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    What's the Best Way to Measure Gluten in Gluten-Free Foods?


    Jefferson Adams


    • A team of researchers recently set out to determine the best way to measure the gluten content of nominally gluten-free foods


    Image Caption: Photo: CC--Bruce Geunter

    Celiac.com 10/16/2017 - In Europe many commercially available, nominally gluten-free foods use purified wheat starch as a base, but what's the best way to way to measure the gluten content of gluten-free foods, particularly those based on purified wheat starch?


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    Currently, the only test for gluten quantitation certified by the Food and Agriculture Organization of the United Nations (FAO) is based on the R5 monoclonal antibody (MAB) that recognizes gliadin, but not glutenin.

    A team of researchers recently set out to determine the best way to measure the gluten content of nominally gluten-free foods, particularly those based on purified wheat starch. The research team included HJ Ellis, U Selvarajah and PJ Ciclitira. They are affiliated with the Department of Gastroenterology, Division of Diabetes and Nutritional Sciences at Kings College London, St Thomas Hospital in London.

    Celiac disease is treated with a strict Gluten-Free Diet (GFD). Gluten is comprised of gliadin, Low (LMWG) and High (HMWG). To estimate gluten content of gluten-free foods, the R5 works by multiplying the R5 gliadin value by two to yield a gluten value.

    The research team raised a panel of monoclonal antibodies to celiac disease toxic motifs. They then assessed the gluten content of three wheat starches A, B, & C that are supplied as standards for the Transia gluten quantitation kit, which is based on a MAB to omega-gliadin. They used separate ELISAs to measure gliadin, Low (LMWG) and High Molecular Weight (HMWG) glutenins.

    They found that the gliadin levels in all three starches were always higher, as measured by one of the antibodies, than the levels measured with the other, and that the ratio between measurements made by the 2 MABs varied from 3.1 to 7.0 fold. The team noted significant differences in glutenin to gliadin ratios for different wheat starches.

    Based on their results, the team suggests that the best way to measure the gluten content of nominally gluten-free foods, especially those containing purified wheat starch, is to first measure gliadin and glutenin, and to then add the values together.

    This is because measurement of gliadin alone, followed by multiplication by two to yield a gluten content, appears to be inadequate for measuring total gluten in processed foods.

    Source:

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  • Related Articles

    Scott Adams
    Celiac.com 01/10/2007 – Celiac disease researchers in Italy and at the Center For Celiac Research in Baltimore, Maryland have conducted a multi center, double-blind, placebo-controlled, randomized trial involving 49 adult individuals who have biopsy-proven celiac disease, and who have been on a gluten-free diet that contains less than 5mg of gluten per day for a minimum of two years. The aim of this study was to determine whether there is a safe threshold for prolonged, daily exposure to minute amounts of gluten. Subjects in the study were divided into 3 groups which were given daily capsules that contained 0mg, 5mg or 50mg of gluten. They were given biopsies and serological screening before and after a gluten challenge. One patient who was given 10mg of gluten daily did experience a clinical relapse, but at the end of the study no significant differences in the IEL count were found between the 3 groups, which lead the researchers to conclude that "(t)he ingestion of contaminating gluten should be kept lower than 50 mg/d in the treatment of celiac disease."
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    Kaukinen K, Salmi T, Huhtala H, et al. Clinical trial: gluten microchallenge with wheat-based starch hydrolysates in celiac disease patients:  a randomized, double-blind, placebo-controlled study study to evaluate safety. Alimentary Pharmacolgy 
    Aliment Pharmacol Ther. 2008 Aug 17.
    Departments of Gastroenterology and Alimentary Tract Surgery, University of Tampere and Tampere University Hospital, Tampere, Finland.


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    Conclusion
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    References
    1. Lo W, Sano K, Lebwohl B, Diamond B, Green PH. Changing presentation of adult celiac disease. Dig Dis Sci 2003; 48:395-8.
    Aliment Pharmacol Ther. 2008; 27:1044-1052. Epub 2008 February 29.



    Jefferson Adams
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    Evidence with this small 60-day dietary study shows that people with celiac disease can safely consume baked goods made from fully hydrolyzed wheat flour, manufactured with sourdough lactobacilli and fungal proteases. This flour shows no toxicicity to patients with celiac disease.
    The team notes that a combined analysis of serologic, morphometric, and immunohistochemical parameters is the most accurate method to assess new therapies for this disorder.
    The results need to be borne out by further study, but, in the future, baked goods made with fully hydrolyzed wheat flour, manufactured with sourdough lactobacilli and fungal proteases may become another option for people with celiac disease.
    Source:

    Clin Gastroenterol Hepatol. 2010 Oct 15. doi:10.1016/j.cgh.2010.09.025

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    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

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    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics

    Jefferson Adams
    Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
    A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.
    For their study, the team collected urine samples from 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIPs and an LFT reader. 
    They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage.
    The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
    Source:
    Gut. 2017 Feb;66(2):250-257.  doi: 10.1136/gutjnl-2015-310148.