Frequently Asked Questions About Celiac Disease

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    Scott Adams
    WHAT IS CELIAC DISEASE?
    Celiac disease is an autoimmune condition that affects around 1.4% of the population (91.2 million people worldwide, and 3.9 million in the U.S.A.). People with celiac disease suffer an autoimmune reaction when they consume wheat, rye or barley. The immune reaction is triggered by certain proteins in the wheat, rye, or barley, and, left untreated, causes damage to the small, finger-like structures, called villi, that line the gut. The damage occurs as shortening and villous flattening in the lamina propria and crypt regions of the intestines. The damage to these villi then leads to numerous other issues that commonly plague people with untreated celiac disease, including poor nutritional uptake, fatigue, and myriad other problems.
    Celiac disease mostly affects people of Northern European descent, but recent studies show that it also affects large numbers of people in Italy, China, Iran, India, and numerous other places thought to have few or no cases.
    Celiac disease is most often uncovered because people experience symptoms that lead them to get tests for antibodies to gluten. If these tests are positive, then the people usually get biopsy confirmation of their celiac disease. Once they adopt a gluten-free diet, they usually see gut healing, and major improvements in their symptoms. 
    CLASSIC CELIAC DISEASE SYMPTOMS
    Symptoms of celiac disease can range from the classic features, such as diarrhea, upset stomach, bloating, gas, weight loss, and malnutrition, among others.
    LESS OBVIOUS SYMPTOMS
    Celiac disease can often less obvious symptoms, such fatigue, vitamin and nutrient deficiencies, anemia, to name a few. Often, these symptoms are regarded as less obvious because they are not gastrointestinal in nature. You got that right, it is not uncommon for people with celiac disease to have few or no gastrointestinal symptoms. That makes spotting and connecting these seemingly unrelated and unclear celiac symptoms so important.
    NO SYMPTOMS
    Currently, most people diagnosed with celiac disease do not show symptoms, but are diagnosed on the basis of referral for elevated risk factors. 

    CELIAC DISEASE VS. GLUTEN INTOLERANCE
    Gluten intolerance is a generic term for people who have some sort of sensitivity to gluten. These people may or may not have celiac disease. Researchers generally agree that there is a condition called non-celiac gluten sensitivity. That term has largely replaced the term gluten-intolerance. What’s the difference between celiac disease and non-celiac gluten-sensitivity? 
    CELIAC DISEASE VS. NON-CELIAC GLUTEN SENSITIVITY (NCGS)
    Gluten triggers symptoms and immune reactions in people with celiac disease. Gluten can also trigger symptoms in some people with NCGS, but the similarities largely end there.

    There are four main differences between celiac disease and non-celiac gluten sensitivity:
    No Hereditary Link in NCGS
    Researchers know for certain that genetic heredity plays a major role in celiac disease. If a first-degree relative has celiac disease, then you have a statistically higher risk of carrying genetic markers DQ2 and/or DQ8, and of developing celiac disease yourself. NCGS is not known to be hereditary. Some research has shown certain genetic associations, such as some NCGS patients, but there is no proof that NCGS is hereditary. No Connection with Celiac-related Disorders
    Unlike celiac disease, NCGS is so far not associated with malabsorption, nutritional deficiencies, or a higher risk of autoimmune disorders or intestinal malignancies. No Immunological or Serological Markers
    People with celiac disease nearly always test positive for antibodies to gluten proteins. Researchers have, as yet, identified no such antobodies or serologic markers for NCGS. That means that, unlike with celiac disease, there are no telltale screening tests that can point to NCGS. Absence of Celiac Disease or Wheat Allergy
    Doctors diagnose NCGS only by excluding both celiac disease, an IgE-mediated allergy to wheat, and by the noting ongoing adverse symptoms associated with gluten consumption. WHAT ABOUT IRRITABLE BOWEL SYNDROME (IBS) AND IRRITABLE BOWEL DISEASE (IBD)?
    IBS and IBD are usually diagnosed in part by ruling out celiac disease. Many patients with irritable bowel syndrome are sensitive to gluten. Many experience celiac disease-like symptoms in reaction to wheat. However, patients with IBS generally show no gut damage, and do not test positive for antibodies to gliadin and other proteins as do people with celiac disease. Some IBS patients also suffer from NCGS.

    To add more confusion, many cases of IBS are, in fact, celiac disease in disguise.

    That said, people with IBS generally react to more than just wheat. People with NCGS generally react to wheat and not to other things, but that’s not always the case. Doctors generally try to rule out celiac disease before making a diagnosis of IBS or NCGS. 
    Crohn’s Disease and celiac disease share many common symptoms, though causes are different.  In Crohn’s disease, the immune system can cause disruption anywhere along the gastrointestinal tract, and a diagnosis of Crohn’s disease typically requires more diagnostic testing than does a celiac diagnosis.  
    Crohn’s treatment consists of changes to diet and possible surgery.  Up to 10% of Crohn's patients can have both of conditions, which suggests a genetic connection, and researchers continue to examine that connection.
    Is There a Connection Between Celiac Disease, Non-Celiac Gluten Sensitivity and Irritable Bowel Syndrome? Large Number of Irritable Bowel Syndrome Patients Sensitive To Gluten Some IBD Patients also Suffer from Non-Celiac Gluten Sensitivity Many Cases of IBS and Fibromyalgia Actually Celiac Disease in Disguise CELIAC DISEASE DIAGNOSIS
    Diagnosis of celiac disease can be difficult. 

    Perhaps because celiac disease presents clinically in such a variety of ways, proper diagnosis often takes years. A positive serological test for antibodies against tissue transglutaminase is considered a very strong diagnostic indicator, and a duodenal biopsy revealing villous atrophy is still considered by many to be the diagnostic gold standard. 
    But this idea is being questioned; some think the biopsy is unnecessary in the face of clear serological tests and obvious symptoms. Also, researchers are developing accurate and reliable ways to test for celiac disease even when patients are already avoiding wheat. In the past, patients needed to be consuming wheat to get an accurate test result. 
    Celiac disease can have numerous vague, or confusing symptoms that can make diagnosis difficult.  Celiac disease is commonly misdiagnosed by doctors. Read a Personal Story About Celiac Disease Diagnosis from the Founder of Celiac.com Currently, testing and biopsy still form the cornerstone of celiac diagnosis.
    TESTING
    There are several serologic (blood) tests available that screen for celiac disease antibodies, but the most commonly used is called a tTG-IgA test. If blood test results suggest celiac disease, your physician will recommend a biopsy of your small intestine to confirm the diagnosis.
    Testing is fairly simple and involves screening the patients blood for antigliadin (AGA) and endomysium antibodies (EmA), and/or doing a biopsy on the areas of the intestines mentioned above, which is still the standard for a formal diagnosis. Also, it is now possible to test people for celiac disease without making them concume wheat products.

    BIOPSY
    Until recently, biopsy confirmation of a positive gluten antibody test was the gold standard for celiac diagnosis. It still is, but things are changing fairly quickly. Children can now be accurately diagnosed for celiac disease without biopsy. Diagnosis based on level of TGA-IgA 10-fold or more the ULN, a positive result from the EMA tests in a second blood sample, and the presence of at least 1 symptom could avoid risks and costs of endoscopy for more than half the children with celiac disease worldwide.

    WHY A GLUTEN-FREE DIET?
    Currently the only effective, medically approved treatment for celiac disease is a strict gluten-free diet. Following a gluten-free diet relieves symptoms, promotes gut healing, and prevents nearly all celiac-related complications. 
    A gluten-free diet means avoiding all products that contain wheat, rye and barley, or any of their derivatives. This is a difficult task as there are many hidden sources of gluten found in the ingredients of many processed foods. Still, with effort, most people with celiac disease manage to make the transition. The vast majority of celiac disease patients who follow a gluten-free diet see symptom relief and experience gut healing within two years.
    For these reasons, a gluten-free diet remains the only effective, medically proven treatment for celiac disease.
    WHAT ABOUT ENZYMES, VACCINES, ETC.?
    There is currently no enzyme or vaccine that can replace a gluten-free diet for people with celiac disease.
    There are enzyme supplements currently available, such as AN-PEP, Latiglutetenase, GluteGuard, and KumaMax, which may help to mitigate accidental gluten ingestion by celiacs. KumaMax, has been shown to survive the stomach, and to break down gluten in the small intestine. Latiglutenase, formerly known as ALV003, is an enzyme therapy designed to be taken with meals. GluteGuard has been shown to significantly protect celiac patients from the serious symptoms they would normally experience after gluten ingestion. There are other enzymes, including those based on papaya enzymes.

    Additionally, there are many celiac disease drugs, enzymes, and therapies in various stages of development by pharmaceutical companies, including at least one vaccine that has received financial backing. At some point in the not too distant future there will likely be new treatments available for those who seek an alternative to a lifelong gluten-free diet. 

    For now though, there are no products on the market that can take the place of a gluten-free diet. Any enzyme or other treatment for celiac disease is intended to be used in conjunction with a gluten-free diet, not as a replacement.

    ASSOCIATED DISEASES
    The most common disorders associated with celiac disease are thyroid disease and Type 1 Diabetes, however, celiac disease is associated with many other conditions, including but not limited to the following autoimmune conditions:
    Type 1 Diabetes Mellitus: 2.4-16.4% Multiple Sclerosis (MS): 11% Hashimoto’s thyroiditis: 4-6% Autoimmune hepatitis: 6-15% Addison disease: 6% Arthritis: 1.5-7.5% Sjögren’s syndrome: 2-15% Idiopathic dilated cardiomyopathy: 5.7% IgA Nephropathy (Berger’s Disease): 3.6% Other celiac co-morditities include:
    Crohn’s Disease; Inflammatory Bowel Disease Chronic Pancreatitis Down Syndrome Irritable Bowel Syndrome (IBS) Lupus Multiple Sclerosis Primary Biliary Cirrhosis Primary Sclerosing Cholangitis Psoriasis Rheumatoid Arthritis Scleroderma Turner Syndrome Ulcerative Colitis; Inflammatory Bowel Disease Williams Syndrome Cancers:
    Non-Hodgkin lymphoma (intestinal and extra-intestinal, T- and B-cell types) Small intestinal adenocarcinoma Esophageal carcinoma Papillary thyroid cancer Melanoma CELIAC DISEASE REFERENCES:
    Global Prevalence of Celiac Disease: Systematic Review and Meta-analysis. Clinical Gastroenterology and Hepatology 2018;16:823–836 Celiac Disease Center, Columbia University Gluten Intolerance Group National Institutes of Health U.S. National Library of Medicine Mayo Clinic University of Chicago Celiac Disease Center
    Jefferson Adams
    Image Caption: Image: CC--kae71463
    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:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.
    Dr. Ron Hoggan, Ed.D.
    Image Caption: Image: CC--Chris Phutully
    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.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    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
    Image Caption: Image: CC--NIAID
    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
    Image Caption: Image: CC--Ed Uthman
    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
    Image Caption: Image: CC--Retinafunk
    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.
    Jefferson Adams
    Image Caption: Image: CC--J Brew
    Celiac.com 06/11/2018 - Untreated celiac disease causes damage to the small intestine, which can interfere with proper nutrient absorption. Most patients can recover proper nutritional absorption via vitamins and mineral therapy, according to the CDF. Avoiding gluten is key. However, many people with celiac disease may not know that their pharmacist might just be one of their best allies in the fight to avoid gluten.
    Currently, there are no rules that require drug manufacturers to disclose the source of medication ingredients. Consumers can contact the manufacturer directly with questions, and some drug companies strive for clear, helpful answers, but getting correct information can be challenging.  Many times though, an answer won't address possible cross contamination during the manufacturing process.
    This is where pharmacists can be a strong ally for patients with celiac disease. Here are a few way that pharmacists can help people with celiac disease to avoid hidden gluten in their prescriptions and over-the-counter drugs.
    The first thing pharmacists can do is to check ingredients on prescription medications these patients are taking. They can also share related information to help educate patients, and to improve their choices, and speak with drug manufacturers on patients’ behalf. In addition to assisting with prescription medicines, pharmacists can offer recommendations on vitamins and supplements. 
    As with prescription drugs, both doctors and patients should do their best to review the ingredients used to manufacture vitamins and supplements, and to share this information with celiac patients.
    So, if you have celiac disease, definitely consider enlisting your pharmacist in an effort to get complete drug and supplement information. This simple tactic can help you to remain gluten-free during your course of drug treatment, however long that may last?
    Do you have a story about gluten in prescription drugs or supplements? Do you use your pharmacist to help you better understand your gluten-free drug and supplement options? Share your story with us.
    Source:
    medscape.com
    Jefferson Adams
    Image Caption: Image: CC--Helen_Harrop
    Celiac.com 06/09/2018 - If you haven’t tried savory porridge, then you’ve been missing out. This combination of brown rice, steel cut oats and quinoa makes a nice introduction. The perfectly boiled egg takes it to the top. Dress it up with as many vegetables as you like. You can make it a day or two ahead of time, and just top with vegetables to make a tasty, portable lunch. 
    Ingredients:
    4 large eggs, room temperature ⅓ cup brown rice, rinsed well ⅓ cup red quinoa, rinsed well ⅓ cup steel cut oats, rinsed well 2 ounces fresh pea sprouts 2 medium shallots, peeled, halved through root 1 1” piece ginger, peeled, crushed ¼ cup gluten-free tamari or soy sauce Kosher salt, freshly ground pepper 2 teaspoons toasted sesame oil, divided 2 radishes, thinly sliced 1 small Persian cucumber, diced 1½ cups spinach, wilted  Sliced almonds, more fresh pea shoots, fresh cilantro leaves, and chopped scallions, as desired Directions:
    Bring shallots, ginger, rice, quinoa, oats, and 4 cups water and 4 cups of chicken broth to a boil in a large saucepan, reduce heat, and simmer for about 1½–2 hours, stirring often after the first hour of cooking to prevent sticking. 
    Cook until mixture is thick like porridge and rice is very soft, and beginning to break down. 
    Stir in more water as needed to achieve desired thickness. 
    Discard shallots and ginger and stir in soy sauce; season with salt and pepper. 
    Add pea shoots and cook just until shoots are wilted and tender, about 1 minute.
    Meanwhile, bring a large saucepan of water to a boil, then carefully add eggs. 
    Boil exactly 6 minutes, then transfer eggs to a large bowl of ice water; saving hot water for wilting the spinach. 
    Let eggs cool and peel.
    Serve porridge drizzled with oil and topped with soft-boiled eggs, wilted spinach, cucumber, radishes, peanuts, cilantro, and scallions, as desired.
    Note: You can cook the rice and quinoa up to 2 days ahead. Reheat in the microwave before adding soy sauce and remaining ingredients.
    Jefferson Adams
    Image Caption: Here you can see the use of "GF" in both marks.
    Celiac.com 06/08/2018 - A spat over gluten-free symbols turned legal recently, when Bob’s Red Mill filed a lawsuit against the Gluten Intolerance Group of North America in U.S. district court in Portland. Bob’s Red Mill is looking to continue using their current gluten-free logo without seeking permission from, or paying money to, the Gluten Intolerance Group (G.I.G.), which verifies and certifies gluten-free products through its Gluten-Free Certification Organization program. To date, the program has certified more than 30,000 products in 29 different countries.
    For its gluten-free labeling, Bob’s Red Mill currently uses a gluten-free circle symbol with “gluten-free” in larger letters in the middle. Above and below the gluten-free, in smaller font are the words “GLUTEN” and “FREE,” respectively. For their certification label, The Gluten Intolerance Group uses a similar “gluten-free” in a circle, with the words “Certified” and “Gluten-Free” in smaller letters above and below the circle, respectively.
    Bob’s Red Mill said in court documents that on May 17 it received a cease and desist e-mail from the G.I.G. The e-mail stated that G.I.G. has used their mark consistently in commerce since 2005, and demanded that Bob’s cease using their logo, saying it was similar to the G.I.G.’s logo and could confuse consumers into thinking the Group had certified the Bob’s Red Mill products, which it had not. The Food and Drug Administration’s says that a product labeled gluten-free must have less than 20 parts per million, and Bob’s Red Mill says they adhere to that standard.
    In court document, Bob’s said that “complying with G.I.G.’s demand would require a significant redesign and marketing process,” and that the “potential damages exceed $75,000.” The suit by Bob’s Red Mill claims that G.I.G. abandoned its application to register its gluten-free mark with the U.S. Patent and Trademark Office on Feb. 13 of this year, and asks the court to declare that G.I.G.s gluten-free mark is unenforceable and merely descriptive.
    Basically, Bob’s seems to be launching a preemptive lawsuit to put G.I.G. on its heels before G.I.G has the chance to sue Bob’s. Stay tuned to see if this suit actually makes it to a trial, or if cooler heads prevail and the two sides work something out.
    The Gluten Intolerance Group was founded in 1974, and offers consumer support, advocacy and education to the gluten-free community. Bob’s Red Mill was founded in 1978, is a global provider of gluten-free milled grain products, and certified-organic milled grain products.
    Disclosure: Bob's Red Mill and G.I.G. have been sponsors of Celiac.com.
    Mica Adams
    Celiac.com 06/07/2018 - Mica is off for the Summer and wants to share her super easy oven baked gluten-free mac-n-cheese recipe.
    This recipe is pure comfort food that will make almost anybody happy!
    Below is the recipe, and here is the video version:

    Ingredients:
    1 pound uncooked gluten-free macaroni (use Schar penne)
    4 eggs
    3 cups (2 cans) evaporated milk
    2 cups water
    2 tablespoons butter, melted
    ⅓ pound shredded American cheese
    ⅓ pound shredded cheddar cheese
    ⅓ pound shredded Monterey Jack cheese
    2 teaspoons gluten-free mustard
    1 teaspoon salt
    ½ teaspoon ground white pepper
    Directions:
    Heat the oven to 350 degrees F (175 degrees C).
    In a large shallow baking dish, toss
    Mix uncooked macaroni and melted butter together, making sure the macaroni and the inside of the dish are both thoroughly coated. Add cheese, and stir until evenly mixed.
    In a medium bowl, mix the evaporated milk, water, eggs, mustard powder, salt, and white pepper.
    Pour over the macaroni, and bake uncovered for 45 minutes, or until it is firm in the middle.
    Remove from the oven, and let cool for 5-10 minutes before serving.
    Jefferson Adams
    Image Caption: Image: CC--J.K. Califf
    Celiac.com 06/06/2018 - Endometriosis is an often painful medical condition in which tissue that normally lines the inside of your uterus, known as the endometrium, begins to grow outside the uterus. There is a bit of research data to support the idea that a gluten-free diet can improve the symptoms of endometriosis for some people. Mainly a 2012 clinical study that showed 75 percent of endometriosis patients reported major improvements after 12 months without gluten.
    That bit of news has prompted more than a few women to try the diet, and more than a few to blog about it. One example is this blog entry by Lindsay Burgess. According to Burgess, She adds that gluten can “increase inflammation and can also cause digestive issues such as bloating and constipation,” which are common complaints from many who suffer from endometriosis.
    The basic theory is that endometriosis involves a good deal of inflammation, and that a gluten-free diet will somehow help to reduce inflammation in general, and that the overall result will be a reduction of symptoms and an overall improvement in the endometriosis. Burgess says the endometriosis diet is largely about “cutting down/out inflammatory foods and replacing them with foods that can really support our bodies.” 
    So, it’s not just about eliminating gluten, it is also about eating foods that promote overall health. Nothing wrong with promoting overall health by eating more nutritious foods. A more general question might be: Can eating a more nutritious diet help to improve overall health and thus help to improve symptoms of endometriosis? 
    Perhaps, but eating a more nutritious diet is always a good idea. There’s still no solid medical evidence to show that eliminating gluten alone will help to improve endometriosis, tough, it’s certainly worth a try.
    Remember, though, that many gluten-free foods are highly processed, and many are high in salt, sugar and fat, compared with their non-gluten-free counterparts. That means that simply giving up gluten likely won’t improve your diet, to say nothing of your endometriosis.
    So, the take away here is that eating a more nutritious diet is never a bad idea, and that diet can include gluten-free foods, and these foods may improve your general health or your endometriosis.
    Endometriosis can be a painful, frustrating experience, but going gluten-free is unlikely to improve your condition, and very unlikely to “cure” it. Officially, for people who do not have medical condition that requires them to avoid gluten, it’s probably best to resist the gluten-free diet.
    So, the short of it is that, if you wish to eat gluten-free, then go ahead. But if you don’t have celiac disease or some other gluten sensitivity, don’t expect health or medical miracles, even for endometriosis.
    Any benefits gained by a more nutritious diet can likely be gained with a diet that is not gluten-free. Of course, a balanced and nutritious gluten-free diet likely won’t harm you. Otherwise, you can choose to eat an anti-inflammatory diet that is not gluten-free and probably get similar results. 
    In any case, be careful, choose carefully, and pay attention to your body.
    There’s a good article on this at EndometriosisNews.com.
    They also have a helpful link about getting started on a gluten-free diet for endometriosis. 
    Jefferson Adams
    Image Caption: Image: CC--Charles Haynes
    Celiac.com 06/05/2018 - It’s never a bad idea to have a great fresh salsa recipe on hand as summer approaches. This happy salsa blends roasted tomatillos, yellow mangos pineapple, and onion with fresh fruit and a dash of jalepeño for a tasty salsa treat.
    Ingredients: 
    Two 8-ounce yellow Ataulfo mangoes, seeded, peeled and chopped—about 2 cups 10-12 medium tomatillos (10 ounces total), husked, rinsed and finely chopped—about 1½-2 cups 10-12 ounces fresh pineapple chunks, peeled, cored and chopped—about 2 cups (larger chunks okay for roasting, smaller for adding later) ½ medium red onion, halved, diced small 1 small or ½ large jalapeño or Serrano pepper, stemmed, seeded Small handful cilantro Juice of 2-3 fresh limes, more as needed 1 teaspoon kosher salt, or more as needed Note: Goes great with guacamole!
    Directions:
    In a cast iron skillet or pan, roast 8-10 tomatillos, pineapple chunks, jalapeño and 2 onion halves.
    Combine about 1 cup of mango, roasted tomatillos, roasted pineapple, 1 red onion half, pepper, cilantro, lime juice and salt in blender and purée until smooth.
    Pour into a large bowl, and add remaining chunks of fresh mango, pineapple, and tomatillo, along with the diced onion.
    Adjust flavor with additional ingredients or salt, as needed.
    Serve with tortilla chips and guacamole, as desired.
    Jefferson Adams
    Image Caption: Image: CC--Paul VanDerWerf
    Celiac.com 06/04/2018 - Rates of contamination in commercial food advertised as gluten-free are improving, but nearly one in ten still show unacceptable levels of gluten. As part of a government mandated food sampling program, the city of Melbourne, Australia recently conducted a survey of 127 food businesses advertising gluten-free options. 
    For the tests, government officers conduct unannounced site visits and take a sample of at least one food item declared to be gluten-free.  Ridascreen Gliadin R5 ELISA analysis showed that 14 of 158 samples (9%) contained detectable gluten in excess of the official Food Standards Australia New Zealand (FSANZ) definition of gluten-free.
    Nine of the 14 samples (6% overall) registered gluten above 20 parts per million, which exceeds the official threshold for foods labeled gluten-free in Europe and the United States. At one business, food labeled gluten-free registered above 80 ppm, even though they were asked directly for a gluten-free sample. These findings confirm the lack of understanding reported by many people with celiac disease.
    The good news is that rates of gluten non-compliance has improved over earlier audits, from 20% of samples in 2014 to 15% of samples in 2015. The survey team notes that one-third of the businesses in this study had previously been audited) and education seems to be paying off. 
    In one burger chain alone, four of five venues which were non-compliant in 2014, were fully compliant in 2015 and 2016.  The survey results showed that businesses that provided gluten-free training for staff showed 75% better odds of compliance. The overall good news here is that gluten-free compliance in commercial food businesses has improved steadily since the first surveys in 2014.
    One in ten odds of getting gluten contamination from food labeled gluten-free is still to high, but even though there is room for improvement more and more businesses are providing gluten-free training for their staff, and those that do are reaping benefits. Look for this trend to continue as more businesses offer training, gluten-free and celiac disease awareness increases, and more consumers demand safe gluten-free foods.
    Read more at: The Medical Journal of Australia
    Jefferson Adams
    Image Caption: Image: CC--Keith McDuffee
    Celiac.com 06/04/2018 - Spring means fresh vegetables, and fresh vegetables mean soup. Minestrone soup is one of the great dishes of spring. There are many versions, and many of them are delicious. I tend to favor those with a lighter touch. This version makes a clear, light, delicious minestrone broth that is perfect for showing off your fresh garden vegetables. The gluten-free meatballs help take this soup to eleven. 
    Ingredients:
    3 ounces ground beef 3 ounces ground pork 5 cups chicken broth ½ cup fresh gluten-free breadcrumbs 6 tablespoons finely grated Parmesan, divided, plus more for garnish 1 large egg, whisked 4 garlic cloves, 2 minced, 2 sliced thin 2 tablespoons chopped fresh chives 2 tablespoons extra-virgin olive oil 1 teaspoon Italian dried seasoning 1 leek, white and pale-green parts only, cut into ¼-inch rounds 1 cup carrots, peeled and cut to ½-inch rounds 1 cup (packed) baby spinach Kosher salt, freshly ground pepper Directions:
    Mix chicken, beef, egg, gluten-free breadcrumbs,, Italian seasoning, 3 tablespoons Parmesan, 2 minced garlic cloves, chives, ¾ teaspoon salt, and ¼ teaspoon pepper in a medium bowl. 
    Form into meatballs ½-inch-diameter.
    Heat oil in a small pot over medium heat. Cook meatballs about 3 minutes, until golden brown. 
    Move meatballs to a paper towel to drain away cooking oil.
    Add leek to pot and cook, stirring often, until beginning to soften, about 3 minutes. 
    Add 2 thinly sliced garlic cloves; cook for 1 minute. 
    Add broth and 2 cups water; bring to a boil. 
    Stir in carrots, add meatballs, and simmer until carrots are tender, and meatballs are cooked through, about 3 minutes. 
    Add spinach and remaining 3 tablespoons Parmesan; stir until spinach wilts and Parmesan melts. 
    Season with salt and pepper.
    Ladle soup into bowls. Garnish with grated Parmesan.
    Jefferson Adams
    Image Caption: Image: CC--Gage Skidmore
    Celiac.com 06/01/2018 - Sharon Stone is gluten-free and glamorous. Even at 59, the veteran screen star manages to look great and keep landing new work. Stone is in the news recently, promoting her work in two new projects.
    Stone currently stars in Steven Soderbergh’s innovative murder mystery “Mosaic,” which began as an app and evolved into a full-blown HBO mini-series. She also stars in the romantic comedy “All I Wish,” which premiered at the end of March. 
    A recent article in the New York Times details Stone’s picks for makeup, hair and beauty products, along with some tips on diet and fitness. 
    Among her diet tips, the seasoned star shares the fact that she has celiac disease, so she eats gluten-free. She also avoids processed food, caffeine, and rarely drinks soda or alcohol.
    For more on Sharon Stone, including her beauty and health routines, check out other recent articles.
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    Jefferson Adams
    Image Caption: Image: CC--mandam
    Celiac.com 05/31/2018 - Explaining the genetics of many diseases is challenging because most genetic associations occur in regulatory regions that just aren’t very well understood and documented. In an effort to provide better genetic information about certain regulatory regions, a team of researchers recently used new computational methods to demonstrate that transcription factors (TFs) occupy multiple loci associated with individual complex genetic disorders. Their work has important implications for celiac disease, and numerous other medical disorders.
    The research team included John B. Harley, Xiaoting Chen, Mario Pujato, Daniel Miller, Avery Maddox, Carmy Forney, Albert F. Magnusen, Arthur Lynch, Kashish Chetal, Masashi Yukawa, Artem Barski,  Nathan Salomonis, Kenneth M. Kaufman, Leah C. Kottyan and Matthew T. Weirauch.
    They are variously affiliated with the Center for Autoimmune Genomics and Etiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; the Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; the Division of Developmental Biology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; the Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA; US the Department of Veterans Affairs Medical Center, Cincinnati, OH, USA; the Division of Biomedical Informatics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; the Division of Allergy & Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; and the Division of Human Genetics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA.
    The group conducted an assessment of 213 phenotypes and 1,544 TF binding datasets that identified 2,264 relationships between hundreds of TFs and 94 phenotypes, including androgen receptor in prostate cancer and GATA3 in breast cancer.  In one interesting finding, the team noted that the gene loci for systemic lupus erythematosus risk are occupied by the Epstein–Barr virus EBNA2 protein, along with many co-clustering human TFs, which suggests gene–environment interaction.
    Similar EBNA2-anchored connections are seen in multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, juvenile idiopathic arthritis and celiac disease.  Allele-dependent DNA binding and downstream effects on gene expression support genetic mechanisms dependent on EBNA2. These results indicate that such mechanisms are operating across risk loci within disease phenotypes, which offers a new hypothesis for the origins of numerous diseases, including celiac disease.
    Such complex gene–environment interactions may help explain the origins of numerous autoimmune diseases. Specifically, Epstein–Barr virus (EBV) infection is associated with the autoimmune mechanisms and epidemiology of systemic lupus erythematosus (SLE), increasing SLE risk by as much as 50-fold in children. 
    Despite strong associations between EBV and multiple autoimmune diseases, the underlying molecular mechanics are not understood. That said, genome-wide association studies (GWAS) have identified more than 50 possible European-ancestry SLE susceptibility loci, offering strong support for germline DNA polymorphisms altering SLE risk. 
    The team’s analyses found strong connections with an EBV gene product (EBNA2), offering a potential origin of gene–environment interaction, along with a set of human transcription factors and cofactors (TFs), in SLE and six other auto-immune diseases. 
    The team presents allele- and EBV-dependent TF binding interactions and gene expressions that nominate cell types, molecular agents and environmental factors to disease mechanisms for more than 85 diseases and physiological phenotypes. The team’s analysis suggest that numerous causal autoimmune combinations may act through allele-dependent binding of these proteins, altering downstream gene expression. 
    These results offer promise for the development of future therapies for manipulating the action of these proteins in individuals harboring risk alleles at EBNA2-bound loci.
    The team’s current current data point to particular TFs and cell types for 94 phenotypes, offering ways to verify, via experiment and exploration, the potential molecular and cellular origins of disease risk, potentially including celiac disease. 
    As new genetic association and TF binding data are collected, approaches such as this will undoubtedly identify additional disease mechanisms. As researchers gain an understanding of the genetics behind the origins of numerous diseases, look for them to make progress on new methods of testing, diagnosis and treatment of many of these conditions.  
    Source:
    NATURE GENETICS | VOL 50 | MAY 2018 | 699–707 
    Jefferson Adams
    Image Caption: Image: CC--Breville USA
    Celiac.com 05/30/2018 - One of the key aspects of non-celiac gluten sensitivity (NCGS) is that patients are diagnosed partly by the absence of celiac disease. That is, patients with NCGS, whatever their symptoms, do not have celiac disease. But could those patients still have some kind of gut damage, or permeability issues? Do people with non-celiac gluten sensitivity have distinct duodenal histological features? Researchers are seeking a better understanding of this still undefined condition.
    Some researchers have suggested that histology may play a key role in NCGS, but there is still no consensus. A recent review by Bardella et al. revealed that histology is not always reported in NCGS studies, and exclusion of celiac disease is generally done by showing negative serology and/or genetic typing. 
    In June 2015, researchers published what is now called the Salerno Experts’ criteria, which proposes a double (or single)-blind, placebo-controlled, (DBPC), crossover gluten challenge as the gold standard to NCGS diagnosis
    In order to investigate histological findings of people with suspicion of NCGS, we retrospectively evaluated duodenal biopsies of a cohort of patients undergoing clinical diagnostic algorithm for NCGS as proposed by the Salerno consensus.
    The research team included B Zanini, V Villanacci, M Marullo, M Cadei, F Lanzarotto, A Bozzola, and C Ricci. They are variously affiliated with the Gastroenterology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Viale Europa 11, 25123, Brescia, Italy; and with the Institute of Pathology Spedali Civili, Piazzale Spedali Civili 1, 25123, Brescia, Italy.
    Their team’s main goal was to underline that the peculiar IEL distribution and the increased eosinophil count may represent a valid warning that help to identify patients with NCGS, given the absence of serological markers for NCGS. 
    The team also performed a CD3 immunohistochemical evaluation of T lymphocytes confirming that the IEL numbers were normal, but their distribution is peculiar, as noted by the clusters of T lymphocytes in the superficial epithelium and linear disposition of T lymphocytes in the deeper part of the mucosa above the muscularis mucosae. 
    They also note that their failure to fully match study subjects with placebo challenge is a limitation of this study, but stress the current uncertainty of the actual clinical diagnostic algorithm as supported by recent reviews of the literature. The team’s observations led them to note that histology may play a similar role in NCGS diagnosis as it does in celiac diagnosis. 
    Researchers do know that, unlike with celiac disease, there is an absence of damage or change to intestinal mucosa in patients with NCGS, especially an absence of villous atrophy. In addition, the morphological exclusion of celiac disease is a crucial assessment, because some patients classified as NCGS show increased duodenal IEL count (> 25 IELs/100 enterocytes), corresponding to Marsh I, or grade A lesions of celiac histological classification.
    To properly diagnose NCGS, the team says it’s very important to confirm these features, to rule out any type of organic malabsorption diseases, and to definitively rule out celiac disease, via a negative celiac disease serology.
    Taken as a whole, the team’s results provide evidence that both intraepithelial lymphocytes and eosinophils play a role in the physiopathology behind NCGS. They are calling for more studies to confirm their findings and to determine whether the results they observed were specific to NCGS.
    Source:
    Virchows Arch. 2018 Apr 4. doi: 10.1007/s00428-018-2346-9
    Jefferson Adams
    Image Caption: Image: CC--Robert Couse-Baker
    Celiac.com 05/29/2018 - The quest for gluten-free product glory just took an interesting turn. Certainly, the explosion of gluten-free products, and their corresponding popularity among consumers is not news. Gluten-free products are a multi-billion dollar industry, and the vast majority of gluten-free products are purchased by people who do not have celiac disease or a dietary sensitivity to gluten.
    Consumers can now buy nearly every kind of product imaginable in a gluten-free version. There are gluten-free make-ups, gluten-free shampoos, conditioners, and lotions. There’s even been some research to suggest that gluten in orthodontic retainers might be an issue, and so maybe we can expect to see gluten-free retainers soon. 
    But gluten-free condoms? Yes, gluten-free condoms are a thing. And not just one single thing. Numerous organic condom manufacturers are touting their condoms as gluten-free. Brands include Glyde, Green Condom Club, Sustain, and now Lola.
    Lola is an all-natural personal care company that just launched a line of condoms that claim to be free of paraben, fragrance, casein, and, of course, gluten. 
    Do condoms actually have gluten in the first place? Maybe not.
    According to Lola co-founders Alex Friedman and Jordana Kier, while most condoms don't contain gluten, those that contain lubricant might. That’s because gluten is commonly used as an emulsifier, stabilizer, and/or filler in personal care products. Because the Food and Drug Administration classifies condoms as medical devices, condom regulations don’t require manufacturers to declare gluten as an ingredient. 
    Certainly there are numerous areas where hidden gluten can be a concern for some consumers, especially those with celiac disease or gluten-sensitivity. And personal beauty care products, prescription and over the counter drugs, and other health care products are one of those areas. Making a strong claim to be gluten-free may be a way for manufacturers like Lola to differentiate itself from products that may contain gluten, or other products that may not include gluten, but may also not declare that clearly. 
    So, for anyone worried about such things, and willing to pay a premium price (a 12 pack of Lola’s gluten-free condoms retail for $11), then gluten-free condom bliss awaits you; or something like that.
    What do you think? Are gluten-free condoms a genuine product advance? Just another marketing gimmick? A product you would try?
    More info is at: menshealth.com
    Jefferson Adams
    Image Caption: Image: CC--glasseyes view
    Celiac.com 05/28/2018 - Myasthenia gravis is a medical condition caused by a disturbance in the communication between nerves and muscles. Symptoms include weakness of arm or leg muscles, double vision, drooping eyelids, and difficulties with speech, chewing, swallowing and breathing. There is no cure for myasthenia gravis, but treatment can help symptoms to improve. 
    Some case reports have indicated a connection between celiac disease and myasthenia gravis (MG). A team of researchers recently set out to determine if those reports are accurate, and, if so, what the connection might be between celiac disease and risk for myasthenia gravis.
    The research team included Sujata P. Thawani, Thomas H. Brannagan, Benjamin Lebwohl, Peter H. R. Green, and Jonas F. Ludvigsson. They are variously affiliated with the Department of Neurology, New York University School of Medicine, New York, NY USA; the Peripheral Neuropathy Center, Neurological Institute, Columbia University, College of Physicians and Surgeons, New York, NY USA; the Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY USA; the Department Medical Epidemiology and Biostatistics, Karolinska Institutet, 171 77 Stockholm, Sweden; the Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden; and with the Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK.
    The team found 29,086 people who had celiac disease in Sweden between 1969 to 2008. The team then compared these individuals with 144,480 matched control subjects. They used Cox regression to estimate hazard ratios (HRs) for future MG, as identified through ICD codes.
    Their study period covered 326,376 person-years of follow-up in celiac patients. Over that period, they found 7 cases of MG, for a total of 21 cases per million person-years. In the control group, the team found 22 cases of MG over 1,642,273 years of follow-up, for a total of 14 cases per million person-years, which yielded an HR of 1.48 (95% CI = 0.64–3.41). 
    The HRs did not change when stratifying for age, sex or calendar period. HRs were highest in the first year after follow-up, though insignificant. 
    Individuals with celiac disease showed no increased MG risk for more than 5 years after celiac diagnosis (HR = 0.70; 95% CI = 0.16–3.09).
    Fortunately, this study showed no increased risk for myasthenia gravis in celiac disease patients.
    Source:
    BMC Neurol. 2018; 18: 28.Published online 2018 Mar 12. doi:  10.1186/s12883-018-1035-2
    Jefferson Adams
    Image Caption: Image: CC--Patrick Nuetzel
    Celiac.com 05/26/2018 - If you haven’t tried a savory pancake, then you’ve been missing out. In many places in the world, savory pancakes are more common than the sweet pancakes. They make a great lunch or dinner twist. This gluten-free version combines scallions and peas, but feel free to add or subtract veggies at will. Serve pancakes them warm with butter for a delicious twist on lunch or dinner.
    Ingredients:
    3 large eggs 1 cup cottage cheese ½ stick salted butter, melted ¼ cup all-purpose gluten-free flour 2 tablespoons vegetable oil plus more for skillet 1 cup shelled fresh or frozen peas, thawed 4 scallions, thinly sliced, plus more for serving 1 teaspoon kosher salt plus more, as desired Directions:
    If using fresh peas, blanch the peas about 3 minutes in a small saucepan of boiling salted water until tender, about 3 minutes (don’t cook frozen peas). Drain well.
    In a blender, add eggs, cottage cheese, flour, 2 tablespoons oil, and 1 teaspoon salt, and purée until smooth. 
    Transfer batter to a medium bowl and stir in peas and scallions. 
    Batter should be thick but pourable; stir in water by tablespoonfuls if too thick.
    Heat a lightly oiled large nonstick skillet over medium heat. 
    Working in batches, add batter to skillet by ¼-cupfuls to form 3-inch-4-inch rounds. 
    Cook pancakes about 3 minutes, until bubbles form on top. 
    Flip and cook until pancakes are browned on bottom and the centers are just cooked through, about 2 minutes longer.
    Serve pancakes drizzled with butter and topped with scallions.
    Inspired by bonappetit.com.
    Jefferson Adams
    Image Caption: Image: CC--Richard Masoner
    Celiac.com 05/25/2018 - People with celiac disease need to follow a lifelong gluten-free diet. However, once their guts have healed, they can still be sensitive to gluten. Sometimes even more sensitive than they were before they went gluten-free. Accidental ingestion of gluten can trigger symptoms in celiac patients, such as pain in the gut and diarrhea, and can also cause intestinal damage. 
    A new drug being developed by a company called Amgen eases the effects of people with celiac disease on a gluten-free diet. Researchers working on the drug have announced that their proof-of-concept study shows AMG 714, an anti-IL-15 monoclonal antibody, potentially protects celiac patients from inadvertent gluten exposure by blocking interleukin 15, an important mediator of celiac disease, and leads to fewer symptoms following gluten exposure.
    The drug is intended for people with celiac disease who are following a gluten-free diet, and is designed to protect against modest gluten contamination, not to permit consumption of large amounts of gluten, like bread or pasta.
    AMG 714 is not designed for celiac patients to eat gluten at will, but for small, incidental contamination. Francisco Leon, MD, PhD, study director and consultant for Amgen, says that their team is looking at AMG 714 “for its potential to protect against modest contamination, not deliberately eating large amounts of gluten, like bread or pasta.” 
    Amgen hopes that AMG 714 will help celiac patients on a gluten-free diet to experience fewer or less sever gluten-triggered events.
    Findings of the team’s first phase 2 study of a biologic immune modulator in celiac disease will be presented at the upcoming Digestive Disease Week 2018. 
    Read more at ScienceDaily.com
    Jefferson Adams
    Image Caption: Image: CC--Eugene Peretz
    Celiac.com 05/24/2018 - England is facing some hard questions about gluten-free food prescriptions for people with celiac disease. Under England’s National Health Plan, people with celiac disease are eligible for gluten-free foods as part of their medical treatment. 
    The latest research shows that prescription practice for gluten-free foods varies widely, and often seems independent of medical factors. This news has put those prescribing practices under scrutiny.
    "Gluten free prescribing is clearly in a state of flux at the moment, with an apparent rapid reduction in prescribing nationally," say the researchers. Their data analysis revealed that after a steady increase in prescriptions between 1998 and 2010, the prescription rate for gluten free foods has both fallen, and become more variable, in recent years. Not only is there tremendous variation in gluten free prescribing, say the researchers, “this variation appears to exist largely without good reason…”
    Worse still, the research showed that those living in the most deprived areas of the country are the least likely to be prescribed gluten-free products, possibly due to a lower rate of celiac diagnosis in disadvantaged groups, say the researchers.
    But following a public consultation, the government decided earlier this year to restrict the range of gluten free products rather than banning them outright. As research data pile up and gluten-free food becomes cheaper and more ubiquitous, look for more changes to England’s gluten-free prescription program to follow. 
    Read more about this research in the online journal BMJ Open.
    Jefferson Adams
    Image Caption: Image: CC--Marco Verch
    Celiac.com 05/23/2018 - Yes, we at Celiac.com realize that rye bread is not gluten-free, and is not suitable for consumption by people with celiac disease!  That is also true of rye bread that is low in FODMAPs.
    FODMAPs are Fermentable Oligosaccharides, Disaccharides, Monosaccharides and Polyols. FODMAPS are molecules found in food, and can be poorly absorbed by some people. Poor FODMAP absorption can cause celiac-like symptoms in some people. FODMAPs have recently emerged as possible culprits in both celiac disease and in irritable bowel syndrome.
    In an effort to determine what, if any, irritable bowel symptoms may triggered by FODMAPs, a team of researchers recently set out to compare the effects of regular vs low-FODMAP rye bread on irritable bowel syndrome (IBS) symptoms and to study gastrointestinal conditions with SmartPill.
    A team of researchers compared low-FODMAP rye bread with regular rye bread in patients irritable bowel syndrome, to see if rye bread low FODMAPs would reduce hydrogen excretion, lower intraluminal pressure, raise colonic pH, improve transit times, and reduce IBS symptoms compared to regular rye bread. The research team included Laura Pirkola, Reijo Laatikainen, Jussi Loponen, Sanna-Maria Hongisto, Markku Hillilä, Anu Nuora, Baoru Yang, Kaisa M Linderborg, and Riitta Freese.
    They are variously affiliated with the Clinic of Gastroenterology; the Division of Nutrition, Department of Food and Environmental Sciences; the Medical Faculty, Pharmacology, Medical Nutrition Physiology, University of Helsinki in Helsinki, Finland; the University of Helsinki and Helsinki University, Hospital Jorvi in Espoo, Finland; with the Food Chemistry and Food Development, Department of Biochemistry, University of Turku inTurku, Finland; and with the Fazer Group/ Fazer Bakeries Ltd in Vantaa, Finland.
    The team wanted to see if rye bread low in FODMAPs would cause reduced hydrogen excretion, lower intraluminal pressure, higher colonic pH, improved transit times, and fewer IBS symptoms than regular rye bread. 
    To do so, they conducted a randomized, double-blind, controlled cross-over meal study. For that study, seven female IBS patients ate study breads at three consecutive meals during one day. The diet was similar for both study periods except for the FODMAP content of the bread consumed during the study day.
    The team used SmartPill, an indigestible motility capsule, to measure intraluminal pH, transit time, and pressure. Their data showed that low-FODMAP rye bread reduced colonic fermentation compared with regular rye bread. They found no differences in pH, pressure, or transit times between the breads. They also found no difference between the two in terms of conditions in the gastrointestinal tract.
    They did note that the gastric residence of SmartPill was slower than expected. SmartPill left the stomach in less than 5 h only once in 14 measurements, and therefore did not follow on par with the rye bread bolus.
    There's been a great deal of interest in FODMAPs and their potential connection to celiac disease and gluten-intolerance. Stay tuned for more information on the role of FODMAPs in celiac disease and/or irritable bowel syndrome.
    Source:
    World J Gastroenterol. 2018 Mar 21; 24(11): 1259–1268.doi:  10.3748/wjg.v24.i11.1259
    Jefferson Adams
    Image Caption: Image: CC--Oak Ridge National Laboratory
    Celiac.com 05/22/2018 - Proteins are the building blocks of life. If scientists can figure out how to create and grow new proteins, they can create new treatments and cures to a multitude of medical, biological and even environmental conditions.
    For a couple of decades now, scientists have been searching for a biological Rosetta stone that would allow them to engineer proteins with precision, but the problem has remained dauntingly complex.  Researchers had a pretty good understanding of the very simple way that the linear chemical code carried by strands of DNA translates into strings of amino acids in proteins. 
    But, one of the main problems in protein engineering has to do with the way proteins fold into their various three-dimensional structures. Until recently, no one has been able to decipher the rules that will predict how proteins fold into those three-dimensional structures.  So even if researchers were somehow able to design a protein with the right shape for a given job, they wouldn’t know how to go about making it from protein’s building blocks, the amino acids.
    But now, scientists like William DeGrado, a chemist at the University of California, San Francisco, and David Baker, director for the Institute for Protein Design at the University of Washington, say that designing proteins will become at least as important as manipulating DNA has been in the past couple of decades.
    After making slow, but incremental progress over the years, scientists have improved their ability to decipher the complex language of protein shapes. Among other things, they’ve gained a better understanding of how then the laws of physics cause the proteins to snap into folded origami-like structures based on the ways amino acids are attracted or repelled by others many places down the chain.
    It is this new ability to decipher the complex language of protein shapes that has fueled their progress. UCSF’s DeGrado is using these new breakthroughs to search for new medicines that will be more stable, both on the shelf and in the body. He is also looking for new ways to treat Alzheimer’s disease and similar neurological conditions, which result when brain proteins fold incorrectly and create toxic deposits.
    Meanwhile, Baker’s is working on a single vaccine that would protect against all strains of the influenza virus, along with a method for breaking down the gluten proteins in wheat, which could help to generate new treatments for people with celiac disease. 
    With new computing power, look for progress on the understanding, design, and construction of brain proteins. As understanding, design and construction improve, look for brain proteins to play a major role in disease research and treatment. This is all great news for people looking to improve our understanding and treatment of celiac disease.
    Source:
    Bloomberg.com

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    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:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.
    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.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    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.