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    Celiac the Mysterious and the Medical Need for Gluten Free Diet


    Melissa Reed
    Image Caption: Photo: CC--Orin Zebest

    Celiac.com 08/10/2014 - Gluten comes from the Latin word for glue. It is a protein in wheat and other grains. It will elicit an autoimmune response in celiacs. Other grains like barley, rye and spelt contain gluten as well. In wheat products, the difficult part for celiacs to digest is gliadin. Some fad diets may try to claim glaidin is new, but it is not, and to dispel another myth there isn’t any wheat on the market that is genetically modified.


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    Photo: CC--Orin ZebestCeliac diease isn't diagnosed as often as it should be. In turn, individuals suffer with it for years, not knowing what to do or how to feel better. Celiac disease is often misdiagnosed for different ailments that have similar symptoms. It can seem to be mysterious, since often it takes time to find out what issue is causing the entire ruckus. There are several symptoms that overlap between celiac and other autoimmune disorders, like Type 1 diabetes, IBS, Crohn's and Hashimoto Thyroiditis. Celiac disease and other autoimmune disorders are known to have neurological effects that sometimes result in ataxia, numbness and pain, so Lupus, rheumatoid arthritis or similar disorders often get confused for celiac.To make it more confusing some autoimmune disorders can be triggered by untreated celiac disease.

    Celiac is a genetic disease that is not contagious, but it does medically require a gluten-free diet. An individual with celiac must be careful to read labels on all products they consume. They must be aware of co-mingling of food ingredients in preparation of their meals and must be diligent to not ingest a crumb of gluten!

    There are individuals that don't have the genetic makeup for celiac disease, but yet seem to be unable to digest gluten. Those individuals are considered gluten sensitive. There unfortunately are no tests or strict criteria to diagnose gluten sensitivity, according to a recent Webinar from National Foundation for Celiac Awareness. The gluten sensitivity issue is not yet as clearly defined as celiac disease. Some individuals with gluten sensitivity do have a problem digesting gluten, but it often is just not as severe as the gluten autoimmune reaction that happens to those with celiac disease.

    If you feel you may need a gluten-free diet, do not start one until you see a doctor who will likely recommend that you get screened for celiac disease. A celiac diagnosis begins with a blood test. If the test is positive then your doctor may direct you to a specialist for more testing, and after diagnosis send you to visit a Registered Dietitian or advise you to start a gluten-free Diet. Again, please do not start a gluten-free diet before your doctor does a test for celiac, it may make your test results inaccurate.

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    Everything in this article is accurate. The genetically modified wheat of today has many doctors choosing not to eat food products that contain wheat. This practice is kept under the radar from the public for fear of retribution from the wheat lobby in Washington.

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    This article is incorrect! Most wheat available in the US market is GMO! The only exceptions are wheat sources from non-government subsidized farmers! What an outrage that the people who want to help those suffering with this disease either don't know the facts or purposefully mislead the very population they hope to help. GMOs should be clearly labeled on our foods so we can choose! GMO foods are toxic to everyone

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  • Related Articles

    Scott Adams
    An article on celiac disease by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health, Bethesda, Maryland, at http://www.niddk.nih.gov/health/digest/pubs/celiac/index.htm states the following:
    In Italy, where celiac disease is common, all children are screened by age 6 so that even asymptomatic disease is caught early. In addition, Italians of any age are tested for the disease as soon as they show symptoms. As a result of this vigilance, the time between when symptoms begin and the disease is diagnosed is usually only 2 to 3 weeks. In the United States, the time between the first symptoms and diagnosis averages about 10 years.

    Scott Adams
    Am J Gastroenterol. 2002;97(11):2702-2704, 2785-2790
    Celiac.com 04/30/2003 - The results of a population-based study published in the November 2002 edition of the American Journal of Gastroenterology indicate that it is time to change celiac disease screening methods. Karoly Horvath, MD, PhD, from the University of Maryland School of Medicine in Baltimore, and Ivor D. Hill, MD, from Wake Forest University School of Medicine in Winston-Salem, North Carolina, found that testing first for tissue transglutaminase (tTG) antibodies followed by endomysial antibodies may eliminate the need to screen using antigliadin IgA.
    Using a community-based population the researchers screened the blood of 1,000 consecutive subjects (age 16 to 71 years, 497 women) using the three tier classic screening which looks at IgG and IgA antigliadin antibodies, followed by endomysial antibodies (EmA) and total serum IgA in positive patients, and finally at intestinal biopsies of patients with positive EmA. The study screening protocol consisted of the use of a commercial guinea pig anti-tTG antibodies and total serum IgA, the with EmA (IgA and/or IgG) for positive patients followed by intestinal biopsies.
    The classic screening found five patients who were eligible for intestinal biopsy, and celiac disease was confirmed in all five. The study group yielded the five patients identified in the classic screening, plus two more with positive IgG antigliadin antibodies and normal total serum IgA (both were positive for EmA).
    Juan C. Gomez, MD, and colleagues from San Martin Hospital in La Plata, Argentina write: "Our data showed that a new screening protocol using [anti-tTG] as first line followed by endomysial antibodies is a cost-effective screening and yielded more realistic figures of prevalence for celiac disease in a community setting than the classic three-level sequential evaluation using antigliadin antibodies." In addition to being more sensitive than the classic method of detection, the new screening protocol is cheaper: $3,006 per new patient detected vs. $4,687. Further: Although we still did not perform intestinal biopsy on all those subjects with positive anti-tTG tests but negative EmA, current evidence appears to suggest that the addition of EmA to the seropositive anti-tTG patients might have a key role in the simplified screening avoiding unnecessary biopsies, although the researchers still recommend using a biopsy to confirm diagnosis until the new protocol can be standardized.
    In conclusion: We recommend using the anti-tTG as the initial test in both population screening studies and for individual cases suspected of having celiac disease on the basis of symptoms or conditions associated with the condition...(T)hose with positive results should be tested for EmA as a second step in the screening process and, if positive, should undergo an intestinal biopsy for confirmation of the diagnosis.

    Jefferson Adams
    Celiac.com 11/16/2009 - Could unknown benefits from one of the oldest parasites of the human digestive tract hold the key to cure for celiac disease?
    Australian scientists think so. Encouraged by successful treatments of Crohn's and ulcerative colitis by American researchers using a pig whipworm (Trichuris sues), a team of Australian researchers is recruiting volunteers with celiac disease for trials using human hookworm (Necator americanus).
    The researchers have undertaken a similar preliminary study using a human hookworm in Crohn's patients.
    Researchers hypothesize that the disappearance of intestinal parasites from humans in developed countries may be responsible for the upsurge in many diseases including Celiac Disease, Crohn's, ulcerative colitis, asthma and hay fever.
    Using a small group of healthy people with celiac disease, the investigators will look to see if human hookworm interferes with the human immune reaction to gluten.
    Parasites survive partly by interfering with the host's immune response. The mechanisms they use to accomplish this are similar to those required by a person to regulate against the so-called autoimmune disorders, wherein the body begins to fight against itself.
    The investigators suspect that when parasites are excluded from the environment, some individuals become sufficiently self-reactive to develop an autoimmune disease.
    Using a small group of healthy people with celiac disease, the investigators will test if a human hookworm, Necator americanus, inhibits immune responsiveness to gluten.
    Specifically, they will examine whether hookworm infection will change the immune processes and suppress gluten sensitivity in people with celiac disease.
    Celiac disease is a good model for studying Crohn's disease because both involve similar immune changes. However, celiac patients are usually healthier overall, and, importantly, are not taking powerful immune suppressive drugs, and the provocative antigens (molecules that engage the immune system and provoke the disease) are well known and can be administered or cut out at will.
    In addition to directly benefitting celiac disease sufferers, this study may provide potential guidance in the use of hookworms to control inflammatory bowel disease.
    The study is open to people with proven celiac disease who reside in Brisbane, Australia. Those who enroll will be required to avoid gluten for six months.
    The blinded study will compare disease activity and immunity after a controlled break from the gluten-free diet in celiac patients, before and after hookworm infection.
    The team will use conventional and experimental methods to examine the disease severity and the immune system of celiac subjects before and after being inoculated with N. americanus.
    They will then compare immunity levels of the study subjects
    against those of matched, celiac control subjects (not infected with hookworm), before and after eating four pieces of standard white bread each day for three to five days.
    The initial study group will be small. The researchers will recruit ten subjects for each arm of the study, for a total of twenty.
    Initially, ten larvae will be placed on the skin under a light dressing for thirty minutes, followed by five more after twelve weeks.
    The researchers intend to asses whether the hookworm infection will change the immune processes and suppress gluten sensitivity in people with celiac disease. Outcomes to be measured will be those that reflect the activity of celiac disease.
    Stay tuned to see if hookworm therapy will be coming to a gastroenterologist near you! Tell us what you think. Would you sign up? Comment below.
    Source:
    ClinicalTrials.gov


    Jefferson Adams
    Celiac.com 10/24/2012 - Doctors can face challenges when attempting to diagnose celiac disease in patients who have already begun a gluten-free diet, and/or when the results of tests are inconsistent.
    To better understand this problem, a group of researchers set out to assess the benefits of an in vitro gliadin challenge.
    The research team included Raffaella Tortora, MD, Ilaria Russo, PhD, Giovanni D. De Palma, MD, Alessandro Luciani, PhD, Antonio Rispo, MD, Fabiana Zingone, MD, Paola Iovino, MD, Pietro Capone, MD and Carolina Ciacci, MD.
    The study cohort included 57 patients without celiac disease, 166 patients with untreated celiac disease, 55 patients with celiac disease on a gluten-free diet, and 59 patients with challenging diagnosis.
    The team provided all patients with endoscopy for collection of duodenal samples, which served for the diagnosis of celiac disease and for the in vitro evaluation of the gliadin-induced mucosal expression of seven inflammatory markers: PY99, ICAM-1 (intercellular cell adhesion molecule), HLA-DR, CD3, CD25, CD69, and transglutaminase 2 IgA.
    Diagnostic work-up for celiac disease included the search of specific serum antibodies. Researchers asked patients in the challenging diagnosis group to stop gluten-free diet to facilitate the search for these antibodies under untreated conditions.
    They used the area under the receptor-operated curve (ROC) for statistical analyses on accuracy.
    For patients with and without celiac disease (not including those on a gluten-free diet) HLA-DR offered the best accuracy for diagnosing celiac disease (area under ROC = 0.99).
    Combining the data from the HLA-DR with data of other markers did not increase test accuracy.
    The team found similar results in the 39 patients of the difficult diagnosis group undergoing the search celiac disease-speciï¬c antibodies under untreated conditions.
    In vitro testing of mucosal HLA-DR to gliadin is an accurate tool for the diagnosing celiac disease, and also works in patients who are hard to diagnose.
    Source:
    Am J Gastroenterol 2012; 107:111–117; doi:10.1038/ajg.2011.311; published online 27 September 2011

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
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    Cover and refrigerate for at least 1 hour. 
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    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
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    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    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.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    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.