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    Common Cookware Cross-contamination with Gluten Post Customary Sanitation Study


    Eleanore Dara


    • Journal of Gluten Sensitivity Autumn 2012 Issue


    Image Caption: Image: CC--Nicki Dugan Pogue

    Celiac.com 09/22/2017 - Misdiagnosed my sophomore/ junior year of High School, 3 years ago, with celiac disease, I became obsessed with the science of this ailment and how it was supposedly affecting me. I was shocked by how little is known about this autoimmune disease and the many gaps in research done on it. One such gap is that of cross-contamination in the household, where it is likely to have a daily impact on those following gluten-free diets. Because of this, I decided to help fill this gap in scientific knowledge with a manageable project based on cross-contamination in the home, asking whether one can share common kitchen cookware that is used with gluten containing foods, or if people, to help maintain a gluten-free diet, need designated ones for their food preparation.


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    Either way that this research played out would be beneficial to the gluten-free community. For example, some families with members on gluten-free diets will spend a lot of money to buy all new ‘gluten-free' designated cookware and utensils to help minimize cross-contamination. Part of the relevancy of this project is economical, as designated cookware can be very costly. Despite the cost, other factors affect the value of this research, including the impracticality of having a double set of kitchen appliances, which would be very bulky and impractical for those with limited space. Another factor that influences the significance of this project is beyond one's home; celiac disease brings a lot of social stress. By assuring there is limited or no cross-contamination from common kitchen appliances after customary washing, these individuals would be able to have some confidence when eating at friends' or families' homes. On the other end, if this research shows that there is cross-contamination with shared supplies it will highlight the need for dedicated ones to maintain a strict gluten-free diet. Just because a gluten-free recipe is used, a given dish may not be genuinely gluten free if there is contamination from cookware.

    Hazards and Concerns
    To fully understand the hazards of gluten contamination, a few things must first be established: What is gluten? Who is it harmful to? How and to what extent must it be avoided? How does cross-contamination occur?

    What is Gluten?
    The United States Food and Drug Association (FDA) have been trying to define "gluten" for years. The current proposed definition is, "the proteins that naturally occur in a ‘prohibited grain' that may cause adverse health effects in persons with celiac disease."(1) These prohibited grains are any species belonging to triticum, hordeum and secale or more commonly called respectively: wheat, barley, and rye, though other prohibited grains exist as hybrids of any of the three.(2) That being said, not all proteins in these three types of grains are toxic to those with celiac disease as there are two parts to glutens: prolamins, the immunotoxic ones, and glutenins, the safe ones.(3) The prolamins in the three main prohibited grains, wheat, barley, and rye, are gliadin, hordein, and secalin.(4)

    Who Does Gluten Harm?
    Gluten is toxic to certain individuals with celiac disease, an autoimmune disease that also goes by the names of: coeliac disease, celiac sprue, nontropical sprue, and gluten-sensitive enteropathy.(5) A Thomson Healthcare Company study estimated that up to 1.5 Million Americans, or one in 133 people, have celiac disease, though other individuals avoid gluten as well, such as those with gluten intolerance, or other ailments where a gluten-free diet is believed to lessen their symptoms.(6) This strict abstention from gluten is because celiac disease cannot be cured, or mediated with medication as yet. The only way to help those affected is by following this strict diet.

    How and to What Extent Must it be Avoided?
    Foods that contain wheat, rye, and barley, or any hybrid of these grains contain gluten. Gluten is a very common protein in foods, whether from bread, or as an additive to provide a thicker texture, such as in soups. This versatility makes processed foods, in the eyes of those on gluten-free (gluten-free) diets, something to be wary of. Because of this caution, companies want their products to be certified gluten-free, which according to the FDA calls for

    Despite current unknowns regarding contamination, a strict gluten-free diet must exclude all foods that contain gluten and minimize cross-contamination. This means from eating out, to staying in, gluten must be avoided. Topical products where gluten is added, such as in some lotions or body washes, should also be avoided. Despite the widespread use of gluten there are gluten-free grains and foods, such as beans, rice, millet, corn, amaranth, and soy.

    How Does Cross-contamination Occur?
    Cross-contamination is a term usually directed toward accidental spread of bacteria due to not cooking food, washing hands or materials. However, in this article it refers to the accidental transfer or content of gluten, the protein that is toxic to those with celiac disease.

    In my personal experience and research on celiac forums, when a member of a family goes gluten-free the family will most likely continue eating a regular diet. In addition, as the average time it takes to be diagnosed from the first onset of symptoms is 10 years in the United States, these families have kitchen supplies that they have been using with gluten.(8) With little public knowledge about celiac disease and going gluten-free, people tend to overlook cross-contamination. Theoretically, in the simple act of making a sandwich with gluten-free bread there are many different ways for it to become contaminated. For example, from a shared jar of peanut butter or jelly with crumbs accidentally getting into it and then dipped out onto the gluten-free bread, or crumbs on the surface it's prepared on sticking to the gluten-free bread.

    Research Investigation
    The investigation of common kitchen appliances that are frequently exposed to gluten and cleaned by customary sanitation techniques calls for the conduction of an enzyme linked immunoassay (ELISA) test when using them to prepare gluten-free food. Various well used kitchen appliances, wood and plastic cutting boards, cast iron skillets, both seasoned and unseasoned, Teflon and aluminum pans, and ceramic and glass bowls were contaminated with gluten, using whole wheat flour slurry, and then washed by their standard cleaning technique, either scrubbing with hot soapy water, or wiping with a paper towel and water.

    Afterward a certified gluten-free substance, in this case millet flour, was added and let sit to allow adherence of any gluten remaining on the ‘cleaned' surface. Figure 1 illustrates the extraction solutions that were made from the samples and injected into the Microwell plates with the anti-body coating and the various washes of the ELISA test.

    Then, the gliadin, if present, bound to the walls of the wells due to its antibody coating and the wells were washed to eliminate remaining parts in the well. Next, the enzyme Horseradish Peroxidase, or HRP enzyme, adheres post-injection to any gliadin present as an amplifier and is again washed to remove extra parts. Lastly, a 3,3', 5,5'-Tetramethylbenzidine, or TMB substrate was added which turns blue in the presence of a peroxidase, in this case the adhered HRP enzyme, which can only be there if there was gliadin to attach to. This color after a acid stop solution, which turns it yellow, is added is then assessed using a Microwell plate reader for its absorbency which, when compared with a standards curve made from known samples, by the company, will be used to determine the gluten content, in parts per million, of all the samples individually.

    Results
    Intuition may lead one to think that well developed standard cleaning techniques for most appliances, and the difficulty in transferring proteins to a gluten-free medium from a surface that has been cleaned, will make gluten cross-contamination unlikely. However, due to factors such as porosity and oiliness, some surfaces may harbor gluten. Typically, far less rigorous cleaning techniques are used on the seasoned cast iron skillet and it is very porous and oily so the gluten proteins have a better chance of binding to it and then transferring to a gluten free medium. Given the test results of the ELISA test, this is mostly true. Despite the logic being the same, and it being the intuitive most likely candidate for cross-contamination a different appliance with the same sanitation technique proved to exceed the gluten parts per million limit where as the cast iron did not.

    The only absorbency ratings from the samples that interpolated to be greater than the 20 ppm of gluten allowance were two extractions from the Teflon pan. All other ratings, including two other Teflon pan extractions, were below the limit.

    Conclusion
    Ninety-four percent of the sample extractions showed less than the 20 parts per million of gluten which is the threshold for something to be declared gluten-free. Teflon had half of its extractions above the limit, as such Teflon should be deemed cross-contaminated. However, the Teflon's other extraction samples had well below 20ppm. This could have been due to the sample's gluten free sample being rather large and thus only part of it could have gotten contaminated (positive cross-contamination) and other parts not (negative cross-contamination). All others samples were classified as gluten-free due to being below the 20ppm allowance.

    In conclusion, the values of gluten cross-contamination, in ppm, were too small to hinder the integrity of the gluten-free medium in all but Teflon. Thus, to the extent of the experiment done, having tested only eight different kitchen appliances, with only two different sanitation techniques, common kitchen appliances that are frequently exposed to gluten, can be cleaned by customary methods and used to prepare gluten-free food with the exception of Teflon appliances.

    This research project could be extended by more trials. For example, eight types of common kitchen appliance were used, but only one appliance was used to represent each type. More trials could be done within each type, using different brands, variations in extent of wear, etc. In addition, the only type of contaminant used was whole-wheat slurry. Other forms of contaminant should be tested as well, to show the universality of the cross-contamination, or lack thereof. This should include different gluten-containing substances, as well as some dry and some wet.

    Unfortunately, this research question will have exceptions as the extent of washing and wear on an appliance is a more subjective issue. This means that even if it is found on a larger scale that certain appliances have been found to be safe for producing gluten-free foods, it should still be avoided when possible for those with celiac disease as if not washed properly; it could go beyond the 20ppm allowance and be immunotoxic to these individuals.

    Vested interest is always a concern with research, and thus it must be pointed out that no company or university holds any interest in this project and no help was given financially or academically, only that The University of Detroit Mercy allowed me to use their lab for the duration of the experiment and Microwell plate reader. In addition, both sides of the results would prove beneficial, so the data were not interpreted with a bias toward any desired result.

    Eleanore Dara is a "rising scientist" and is an incoming biochemistry student on a Research Track Major at the University of Scranton in Pensnsylvania.

    References:

    1. "Questions and Answers on the Gluten-Free Labeling Proposed Rule." U S Food and Drug Administration. N.p., 23 Jan. 2007. Web. 31 Jan. 2011.  https://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/Allergens/ucm362880.htm 
    2. Ibid.
    3. Amaya-González, et al. "Amperometric Quantification of Gluten in Food Samples Using an ELISA Competitive Assay and Flow Injection Analysis." Electoanaylsis 23.1 (2010): 108+. Wiley Online Library. Web. 8 Mar. 2011.
    4. "What Is Gliadin? What Is Its Role In Gluten Sensitivity?." Gluten Free Around The World, Traditional Foods Make Eating an Adventure. N.p., n.d. Web. 25 Mar. 2012. http://www.gluten-free-around-the-world.com/gliadin.html 
    5. Snyder, Cara et al. "Celiac Disease Coeliac Disease, Celiac Sprue, Nontropical Sprue, Gluten-Sensitive Enteropathy." The National Center for Biotechnology Information. N.p., 3 June 2008. Web. 31 Jan. 2011.
    6. Cerrato, Paul L. "Gluten Intolerance: more common than thought. (Complementary Therapies Update)." RN 66.8 (2003): 23. General One File. Web. 28 Mar. 2011.
    7. "Questions and Answers on the Gluten-Free Labeling Proposed Rule." U S Food and Drug Administration. N.p., 23 Jan. 2007. Web. 31 Jan. 2011.   https://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/Allergens/ucm362880.htm 
    8. Adams, Scott. "USA - Average Time to Diagnosis = 10 Years - Celiac.com." Celiac Disease & Gluten-free Diet Information at Celiac.com. Scott Adams, 26 July 1996. Web. 16 Feb. 2012. http://www.celiac.com/articles/48/1/USA---Average-Time-to-Diagnosis--10-Years/Page1.html.
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    Guest Dick Lunde

    Posted

    Four years ago when I got diagnosed (biopsy confirmed), I stopped using a cast iron skillet that I'd used for various things, but most frequently for skillet-sizzled corn bread, using a recipe that contained wheat flour. But I thought there should be a way to clean the pan adequately. So eventually I filled it with water, added some dishwasher detergent and simmered that for an hour or so, which quite successfully stripped it of any seasoning. Then I went over it with an SOS pad and washed it with ordinary dish detergent (not dishwasher detergent as before). I re-seasoned it with multiple coats of flax seed oil, and have used it since for a modified, gluten-free version of the cornbread a few times. I've noticed no symptoms of being glutened from eating that cornbread, and I do get glutened occasionally by other things (once by oyster sauce-- who knew it came in glutenous and gluten-free versions?). So I believe the conventional wisdom that cast iron can't be cleaned up short of running it through the self-cleaning cycle of an oven is wrong. If I read this research correctly, I may not even have had to re-season the pan. And I think it's really great that someone is doing some research on cooking utensils. I suspect a lot of money has been wasted on new utensils when people have had to go gluten free. I've also wondered if gluten (or gliadin, or whatever form is retained by at least the teflon-coated utensils) is soluble in (or can be denatured by) any commonly available solvents or in/by water solutions of any common household chemicals. Another question of interest is how many times a gluten-contaminated vessel (such as the teflon-coated ones that were mentioned in the article) can contaminate something cooked in them if they're not further exposed to wheat (etc.).

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    Guest Leslie Hutton

    Posted

    I second Dick Lund's post. I stripped and re-seasoned my cast iron and stainless cookware when I had to go on a gluten free diet. I kept my wooden cutting board and the wooden spoons that my mother used. I've never noticed any problems using this cookware. My only question would be if it would be better to heat the metal pans during the gluten soak in order to replicate actual cooking conditions. Porosity and gluten absorbance may be altered at high temperatures used to fry chicken or stir fry noodles for example.

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    Having dealt with my husband's celiac for years I have a few tips about cookware. I found these out by trial and error. Most mixing bowls, plates, utensils, etc are perfectly fine with normal washing as long as they are glass, ceramic or metal. Plastic holds gluten in crevices and should not be used. This is true of cutting boards, mixing bowls, etc. Never had a problem with cast iron skillets. Use 2 toasters. Jars of jam or peanut butter or anything dippable, I place a small bowl of it on the table for guests as they cannot remember not to put the knife back in, then I finish that portion myself and the jar remains gluten-free. Any work on counter is on paper plates such as making sandwich. We use paper plates and cups a lot which also helps. Hope this helps people, I have been dealing with it a long time.

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    Guest Joanna Davis

    Posted

    As a 73 year old celiac who was not diagnosed until two years ago, I scoured all my cast iron skillets with non-iodized salt. This is the method I use to clean them each use, no detergent. I heat them each time before using them and have never experienced any issues. I am a very sensitive celiac. I sterilized all my baking pans and cookware in the dishwasher, did not throw anything away. I cleaned all my wooden spoons and cutting boards by scrubbing thoroughly and using boiling water to rinse, then dried them in the oven at 200 degrees. Also no problems. We do use separate toasters. I have double ovens, one strictly for gluten free baking. Separate tubs of margarine, peanut butter and jam jars. Only squeeze bottles for safe condiments in preparing foods. Pots and pans are washed in the dishwasher and sanitized. I store all left over foods in separate canning jars to avoid cross contamination in the refrigerator. I do not own Teflon cookware, never liked it. Thank you Elenore Dara for an insightful article. Keep up the good work. Going gluten free is a challenge on so many levels. I have given up eating out and I am a rabid label reader. I send emails all the time to companies that say gluten free and hide gluten in ingredients that are obviously made with gluten. Restaurants are the worst. I react to anything made with seaweed, i.e. MSG, carrageenan, alginate and agar as do many celiacs, these ingredients are in nut milks, dairy products of all kinds and baked goods. Carrageenan is a cheap emulsifier and the food industry loves it.

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    It would be interesting to test used cookware that has a long history of being exposed to gluten and then used to cook gluten free food. This isn't something killed off by heat like a bacteria. The cooking process may bind gluten to a pot? Or perhaps release it? Also running items trough a common dish washer machine where lots of gluten exposure takes place, like in a Italian restaurant.

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    Guest Mrs. Bright

    Posted

    Love your article. It's been rough being the only gluten free person in the family. I'm finding out the hard way that seasonings can be contaminated even though the ingredient list does not show any Gluten ingredients. When my husband would season our food with Lawry's Seasoning I would get sick ever time. I finally called the company that makes Lawry's and asked them what ingredients are making my sick... well the guy tells me technically all the ingredients are Gluten Free BUT the machine they run the seasonings thru does contain wheat products. So I'm learning just because it doesn't list a Gluten items doesn't make it Gluten Free. I also learned this with Yellow Rice. Same problem. Anything that is processed may have Gluten UNLESS it has the gluten-free listed on the label and has been approved a gluten-free item.

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    Gryphon Myers
    Celiac.com 07/16/2013 - Gluten has a way of popping up in some very unexpected products.  Peers (whether online or otherwise) are sometimes our best resource for information regarding these oft-overlooked gluten-containing products, but sometimes speculation gets passed along the grapevine as fact. This has led to some very believable, but ultimately questionable rumors. Alcohol in particular has some of the most persistent rumors regarding gluten content. This is likely because the processes involved with alcohol production are confusing and widely misunderstood. With this article, I hope to address and clear up a few of the most persistent gluten-free alcohol misunderstandings that you've certainly heard before.
    Misunderstanding #1: “Not all wine is gluten-free: some vintners age their wine in barrels that are sealed with a wheat paste. This paste contaminates the wine, making it dangerous for consumption by celiac disease sufferers.”
    This is a big one. Wine is naturally gluten-free, but the fact that some vintners use wheat paste to seal their barrels has led many to cut wine out of their diets as a precautionary measure. It's a plausible idea, as some vintners do in fact use wheat paste to seal their barrel heads. However, there are a few key points here that you should consider before cutting wine out of your diet entirely:
     
    Because the Tobacco Tax and Trade Bureau currently disallows gluten-free labeling of alcoholic beverages if the producer used “storage materials that contained gluten,” any wine that is labeled gluten-free was aged using a barrel alternative and carries no risk of contamination. Wines that aren't labeled gluten-free might still be aged using barrel alternatives. Roughly speaking, the more expensive ($12+) Cabernet Sauvignons, Merlots, Zinfandels and red blends are more likely to be aged in oak barrels (and for a longer period of time). The amount of wheat paste used to seal barrel heads is minimal. It is not the staves of the barrels that are sealed with a wheat flour paste, but the barrel heads.  Furthermore, most wineries thoroughly pressure wash all barrels with boiling hot water before they are used. The last thing vintners want is a contaminated product. In order to lay this contamination issue to rest, Tricia Thompson tested a single winery's Cabernet Sauvignon and Merlot, which she was told by the winery were their two wines that spent the most time in wheat-sealed oak barrels. She tested each wine four times: twice with the Sandwich R5 ELISA test, and twice with the competitive R5 ELISA test. The competitive R5 ELISA is the current standard for detecting hydrolyzed (broken down) gluten, while the sandwich R5 ELISA is the current standard for detecting non-hydrolyzed gluten (1). Combined, the tests can reliably test for any possible form of gluten contamination.
    Both extractions of both wines came back with the lowest possible results for both tests:
    Cabernet Sauvignon
    Sandwich R5 ELISA extraction 1: < 5 ppm gluten
    Sandwich R5 ELISA extraction 2: < 5 ppm gluten
    Competitive R5 ELISA extraction 1: < 10 ppm gluten
    Competitive R5 ELISA extraction 2: < 10 ppm gluten Merlot
    Sandwich R5 ELISA extraction 1: < 5 ppm gluten
    Sandwich R5 ELISA extraction 2: < 5 ppm gluten
    Competitive R5 ELISA extraction 1: < 10 ppm gluten
    Competitive R5 ELISA extraction 2: < 10 ppm gluten Conclusion: Wine that is aged in oak barrels contains less gluten than we are currently capable of testing for, whether hydrolyzed or not.
    At this point, a lot of people will begin to shake their heads: “If wine is gluten-free, then why do I get sick when I drink __________ wine?” The likely answer is that you are reacting to something else! Many winemakers use egg whites as a clarifying agent. The amount of egg used is far more substantial than any wheat paste that might have leaked into the wine, so if you know eggs are a problem, this is likely what you are reacting to.  
    If you don't have a problem with eggs, you could also be reacting to sulfites. Many people have problems with them, and some winemakers use them as preservatives.
    Sometimes, it's best to go out and get information directly from the winemaker. They can tell you more about their aging process, and shed light on what may or may not be making you sick.

    Misunderstanding #2: “Distilled spirits that are derived from gluten-containing ingredients can be contaminated with gluten. Only distilled spirits made from non-gluten-containing ingredients, like potatoes, are safe for consumption by celiacs.”
    This idea was likely propagated due to a misunderstanding of the distillation process. Here, I will refer to Megan Tichy, Ph.D's highly informative and clearly written description of the distillation process (2). It is a great read for those who are unclear on the process, and makes it very evident why all distilled spirits are gluten-free by definition.
    To borrow Dr. Tichy's analogy, the distillation process is like boiling a kettle of water with sand at the bottom of it. Let's say you were to collect the water that boiled away as steam using a condensing tube. After boiling the entire kettle away, you would be left with a kettle with nothing but sand at the bottom of it, and a second container of pure distilled water.  There is no way the distilled water could contain any sand, as sand doesn't evaporate. In the same way, gluten doesn't evaporate, and gets left at the bottom of the 'kettle' during distillation. The likelihood of distilled alcohol being contaminated with gluten is about the same as the likelihood of you getting sand in your new cup of perfectly clean water: it would almost have to be intentional! Also keep in mind that many spirits are double, or even triple distilled. Gluten contamination over the course of a single distillation is already highly unlikely, but after consecutive distillations, it is virtually impossible.
    To this, you might ask, “But what if they were to add other ingredients afterward? Those might contain gluten, right?” That's a perfectly valid concern, and yes, you should be concerned about any added ingredients. However, distilled spirits are almost always marketed based on their purity; this is why they go to all the trouble of double and triple distilling in the first place! Manufacturers of spirits want the most concentrated alcoholic product possible, so it is not exactly in their best interest (nor in common practice) to go adding more ingredients. Even so, you should always be mindful of ingredients lists, and cross check them against a reliable gluten-containing ingredients list (such as ours [3]).
    Despite the fact that distilled spirits derived from grains are necessarily gluten-free, some people still seem to have problems with them. I don't have a ready explanation for this, as scientifically, it doesn't make sense. Celiac disease is triggered by gluten, and distilled alcohol contains no gluten. Here is a quick checklist to help rule out reasons why you may or may not react to such drinks:
    [ ] Have you checked for cross contamination possibilities (glass, container, ice cubes, dish washing liquid, drying towel, etc.)?
    [ ] Are you sure that you do not react to distilled alcoholic beverages that are not derived from grains (e.g. potato vodka)? (It could be a reaction to potent alcohol in general.)
    [ ] Did you pour the drink yourself?
    [ ] Are you sure you are not adding anything to the drink that could be cross contaminated or contain gluten?
    [ ] Have you checked the ingredients list against a reliable gluten-containing ingredients list?
    [ ] Have you considered any other allergies you have or might have?
    [ ] Have you contacted the manufacturer for their official response regarding gluten content?
    Oftentimes (especially soon after adopting GFD), the gut is still sensitive and cannot handle alcohol at high proof levels. If you had a bad experience with distilled spirits derived from grain early on in your GFD regimen, you might want to consider giving it another try after your villi have had a chance to heal. You really should not have a reaction once your gut is adjusted to the gluten-free diet. I know it is hard to trust a product derived from wheat, but distillation really, truly does remove all gluten, and it does so every single time.
    Misunderstanding # 3: “'Low gluten' or 'gluten-removed' beers are unsafe, as gluten tests underestimate gluten content in beer. This is because the brewing process breaks the gluten molecules down into pieces that are too small for gluten tests to detect, but are still harmful.”

    This is a point of fierce contention in the gluten-free community, and probably the most confusing argument to follow, as it all surrounds the validity of a variety of super scientific testing procedures. There isn't even a clear answer or 'winner' here, but I'm going to try and break all the information down for you, so you can make an informed decision about these products for yourself.
    The main beef that people seem to have with gluten-removed beers is that they are derived from gluten-containing ingredients, and the gluten removal process is oftentimes undisclosed. This is an offshoot of the same distrust people feel toward distilled spirits, though perhaps a little more warranted given the fact that distillation is a very well documented and 100% reliable form of gluten removal, whereas as far as we know, these brewers are removing gluten using magic and fairy dust.
    The reality is that these brewers (Widmer Brothers, Estrella Damm, Lammsbraeu, to name a few) are removing the gluten from their beer using one or the other, or perhaps a combination of two methods: filtration, and enzymes. Superfine filters can remove gluten particles from the beer, while added enzymes can target gluten particles, causing them to break down to a harmless state more quickly.
    Whatever their methods, these beers need to have their gluten content verified using scientific testing procedures in order to be considered safe for consumption by celiacs. This is where things start to get murky.
    As Tricia Thompson, MS, RD writes on her blog, Gluten-Free Dietitian, the current standard for testing gluten content in foods is a sandwich ELISA test (4). The R5 and omega-gliadin versions of the test are the most widely used, and both have been validated in collaborative trials.
    While sandwich ELISA tests are reliable for detecting gluten in heated and non-heated food items, they are notoriously unreliable for detecting hydrolyzed gluten. Many see this as reason not to trust gluten-removed beers: the fermentation process hydrolyzes gluten in beer, so sandwich ELISA tests cannot accurately quantify their gluten content. If the test is unreliable, we are back where we started, with a once-gluten-containing product that has supposedly been rendered gluten-free by unexplained and unverifiable means; it's a hard pill to swallow!
    However, the sandwich R5 ELISA's weaknesses are well documented and widely known. Most of these brewers are using an entirely different test that was specifically designed to detect partial gluten fragments (peptides) that may still be harmful to the gluten-sensitive. The competitive R5 ELISA is the standard test used to detect these peptides, and although it has not been validated yet, many published studies have found the competitive R5 ELISA to be a reliable indicator of hydrolyzed gluten (5) (6) (7).
    This would all seem well and good since many of these beers test well under the proposed FDA limit of 20ppm gluten content with the competitive R5 ELISA. (As an aside, studies have shown 20 ppm to be an adequately conservative standard for most celiacs [8]). Unfortunately, the discussion doesn't end there. A recent Australian study tested a broad range of both beers brewed from alternate grains (sorghum, millet, etc.), and gluten-removed beers, and found that most gluten-removed beers contained significant levels of barley gluten (hordein) fragments, while beers brewed with alternative grains did not (9). 
    Many have inferred two things from this study: 1) gluten-removed beers are unsafe, and 2) R5 ELISA testing under-reports, or is incapable of testing for the barley gluten, hordein. I would posit that these are both hasty conclusions to make, as the study begs the following questions:
    How much gluten are we talking about?
    It isn't entirely clear from the study what 'significant' levels are, as it quantifies hordein levels on a relative scale, but not in terms of ppm. Yes, it is clear from the study that truly gluten-free beers contain less hordein than gluten-removed beers. It would also seem that some hordein families are just as present in gluten-removed beers as in standard beers whose brewers make no claims as to their gluten content. But this does not mean that any of the beers are over the 20ppm standard. The study actually states that the gluten-removed beers were tested to under 10 ppm, but then indirectly implies that they were not actually under that threshold. This is not necessarily true though! One recent study found that around 50% of standard beers on the market actually test to under 20 ppm gluten content (10). In other words, the average gluten content of beer is lower than you might think. Just because gluten-removed beers may be closer to the average on the study's relative scale than might look safe, this does not mean they contain gluten at levels that would be harmful to the average celiac. Furthermore, the toxicity of hordein and hordein peptides for celiacs still hasn't been conclusively quantified (11).

    Is R5 ELISA really that unreliable?
    The study also makes some interesting claims about the limits of R5 ELISA testing procedures. Specifically, it claims that “The R5 antibody is unable to accurately detect and quantify barley gluten (hordeins) in beer.” This is a slightly misleading statement. It is true that the sandwich R5 ELISA can be inaccurate when detecting hordein levels, but it actually overestimates them, so long as they are not hydrolyzed. Furthermore, that is the sandwich ELISA; there is much evidence to suggest that the competitive R5 ELISA provides an accurate measurement of hordein peptides (6) (7) (12). Conversely, this study employed multiple reaction monitoring mass spectrometry, a testing procedure that has not been validated for gluten testing of foods or fermented alcoholic beverages. I would say that the competitive R5 ELISA has a more proven track record when it comes to testing for hydrolyzed gluten in beer.
    What does it all mean then? Should I drink gluten-removed beer or not?
    Well, that's up to you, of course. As I said before, this is a hotly debated and highly contentious issue in the gluten-free world right now, so I'm hesitant to take one side or the other. If you suffer from refractory sprue, or some other severe form of gluten intolerance, I would advise you to stay away, as the risk simply isn't worth it for you. For more mild sufferers of celiac disease or wheat sensitivity though, if you really miss the taste of beer and gluten-free beers just aren't doing it for you, there is no solid evidence to discredit the results of competitive R5 ELISA testing. Find a beer that is batch tested to under 20 ppm using this test (not sandwich R5 ELISA, though it wouldn't hurt if it was tested by both), try a few sips, and see if you react.
    I've tried to provide all the key information so you can make an informed decision about these beers for yourself, but it never hurts to do your own research! Just know that there are a lot of biased and outdated sources out there; the more recent and scientific the study, the better!
    References:
    (1) Thompson, Tricia, MS, RD. “Wine Aged in Oak Barrels Sealed with Wheat Paste: Test Results for Gluten Contamination.” GlutenFreeDietitian.com, 10 Oct. 2012. Web. 20 Dec. 2012.
    (2) Tichy, Megan, PhD. “Distilled Spirits (Grain Alcohols) and Vinegar: Are they Gluten-Free?” Celiac.com, 26 Aug. 2009. Web. 20 Dec. 2012.
    (3) Adams, Scott. “Unsafe Gluten-Free Food List (Unsafe Ingredients).” Celiac.com, 27 Nov. 2007. Web. 20 Dec. 2012.
    (4) Thompson, Tricia, MS, RD. “Standards for testing food for gluten: Issues that need addressing.” GlutenFreeDietitian.com, 6 Aug. 2012. Web. 20 Dec. 2012.
    (5) Thompson, Tricia, MS, RD. “Beer: Why it is so hard to assess fermented and hydrolyzed products for gluten.” GlutenFreeDietitian.com, 24 Jul. 2012. Web. 20 Dec. 2012.
    (6) Gessendorfer, Benedict, et al. “Preparation and characterization of enzymatically hydrolyzed prolamins from wheat, rye, and barley as references for the immunochemical quantitation of partially hydrolyzed gluten.” Analytical and Bioanalytical Chemistry 395.6 (Nov. 2009): 1721-1728. Web. 20 Dec. 2012.
    (7) Haas-Lauterbach, S, et al.”Gluten fragment detection with a competitive ELISA.” Journal of AOAC International 95.2 (2012): 377-381. Web. 20 Dec. 2012.
    (8) Thompson, Tricia, MS, RD. “How much gluten is 20 parts per million?” GlutenFreeDietitian.com, n.d. Web. 20 Dec. 2012.
    (9) Colgrave, Michelle, et al. “What is in a Beer? Proteomic Characterization and Relative Quantification of Hordein (Gluten) in Beer.” Journal of Proteome Research 11.1 (2012): 386-396. Web. 20 Dec. 2012.
    (10) Cane, Sue. “Gluten-free beer 2011. How is it made? How is its gluten content tested? And is it really safe for coeliacs?” FoodsMatter.com, 2011. Web. 20 Dec. 2012.
    (11) Thompson, Tricia, MS, RD. “Barley enzymes in gluten-free products.” GlutenFreeDietitian.com, Jun. 2009 (updated 3 Feb. 2011). Web. 20 Dec. 2012.
    (12) Guerdrum, Lindsay, Bamforth, Charles. “Levels of gliadin in commercial beers.” Food Chemistry  129.4 (2011): 1783-1784. Web. 20 Dec. 2012.

    Kay A. Chick, Ed.D.
    Celiac.com 11/15/2016 - Do you know someone who has lived with celiac disease for over eighty years? Someone who lived on nothing but mashed bananas for a year? Someone who continued to eat gluten for over 30 years because doctors didn't know how to treat a celiac diagnosis? Someone who experienced serious physical, emotional, and family challenges as a result? Well, I met such an individual at the International Celiac Symposium in Chicago in the fall of 2013. Clara (a pseudonym) attended my poster session, The Educational, Social, and Family Challenges of Children with Celiac Disease: What Parents Should Know. As she stood before my poster with tears in her eyes she began to say, "This is me. This is me." Through a brief conversation then, and several lengthy telephone interviews that followed, she shared her incredible story with me and gave me permission to share it with you.
    Clara was born in 1933 on a citrus ranch in California and was the youngest of five children. She was very sick as a baby with what her family thought was a "terrible case of the flu." She lost muscle tone, had wrinkly skin, and some mornings she didn't move or even open her eyelids without the help of her mother. She looked malnourished and had a distended stomach. When she was two, her parents took her to Dr. Victor E. Stork, but he was not sure what the problem might be. A few weeks later, the doctor attended a conference where he described Clara's symptoms. He learned of another child with similar symptoms who had been diagnosed with celiac disease and fed nothing but mashed bananas. After Dr. Stork informed Clara's parents, Clara's father purchased a big hook and drove to the Long Beach docks to buy bananas. He hung bunches of bananas on their back porch to ripen and she was fed nothing but mashed bananas for over a year. What started as half a teaspoon at a time quickly grew until she was eating many bananas each day. This part of Clara's story greatly intrigued me, as I had just read the research of Sidney Haas. In the 1920s Hass successfully treated eight children who were "anorexic" from celiac disease with the banana diet while untreated children did not survive (Guandalini, 2007).
    Growing up, Clara was a happy child but had no appetite and didn't enjoy food. She was very small for her age and, at times, was made to stay at the dinner table until she ate everything on her plate. Clara's mother, a practical nurse, thought she might be allergic to fat. The family kept a quarter of a beef in a freezer locker 25 miles away and her mother scraped the fat off the beef before giving it to Clara. She was also made to finish her breakfast, typically oatmeal, toast, and orange juice, before going to school in the morning. Clara routinely had vomiting and diarrhea each morning, and didn't understand why this didn't happen to other children. She missed school often because she had abdominal discomfort and was weak. Clara hid in the girls' restroom during recess and physical education so she wouldn't have to participate. Since she was unsuccessful at athletics she found it easier to sit on a toilet with her feet pulled up so no one would see her.
    Clara continued to miss a great deal of school but was required to do her school work at home. During second grade she worked ahead, completing both second and third grade work. Consequently, she was allowed to skip third grade, which only accentuated her small size. When she entered high school people thought she was in third or fourth grade. After entering puberty at age 14 she finally acquired an appetite and began to grow much taller. At this point in her life, Clara decided that she would never be sick again. She graduated from high school in 1950, after acting in dramatic productions, serving as president of the Girls' League, and planning the ten year class reunion.
    Clara married at age twenty, between her junior and senior years in college. She had few symptoms during this time and was hired as a kindergarten teacher. Her husband was drafted and she taught in several different places on the west coast while he was in the service. During this time, Clara had a baby girl followed by two miscarriages. Three weeks after the birth of their second child Clara became very ill and lost her hair. They had no insurance and she lost a dramatic amount of weight. She weighed only 80 pounds and her husband had to carry her from the bed to the couch. The vomiting and diarrhea got worse and her mother had to take care of her babies. She was on heavy doses of medication and her doctors thought her gastrointestinal problems "were all in her head."
    Clara's speech became "jumbled" and she was not making sense. Her doctor sent her to a psychiatrist who placed her in a "sanitarium." She was hospitalized for several months where she felt very isolated and alone. Her relatives weren't told where she was and her father would not allow her mother to visit her. At the sanitarium Clara received shock treatments every three days, ten in all. Her sister offered her son's college fund to pay the sanitarium bill so that Clara would be allowed to leave.
    When Clara returned home she found she had lost much of her memory. She didn't remember how to hold a knife and her daughter, who was three, taught her how to tie her shoes. She was on sedatives and slept much of the time. She does not know how she took care of her children during this time. Clara and her husband had little money, so she took in ironing and taught preschool. It took them twelve years to pay off the hospital bills.
    It was fifteen years after this experience, and two babies later, that Clara finally got treatment for her celiac disease. She was hospitalized at UCLA Medical Center for a month while more tests and an intestinal biopsy were completed. It was 1972, and she was now 39 years old. The gastroenterologist finally confirmed the diagnosis of celiac disease and told her that she would never be able to eat pie, bread, or cake ever again. Clara was so thrilled that it was "just food" that would make a difference and not cancer. The doctor told her that there was no reason why she was still alive. Within two months she was noticing a difference and had gained weight. Clara was able to go back to teaching part-time and started teaching full-time in 1981.
    After her celiac diagnosis Clara did her best to avoid grains completely. One doctor told her to eat wheat germ, a product she clearly was correct in avoiding. In the 1970s she tried to make bread with rice, but her attempts were very unsuccessful. Clara started a support group in 1984 which was part of the Celiac Sprue Association. Little by little the group started receiving information on eating gluten-free, as many of these foods were readily available in Europe. By 1988 there were some gluten-free foods available in California. Clara experimented with cooking and breads and tested recipes for Carol Fenster's cookbooks. Her household today is totally gluten-free, with the exception of a loaf of bread for her husband. She and her husband traveled extensively after their retirement, visiting every state except Hawaii, along with the Caribbean and Australia.
    As far as lessons learned, Clara believes that people should listen to each other. She says, "If a person says, I feel horrible, someone should listen. The medical profession didn't listen to me. They said it was all in my head. If they had listened I could have been helped." It is unfortunate that her doctors didn't listen, as Clara could have been diagnosed much sooner. Willem-Karel Dicke first published an article on the importance of a gluten-free diet for the treatment of celiac disease in 1941 (Berge-Henegouwen & Mulder, 1993).
    Since my own celiac diagnosis came within two months of the onset of symptoms, I marvel at how someone could live for 39 years while still eating gluten. I think about the lessons to be learned from Clara's story. I consider the advancements that have been made in the diagnosis and treatment of celiac disease and the ease with which I'm able to eat gluten-free. And I send a reminder of the importance of early detection and the physical and emotional consequences that individuals like Clara face when a celiac diagnosis is delayed.
    References:
    Guandalini, S. (2007). A brief history of celiac disease. Impact, 7, (3), 1-2. Van Berge-Henegouwen, G. P., & Mulder, C.J. (1993). Pioneer in the gluten-free diet: Willem-Karel Dicke 1905-1962, over 50 year of gluten-free diet. Gut, 34, 1473-1475.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/30/2017 - Dear attending physician:
    If you are reading this it is because your patient either expects you to refuse or you have refused to test them for celiac disease. You may believe, in keeping with prior training, that this patient does not display the signs or symptoms associated with celiac disease. However, the symptom complex of celiac disease has recently undergone dramatic changes, beginning with the understanding that celiac disease is a systemic, rather than an intestinal ailment. World renowned researchers have weighed in on this issue, with peer reviewed reports that repeatedly establish the protean manifestations of celiac disease. They defy prior algorithms for symptom assessment toward diagnosing celiac disease. In the past, undiagnosed celiac patients were often identified as asymptomatic because their symptoms were simply not diarrhea, abdominal bloating, and muscle wasting. However, the Celiac Disease Center at the University of Chicago lists more than 300 presenting symptoms of celiac disease (1). The same group also offers a list of symptoms that demonstrate the wide range of apparently unrelated symptoms that can indicate celiac disease, only the first two of which represent these classical symptoms (2).
    Recurring abdominal bloating and pain Chronic or recurrent diarrhea Constipation Nausea or emesis Liver and biliary tract disorders (increased serum transaminases, primary sclerosing cholangitis) Weight loss Pale, foul-smelling stool Iron-deficiency anemia unresponsive to iron therapy Fatigue Failure to thrive or short stature Delayed puberty Arthralgia Tingling numbness in the legs Pale sores inside the mouth Dermatitis herpetiformis Abnormal dentition (tooth discoloration, loss of enamel) Unexplained infertility or recurrent miscarriage Osteopenia or osteoporosis Peripheral neuropathy Psychiatric disorders (anxiety or depression) Please remember that any one or more of the above symptoms and/or ailments may indicate untreated celiac disease, so testing for celiac disease is an important, inexpensive step toward assisting a patient to resolve these troubling, sometimes debilitating, symptoms.
    Overweight and obesity may also indicate underlying celiac disease. Today's affluence and accompanying food surpluses permit people who are not absorbing nutrients efficiently to eat enough to more than compensate for otherwise calorically deficient diets. Thus, only a minority of celiac disease cases present with classical symptoms in most of the first world. In fact, some reports indicate that overweight patients with celiac disease are as common as those who are underweight ( 3, 4, 5). This is why researchers have long employed the iceberg metaphor to describe the mass of people with celiac disease. The vast majority these people with celiac disease remain undiagnosed (6). Until sensitive and specific serological screening tools became available, very few cases were diagnosed and celiac disease was erroneously considered rare.
    In addition to alleviating quite a lot of human suffering, early detection offers some rather large economies for the health care system, as many of the more serious ailments that often befall those with untreated celiac disease may be averted through these inexpensive serological tests and subsequent prescription of a strict gluten free diet.
    Prior to the therapeutic use of a gluten free diet, mortality was reported at 36% among 73 children with celiac disease (7). Admittedly, it is likely that these were the more serious cases and perhaps some cases of misdiagnosis. However, even as recently as 1989, adult celiac patients experienced almost double the early mortality rate seen in the general population (8), so an early diagnosis and treatment of celiac disease is not just helpful in mitigating current symptoms, it is a powerful form of preventive medicine that is coincidental to the appropriate diagnosis and treatment of celiac disease.
    Let me expand on that last comment a little further. Chronic depression (9), ADHD (10), neurological (11) and neuromuscular disorders(12) treatment-resistant iron deficiency (13, 14), impaired lung function (15, 16) a variety of lymphomas including B cell and T cell (17, 18, 19) and adenocarcinomas (20, 21) dental enamel defects (22, 23) autoimmune thyroid disease (24, 25 ) autoimmunity in general (26) type 1 diabetes (27, 28) kidney disease (29) liver disease (30, 31) skin disease (32, 33) seizure disorders (34) gait disorders (35) obesity (36) fatigue (37) anxiety (38) infertility (39) osteoporosis (40) learning disorders (41, 42) aphasia (43) and many more such sequels to untreated celiac disease (44) impose an enormous economic burden on our health system and education system. This burden weighs on most levels of government, private insurance companies, families, and individuals. Much of this unnecessary cost is ultimately passed along to taxpayers and/or are incorporated into insurance premiums. We all pay.
    And the human costs are even greater. Attention deficits and learning disabilities impose life-long inhibitions on success and are corrosive to self esteem. Depression robs us of individual, economic and social achievements, as well as denying us the day-to-day pleasures of life. Similarly, anxiety and infertility are socially isolating and heartbreaking, each in their own ways. Neurological and seizure disorders, including gait disorders, can inhibit our mobility and/or our safe function in this increasingly complex and fast-paced society. Impaired lung function can prohibit or interfere with normal, desirable activities ranging from pleasant walks, sports, and even having sex. Lymphomas and adenocarcinomas can have rapidly fatal consequences. The individual and familial consequences are often devastating. Type 1 diabetes tethers us to insulin injections and requires that we maintain a careful balance between carbohydrate intake and insulin injections. The challenges of this diet dwarfs the inconvenience of a gluten free diet, and a late celiac diagnosis may require that some people comply with both sets of dietary constraints. Skin disease can also exact an enormous social toll, and this is ignores the discomfort and embarrassment of constant itching and scratching, as well as the pain associated with the most common skin diseases connected to celiac disease. Similarly, obesity is not only socially excluding, it poses its own sets of health hazards and life shortening penalties. As osteoporosis becomes more and more common, we can see that society's increasing nutritional dependence on gluten grains may well have set the stage for this degenerative condition, often requiring painful and expensive joint replacement surgeries as our bones gradually crumble and shrink. The dramatic loss of our ability to produce intelligible speech, called aphasia, is by no means the least of this list. The horrific nightmare of being unable to speak to others and have them understand us has been the lived experience of at least one individual. His speech slowly returned after his celiac diagnosis and some time on a gluten free diet. Too many of us are not so lucky.
    Many of us see ourselves, and our symptoms, in the many posts, blog comments, listservs and websites that discuss celiac disease. Yet outdated medial training can create barriers to patients seeking testing. However, given the above, peer reviewed data and expert opinions, it is difficult to imagine any reasonable argument for refusing to test a patient who requests serological testing for celiac disease. The cost is minimal and the potential benefits to those who are diagnosed, and our society, are enormous.
    Current data suggest a prevalence of celiac disease in the general population at somewhere around 1%, based on serological testing for selective antibodies. However, newly emerging data suggest that a portion of the population that is at least six or seven times the size of the group with celiac disease mounts an innate immune response to gluten grains. The careful characterization of one pathway for activating intestinal inflammation by non-gluten components of these grains, leaves open the possibility of "gliadin-dependent signaling pathways that still remain to be characterized" (45).
    Other forms of non-celiac gluten sensitivity, as signaled by IgG class antibodies against gliadin, are seen in 10% to 12% of the general population. Whether these segments of the population with non-celiac gluten sensitivity overlap or are distinct has yet to be determined, so it remains unclear whether they form 10% of our population, or as much as 19% of our culture. Finally, based on a new book by the world renowned pediatric gastroenterologist and allergist, Dr. Rodney Ford, titled Gluten: Zero Global, there is considerable evidence to suggest that, with their many other anti-nutrient, addictive, allergenic, and blood-glucose altering features, gluten grains are a questionable macronutrient food source for humans (46).
    Thus, testing for non-celiac gluten sensitivity, may offer many of the benefits that testing for celiac disease offers. Your patient and I are asking that you heed the above data from your professional literature and the first dictum of your profession, by 'first doing no harm', and ordering testing for celiac disease and non-celiac gluten sensitivity.
    Sincerely,
    Dr. Ron Hoggan, Ed. D.
    Sources:
    1. http://www.cureceliacdisease.org/wp-content/uploads/2011/09/CDCFactSheets10_SymptomList.pdf
    2. http://www.cureceliacdisease.org/medical-professionals/guide/symptoms
    3. Dickey W, Kearney N. Overweight in celiac disease: prevalence, clinical characteristics, and effect of a gluten-free diet. Am J Gastroenterol. 2006 Oct;101(10):2356-9
    4. Tucker E, Rostami K, Prabhakaran S, Al Dulaimi D. Patients with coeliac disease are increasingly overweight or obese on presentation. J Gastrointestin Liver Dis. 2012 Mar;21(1):11-5
    5. Cheng J, Brar PS, Lee AR, Green PH. Body mass index in celiac disease: beneficial effect of a gluten-free diet. J Clin Gastroenterol. 2010 Apr;44(4):267-71.
    6. Katz KD, Rashtak S, Lahr BD, Melton LJ 3rd, Krause PK, Maggi K, Talley NJ, Murray JA. Screening for celiac disease in a North American population: sequential serology and gastrointestinal symptoms. Am J Gastroenterol. 2011 Jul;106(7):1333-9. doi: 10.1038/ajg.2011.21. Epub 2011 Mar 1.
    7. Hardwick C. 1989, as described in Holmes GKT. Non-malignant complications of coeliac disease. Acta Paediatr Suppl. 412: 68-75. 1996.
    8. Logan RF, Rifkind EA, Turner ID, Ferguson A. Mortality in celiac disease. Gastroenterology. 1989 Aug;97(2):265-71.
    9. Zipser RD, Farid M, Baisch D, Patel B, Patel D. Physician awareness of celiac disease: a need for further education. J Gen Intern Med. 2005 Jul;20(7):644-6.
    10. ADHD (10),Niederhofer H. Association of attention-deficit/hyperactivity disorder and celiac disease: a brief report. Prim Care Companion CNS Disord. 2011;13(3).
    11. neurological and neuromuscular disorders (11, 12,) Currie S, Hadjivassiliou M, Clark MJ, Sanders DS,
    12. Wilkinson ID, Griffiths PD, Hoggard N. Should we be 'nervous' about coeliac disease? Brain abnormalities in patients with coeliac disease referred for neurological opinion. J Neurol Neurosurg Psychiatry. 2012 Dec;83(12):1216-1221.
    13. Hadjivassiliou M, Chattopadhyay AK, Davies-Jones GA, Gibson A, Grünewald RA, Lobo AJ. Neuromuscular disorder as a presenting feature of coeliac disease. J Neurol Neurosurg Psychiatry. 1997 Dec;63(6):770-5.
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    Prevalence of celiac disease, Helicobacter pylori and gastroesophageal reflux in patients with refractory iron deficiency anemia. J Trop Pediatr. 2008 Feb;54(1):43-53.
    15. Cekın AH, Cekın Y, Sezer C. Celiac disease prevalence in patients with iron deficiency anemia. Turk J Gastroenterol. 2012 Oct;23(5):490-5.
    16. Robertson DA, Taylor N, Sidhu H, Britten A, Smith CL, Holdstock G. Pulmonary permeability in coeliac disease and inflammatory bowel disease. Digestion. 1989;42(2):98-103.
    17. Edwards C, Williams A, Asquith P. Bronchopulmonary disease in coeliac patients. J Clin Pathol. 1985 Apr;38(4):361-7.
    18. Bautista-Quach MA, Ake celiac disease, Chen M, Wang J. Gastrointestinal lymphomas: Morphology, immunophenotype and molecular features. J Gastrointest Oncol. 2012 Sep;3(3):209-25.
    19. Leslie LA, Lebwohl B, Neugut AI, Gregory Mears J, Bhagat G, Green PH. Incidence of lymphoproliferative disorders in patients with celiac disease. Am J Hematol. 2012 Aug;87(8):754-9.
    20. Elfström P, Granath F, Ekström Smedby K, Montgomery SM, Askling J, Ekbom A, Ludvigsson JF. Risk of lymphoproliferative malignancy in relation to small intestinal histopathology among patients with celiac disease. J Natl Cancer Inst.2011 Mar 2;103(5):436-44.
    21. Benhammane H, El M'rabet FZ, Idrissi Serhouchni K, El Yousfi M, Charif I, Toughray I, Mellas N, Riffi Amarti A, Maazaz K, Ibrahimi SA, El Mesbahi O. Small bowel adenocarcinoma complicating coeliac disease: a report of three cases and the literature review. Case Rep Oncol Med. 2012;2012:935183.
    22. Vecchio R, Marchese S, Gangemi P, Alongi G, Ferla F, Spataro C, Intagliata E. Laparoscopic treatment of mucinous adenocarcinoma of jejunum associated with celiac disease. Case report. G Chir. 2012 Apr;33(4):126-8.
    23. El-Hodhod MA, El-Agouza IA, Abdel-Al H, Kabil NS, Bayomi KA. Screening for celiac disease in children with dental enamel defects. ISRN Pediatr. 2012;2012:763783.
    24. Erriu M, Sanna S, Nucaro A, Orrù G, Garau V, Montaldo C. HLA-DQB1 Haplotypes and their Relation to Oral Signs Linked to Celiac Disease Diagnosis. Open Dent J. 2011;5:174-8.
    25. Cats EA, Bertens AS, Veldink JH, van den Berg LH, van der Pol WL. Associated autoimmune diseases in patients with multifocal motor neuropathy and their family members. J Neurol. 2012 Jun;259(6):1137-41.
    26. Bardella MT, Elli L, De Matteis S, Floriani I, Torri V, Piodi L. Autoimmune disorders in patients affected by celiac sprue and inflammatory bowel disease. Ann Med. 2009;41(2):139-43
    27. Nass FR, Kotze LM, Nisihara RM, de Messias-Reason IT, Utiyama SR. Autoantibodies in relatives of celiac disease patients: a follow-up of 6-10 years. Arq Gastroenterol. 2012 Jul-Sep;49(3):199-203.
    28. Saadah OI, Al-Agha AE, Al Nahdi HM, Bokhary RY, Bin Talib YY, Al-Mughales JA, Al Bokhari SM. Prevalence of celiac disease in children with type 1 diabetes mellitus screened by anti-tissue transglutaminase antibody from Western Saudi Arabia. Saudi Med J. 2012 May;33(5):541-6.
    29. Van den Driessche A, Eenkhoorn V, Van Gaal L, De Block C. Type 1 diabetes and autoimmune polyglandular syndrome: a clinical review. Neth J Med. 2009 Dec;67(11):376-87.
    30. Welander A, Prütz KG, Fored M, Ludvigsson JF. Increased risk of end-stage renal disease in individuals with coeliac disease. Gut. 2012 Jan;61(1):64-8.
    31. Drastich P, Honsová E, Lodererová A, Jarešová M, Pekáriková A, Hoffmanová I, TuÄková L, Tlaskalová-Hogenová H, SpiÄák J, Sánchez D. Celiac disease markers in patients with liver diseases: A single center large scale screening study. World J Gastroenterol. 2012 Nov 21;18(43):6255-62.
    32. Massironi S, Rossi RE, Fraquelli M, Bardella MT, Elli L, Maggioni M, Della Valle S, Spampatti MP, Colombo M, Conte D. Transient elastography in patients with celiac disease: a noninvasive method to detect liver involvement associated with celiac disease. Scand J Gastroenterol. 2012 Jun;47(6):640-8
    33. Caproni M, Bonciolini V, D'Errico A, Antiga E, Fabbri P. Celiac disease and dermatologic manifestations: many skin clue to unfold gluten-sensitive enteropathy. Gastroenterol Res Pract. 2012;2012:952753.
    34. Criado PR, Criado RF, Aoki V, Belda W Jr, Halpern I, Landman G, Vasconcellos C. Dermatitis herpetiformis: relevance of the physical examination to diagnosis suspicion. Can Fam Physician. 2012 Aug;58(8):843-7.
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    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    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