict gluten-free diet, and in a control group of healthy children.

    They found that the two groups of celiacs showed significantly higher overall levels of 8-oxodG in DNA isolated from the leukocytes and from the urine samples than did the control subjects, without regard to diet. There was no significant difference  between treated and untreated celiacs. That means being on a gluten-free diet offered no protection from oxidative DNA damage for all children with celiac disease.

    One key difference was that the untreated celiac children showed significantly lower levels of retinol and α-tocopherol, vitamin A and E, compared to the treated celiac children. Between group difference of 0.31 and 3.76 µmol/l, respectively, suggests that a gluten-free diet offers some protection against oxidative damage in treated celiacs.

    From the results indicate that oxidative stress and/or oxidatively damaged DNA in celiac patients cannot be explained by diet alone, and that factors independent of diet play an important role.

    Supplemental vitamin A and E in celiac disease patients may help minimize the risk of cancer development.

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    Guest CeliBelli

    Posted

    What neither the study abstract, nor this restatement of it, disclose is how long the children had been on the gluten free diet. Had all children in group 'b' been on a gluten free diet since birth? Or had they been diagnosed subsequent to birth, and therefore exposed to gluten for some length of time? In addition, there is no mention of the mothers of these children. If the children were gluten free from birth, were their mothers living gluten free while pregnant?

     

    It seems to me that in order to draw the conclusion that the DNA damage cannot be attributed to diet alone, a study would have to control for these factors. If they want to draw conclusions regarding whether or not diet or something else is at work on the DNA of Celiac children, they would have to use a group of children whose mothers had observed strict gluten free diets throughout pregnancy and who then themselves were on strict gluten free diets from birth.

     

    If they did exercise such strict controls, they do not mention it in their abstract, and Mr. Adams does not probe the study for it. Without such strict controls, the study's conclusion that something other than diet is impacting DNA cannot be considered valid.

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    Guest Gloria Brown

    Posted

    The influence of gluten ingested from airborne sources needs to be considered when celiac on gluten free and non-gluten free diets are being studied.

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    More proof that we don't really understand celiac yet. We're only seeing one piece of it (the damage to the stomach and digestion, the autoimmune syndrome). People with celiac are more likely to have problems with yeast overgrowth, heavy metal toxicity, fibromyalgia, etc., even long after they've eliminated all gluten from their diets. I really hope the medical communities will pick up on this and start looking at celiac more holistically.

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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 Dangerous Grains by James Braly, MD and Ron Hoggan, MA.

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    Virchows Archive, Volume 456, Number 3 / March, 2010

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    Gluten-Free Dietary Compliance and Psychosocial Challenges in Indian Children with Celiac Disease
    Celiac.com 07/20/2010 - Anyone who's tried to maintain a gluten-free diet for celiac disease or other reasons can likely tell stories about the difficulties and challenges they face on a regular basis. Still, very little research has been done regarding the psychological and social challenges faced by people with celiac disease who are attempting to follow a gluten-free diet.
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    Source:

    Indian Journal of Pediatrics 2010 Jun;77(6):649-54. DOI 10.1007/s12098-010-0092-3

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    HLA-DQ2 and -DQ8 Genotypes in Libyan Children with Celiac Disease
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    Lastly, the prevalence of HLA-DQ2 and -DQ8 genes was higher among the Libyan general population that among the Italian population, which suggests a strong genetic predisposition to celiac disease among the Libyan population.
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    Digestive and Liver Disease 42 (2010) 425–427

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    Source:
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