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      Frequently Asked Questions About Celiac Disease   04/07/2018

      This Celiac.com FAQ on celiac disease will guide you to all of the basic information you will need to know about the disease, its diagnosis, testing methods, a gluten-free diet, etc.   Subscribe to Celiac.com's FREE weekly eNewsletter   What are the major symptoms of celiac disease? Celiac Disease Symptoms What testing is available for celiac disease?  Celiac Disease Screening Interpretation of Celiac Disease Blood Test Results Can I be tested even though I am eating gluten free? How long must gluten be taken for the serological tests to be meaningful? The Gluten-Free Diet 101 - A Beginner's Guide to Going Gluten-Free Is celiac inherited? Should my children be tested? Ten Facts About Celiac Disease Genetic Testing Is there a link between celiac and other autoimmune diseases? Celiac Disease Research: Associated Diseases and Disorders Is there a list of gluten foods to avoid? Unsafe Gluten-Free Food List (Unsafe Ingredients) Is there a list of gluten free foods? Safe Gluten-Free Food List (Safe Ingredients) Gluten-Free Alcoholic Beverages Distilled Spirits (Grain Alcohols) and Vinegar: Are they Gluten-Free? Where does gluten hide? Additional Things to Beware of to Maintain a 100% Gluten-Free Diet What if my doctor won't listen to me? An Open Letter to Skeptical Health Care Practitioners Gluten-Free recipes: Gluten-Free Recipes
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    DOCTOR, HOW DO I FEEL?


    Dr. Ron Hoggan, Ed.D.


    • Journal of Gluten Sensitivity Summer 2014 Issue


    Celiac.com 09/20/2016 - A surprising research report from Australia that explores non celiac gluten sensitivity (1) has given rise to a number of journalistic offerings that range between offensive and downright silly, while the reporters who wrote them appear to have somewhat compromised reading skills (3, 4). That is not to say that the research report is without problems. However, at least that report requires a close reading to identify its most troubling elements (1). Specifically, it suggests that patients who claim to feel better on a gluten free diet are either deluded or confused. The research implies that these patients may actually feel better because they have reduced their consumption of the starch in the gluten grains they are avoiding. That doesn't qualify as justification for either "fake" or "b$#@@#$$" (2, 3) as stated in the titles of the above journalistic offerings. The central thrust of the research report is that their investigations showed no evidence of benefits for patients who follow a gluten free diet due to the patients' belief that they are sensitive to gluten. These researchers could have said something indicating that a low FODMAPs diet might work better to help the person with NCGS [non celiac gluten sensitivity], as it not only eliminates gluten, but it also eliminates the associated starches, and a host of other sugars and starches that may also be contributing to their digestive symptoms. But they didn't. They said, instead, that they found ".....no evidence of specific or dose-dependent effects of gluten in patients with NCGS placed on a low FODMAPs diet" (1).


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    First, let's be clear about what the acronym FODMAP means. It stands for fermentable, oligosaccharides, disaccharides, monosaccharides, and polyols. They are groups of sugars and starches that can induce or exacerbate gastrointestinal symptoms. But most of the gluten grains are made up of such starches (which are quickly turned to sugar as soon as we ingest them). The protein content is relatively small. Flours made from all forms of wheat and rye are high in FODMAPs (4). These people were not masquerading as having celiac disease. Neither were they trying to mislead anyone. They simply found that they feel better when avoiding gluten grains. So why the profanity and accusations embedded in the headlines of these articles (2, 3)?

    Avoidance of these foods will often help those with digestive problems. But this can happen for a variety of reasons. For instance, in a person with lactose intolerance, that individual has stopped or reduced production of the brush border enzymes (lactase) that are needed to break apart the two constituent sugars that form lactose (galactose and glucose) the sugar found in milk. The lactose molecule, a disaccharide (di = two and saccharide = sugar) is too large to be absorbed through the cells (enterocytes) that line the intestinal wall, and then into the bloodstream. While humans may not be able to digest these larger molecules of lactose, many of the bacteria that live in our intestines do so with little problem. These microscopic residents of our GI tracts multiply rapidly in the presence of so much available food. The enormous and growing numbers of these microbes, combined with their rapid digestion of lactose, produces considerable quantities of methane gas. The resulting symptoms we experience include gut pain, flatulence, smelly stools, and diarrhea. The low FODMAP diet excludes or limits oligosaccharides (from 3 to 6 units of simple sugars) disaccharides, and monosaccharides. It also excludes sugar alcohols and fermentable foods which can produce acids, gases and/or alcohols.

    Thus, only the gluten family of proteins should have been used to "challenge" the research subjects in this study (1) that is causing all the fuss. But that wasn't done.

    As may be very quickly ascertained from the interview with Sachin Rustgi, in the spring issue of this journal, there are many structural variations in each of the families of glutens and in specific gluten structures of each strain of each of the gluten-containing grains (5). In fact, Biesiekierski et al openly acknowledge that they purchased the refined gluten they used in their study from a different supplier than was used in a previous study, conducted by some of the same researchers, that confirmed the presence of non celiac gluten sensitivity (6). The later study used a form of gluten that may not have diverged much from the original, as the research group was able to state that the glutens from both studies were similar. However, they also acknowledged that they did not characterize the other, non-gluten components of the gluten they used, either. Thus, there are two possible confounding factors just in the gluten component used in this study. Small differences in the gluten protein structures may have been sufficient to cause the dramatically different result, or some added or missing non-gluten component of the gluten purchased may have caused the different result. We have no way of telling if, or to what extent, either of these factors may have played in the different findings. Without more careful work, neither could the Biesiekierski et al research group (1).

    It is not news to many of us who are gluten sensitive that differing families of gluten can produce differing symptoms and will sometimes elicit no symptoms at all. Some of us, including those with celiac disease, also react to corn and/or rice glutens, despite very clear medical statements that this is not part of our gluten-induced disease. So some of us have a more generalized reaction to gluten, while others are reacting only to sub-groups of gluten. Still others may cross react with similar proteins from other foods. Yet I can't help but believe that when such foods cause virtually identical digestive symptoms, there is some kind of connection to our problem with digesting and metabolizing gluten. Narrow medical definitions notwithstanding, each individual who struggles with this digestive issue must find her or his best answers through trial and error. Rigid journalists who genuflect at the altar of allopathic medicine will be unable to help us navigate this hazardous swamp. Neither will researchers with pre-conceived notions, who try to conduct dietary studies in a manner developed for pharmaceutical trials.

    For instance, Sachin Rustgi acknowledged that some biopsy-diagnosed celiacs will not react to a given strain of gluten grains while others with celiac disease will mount an immune reaction against the same strain (5). So each of us may be sensitized to different short strings of amino acids that form part of one or more of the family of gluten proteins or one or more of its sub-groups. This is wholly congruent with the science that explains and depicts selective antibody formation and activation.

    And that is only one part of the complexity here. Research that tries to formulate a strain of wheat that will not trigger gluten-induced illnesses must eliminate all sensitizing agents that each person with celiac disease may respond to with selective antibody production, while trying to retain the characteristics that produce the desired taste, smell, and nutrient content. Also, few of us with gluten issues need to be told that other foods can cause us to experience similar symptoms, or exacerbate, or vary, our symptoms. It can sometimes be a very confusing quagmire where it is difficult to identify the source of our symptoms.

    Further, Biesiekierski and colleagues overtly acknowledge that their focus on fatigue might have produced better insight into NCGS by revealing "why those who follow a GFD feel better" if they had asked their question differently (1). They also acknowledge the possibilities that gluten may only cause symptoms in combination with FODMAPs, or that FODMAPs cause gut problems which result in a gluten-induced loss of a sense of wellness. Their comments in this regard commendably reflect a willingness to look beyond the surface in this matter. I would go further, based on Scott Adams' interview of Sachin Rustgi (5) and assert that not all genetic strains of wheat gluten will elicit symptoms of celiac disease in a given individual with biopsy-proven celiac disease, never mind those with NCGS. So the researchers' failure to account for patient-to-patient variability, as is seen in celiac disease, along with specific wording of questions about symptoms are yet two more confounding factors in this study. Perhaps a mixture of several forms of gluten, bereft of contaminants, would have been a better choice for Biesiekierski's group. And other precautions in formulating their questions might have been useful. But there are many more problems with this report.

    Extensive Review by Expert Panel
    Dr. Carlo Catassi and a large group of widely recognized celiac experts published a comprehensive review of the medical literature on the topic of non-celiac gluten sensitivity in September of last year. Therein, they state that: " Lack of biomarkers is still a major limitation of clinical studies, making it difficult to differentiate NCGS from other gluten related disorders" (7). Conversely, the Australian group led by Biesiekierski, asserts in their report which was published the previous month, that "Generally, NCGS is viewed as a defined illness, much like celiac disease, where gluten is the cause and trigger for symptoms" (6). At least one of these groups is confused about whether or not non celiac gluten sensitivity is well defined and well understood.

    As a student of this literature myself, I would assert that the consensus view is that this form of gluten sensitivity is far from being either well defined or well understood. In fact, there is still a great deal that is not understood even about celiac disease. Non celiac gluten sensitivity has only recently begun to be widely recognized in circles of gastrointestinal researchers. Further, the Biesiekierski group's extensive use of celiac-related antibody tests appears to ignore the widely held view that biomarkers are one of the great impediments to understanding non celiac gluten sensitivity. I would also add that while I have often argued for the use of IgG class anti-gliadin antibodies as a marker of many cases gluten sensitivity (also see Jean Duane's article in this issue) with or without symptoms, I have also maintained that there are many cases in which these antibodies are not found, yet the patient will frequently benefit from removal of gluten from her/his diet.

    A further weakness of the Biesiekierski et al study is that each of the intervals during which the low FODMAP diet (2 weeks), the gluten-containing diet at 16 grams/day (for 1 week), the low gluten diet at 2 grams /day (for 1 week), and the whey-containing diet 16 grams/day ( for 1 week) all ran for periods of time that were just too short to produce measurable serological findings in people with celiac disease. Even the washout period of 2 weeks was a minimal duration. Also, the three days allotted for the re-challenge trial was certainly too brief to produce meaningful results. Some celiac disease researchers report that only about 50% of their research subjects, all of whom had biopsy diagnosed celiac disease, produced celiac-associated antibodies after a two week challenge: "Antibody titres increased slightly from baseline to day 14 of GC [gluten challenge] but markedly by day 28" (8). This puts the one week duration of the Biesiekierski study into perspective - it is a choice that may have been directed at a specific research result. By day 28 of the Leffler et al study, 75% of the celiac patients showed markedly increased celiac associated antibodies. Thus, a single week of gluten challenge, as was used in the Biesiekierski et al study would be unlikely to produce any measureable changes in serum antibodies, even among people with celiac disease, who should reasonably be expected to react most quickly and strongly to gluten ingestion. Those with biopsy diagnosed celiac disease form the group that is currently thought to mount a much more serious and vigorous immune reaction to gluten than that seen in those with non celiac gluten sensitivity. While I do not necessarily agree with that perspective, it is wholly unreasonable to expect a reaction from a group of NCGS patients in one quarter of the time it is seen in only 75% of celiac patients.

    This Leffler et al study (8) also indicates that these celiac patients were reporting symptoms within three days of beginning the gluten challenge. Thus, it seems especially surprising that self-diagnosed gluten sensitivity would be such a contentious issue that would incite such rancorous responses as those mentioned earlier (2, 3). Because NCGS is not well characterized or understood, allowing only one week for gluten ingestion to cause symptoms, if that is our only measurement of gluten's impact on their health, might work with about three quarters of celiac patients, if antibodies are measured after 28 days, but how can anyone say that it is appropriate for NCGS? Further, the use of tests, especially serological antibodies, takes the focus off of symptoms and undermines the patients' reports of symptoms, suggesting that their claims of gluten sensitivity are either misguided or duplicitous. Meanwhile, the ~25% of those with biopsy diagnosed celiac disease had not yet produced celiac associated serum antibodies, even after four weeks of gluten challenge.

    We do not need physicians to tell us how we feel.

    While most of the limitations to the Biesiekierski et al study were actually mentioned in their report, those journalists who formulated articles and inflammatory titles that included the terms "fake" (2) and "b$#@@#$$" (3) seem to have missed reading those parts of this report. Further, they took such statements as "These data suggest that NCGS, as currently defined, might not be a discrete entity or that this entity might be confounded by FODMAP restriction" to mean that there is no such thing as NCGS. However, those of us with reading skills above the middle-school level will recognize that Biesiekierski and colleagues qualified their statement in several important ways, suggesting that FODMAP restriction could be a confounding variable or that the current definition of NCGS may need to be adjusted, or the possibility that the gluten they used may not have been appropriate. One must wonder whether these journalists are that challenged when it comes to reading? Or are they trying to raise readership? Perhaps their ads sell according to how many hits and responses their websites garner. Thus, it may make sense to offend groups that are likely to post responses to their site, as a strategy aimed at raising their advertising revenue. I can't see what other limitation or motivation there might be to so dramatize these research findings with little regard for what the researchers actually said. On another level, I hope that the field of Journalism has not become so crass that they don't bother to exercise even a modicum of critical thought when reading reports of research results. That, after all, is their function in democratic societies. They are supposed to offer insightful commentaries on current trends in politics, science, education, law enforcement, and various other facets of our democratic cultures. It is difficult to find thoughtfulness or insight in the terms "fake" and "b$#@@#$$". It is also difficult to see such reports being published when a retrospective study I was involved in remains unpublished. Perhaps that is due to the finding that the gluten free diet had a very positive impact on the behavior and scholastic performance of many children.

    The gluten sensitive community has come a long way, but many biased journalists, physicians, and researchers continue to resist the notion that gluten is a food that harms many people.

    Sources:

    1. Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology. 2013 Aug;145(2):320-8.e1-3.
    2. https://ca.shine.yahoo.com/gluten-intolerance-is-fake-093131285.html
    3. http://kitchenette.jezebel.com/gluten-sensitivity-is-apparently-b$#@@#$$-1577905069
    4. http://stanfordhospital.org/digestivehealth/nutrition/DH-Low-FODMAP-Diet-Handout.pdf
    5. Adams S. Discussion with Assistant Resident Research Professor Sachin Rustgi on the Genetic Modification of Wheat to Make it Safe for Celiacs. Jrnl Glut Sens. 2014. Spring; 13 (2): 11-13.
    6. Biesiekierski JR, Newnham ED, Irving PM, Barrett JS, Haines M, Doecke JD,Shepherd SJ, Muir JG, Gibson PR. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. 2011 Mar;106(3):508-514.
    7. Catassi C, Bai JC, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano A. Non-Celiac Gluten sensitivity: the new frontier of gluten related disorders. Nutrients. 2013 Sep 26;5(10):3839-53.
    8. Leffler D, et al. (2013) Kinetics of the histological, serological and symptomatic responses to gluten challenge in adults with coeliac disease. Gut 62(7):996–1004.


    Image Caption: Image: CC--Ansel Edwards
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    Guest Thomas Hessley

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    It took me approximately 6 weeks to "start feeling better" after adopting the gluten-free diet. I "felt" awful for the first 50 years of my life, and after 22 years on the gluten-free diet, there is absolutely no incentive to "cheat".

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    Dr. Ron Hoggan, Ed.D.
    Celiac.com 05/01/2015 - In his article titled "Against the Grain," published in the November 3, 2014 issue of The New Yorker, Michael Specter likens the Gluten and Allergen Free Expo to "a travelling medicine show" in the first paragraph (1). Just in case a reader was half asleep and missed the bias embodied in that phrase, Specter ends the same first paragraph with: "There was even gluten-free dog food." It's hard to miss the harsh, cynical tone, and it is a shame that he usurped the name of Melissa Diane Smith's informative book to title his invective.
    What, we must wonder, is the source of his bias? He does offer some detailed explanations of the bond between glutenin and gliadin, and how carbon dioxide from the fermentation process is trapped as bread and other pastry rises, making light, fluffy bread and pastry. He has done some detailed, even impressive investigation into cooking with gluten. However, he also asserts that wheat-breeding practices haven't induced any changes that might explain the increased incidence of celiac disease since World War II. He then goes on to say: "But something strange is clearly going on. For reasons that remain largely unexplained, the incidence of celiac disease has increased more than fourfold in the past sixty years." Mr. Specter acknowledges that celiac disease is on the rise and, according to Specter, there have not been any major changes to the genetics of wheat that might explain this increase.
    This perspective appeared in a very prestigious, highly regarded publication—The New Yorker. Many people will believe these claims just because of where they were published. And here is the problem I have with that. Mr. Specter has the genetic information all wrong: Norman Borlaug was awarded a plethora of honors for his work in developing more than 6,000 new wheat hybrids, which included several strains of disease resistant, semi-dwarf wheat that increased per-acre yields by seven to ten fold, thereby leading to wheat independence in a number of third world nations. For these scientific accomplishments he was awarded the Nobel Peace Prize, the Presidential Medal of Freedom, and a Congressional Gold Medal. Several books have been written about Dr. Borlaug and his achievements, and several foreign governments, science academies, and institutions have bestowed him with awards, honorary degrees and memberships. Borlaug has even had streets, university wings, and assorted other places and artifacts named after him and has even been mentioned in popular television shows. He has been called the father of the "green revolution" and has enjoyed very widespread recognition for having been instrumental in saving many millions of lives through increasing the world's food supply in the form of wheat. It is my belief that this venerable and compassionate man of science deserved every honor that was bestowed on him (2).
    However, I also think that it besmirches Dr. Borlaug's memory when Specter dismisses all those genetic changes to wheat as a possible factor in "the growing number of cases" of celiac disease based on the statement by Dr. Donald Kasarda that he was unable to find "evidence that a change in wheat-breeding practices might have led to an increase in the incidence of celiac disease". One person's failure to find evidence for something does not prove the absence of that phenomenon. Mr. Specter also quotes Dr. Joseph Murray, the very popular and famous (at least in the gluten sensitive community) gastroenterologist at the Mayo Clinic, as an expert in wheat genetics, and quotes Dr. Murray as asserting that wheat genetics haven't changed much over the past fifty years. I'm skeptical that Dr. Murray would profess expertise in the realm of cereal grain genetics. Regardless of whether this is Mr. Specter's construct, or Dr. Murray did actually make this claim to expertise in wheat genetics and the assertion that little has changed in wheat genetics since World War II, the statement is at least incorrect when it comes to wheat genetics.
    The conundrum Mr. Specter has created by ignoring Dr. Borlaug's work sets up an article in which he attacks what he calls "gluten anxiety". He says that "nearly twenty million people contend that they regularly experience distress after eating products that contain gluten." The implication is clear. Mr. Specter would have us believe that these people are confused about changes to how they feel, and/or whether those changes resulted from switching to a gluten-free diet—apparently all twenty million of them are so confused that they now need Mr. Specter to lead them out of the darkness of their own self-delusion, and begin to appreciate that wheat, in its present genetic form, has been consumed for at least 10,000 years and it's "a staple food that has sustained humanity for thousands of years". I'd like to point out that the Levant, where wheat was first grown, was not host to all of humanity at that, or any other time. Many humans, after leaving Africa about 85,000 years ago, evolved in a variety of environmental niches where gluten grains have not been available until quite recently.
    And there are many genetic variations of wheat. Which ones, I wonder, is Mr. Specter saying have been with us for so long? Contrary to his assertions, it is this variability that serves as one of the greatest barriers to the development of genetic strains of wheat that are "safe" for consumption by people with celiac disease. Dr. Sachin Rustgi, one of the scientists who is trying to develop such a safe wheat also said that: "Different celiac patients are sensitive to different 'gluten' proteins (prolamins). If one feeds peripheral blood cells sampled from a patient or a small group of patients (from a specific geographical location) with gluten proteins derived from a wheat genotype, it is expected either to see a reaction (monitored by the production of interferon gamma) or no apparent effect. But in the latter case it does not mean that the wheat genotype is non-toxic to all celiac patients" (3). Since different proteins or protein fractions (peptides) are recognized by different celiac patients' immune systems, there is an enormous number of peptides and proteins that are potentially toxic to at least some people with celiac disease. Extrapolating from that point, people with non celiac gluten sensitivity may well be reacting to any of the proteins or derivative peptides from any of the multitudinous variants of wheat.
    Mr. Specter also makes the claim that: "Humans have been eating wheat, and the gluten in it, for at least ten thousand years." Yet the geneticist, Dr. Martin Richards, and his colleagues report that about three quarters of Europeans are descendants of hunter-gatherers, rather than the early farmers from the Levant (4). So a large majority of people of European descent have not been eating cereal grains for more than 10,000 years. Just how long they have been consuming them depends on where they lived in Europe, which may explain the variability in the frequency of celiac disease across Europe. It is worthy of note that incidence of celiac disease is particularly increased in Scandanavia, Scotland, and Ireland, where climate and topography combined to make cereal grain cultivation more difficult. Thus, one might reasonably interpret this to suggest that these populations experienced limited past exposure to these grains. It is only with modern transportation systems, combined with the abundant excesses of wheat made possible by the work of Dr. Norman Borlaug and many others, in addition to the erroneous belief that wheat is a healthy food, that we now have almost worldwide over-consumption of gluten grains. Increased consumption has led to the increased frequency of celiac disease in these relatively grain-naive populations.
    Much of the rest of the world's populations have only recently begun to eat these grains. Even in the lowlands of England, where grain cultivation is relatively easy and successful, these grains have only been there for the about the last 5,000 years. Worldwide exposure to these grains varies somewhere between several thousands of years to less than 100 years. And what data supports the notion that even 10,000 years is sufficient time for humans to make the complex adaptation to eating them? Dr. Marlene Zuk has implicitly made such a claim, through reporting on much more rapid adaptations to adult consumption of dairy products (5). However, since we are mammals, and are almost universally able to consume human milk as infants, the adaptation required for the digestion of lactose into adulthood is, comparatively speaking, quite minor. Still, more than two thirds of the world's populations are unable to do so. Mr. Specter's resistance to recognizing gluten as a dietary hazard appears to be rooted in bias, rather than a thoughtful examination of the relevant data.
    It also appears that Mr. Specter either failed to learn, or failed to mention, that humans do not have the necessary complement of digestive enzymes needed to break some of the bonds between amino acids in the storage proteins of gluten grains, so we can fully digest them (6). Surely, if we were fully adapted to eating them, we should be able to digest these proteins.
    Nonetheless, Mr. Specter repeatedly disparages and dismisses the disease entity of non-celiac gluten sensitivity, and goes on to say: "The most obvious question is also the most difficult to answer: How could gluten, present in a staple food that has sustained humanity for thousands of years, have suddenly become so threatening?" Of course, this question is only difficult to answer if one ignores the many genetic manipulations of gluten grains and a substantial body of medical research into a variety of human ailments.
    For instance, Dr. Curtis Dohan and his colleagues were the first to publish a report on the connection between some cases of schizophrenia and gluten grains titled "Relapsed schizophrenics: more rapid improvement on a milk- and cereal-free diet" in 1969 (7). This research was conducted in a locked psychiatric ward. Similarly, seven years later, Singh and Kay followed with publication of an affirming research report that, using a different study design, identified wheat as a pathogenic factor in some cases of schizophrenia (8). This work was also conducted in a locked ward where total control of the patients' food intake could be controlled. Further, neither of these reports asserted a connection between celiac disease and schizophrenia. Over the following two decades, several reports, based on sloppy, poorly designed research, were published in the medical literature, and the notion that gluten grains could be a factor in schizophrenia was quickly forgotten. Mr. Specter would have been pleased with these latter reports. Another critic of Dr. Dohan's work, Dr. Donald Kasarda, a cereal scientist at the USDA, was quite happy to make statements such as: "Dohan wasn't much of a scientist" (9). Yet it was this same individual, Don Kasarda, whose name appeared as one of the authors of a report that asserted that a subset of schizophrenic patients mount a novel immune reaction against gluten (10). Dr. Dohan and his colleagues discovered a disease process, and an effective treatment for it, forty years ahead of the group that Dr. Kasarda worked with. Yet the earlier work was unscientific—until the publication of the work led by Dr. Samaroo, with contributions from Dr. Kasarda. Did Dr. Dohan suddenly become competent? Or is there another, more reasonable explanation? I don't understand the contradictions here.
    I'm also struggling to understand Mr. Specter's quoting Dr. Kasarda in his attack on non celiac gluten sensitivity. After all, Dr. Kasarda was one of the authors who published the report of non celiac gluten sensitivity in a subset of schizophrenic patients.
    On another front, Dr. Marios Hadjivassiliou and colleagues have been reporting, over the last twenty years, on celiac disease and non-celiac gluten sensitivity in connection with a variety of neurological diseases. These include depression, cerebral palsy, neurological dysfunction, alcohol induced cerebellar degeneration that results in gluten sensitivity, ataxia, ganglionopathy, a gluten induced condition that mimicks amyotrophic lateral sclerosis, inflammatory myopathy, chorea, headaches, balance disturbances, and neuromuscular disorders. They have also reported that antibodies against one of the protein families in gluten are found in the brain (IgG class anti-gliadin antibodies) and they also attack brain tissues (11). Others have reported connections between gluten and seizure disorders in non-celiac gluten sensitivity (12), and cerebral calcifications with seizures (13). Further, several forms of gluten induced brain damage have been reported in the context of celiac disease, which suggests a similar dynamic for those with non-celiac gluten sensitivity and brain damage. Gluten induced brain disorders include headache/migraine, attention-deficit/hyperactivity disorder, epileptic seizures, mental retardation, cerebellar ataxia and behavior disorders (14) in the context of celiac disease. Any and all of these may also suggest a similar dynamic for those with NCGS.
    I have worked with learning disabled students who have shown remarkable recoveries on a gluten-free diet, similar to those described by Alexandra Blair, in her 2003 Times article about dyslexic children who improved enormously on a gluten-free diet (15). Unfortunately, these data were not published in the peer reviewed literature, so they are unlikely to persuade researchers to investigate this matter further. Nonetheless, given the data on gluten's impact on neurological and brain tissues, it does seem very possible that many learning disabilities are, at least partly, the result of non-celiac gluten sensitivity, and that they may benefit from gluten avoidance. Time and space limitations prevent me from exploring the research that identifies the psychoactive properties of protein fractions in wheat, first identified by Christine Zioudrou et al, in her 1979 publication (16), or the Hudson and colleagues' report in 1976 showing that a single subgroup of gluten proteins, called gliadins, are toxic to any of a wide variety of human cells (17). Yet Mr. Specter, calling it "gluten anxiety" would have us dismiss all of this and much, much, more peer reviewed research that identifies gluten as toxic to many people who do not have celiac disease.
    It has never been clear to me why people such as Mr. Specter are quite willing to attack new ideas and discoveries that others have made on their quest for improved health. The attackers seem to want to mock those of us who have found an answer for ourselves. He interviewed several people, whom he quoted in his article, who were just convinced that they felt better when avoiding gluten. Mr. Specter derides those gluten sensitive individuals who were generous enough with their time to allow him to interview them, apparently at the Gluten Free Expo he attended, then compared with "a travelling medicine show". It is difficult to tell whether Mr. Specter was making news or reporting it when he interviewed these people.
    Please recall the fall issue of the Journal of Gluten Sensitivity, in which I explored the flaws of the research by Dr. Biesiekierski and colleagues in Australia (18). Mr. Specter cites Professor Gibson, one of the authors of the same study, as one of his sources for discrediting the notion of non-celiac gluten sensitivity. Mr. Specter goes on to present himself as having a superior insight into the issue of non-celiac gluten sensitivity, attacking Dr. William Davis, cardiologist and author of the popular book, Wheat Belly (19), and Dr. David Perlmutter, a neurologist and author of the similarly popular book, Grain Brain (20). Are we to ignore the now thousands of researchers whose peer reviewed reports are now characterizing non-celiac gluten sensitivity as a disease entity? And should we ignore the scores of popular books asserting the same thing? Or should we ignore Mr. Specter and the flawed research from Australia? I know what I'm going to do.
    Sources:
    Specter M. Against the Grain. The New Yorker. Nov 3, 2014. http://en.wikipedia.org/wiki/Norman_Borlaug Adams S. Discussion with Assistant Research Professor Sachin Rustgi on the genetic modification of wheat to make it safe for celiacs. Journal of Gluten Sensitivity. 2014; 13(2): L11-14. Richards M, Macaulay V, Hickey1 E, Vega1 E, Sykes B, Guida V, Rengo C, Sellitto D, Cruciani F, Kivisild T, Villems R, Thomas M, Rychkov S, Rychkov O, Rychkov Y, Gölge M, Dimitro D, Hill E, Bradley D, Romano V, Calì F, Vona G, Demaine S, Papiha S, Triantaphyllidis C, Stefanescu G, Hatina J, Belledi M, Di Rienzo A, Novelletto A, Oppenheim A. Tracing European Founder Lineages in the Near Eastern mtDNA Pool. American Journal of Human Genetics, 2000; 67; 5: 1251–1276. Zuk M. Paleofantasy. Norton, NY: 2013. Kagnoff M. Diagnosing Celiac Disease. CSA/USA, Seattle, WA., Oct. 3-5, 1997. Dohan F, Grassberger J, Lowell F, Johnson H, Arbegast A. "Relapsed schizophrenics: more rapid improvement on a milk- and cereal-free diet" British Journalof Psychiatry. 1969; 115: 595-596. Singh M & Kay S.: 1976, "Wheat gluten as a Pathogenic factor in Schizophrenia" Science. 1976: 191; 401-402. Kasarda, D. private communication. Samaroo D, Dickerson F, Kasarda DD, Green PH, Briani C, Yolken RH, Alaedini A. Novel immune response to gluten in individuals with schizophrenia. Schizophr Res. 2010, May;118(1-3):248-55. Hadjivassiliou M1, Mäki M, Sanders DS, Williamson CA, Grünewald RA, Woodroofe NM, Korponay-Szabó IR.Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia.Neurology. 2006 Feb 14;66(3):373-7. Bruni O, Dosi C, Luchetti A, Della Corte M, Riccioni A, Battaglia D, Ferri R. An unusual case of drug-resistant epilepsy in a child with non-celiac gluten sensitivity.Seizure. 2014 Sep;23(8):674-6. Calvani M Jr1, Parisi P, Guaitolini C, Parisi G, Paolone G.Latent coeliac disease in a child with epilepsy, cerebral calcifications, drug-induced systemic lupus erythematosus and intestinal folic acid malabsorption associated with impairment of folic acid transport across the blood-brain barrier.Eur J Pediatr. 2001 May;160(5):288-92. Diaconu G, Burlea M, Grigore I, Anton DT, Trandafir LM Celiac disease with neurologic manifestations in children. Rev Med Chir Soc Med Nat Iasi. 2013 Jan-Mar;117(1):88-94.) Blair A. Wheat-free diet gives food for thought. The Times. (of London) June 12, 2004. Zioudrou C, Streaty RA, Klee WA. Opioid peptides derived from food proteins. The exorphins. J Biol Chem. 1979 Apr 10;254(7):2446-9. Hudson, D., Purdham, D., Cornell, H., Rolles, C. Non-specific cytotoxicity of wheat gliadin towards cultured human cells. The Lancet February 14, 1976. 339-341. Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology. 2013 Aug;145(2):320-8.e1-3. Davis W. Wheat Belly. Rodale Inc. NY, 2011. Perlmutter D. Grain Brain. Little, Brown & co. NY, 2013.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 10/16/2015 - Y Net News, under their "Health & Science" banner, published an article titled "Israeli researchers propose link between gluten and ALS", on April 17, 2015 (1). ALS refers to amyotrophic lateral sclerosis, or Lou Gehrig's disease, also known as motor neuron disease. Authorship of this article is attributed to the news agency, Reuters. The article refers to a study in which the investigators identify an autoimmune dynamic in the brain (2). The Y Net News article quotes one of these investigators as warning ALS patients against experimenting with a gluten-free diet: "Patients should not be tempted to use a gluten-free diet without clear evidence for antibodies, because an unbalanced diet might harm"(1). This is the kind of advice that frequently appears in the popular media. There can be little doubt that a gluten-free can be unhealthy, just as gluten containing diets can be unhealthy. When contacted on this issue, Dr. Drory said that "Patients with ALS tend to lose weight due to symptoms of their disease and it is well known that weight loss has a negative influence on disease progression and survival. Therefore it is very important for these patients not to lose weight" (3). Although Dr. Drory did not mean to impugn the gluten-free diet for the general population, she is legitimately concerned about the longevity and health of ALS patients, so she believes that only those with positive antibody tests should try the diet, and then only under the supervision of a dietitian. Reuters, on the other hand, have not responded to my request, through Y Net News, to contact the author of this article.
    While Dr. Drory's concerns are reasonable, I think that she has missed an important feature of the gluten-free diet and she puts too much faith in the connection between TG6 and ALS [an abbreviation for a recently discovered enzyme named tissue transglutaminase six] apparently believing that it will identify all ALS patients who might benefit from avoiding gluten. However, if we can judge based on those who have celiac disease, it is a diet that is more likely to increase the body mass of someone who is underweight. Dr. Drory also seems to have missed the sentiment expressed in the abstract of her own report. It says: "The data from this study indicate that, in certain cases, an ALS syndrome might be associated with autoimmunity and gluten sensitivity. Although the data are preliminary and need replication, gluten sensitivity is potentially treatable; therefore, this diagnostic challenge should not be overlooked" (1). Thus, when dealing with an otherwise irreversible and unstoppable disease, patients are cautioned not to try the diet without these marker antibodies which the authors identify as "preliminary" findings.
    Dr. Drory's caution also assumes that dietitians will generally be competent to guide the ALS patient in their gluten-free diet. However, it is important to recognize that the neurological patient needs to be even more strict with the diet than a person with celiac disease, and there are many uncertainties and debates around this diet. The average dietitian may not be up to date with the application of the gluten-free diet for such conditions, or the relevant controversies, or their application. Also, the beneficial results of a gluten-free diet are widespread across so many ailments and much medical research currently lags well behind patients' positive experiences. This is what has led to the continuing debate about the frequency and importance of non-celiac gluten sensitivity. Until very recently, it was usually given no attention at all. Further, since "gluten sensitivity is potentially treatable," and the current life expectancy for an ALS patient is about 2 years, it seems irresponsible to warn patients to wait for further research results before trying a gluten-free diet.
    This latter sentiment captures the essence of my current view of the gluten-free diet. Until I was diagnosed with celiac disease, more than twenty years ago, I would have ignored Dr. Drory, and subscribed to the bias inherent in the Y Net News article. Sadly, I used to dismiss people who talked about diet in the same way that I responded to those who talked about "astro travel" and Astrology. I viewed them as foolish concepts that were popular fads among drug-crazed hippies of the 1960s and 1970s, and other similarly deranged individuals. I still question many other diets, astro travel, and Astrology, but hope I do not do so with the same arrogant certitude of my youth.
    You see, I experienced a startling change of perspective shortly after I was diagnosed with celiac disease. Just three days after beginning the gluten-free diet, I awoke to an altered state of consciousness. The closest I can get to describing it is that I felt somewhat like I remember feeling as a kid when I awoke on Christmas morning. I felt optimistic, hopeful, and I looked forward to the day ahead. That was a big change. I was used to waking up feeling tired, depressed, and usually with a sense of foreboding about the coming day. I also found, after about the first six months or so of avoiding gluten, that my mind was becoming sharper, I was more aware of my surroundings, and my memory seemed to improve. My reflexes also seemed quicker. My sense of balance got better and my reaction time was faster. When I looked at others, I saw that many people were similarly challenged and didn't seem to be aware of their limitations—or perhaps they had just become used to them. Thus, I now believe that many people unknowingly suffer from the myriad harms induced or facilitated by gluten consumption. I also see, given the many venues in which the diet made a difference for me, why others might be skeptical.
    But how did Dr. Drory get from the notion that since gluten sensitivity is treatable, and should therefore be investigated as a potential factor in some cases of ALS, to the notion that ALS patients should be cautioned against experimenting with a gluten-free diet because it can cause weight loss? The gluten-free diet can be an effective weight loss strategy for some people. As I have mentioned in previous columns, the gluten-free diet seems to reduce the appetites of overweight individuals with celiac disease by about 400 calories per day. Equally, underweight celiac patients usually gain weight. Dr. Drory's concern about weight loss for those with ALS might be well founded if it was a universally good weight loss strategy. But it isn't. The data regarding weight loss on a gluten-free diet are only available, to my knowledge, with regard to celiac patients, where underweight patients almost always gain weight and about half of overweight patients lose weight. She also thinks that experimentation without a positive antibody test and the oversight of a dietitian might be risky. So her concerns may not be as valid as they first appear. If those ALS patients are gluten sensitive, then they might behave similarly to those with celiac disease, at least with regard to weight gain and loss. Further, how can anyone say, without trying it, that a gluten-free diet would not benefit those ALS patients who do not show TG6 antibodies?
    The Reuters article goes on from there to state: "It’s also worth remembering that an association is not the same as a cause. At least one earlier study concluded that there was no association between TG6 antibodies and either neurological disease or gluten itself" (1). The preceding comment refers to a retrospective research report in which the records of patients, on a Swedish data-base, who had been diagnosed with celiac disease, were further examined for an additional diagnosis of ALS (4). This is more than a little strange, since the very study the Reuters journalist used to distinguish between associations and causality, seeks only evidence of an association between the ALS and celiac disease. The notion that correlation is not causation is valid. However, using a study that looks for a correlation between celiac disease and ALS is not a reasonable basis for differentiating between correlation and causation. Neither is it a valid example of a causal relationship.
    Further, it is difficult to imagine a study design that would be less likely to reveal an association between transglutaminase TG6 and any other ailment, than one based on recorded data from a large number of patients who were diagnosed with celiac disease between 1969 and 2008. All, or almost all of these patients were diagnosed prior to the first published report of the discovery and diagnostic utility of transglutaminase 6 (5). So if one looks through records that predate the discovery of TG6 to find evidence of a connection between TG6 and any other disease, one is highly unlikely to find it.
    The abstract of the study that asserts there is no association between these ailments is based on a very weak design. It also ends with the statement: "Earlier reports of a positive association may be due to surveillance bias just after celiac disease diagnosis or expedited diagnostic work-up of ALS" (4). They are so confident of their own findings that they suggest that contrary findings are either due to bias or fast, careless work. I will leave it to the reader to infer whether there is bias among the authors of this report. Additionally, the Y Net News article, by one or more journalists at the Reuters News Agency, reports that this study found no association between TG6 antibodies and ALS, even though the study in question examines data that predates the use of TG6 antibody testing. While the study in question does appear to claim that there is no connection between celiac disease and ALS, the mention of TG6 and whether there is a connection between these antibodies and ALS appears to be information added by Reuters.
    Regardless of this possibly 'added' information, it really is quite a stretch to warn the public or ALS patients of the dangers of a gluten-free diet in reporting about research that has found evidence of a possible connection between ALS and gluten consumption. In a balanced report, the Reuters journalist would have mentioned the seven other research publications that have reported associations, and/or cause to suspect such associations, between gluten and ALS (5-11). It really isn't rocket science. It is just ethical, balanced reporting, which should serve as a minimum standard for an organization that is engaged in reporting the news. Since there are always at least two sides to almost any argument, both sides should at least have been acknowledged. Thus, in addition to the weak study reporting that they didn't find an association, the seven other reports of possible associations really should have been mentioned.
    It would also have been informative to their readers to mention Stephen Hawking, the longest living patient who was diagnosed with ALS. Dr. Hawking is still alive and has been on a gluten-free diet for the last 40+ years (12). He had already lived well beyond the two year life expectancy predicted by his doctors when, in 1963, Hawking's ALS had progressed to the point where he had begun to choke on his food. That is when he eliminated gluten, sugar, and plant oils from his diet. He has continued to avoid gluten for all these years and has also added several vitamins and supplements to his diet. Whether any or all of these measures have made "the" life extending difference, or if it is all of these measures combined that have allowed him to continue for so long, we can't know. Nonetheless, it may be that the gluten-free diet has been a determining factor in Dr. Hawking's longevity in the context of ALS. We also don't know if he would have tested positive for TG6 back when he was first diagnosed. However, he might not still be with us if he had opted to wait for this research to emerge and be confirmed.
    Since Hawking began his self-directed dietary experiment, researchers at the Royal Hallamshire Hospital in Sheffield, UK, have shown that the TG6 antibodies, while present in some celiac patients, are also found in some patients with non celiac gluten sensitivity and either neurological disease or an increased risk of developing one (5).
    Others, reporting a case study, had diagnosed ALS, then identified, diagnosed, and treated co-existing celiac disease with a gluten-free diet. They then retracted their ALS diagnosis saying: "Ultimately, improvement in the patient’s symptoms following treatment for celiac disease rendered the diagnosis of ALS untenable" (6). It would appear that any improvement in ALS symptoms obviates a diagnosis of ALS. It also raises the possibility that some cases of ALS can be effectively treated with a gluten-free diet.
    Similarly, in another case study report, the authors state: "ALS is a condition with relentless progression; for this reason, the simple observation of an improvement in symptoms is most pertinent in rendering the diagnosis of ALS untenable" (7). Again, the patient's ALS symptoms regressed following institution of a gluten-free diet.
    Yet another report that connects ALS with autoimmunity in general states: "The significance of increased premorbid celiac disease in those with ALS, and in family members of patients with MMN [multifocal motor neuropathy] remains unclear at present."(9). Still others have offered genetic evidence of connections between gluten sensitivity and ALS (10).
    Thus, the Reuters article raises an important question. Why are we seeing so many media attacks on those who are taking responsibility for their own health and experimenting with a gluten-free diet? It might come as a surprise to the Reuters journalist to learn that we humans had evolved and spread into most habitable areas of the world long before a few farmers began cultivating grains in regions of what are now known as Iraq and Iran. She/he might also be surprised to learn that we have known, for decades, that variants of wheat, rye, and barley have a deleterious impact on human neurological tissues (13, 14, 15) and that a variety of neurological ailments arise both in the context of celiac disease and non-celiac gluten sensitivity (14).
    The conclusion in the abstract of the 'no relationship' study dismisses reports of opposing findings as either due to "surveillance bias" or "expedited diagnostic work-up" (4). (This latter is a euphemistic statement suggesting that the work that led to these other reports was conducted too quickly and errors resulted.) Whatever your personal view of the attitude expressed there, the greater concern may be that the media continue to identify the gluten-free diet as potentially harmful (1) while researchers and individuals experimenting with a gluten-free diet have found evidence connecting gluten sensitivity with, at least, some cases of ALS (2).
    Over the years, I have heard many reasons for resisting this diet, but the one that is probably the least defensible is the assertion that it is potentially harmful. Almost any dietary regimen can be hazardous, of course, but the assertion that it might cause a harmful dietary imbalance fails to recognize that gluten has only been part of the Human experience for a very short time, in evolutionary terms. The simple fact is that we humans have spent far more of our evolutionary past eating a gluten-free diet than we have spent eating gluten. Some populations have only been eating these grains since European incursions over the last several hundred years. Some of these populations have only been eating it for less than one hundred years. Still others have been eating gluten for a few thousand years. In Israel, where Dr. Drory's study originated, grains were probably incorporated into the diet much earlier than in most of the rest of Europe, probably sometime between 15,000 and 10,000 years ago. It is difficult to imagine that after hundreds of thousands of years of eating a gluten-free diet, that avoiding gluten can pose a health hazard. The Reuters journalist appears to have another axe to grind, but I continue to wonder why we are seeing so many journalists on the attack against the gluten-free lifestyle?
    The driving force behind these journalists' attacks may well be similar to the perspective that I experienced before my diagnosis with celiac disease. Perhaps they suspect, whatever their reasons, that the gluten-free diet has little or no merit, and their only concession is to grudgingly allow that it may be helpful to those with celiac disease. My suspicion is that this attitude is driven by an insecurity. We want to believe conventional wisdom that gluten grains are healthy and that our medical professionals, and the institutions in which they serve, are above reproach. Nobel Laureate, Kary Mullis, is one highly vaunted physician's voice, among many, who dismiss most diets as fads, arguing that we are omnivores whose secret of successful adaptation to a wide variety of environments is the result of our flexibility in sources of nourishment (18). Many of us want to be able to rely on our physicians. We don't want the insecurity of knowing that our medical establishment is a flawed, human institution. The self-directed experimentation with a gluten-free diet poses a threat to that credibility, and hence, our sense of security, especially when it results in improved health. We don't want to feel the resulting uncertainty that comes from doubting the medical cornerstone of our civilization.
    It is not long ago that Don Wiss, myself, and others, argued extensively with physicians and researchers who insisted that the rate of celiac disease in the USA was variously one in 12,000 persons or one in 25,000 people. Sometimes these discussions became quite heated. Some of the people posting to these newsgroups were asking for suggestions for how they might proceed with various health complaints. When Don or I saw a post asking about symptoms that had been reported in the peer reviewed literature, in association with untreated celiac disease, we suggested a trial of a gluten-free diet. Some of the physicians and researchers contacted these individuals privately, saying things to discredit us. It seems doubtful that they would not have said such things where they were likely to be held accountable for what they said. Their reactions, I suspect, were driven by a sense of feeling threatened. As soon as controlled testing was done, it became clear that the rate of celiac disease, among Americans, is at least 1 in 133 Americans, and many of those individuals we advised to try a gluten-free diet might well have had celiac disease. Yet many journalists, physicians, and researchers have a great deal invested in the current status quo. Any threat to the established order is likely to incite the ire of many members of these groups.
    Thus, while others may consider it prudent to await the end of the current debate about ALS and a gluten-free diet, the ALS patient might be better advised to take dietary steps to ensure against weight loss, while trying a strict gluten-free diet. I know what I would do if were diagnosed with ALS...on second thought, since I've been gluten-free for more than twenty years, maybe I won't ever be diagnosed with ALS. I will continue to hope. In the meantime, Thomas Kuhn clearly outlined this stage of acceptance of new ideas in science (19). We appear to be in the "denial" stage, which is the last one before we can expect the emergence of widespread claims that 'we knew it all along'. If so, then broad acceptance is in the offing, and these nay-saying journalists will move on to some other controversial new discovery, and we can be spared the condescending remarks suggesting that the gluten-free diet is a mere placebo and a 'fad diet' for most of those who follow it.
    Sources:
    http://www.ynetnews.com/articles/0,7340,L-4647994,00.html Gadoth A, Nefussy B, Bleiberg M, Klein T, Artman I, Drory VE. Transglutaminase 6 Antibodies in the Serum of Patients With Amyotrophic Lateral Sclerosis. JAMA Neurol. 2015 Apr 13. Drory V. Personal communication via email Ludvigsson JF, Mariosa D, Lebwohl B, Fang F. No association between biopsy-verified celiac disease and subsequent amyotrophic lateral sclerosis--a population-based cohort study. Eur J Neurol. 2014 Jul;21(7):976-82. Hadjivassiliou M, Aeschlimann P, Strigun A, Sanders D, Woodroofe N, Aeschlimann D. Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase. Ann Neurol 2008;64:332-343 Brown KJ, Jewells V, Herfarth H, Castillo M. White matter lesions suggestive of amyotrophic lateral sclerosis attributed to celiac disease. AJNR Am J Neuroradiol. 2010 May;31(5):880-1. Turner MR, Chohan G, Quaghebeur G, Greenhall RC, Hadjivassiliou M, Talbot K. A case of celiac disease mimicking amyotrophic lateral sclerosis. Nat Clin Pract Neurol. 2007 Oct;3(10):581-4. Ihara M, Makino F, Sawada H, Mezaki T, Mizutani K, Nakase H, Matsui M, Tomimoto H, Shimohama S. Gluten sensitivity in Japanese patients with adult-onset cerebellar ataxia. Intern Med. 2006;45(3):135-40. Turner MR, Goldacre R, Ramagopalan S, Talbot K, Goldacre MJ. Autoimmune disease preceding amyotrophic lateral sclerosis: an epidemiologic study. Neurology. 2013 Oct 1;81(14):1222-5. Auburger G, Gispert S, Lahut S, Omür O, Damrath E, Heck M, BaÅŸak N. 12q24 locus association with type 1 diabetes: SH2B3 or ATXN2? World J Diabetes. 2014 Jun 15;5(3):316-27. Bersano E, Stecco A, D'Alfonso S, Corrado L, Sarnelli MF, Solara V, Cantello R, Mazzini L. Coeliac disease mimicking Amyotrophic Lateral Sclerosis. Amyotroph Lateral Scler Frontotemporal Degener. 2015 Feb 3:1-3. Hawking J. Travelling to Infinity: My Life with Stephen. Alma Books, Richmond, UK. 2014.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 12/15/2015 - Newly diagnosed with celiac disease, late in 1993 or early in 1994, I was reading a paper that turned my perception of this disease upside down. I learned that it takes more than susceptible genes and eating gluten to cause celiac disease. There is some added, as yet unknown factor in the onset of celiac disease. The report I was reading suggested that a fairly common viral infection might be that missing co-factor. It went on to say that 89% of subjects with untreated celiac disease also showed blood evidence of a particular viral infection called adenovirus 12, while fewer than 12% of control subjects showed evidence of past or present infection with this virus. It is a microbe that makes its home in our small intestines. The report went on to say that this particular virus contains an amino acid sequence that is identical to a sequence that forms part of a protein in gliadin, which is found in wheat, while similar proteins with the same triggering impact on our immune systems are also found in rye and barley. I was electrified by this insight. It offered a window through which I could begin to understand this enigmatic disease that made me react to a food that almost everyone I knew seemed to tolerate without any problems.
    I looked to see who had written the article. The lead author was listed as M. F. Kagnoff, but my attention was drawn to Donald Kasarda’s name, also listed as an author, because I had seen that name before. Several years later, I attended a CSA/USA conference in Seattle. The name of one of the speakers was familiar. After a little checking, I realized that he was the lead author of the study that had touched off my imagination.
    Dr. Kagnoff’s lecture followed immediately after a presenter who had repeatedly asserted that celiac disease is a very difficult diagnosis. Almost as soon as he got up on stage, Dr. Kagnoff said something to the effect that celiac disease is only a difficult diagnosis if you aren’t looking for it. The room suddenly became very quiet.
    The presentation went well, and he outlined the criteria for diagnosing celiac disease, and stated why he felt that it was a simple diagnosis. The speaker who followed him began by stating that celiac disease is a difficult diagnosis, despite Dr. Kagnoff’s assertions to the contrary. I left that conference with a strong sense of appreciation for Kagnoff on several levels: as a gastroenterologist, as a researcher, and as an independent thinker who was quite willing to offer a dissenting opinion where he disagreed.
    Six or seven years later, a mutual friend introduced me to Marty Kagnoff at a cocktail party in New York city. It was a pleasure to finally meet him in person. I told him that I was most impressed with, and intrigued by his work with adenovirus 12. I also told him that I enjoyed hearing his assertion, at the Seattle conference, that celiac disease is a simple diagnosis. He seemed a little surprised that I was aware of his research from more than twenty years previous, and he said that his work had been eclipsed by newer work that explored other infectious agents. He was interesting and interested, and the three of us engaged in a lively discussion about some of the politics regarding celiac disease and its diagnosis. He was brilliant, creative, and independent; all the things that a researcher should be.
    His passing is a huge loss to the medical profession, the celiac and gluten sensitive community, as well as to the biological research community. His contributions and discoveries shaped much of what we now understand about celiac disease, the intestinal mucosa, and intestinal immunity.
    Source:
    Kagnoff MF, Paterson YJ, Kumar PJ, Kasarda DD, Carbone FR, Unsworth DJ, Austin RK. Evidence for the role of a human intestinal adenovirus in the pathogenesis of coeliac disease. Gut. 1987 Aug;28(8):995-1001

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 07/19/2016 - We know that celiac disease afflicts almost 1% of the general population (1). We also know that about 12% of the general population has non-celiac gluten sensitivity, as indicated by elevated IgG class anti-gliadin antibodies in their blood (2). Although elevated antibodies identified by this test are often dismissed as "non-specific", they are clear evidence that the immune system is mounting a reaction against the most common food in our western diet. It is also true that many people who produce these antibodies and have then excluded gluten from their diets have also experienced improved health. Unfortunately, most of the individuals who have elevated IgG anti-gliadin antibodies and might benefit from avoiding gluten do not know that they are gluten sensitive and/or have celiac disease. Thus, we really don't know how many, or which, school children should be avoiding gluten to optimize their academic potential as they work their way through the education system.
    Approaching this issue from a different angle, we know that between 10% and 15% of the U.S. population has dyslexia (3). About 60% of those with ADHD have dyslexia (3). If we calculate the prevalence of ADHD, at 8.8% of the population (4), then just the ADHD component, it should give us 5.28% of the population with dyslexia. But we can't tell how much overlap there is between this group and the group that constitutes between 10% and 15% of the population that are reported as having dyslexia. These disabilities have been given considerable attention and have been studied for some time, yet we really know little about their causes, except in cases of traumatic brain injury.
    However, there is a startling study, reported in The Times ten years ago, from the Nunnykirk School in Northumberland, U.K. (5). The astounding results of this study continue to cry out for further research and possible replication. After 6 months on a gluten-free diet, testing showed that 11 of the 12 (92%) live-in students had improved their reading and comprehension at more than twice the rate at which regular students are expected to improve. Among the 22 students living in the community and attending this special school for dyslexic students during the day, 17 of them (77%) showed similar improvements (5). To put these results in perspective, special needs teachers are often very proud when they can help students achieve at rates similar to regular students. Doubling the rates of improvement is an astonishingly positive result! And a few of these students leaped ahead at six times the rate of normal students! The numbers of students involved in this study are too small to allow us to extrapolate to other dyslexic populations. And, given that the research was done in the United Kingdom, where definitions of learning disabilities, and other factors may be dissimilar, and that the work was reported in a newspaper instead of a peer reviewed journal, and the startlingly positive nature of these results, we really need further, carefully designed studies to explore this phenomenon.
    The Nunnykirk findings are consistent with the extensive brain and neurological research that has been done at the Royal Hallamshire Hospital at the University of Sheffield, over the last two decades, by Marios Hadjivassiliou and his colleagues. They have found that a strict gluten-free diet can often relieve central and peripheral neurological symptoms.
    Further, many prominent researchers who work with children and adults who have dyslexia characterize it as a neurobiological condition, and can demonstrate, with MRI, altered brain function in dyslexia (8). It is also clear that many cases of dyslexia are at least partly genetically conferred (8, 9). Neither are learning disabilities limited to dyslexia. Although some practitioners lump two or more learning disabilities together, the literature distinguishes between dyslexia, dysgraphia, dyspraxia, dyscalculia, dysphasia/aphasia, auditory processing disorders, visual processing disorders, etc. Some such practitioners not only differentiate between types of learning disabilities, they also differentiate between sub-types of disabilities. For instance, motor dysgraphia (where fine motor speed is impaired), dyslexic dysgraphia (where normal fine motor speed allows them to draw or copy but impairs spontaneous writing) and spatial dysgraphia (where handwriting is illegible due to distortion) can each be identified based on symptoms (10). Similar sub-types are seen in other learning disabilities.
    But what if the findings at Nunnykirk School are broadly applicable to all of these types of learning problems? Or perhaps further research can tell us which types and sub-types of learning disabilities can often be alleviated by a gluten-free diet.
    My own professional observations suggest that the number of students helped by a gluten-free diet would be similar to the proportions seen at Nunnykirk School. I have also observed that as the strictness of the diet increases, so does the number of students who improve. However, the diagnosing professionals are becoming reluctant to differentiate, even between general types of learning disabilities such as dyslexia and dysgraphia. As teachers, we were told that a child had learning disabilities and then, if not specified in the documents we were given, we had to figure out exactly what type of disability they had, then devise or research effective ways of teaching these students. I have done a little of both, but my experience is that this choice varies from one teacher to the next, and one situation to the next. Unfortunately, depending on the individual teacher's workload, teaching background, and personal biases, these children can sometimes be neglected or under-served, a choice that is often dictated by excessive workloads and demands on teachers' time to perform other tasks, especially extensive reporting and supervising sports and other extra-curricular activities.
    Please recall the overlap between dyslexia and ADHD mentioned earlier (3), and consider that there are ten reports of connections between attention deficit disorders and celiac disease published in the peer reviewed medical literature. Now, please recall that about 60% of these ADHD children will have dyslexia (3). Since the current, and past issues, of the Diagnostic and Statistical Manual of Mental Disorders, require that ADHD and learning disorders each be differentiated from any medical condition that might be causing the same symptoms and be alleviated by resolution of the medical condition in question. On that basis alone, almost every child being considered for a diagnosis of learning disorders or ADHD should be thoroughly tested for celiac disease and non-celiac gluten sensitivity.
    Yet, I would be very surprised to learn that this is commonly being done. Thus, we have a situation in which we are forced to rely upon a study conducted by a group of teachers, in cooperation with parents and students, that was published in The Times (5) and we must take action on our own because, as yet, celiac disease and non-celiac gluten sensitivity are not yet being differentiated from ADHD and/or learning disabilities. The really tragic part of this story is that a gluten-free diet, if started early enough, can reduce or completely eliminate all of these problems with learning disabilities and attention deficits, when gluten is the underlying problem.
    If you or your spouse are gluten sensitive, or have celiac disease, do you also have children who struggle in school? Based on the data from Nunnykirk School, current blood tests are probably not sufficient to rule out those who would benefit from a gluten-free diet. For the moment, you may need to institute a trial of a gluten-free diet, as mentioned above, while we await further research in this area. But wouldn't it be valuable for succeeding generations to know, or have a pretty clear idea whether the diet could help? And with what types and/or sub-types of learning disorders? That's where more research could really help. We already know that there is an association between gluten sensitivity and seizure disorders, ataxia and cerebellar degeneration, neuropathy (damage to peripheral nervous system), schizophrenia, depression, migraine, anxiety disorders, autism, multiple sclerosis, myasthenia gravis (an autoimmune neuromuscular disease), and white matter lesions in the brain (11). It should not be surprising if gluten underlies many or most cases of learning disorders and attention deficits. And if research can tell us which cases would be most likely to benefit from the diet, that will be a huge step forward for parents, students, teachers, and government agencies that provide funding for the education of those who are afflicted with these ailments.
    In the meantime, we only have the information that we have. So, despite its many weaknesses, the Nunnykirk investigation of dyslexic children argues for experimental implementation, on a trial basis. I would suggest at least a six-months-long period of strict gluten avoidance to determine whether it will help individuals who suffer from dyslexia and/or other learning disabilities.
    Sources:
    1. Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago S, Elitsur Y, Green PH, Guandalini S, Hill ID, Pietzak M, Ventura A, Thorpe M, Kryszak D, Fornaroli F, Wasserman SS, Murray JA, Horvath K. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study. Arch Intern Med. 2003 Feb 10;163(3):286-92.
    2. Hadjivassiliou M, Grünewald R A, Davies-Jones G A B. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry 2002;72:560-563.
    3. Dyslexia Research Institute http://www.dyslexia-add.org/
    4. National Resource Center on ADHD http://www.help4adhd.org/about/statistics
    5. Blair http://www.thetimes.co.uk/tto/news/uk/article1924736.ece
    6. 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.
    7. Aziz I, Hadjivassiliou M. Coeliac disease: noncoeliac gluten sensitivity--food for thought. Nat Rev Gastroenterol Hepatol. 2014 Jul;11(7):398-9.
    8. Shaywitz SE, Shaywitz BA. The Neurobiology of Reading and Dyslexia. Focus on Basics - Connecting Research & Practice, Volume 5,A: Aug. 2001. http://www.ncsall.net/index.html@id=278.html
    9. Eicher JD, Powers NR, Miller LL, Mueller KL, Mascheretti S, Marino C, Willcutt EG, DeFries JC, Olson RK, Smith SD, Pennington BF, Tomblin JB, Ring SM, Gruen JR. Characterization of the DYX2 locus on chromosome 6p22 with reading disability, language impairment, and IQ. Hum Genet. 2014 Jul;133(7):869-81.
    10. About Education http://specialed.about.com/od/readingliteracy/a/Dyslexia-And-Dysgraphia.htm
    11. Jackson JR, Eaton WW, Cascella NG, Fasano A, Kelly DL.Neurologic and psychiatric manifestations of celiac disease and gluten sensitivity. Psychiatr Q. 2012 Mar;83(1):91-102.
    12. Diaconu G, Burlea M, Grigore I, Anton DT, Trandafir LM. Celiac disease with neurologic manifestations in children. Rev Med Chir Soc Med Nat Iasi. 2013 Jan-Mar;117(1):88-94. PubMed PMID: 24505898.
    13. Niederhofer H. Association of attention-deficit/hyperactivity disorder and celiac disease: a brief report. Prim Care Companion CNS Disord. 2011;13(3). pii: PCC.10br01104PMCID: PMC3184556.
    14. Niederhofer H, Pittschieler K. A preliminary investigation of ADHD symptoms in persons with celiac disease. J Atten Disord. 2006 Nov;10(2):200-4.
    15. Zelnik N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2004 Jun;113(6):1672-6.
    16. Kozłowska ZE. [Evaluation of mental status of children with malabsorption syndrome after long-term treatment with gluten-free diet (preliminary report)]. Psychiatr Pol. 1991 Mar-Apr;25(2):130-4. Polish.
    17. Diaconu G, Burlea M, Grigore I, Anton DT, Trandafir LM. Celiac disease with neurologic manifestations in children. Rev Med Chir Soc Med Nat Iasi. 2013 Jan-Mar;117(1):88-94. PubMed PMID: 24505898.
    18. Niederhofer H. Association of attention-deficit/hyperactivity disorder and celiac disease: a brief report. Prim Care Companion CNS Disord. 2011;13(3). pii: PCC.10br01104. PMCID: PMC3184556.
    19. Niederhofer H, Pittschieler K. A preliminary investigation of ADHD symptoms in persons with celiac disease. J Atten Disord. 2006 Nov;10(2):200-4.
    20. 4: Zelnik N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2004 Jun;113(6):1672-6.
    21. Kozłowska ZE. [Evaluation of mental status of children with malabsorption syndrome after long-term treatment with gluten-free diet (preliminary report)]. Psychiatr Pol. 1991 Mar-Apr;25(2):130-4. Polish.

    Jefferson Adams
    Celiac.com 09/15/2016 - Some doctors and clinicians have reported cases of severe sprue-like enteropathy associated with olmesartan, but, until now, no clear demonstration of an increased risk has been documented by epidemiological studies.
    Now, a French nationwide observational cohort study has shown a connection between severe intestinal malabsorption and the drug olmesartan, according to results presented by a team of researchers. Olmesartan is an angiotensin II receptor antagonist which has been used for the treatment of high blood pressure. Olmesartan is also sold commercially under the name Benicar.
    The research team included Mickael Basson, Myriam Mezzarobba, Alain Weill, Philippe Ricordeau, Hubert Allemand, Francois Alla, and Franck Carbonnel. They are variously affiliated with the French National Health Insurance Fund, Paris, France, and the Université Paris-Sud, Assistance Publique-Hôpitaux de Paris and Gastroenterology unit, Hôpitaux Universitaires Paris Sud, Le Kremlin Bicêtre, France.
    The team set out to assess, in a nationwide patient cohort, the risk of hospitalization for intestinal malabsorption associated with olmesartan compared with other angiotensin receptor blockers (ARB) and ACE inhibitors (ACEIs). From the French National Health Insurance claim database, they included all adult patients initiating ARB or ACEI between 1 January 2007 and 31 December 2012, with no prior hospitalization for intestinal malabsorption, no serology testing for celiac disease, and no prescription for a gluten-free diet product. Their main endpoint was incidence of hospitalization with a discharge diagnosis of intestinal malabsorption.
    The team included 4,546,680 patients, for a total of 9,010,303 person-years, and observed 218 events. Compared with ACEI, the adjusted rate ratio of hospitalization with a discharge diagnosis of intestinal malabsorption was 2.49 (95% CI 1.73 to 3.57, p
    Average length of hospital stay for intestinal malabsorption was longer in the olmesartan group than in the other groups (p=0.02).
    Compared with ACEI, the adjusted rate ratio of hospitalization for celiac disease was 4.39 (95% CI 2.77 to 6.96, p<0.0001).
    These results show that olmesartan is assoc qiated with higher rates of hospitalization for intestinal malabsorption and celiac disease.
    Source:
    Gut. doi:10.1136/gutjnl-2015-309690

    Jefferson Adams
    Celiac.com 11/21/2016 - Even early on, strange inconsistencies caused Dan and Davina Dixon to wonder about her daughter, Rebecca. With dark hair and olive skin, Rebecca looked visibly different from her fair-complected parents. She looked different enough to wonder, as a child, if was adopted, if Dan and Davina were really her biological parents, as they assured her they were.
    Later, in her twenties, Rebecca developed celiac disease, which usually runs in families, even though no one else in their extended family suffered from it. Most of this was merely fodder for curiosity, until the day Davina saw a Facebook post that mentioned how rare it is for parents with blue eyes to have a child with brown eyes.
    Wondering about Rebecca's brown eyes, Davina went to the family doctor, who suggested a blood test. That's when the real mystery began: The blood test revealed that Rebecca's dad, Dan, was not, in fact, her biological father. There was absolutely no doubt. Dan's blood type was AB, while Rebecca's was O-Positive. That makes it impossible for Dan to be her father. A paternity test followed, and confirmed the blood results. There was simply no chance that Dan was Rebecca's biological father.
    Naturally, the Dixons began to search for answers. As reported by Kidspot, Rebecca was raised believing that Dan and Davina were her biological parents. The couple had tried for years to conceive a child. Unsuccessful, they turned to Dr. Norman Barwin, a gynecologist and fertility expert known by many as Canada's "baby god."
    The couple wondered whether there could have been some sort of mix-up in Barwin's office. Eventually, they noticed Rebecca bore a striking resemblance to Dr. Barwin, himself. Soon after that, as CTV News reported, a woman conceived at the same clinic learned that she was genetically related to Barwin. A DNA test confirmed that Rebecca and the woman were half-sisters, and their father was Dr. Barwin. Apparently, Barwin's role as a sperm donor to his own medical practice was kept secret from both sets of parents.
    The Dixon family is now suing Dr. Barwin for negligence and breach of trust. The lawsuit requests that Barwin turn over a DNA sample, to determine if any other children conceived at his clinic are his offspring, and to notify them accordingly.
    Read more at:
    Kidspot.com CTV News  IJR.com

    Jefferson Adams
    Celiac.com 12/05/2016 - Symptomatic suspected gluten exposure is common among patients with celiac disease on a gluten-free diet. A gluten-free diet is the only recommended treatment for celiac disease. Although anecdotal evidence suggests that suspected gluten exposure is common among celiac patients following a gluten-free diet, there is not a great deal of hard data to support that view.
    A team of researchers recently set out to assess the prevalence and characteristics of gluten reactions in people with celiac disease on a gluten-free diet. The research team included JA Silvester, LA Graff, L Rigaux, JR Walker, and DR Duerksen. They are variously affiliated with the St Boniface Hospital in Winnipeg, Canada, the College of Medicine at the University of Manitoba in Winnipeg, Canada, and with the Celiac Research Program at Harvard Medical School in Boston, MA, USA.
    Their team prospectively enrolled adults with biopsy proven, newly diagnosed celiac disease. They then conducted a survey related to diet adherence and reactions to gluten, both at study entry and at 6 months. To measure celiac disease symptoms and gluten-free diet adherence, they used T Celiac Symptom Index, Celiac Diet Assessment Tool (CDAT) and Gluten-Free Eating Assessment Tool (gluten-free-EAT). Of the 105 patients enrolled, 91% reported gluten exposure less than once per month, while the average CDAT score was 9 (IQR 8-11), which suggests good dietary adherence.
    Two out of three patients reported suspected symptomatic reaction to gluten. Most, 63 percent, did not suspect gluten consumption until a reaction occurred. Meanwhile, just under one-third (29 percent) reported that problems happened when ordering in a restaurant.
    Thirty percent of patients say that gluten was consumed from incidental contact, while 10 percent said it was due to eating a major gluten ingredient.
    Average time to symptom onset was 1 hour, though onset ranged from 10 minutes to 2 days. Symptoms lasted about 24 hours on average, and ranged from 1 hour to 8 days. Symptoms typically included abdominal pain (80%), diarrhea (52%), fatigue (33%), headache (30%) and irritability (29%).
    Even with good dietary compliance, most celiac patients following a gluten-free diet suffer from regular adverse reactions to gluten. Eating away from home continues to pose the major risks for accidental gluten exposure.
    The team recommends that physicians treating celiac disease patients should include regular questions regarding gluten reactions as part of their assessment of gluten-free diet adherence.
    Source:
    Aliment Pharmacol Ther. 2016 Sep;44(6):612-9. doi: 10.1111/apt.13725. Epub 2016 Jul 22.

    Jean Duane
    Celiac.com 04/21/2017 - Adults who have gluten sensitivities cohabitating with non-gluten sensitive adults may have a lot of unanswered questions that need to be asked. Dramatic changes in one family member's diet can have profound effects on a household (Bacigalupe & Plocha, 2015). Numerous studies document how parents and children handle everyday living when the child has food intolerances, but very few studies focus on adults living with food sensitivities. Wouldn't you like to know how other adults with food sensitivities adapt and manage over the long haul? Questions like: Does the person with the sensitivity live in fear of cross-contamination? Does the household employ methods to ensure s/he is safe? If so, what are those methods? Do the non-sensitive members of the household feel resentment? Or have they grown weary of compliance over the long haul? How adherent is the sensitive adult? Is it worth a little risk for a little pleasure once in a while? What do these cohabitating adults do to exist gracefully? These questions will be asked in a forthcoming study (on Celiac.com), and the results will be shared with viewers/readers.
    Food allergies affect 15 million Americans (FARE, 2015), which means that adults with food sensitivities have gone from being rare to more commonplace as the population ages (Norling, 2012). Dietary restrictions due to disease will soon become common in many households and this can be problematic because severe dietary constraints are positively associated with diminished family social activities (Komulainen, 2010). Studies indicate that adults cohabitating, when one has food sensitivities and others do not, could potentially result in problems between members of the household creating feelings of uncertainty and potentially less adherence to the diet.
    Regimented dietary requirements affect the quality of life when virtually every bite of food must be scrutinized before consumption. For some households, compliance may fall on the shoulders of the person who cooks. The cook in the household, caregivers, and everyone sharing the same kitchen, must be actively involved in protecting the person with the sensitivities keeping gluten-containing crumbs off the counter, out of condiment jars, thoroughly cleaning utensils, etc. (Crowley, 2012; Bollinger, 2005; Merras-Salmino et al., 2014). Of course, those living with sensitivities know there is a lot more to staying "clean and safe." Family members who share a home with someone with pervasive food sensitivities must express empathy to ensure harmony and compliance (Komulainen, 2010). However, compliance comes with a price -- every meal must be planned and cooked using alternative ingredients to avoid accidental ingestion. This takes diligence, education and ability to accomplish meal after meal (Jackson et al., 1985) especially when allergies are to ubiquitous foods such as dairy, soy, gluten or corn.
    Dietary restrictions can cause misgivings on the part of the other family members, who may feel deprived of their favorite foods, compromised with recipe adaptations, or forced to unwillingly comply with the other person's diet. On the contrary, the person with food sensitivity may feel pressure not to comply with the diet in order to conform to the other adult's culinary demands. In the Jackson et al. study, forty percent of people with Celiac disease did not comply with the diet because it was too difficult (1985). The relationship between the cohabitating adults may be further complicated as trust issues develop between the sensitive adult and the cook, if the sensitive adult suspects foods that make them sick are creeping into their diet. Other food-sensitive adults report non-adherence because it is "too much trouble" and causes "social isolation" (Coulson, 2007). Non-adherence for those with sensitivities can lead to reactions, anaphylactic shock and even to death (Lee et al., 2003). Even those who do not react immediately risk long-term illness with non-compliance.
    In my twelve years experience working with people in this arena, I have observed that dietary adherence in the household seems to go through phases. The first phase is what I'm calling the "transition" stage when a person is newly diagnosed, and everyone in the household is learning the new rules. The second stage is the "status quo" stage where cohabitants understand, and hopefully comply. Finally, the third stage is what I'm terming as 'turbulent' when other adult household inhabitants are feeling weary of compliance, may have doubts about the other's sensitivities, or even rebel. This stage may be triggered by an event that disrupts the "status quo", such as a holiday where traditional foods are expected, and where their gluten-free substitutions may not be as satisfying to the other household members. It may be triggered when the food sensitive adult decides they may be reacting to different foods than they thought before, and want to experiment with dietary changes. Dynamics between cohabitants may become turbulent during these times. After the event, the household adjusts back to equilibrium until the next triggering event, which throws them into a different part of this phase-cycle, where they may cheerfully welcome a "transition," or react with "turbulence." This cyclical pattern seems to continue as cohabitants move in and out of phases as life-events occur. One of the goals of this survey will be to determine the validity of this cycle.
    I also want to test the hypothesis that a component of household compliance may also be associated with the status of the adult who has the dietary restrictions – whether the head of the home enjoys full household compliance, or if a subordinate adult must comply while others are eating the foods s/he are sensitive to. Another factor that may affect compliance is how the sensitive adult was initially diagnosed. Did a medical doctor conduct tests? Or did they read an article, and notice that they had symptoms consistent with gluten sensitivity and decide to go "gluten free?" Does the diagnostic process affect the compliance of the other adult members of the household? There are many factors that need to be assessed in order to help those of us who have food sensitivities who are living with other adults.
    This survey/study will focus on family interactions when dealing with dietary restrictions, with the potential to increase family member's compliance. It will seek to gain insight on the impact food restrictions for one adult has on the rest of the family. This study has social significance because family unity in the future may rely on developing constructs for compliance to address this emerging social problem.
    I'll collect data for this study and then share it with Celiac.com and the Journal of Gluten Sensitivity readers in order to create awareness by thoroughly examining the lifestyle of food sensitive people, shedding light on how social influences affect dietary adherence. As a PhD student at the University of Denver, and an adult with Celiac disease and a lifetime of other food allergies, living with another adult who has no food sensitivities, I know first-hand that it takes cooperation and commitment from everyone to ensure my health. I hope the study can help others improve their quality of life with the insight gained from conducting this study. I'll be launching this study on Celiac.com.
    Thank you to Scott Adams for allowing this study to be conducted on Celiac.com.

  • Recent Articles

    Connie Sarros
    Celiac.com 04/21/2018 - Dear Friends and Readers,
    I have been writing articles for Scott Adams since the 2002 Summer Issue of the Scott-Free Press. The Scott-Free Press evolved into the Journal of Gluten Sensitivity. I felt honored when Scott asked me ten years ago to contribute to his quarterly journal and it's been a privilege to write articles for his publication ever since.
    Due to personal health reasons and restrictions, I find that I need to retire. My husband and I can no longer travel the country speaking at conferences and to support groups (which we dearly loved to do) nor can I commit to writing more books, articles, or menus. Consequently, I will no longer be contributing articles to the Journal of Gluten Sensitivity. 
    My following books will still be available at Amazon.com:
    Gluten-free Cooking for Dummies Student's Vegetarian Cookbook for Dummies Wheat-free Gluten-free Dessert Cookbook Wheat-free Gluten-free Reduced Calorie Cookbook Wheat-free Gluten-free Cookbook for Kids and Busy Adults (revised version) My first book was published in 1996. My journey since then has been incredible. I have met so many in the celiac community and I feel blessed to be able to call you friends. Many of you have told me that I helped to change your life – let me assure you that your kind words, your phone calls, your thoughtful notes, and your feedback throughout the years have had a vital impact on my life, too. Thank you for all of your support through these years.

    Jefferson Adams
    Celiac.com 04/20/2018 - A digital media company and a label data company are teaming up to help major manufacturers target, reach and convert their desired shoppers based on dietary needs, such as gluten-free diet. The deal could bring synergy in emerging markets such as the gluten-free and allergen-free markets, which represent major growth sectors in the global food industry. 
    Under the deal, personalized digital media company Catalina will be joining forces with Label Insight. Catalina uses consumer purchases data to target shoppers on a personal base, while Label Insight works with major companies like Kellogg, Betty Crocker, and Pepsi to provide insight on food label data to government, retailers, manufacturers and app developers.
    "Brands with very specific product benefits, gluten-free for example, require precise targeting to efficiently reach and convert their desired shoppers,” says Todd Morris, President of Catalina's Go-to-Market organization, adding that “Catalina offers the only purchase-based targeting solution with this capability.” 
    Label Insight’s clients include food and beverage giants such as Unilever, Ben & Jerry's, Lipton and Hellman’s. Label Insight technology has helped the Food and Drug Administration (FDA) build the sector’s very first scientifically accurate database of food ingredients, health attributes and claims.
    Morris says the joint partnership will allow Catalina to “enhance our dataset and further increase our ability to target shoppers who are currently buying - or have shown intent to buy - in these emerging categories,” including gluten-free, allergen-free, and other free-from foods.
    The deal will likely make for easier, more precise targeting of goods to consumers, and thus provide benefits for manufacturers and retailers looking to better serve their retail food customers, especially in specialty areas like gluten-free and allergen-free foods.
    Source:
    fdfworld.com

    Jefferson Adams
    Celiac.com 04/19/2018 - Previous genome and linkage studies indicate the existence of a new disease triggering mechanism that involves amino acid metabolism and nutrient sensing signaling pathways. In an effort to determine if amino acids might play a role in the development of celiac disease, a team of researchers recently set out to investigate if plasma amino acid levels differed among children with celiac disease compared with a control group.
     
    The research team included Åsa Torinsson Naluai, Ladan Saadat Vafa, Audur H. Gudjonsdottir, Henrik Arnell, Lars Browaldh, and Daniel Agardh. They are variously affiliated with the Institute of Biomedicine, Department of Microbiology & Immunology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; the Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden; the Department of Pediatric Gastroenterology, Hepatology and Nutrition, Karolinska University Hospital and Division of Pediatrics, CLINTEC, Karolinska Institute, Stockholm, Sweden; the Department of Clinical Science and Education, Karolinska Institute, Sodersjukhuset, Stockholm, Sweden; the Department of Mathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden; the Diabetes & Celiac Disease Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden; and with the Nathan S Kline Institute in the U.S.A.
    First, the team used liquid chromatography-tandem mass spectrometry (LC/MS) to analyze amino acid levels in fasting plasma samples from 141 children with celiac disease and 129 non-celiac disease controls. They then crafted a general linear model using age and experimental effects as covariates to compare amino acid levels between children with celiac disease and non-celiac control subjects.
    Compared with the control group, seven out of twenty-three children with celiac disease showed elevated levels of the the following amino acids: tryptophan; taurine; glutamic acid; proline; ornithine; alanine; and methionine.
    The significance of the individual amino acids do not survive multiple correction, however, multivariate analyses of the amino acid profile showed significantly altered amino acid levels in children with celiac disease overall and after correction for age, sex and experimental effects.
    This study shows that amino acids can influence inflammation and may play a role in the development of celiac disease.
    Source:
    PLoS One. 2018; 13(3): e0193764. doi: & 10.1371/journal.pone.0193764

    Jefferson Adams
    Celiac.com 04/18/2018 - To the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service animals.
    If you’ve flown anywhere lately, you may have seen them. People flying with their designated “emotional support” animals. We’re not talking genuine service animals, like seeing eye dogs, or hearing ear dogs, or even the Belgian Malinois that alerts its owner when there is gluten in food that may trigger her celiac disease.
    Now, to be honest, some of those animals in question do perform a genuine service for those who need emotional support dogs, like veterans with PTSD.
    However, many of these animals are not service animals at all. Many of these animals perform no actual service to their owners, and are nothing more than thinly disguised pets. Many lack proper training, and some have caused serious problems for the airlines and for other passengers.
    Now the major airlines are taking note and introducing stringent requirements for service animals.
    Delta was the first to strike. As reported by the New York Times on January 19: “Effective March 1, Delta, the second largest US airline by passenger traffic, said it will require passengers seeking to fly with pets to present additional documents outlining the passenger’s need for the animal and proof of its training and vaccinations, 48 hours prior to the flight.… This comes in response to what the carrier said was a 150 percent increase in service and support animals — pets, often dogs, that accompany people with disabilities — carried onboard since 2015.… Delta said that it flies some 700 service animals a day. Among them, customers have attempted to fly with comfort turkeys, gliding possums, snakes, spiders, and other unusual pets.”
    Fresh from an unsavory incident with an “emotional support” peacock incident, United Airlines has followed Delta’s lead and set stricter rules for emotional support animals. United’s rules also took effect March 1, 2018.
    So, to the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service and emotional support animals.
    Source:
    cnbc.com

    admin
    WHAT IS CELIAC DISEASE?
    Celiac disease is an autoimmune condition that affects around 1% of the population. People with celiac disease suffer an autoimmune reaction when they consume wheat, rye or barley. The immune reaction is triggered by certain proteins in the wheat, rye, or barley, and, left untreated, causes damage to the small, finger-like structures, called villi, that line the gut. The damage occurs as shortening and villous flattening in the lamina propria and crypt regions of the intestines. The damage to these villi then leads to numerous other issues that commonly plague people with untreated celiac disease, including poor nutritional uptake, fatigue, and myriad other problems.
    Celiac disease mostly affects people of Northern European descent, but recent studies show that it also affects large numbers of people in Italy, China, Iran, India, and numerous other places thought to have few or no cases.
    Celiac disease is most often uncovered because people experience symptoms that lead them to get tests for antibodies to gluten. If these tests are positive, then the people usually get biopsy confirmation of their celiac disease. Once they adopt a gluten-free diet, they usually see gut healing, and major improvements in their symptoms. 
    CLASSIC CELIAC DISEASE SYMPTOMS
    Symptoms of celiac disease can range from the classic features, such as diarrhea, upset stomach, bloating, gas, weight loss, and malnutrition, among others.
    LESS OBVIOUS SYMPTOMS
    Celiac disease can often less obvious symptoms, such fatigue, vitamin and nutrient deficiencies, anemia, to name a few. Often, these symptoms are regarded as less obvious because they are not gastrointestinal in nature. You got that right, it is not uncommon for people with celiac disease to have few or no gastrointestinal symptoms. That makes spotting and connecting these seemingly unrelated and unclear celiac symptoms so important.
    NO SYMPTOMS
    Currently, most people diagnosed with celiac disease do not show symptoms, but are diagnosed on the basis of referral for elevated risk factors. 

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

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

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

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

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

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

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

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

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

    ASSOCIATED DISEASES
    The most common disorders associated with celiac disease are thyroid disease and Type 1 Diabetes, however, celiac disease is associated with many other conditions, including but not limited to the following autoimmune conditions:
    Type 1 Diabetes Mellitus: 2.4-16.4% Multiple Sclerosis (MS): 11% Hashimoto’s thyroiditis: 4-6% Autoimmune hepatitis: 6-15% Addison disease: 6% Arthritis: 1.5-7.5% Sjögren’s syndrome: 2-15% Idiopathic dilated cardiomyopathy: 5.7% IgA Nephropathy (Berger’s Disease): 3.6% Other celiac co-morditities include:
    Crohn’s Disease; Inflammatory Bowel Disease Chronic Pancreatitis Down Syndrome Irritable Bowel Syndrome (IBS) Lupus Multiple Sclerosis Primary Biliary Cirrhosis Primary Sclerosing Cholangitis Psoriasis Rheumatoid Arthritis Scleroderma Turner Syndrome Ulcerative Colitis; Inflammatory Bowel Disease Williams Syndrome Cancers:
    Non-Hodgkin lymphoma (intestinal and extra-intestinal, T- and B-cell types) Small intestinal adenocarcinoma Esophageal carcinoma Papillary thyroid cancer Melanoma CELIAC DISEASE REFERENCES:
    Celiac Disease Center, Columbia University
    Gluten Intolerance Group
    National Institutes of Health
    U.S. National Library of Medicine
    Mayo Clinic
    University of Chicago Celiac Disease Center