The average gluten-containing diet contains roughly 10-40 grams of gluten per day. This figure is based on the amounts of gluten in your average slice of whole wheat bread, which contains around 4.8 grams of gluten (10% gluten by weight), and the amount of gluten in a serving of pasta, which is roughly 6.4 grams of gluten (11% gluten by weight). The smallest amount of gluten which has been shown by a biopsy to cause damage to a celiac is 0.1 gram per day (Catassi et al.). This is approximately the amount of gluten contained in 1/48th of a slice of bread! The biopsies in this study showed an increase in intraepithelial lymphocyte count, one of the earliest signs of damage. The challenge was on 10 patients (children) for 28 days each. Four of the patients showed an increase in IgA antigliadin antibodies. The intestinal permeability test remained normal.
The common list of forbidden grains is: wheat, rye, barley and oats.
Unfortunately, there are variants out there that go by other names. Durum and semolina are names for certain kinds of wheat that have been bred for specific uses. Both spelt and kamut are versions of wheat. (Other names for these: spelt, Polish wheat, einkorn and small spelt). Bulgur is wheat thats been specially processed. Triticale, a grain crossbred from wheat and rye, is definitely on the toxic list. Though corn (maize) is one of those grains that many people -- not just celiacs -- may be allergic to, it is not a grain that is thought to cause damage to the villi in celiacs. It is tolerated by most celiacs. Of the common grains, rice is the favorite as it rarely troubles anyone. Aside from corn and rice, there is a wide variety of other grains that are used in gluten-free cooking. We even use beans and peas (legumes, pulses). The following can be milled into flour: amaranth*, buckwheat* (or kasha), chickpeas (garbanzos), Jobs tears (Hato Mugi, Junos Tears, River Grain), lentils, millet*, peas, quinoa*, ragi, sorghum, soy, tapioca, teff*, and wild rice. Many of these flours are available in health food stores. Some (like rice flour) may be available in grocery stores. (The products marked with an "*" are listed as grains to avoid by some physicians and celiac societies. See the discussion below about anecdotal evidence and possible contamination of flours for more information.) To improve the texture of gluten-free baked goods, most cooks use one or more of the following: xanthan gum, guar gum (though this sometimes has a laxative effect), methylcellulose, or a new product called Clear Gel. These can be obtained either through health food stores, specialty cooks stores, or some of the mail order sources listed below. Oils popular in cooking include: corn, peanut, olive, rapeseed (canola), safflower, soy, and sunflower.
Vijay Kumar, M.D., Research Associate Professor at the University of Buffalo and President and Director of IMMCO Diagnostics: There is no simple answer to this question as the susceptibility of the patient to developing celiac disease is dependent upon several factors. One factor is the amount of gluten intake. Another is the genetic makeup of the individual. However, we feel that several weeks of gluten intake, especially in doses of 2 gm gluten/day, should result in positive serology in patients with celiac disease.
Karoly Horvath, M.D., Ph.D., Associate Professor of Pediatrics; Director, Peds GI & Nutrition Laboratory; University of Maryland at Baltimore: The result of serological tests depends on the diet. Generally, three to six months of a gluten-free diet may result in normal antibody levels in a new patient. A strict gluten-free diet for more than three months may result in inconclusive serological tests in patients, who have started a diet without any diagnostic test. In this case a gluten challenge should be introduced for a proper diagnosis. Each patient has different sensitivity to gluten for reasons that are unclear. The period of gluten challenge and the amount of gluten necessary to provoke serological immune response are individually different. A 0.3 g/kg body weight/day of single gluten challenge causes immunological changes (cellular immunity) in the intestine (J Pediatr Gastroenterol Nutr 1989; 9:176-180) in patients on a gluten-free diet, however, the serological response is much slower. Our recommendation is to ingest at least 0.3 g/kg/day of gluten for two months prior to the serological tests. However, if somebody experiences symptoms during the gluten challenge we recommend to perform serological tests earlier. The protein content of wheat flour is between 7-15% and approximately 90% of the protein content is gluten. That means a slice of bread may have 2-3 g of gluten.
Vijay Kumar, M.D., Research Associate Professor at the University of Buffalo and President and Director of IMMCO Diagnostics: If the tests are performed using well standardized tests with known positive and negative predictive values then you can make the statement that if the serological tests are negative celiac disease can virtually be ruled out. The problem is that some of these assays, especially the gliadin, can give you false positive results. In our laboratory we rarely see positive AGA results in the absence of EMA and ARA antibodies.
Vijay Kumar, M.D., Research Associate Professor at the University of Buffalo and President and Director of IMMCO Diagnostics: It is important for the serum tests to be negative in patients with celiac disease. These tests provide strong indicators that the gluten free diet followed is effective and is free of gluten. Sometimes drugs or other intakes may be contaminated with gluten that may continue sensitization and the disease process which may be subclinically. We and others believe once the diagnosis of celiac disease is confirmed and the patient is on a gluten free diet, repeat tests once in 3-6 months may be sufficient.
Karoly Horvath, M.D., Ph.D., Associate Professor of Pediatrics; Director, Peds GI & Nutrition Laboratory; University of Maryland at Baltimore: If a patient has histologically (endoscopy) and serologically (antibody tests) proved celiac disease, and his/her symptoms disappeared on a gluten-free diet, a repeat biopsy is not necessary. The serological tests are useful tools for estimating the effectiveness of the diet after 3-6 months on a gluten-free diet. The disappearance of antibodies from the blood takes months, if there was not any accidental gluten challenge (dietary mistake).
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.
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
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.
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.
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.
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.
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.
Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023
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.
Alimentary Pharmacology & Therapeutics
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.
Gut. 2017 Feb;66(2):250-257. doi: 10.1136/gutjnl-2015-310148.
Well you approached the SIBO side...what about candida? Stuff actually sets up worse after antibiotics. The good bacteria helps kill the stuff, but antibiotics can make it worse and kill off the good guys. It can cause gas, bloating, cravings for sugar, a almost drunk/hung over feeling. If your diet has been high in carbs/sugars then good chance.
Other thoughts it could be another AI disease or gut issues....some of us get those, I gut Ulcerative Colitis by example with its own set of triggers...in my case this includes the rare sugar triggers.
Could also be your not as gluten free as you think, if your eating out, using a shared kitchen, did not clean out the kitchen and replace certain things you could be still getting it from sources...this diet can take over year to master. Reread the newbie 101 section to be sure.
To be on the safe side go to a whole foods only diet for a bit, also be sure to remove dairy and oats from your diet....the enzymes to break down dairy are from the vili which are damaged, and oats are commonly CCed along with the fact 10% of celiacs react to oats also regardless.
Food intolerance issues and sensitivities...gluten is not our only issue, most of us develop some other kind of food issues with certain foods causing symptoms....keep a food diary, and go to a whole foods only diet, then try certain foods and record changes it might be a spice or something like onions, garlic, tomatoes, potatoes, carbs, soy, corn, etc.
As to the lump I am unsure, hernia? Gas distention? Like hard lump you have to press to feel, or a distended soft lump? Do you have blood in the stool, or signs of bruising, darkening around the lump? Yellish skin, or yellow in the whites of your eyes? I would really see about having a doctor look at it.
I've been diagnosed with celiac and I have been gluten free for the past 9 months, but I have not getting better. The only thing that improved is that I no longer have diarrhea after eating meals. I have bloating after eating, stomach pain, severe dry eye and a lump on my left side below my ribs that is becoming more painful lately.
I am wondering what this lump can be? I've had it since before I was diagnosed but it has only recently been getting painful and feels like it is getting bigger. I had a CT scan a year ago that didn't find anything and the colonoscopy and endoscopy I had that found the celiac disease 9 months ago didn't find anything related to the lump.
I'm wondering what this lump could be. Can it be inflammation from the celiac or is it likely something else?
I'm seeing my gastroenterologist tomorrow and I'm looking for suggestions. He first thought the lump was gas and that I had SIBO / bacterial overgrowth but two weeks of Doxycycline made absolutely no difference for me. I would love to have some ideas of what this could be so I can get him to run some tests on this lump.
Grief is natural and something we have to get through and it was a few years for me. First i just stopped seeing fast food joints. To me they were empty lots. I stopped watching tv with commercials. Thank you Roku, Netflix, Amazon and HBO. Those helped. Dietitian didnt give me anything i didnt know. Read some Celiac and Nutrition books. Things got easier when the hubby agreed the house should be gluten free. No cross contamination and no temptation. Love my crock pot and rice cooker ( going to buy an instant pot next). Hate to cook. Love fresh fruit. Steam veggies in glass bowls in microwave. Boil up dozen eggs always on hand. Found gluten free crackers and popcorn on Amazon. Just search gluten free. Key is to make a bunch of food then freeze it in meal sizes. Always having food cooked or fresh on hand helps cravings. And find favorite snacks to look forward to. All said and done the gluten-free non processed food diet has reversed my heat disease and lowered my diabeties risk. All bad numbers are normal and being 50 that is great.