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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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    IT'S NOT JUST ME


    Dr. Ron Hoggan, Ed.D.


    • Journal of Gluten Sensitivity Summer 2013 Issue


    Celiac.com 02/14/2017 - In 1999, Loren Cordain, the renowned professor of Exercise Physiology at Colorado State University who has since popularized the Paleodiet, published an extensive exploration of why our cultivation and consumption of cereal grains has been disastrous for the human race, resulting in many autoimmune, nutrient deficiency, and other modern diseases (1). Previously, in 1987, the famous physiologist, Jared Diamond characterized humanity's shift to agriculture as "The Worst Mistake in the History of the Human Race" (2). A year later, medical doctor and professor of Anthropology, S. Boyd Eaton and colleagues suggested a mismatch between the human genome and our current agricultural diet/lifestyle (3). And more than a decade prior to that, gastroenterologist, Walter L. Voegtlin, M.D., self published a book apparently asserting, based on his treatments and observations of patients, that dietary avoidance of cereal grains and sugars, offset by increased consumption of meats and animal fats, is an effective treatment regimen for a variety of intestinal ailments including Crohn's disease, colitis, irritable bowel syndrome, and indigestion (4). Each of these perspectives was informed by a different but solidly scientific approach to human health. The academic field of each of these authors varied from Exercise Physiology to Physiology, to Gastroenterology, to Anthropology. Yet each of these specialist researchers arrived at the very similar conclusion that cereal grains are not healthful foods for humans. Their strident declarations to that effect leave little room for doubt. Dr. Cordain acknowledges that the roots of some of his thinking lie with Dr. Eaton and his colleagues. Nonetheless, there is a convergence here, of ideas and insights drawn from separate bodies of data and investigative approaches. While there is some overlap between these scientific disciplines, they all lead to a clear indictment of cereal grains as little more than a starvation food for humans. These scientists point to myriad signs of illness that arise more commonly when populations make the transition to eating diets dominated by grains, especially when the grains are refined and when they are combined with sugar.


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    One critic of this paradigm is the evolutionary biologist, Dr. Marlene Zuk of the University of California at Riverside. According to Alison George at New Scientist, Zuk asserts that the 10,000 years that humans have been cultivating and consuming cereal grains is an adequate time period for humans to evolve an adaptation to these foods (5). But surely this is a Eurocentric view. Simply because some Europeans have been cultivating and consuming cereal grains for ten or more thousands of years does not mean that the entire world's population, or even all Europeans, would or could have adapted to consuming these foods.

    Let's look back to see what we currently know about our human roots and how those early humans spread all over the world. A group thought to number about 200 humans left Africa sometime between 85,000 and 70,000 years ago, during a glacial maximum that lowered worldwide sea levels by about 300 feet below current levels. The enormous glaciers of the time so depleted the oceanic barriers we see today, that these bodies of water were made navigable even with very primitive flotation devices.

    The progeny of this relatively small group of early modern people multiplied and went on to parent almost all of today's non-African people of the world with some 1% to 4% of today's human, non-African genes having been derived from the Neanderthal branch of the hominid tree (6). This predominantly early modern human group's progeny would quickly find its way to Australia, the South Pacific, across Asia, to China, east to the Americas and west across India, finally arriving in Europe, where they would supplant the long-time Neanderthal residents who had survived some of Europe's harsh and inhospitable glaciations but apparently could not survive having our forebears as neighbors.

    While specific paths and dates for exiting Africa, and worldwide patterns and timing of human distribution remain controversial, most experts now accept that indigenous Australians had arrived there at least 60,000 years ago (6). A similarly recent finding places people in the Americas by at least 55,000 years ago, long prior to the date at which the Bering Land Bridge was thought to be available for human movement from Siberia into the Americas (8). This newer, admittedly controversial date raises the likely possibility that people arrived in the Americas, from Asia, by boats or rafts on which they followed the shoreline east to what is now Alaska, then south of the glaciated wastelands of much of what is now Canada. (Or perhaps they arrived by some other means that we have not yet imagined.) But only a small portion of these early Americans would eat wheat, rye, oats, or barley before the last 200 years or so, especially those living on the Great American Plains, or in the frigid north, the dense jungles or places that were otherwise isolated from the encroaching wave of "immigrants" from Europe and beyond. And none of those aboriginal peoples of the Americas were eating these grains prior to 1492. The epidemics of autoimmunity and obesity that may be seen among indigenous Americans are clear reflections of their recent shift to the gastronomic wonders of foods derived from these European grains.

    Further, even among Europeans, grain cultivation and consumption had not uniformly spread across most of Europe until, at most, less than half of the 10,000 years that Zuk says would be sufficient for human adaptation. In Britain, for instance, grain farming was only getting under way about 4,000 years ago, and availability of grains varied according to local geographies and economies. Also, in parts of Scandanavia, wheat bread was a rare treat until after World War II. Some Europeans are thought to have been cultivating grains for even longer than the 10,000 years ago suggested by Cordain, but the evidence is contradictory and accompanied by a range of expert opinions. Further, the health consequences of this nutritional path are consistently seen in the skeletal remains of those early farmers, many of which can now be seen reflected among indigenous peoples of the Americas, as they assimilate our grain and sugar dominated diet. Adaptation to eating grains is not a gentle, joyful process. Early farmers may have produced many more children than their hunting and gathering neighbors, but their lives were shorter, their bodies were less robust, with substantial reductions in stature, and they experienced widespread infectious diseases and ailments driven by nutritional deficiencies.

    By the time grains became a cash crop for many European farmers, cereals were disproportionately consumed by affluent urbanites. Those who were large consumers of cereal grains did not include all Europeans, even where yields were prodigious. In more remote, northerly, or mountainous areas, cereal grains, or foods made from them, were likely a rare treat rather than a daily staple.

    Jared Diamond points out, that in addition to "..... malnutrition, starvation, and epidemic diseases, farming helped bring another curse upon humanity: deep class divisions." He goes on to argue that only with farming and the storage and accumulation of food can Kings "and other social parasites grow fat on food seized from others". He also presents evidence that farming led to inequality between men and women. Conversely, contemporary hunter-gatherers have repeatedly been shown to be quite egalitarian, both regarding gender and political leadership (9).

    Roger Lewin is another critic of the health impact of European grain cultivation on humans. He points out that even in the very heart of the Fertile Crescent, where agriculture got its start, there was not a uniform adoption of farming. One agricultural center at Abu Hureyra, experienced two cycles of abandonment, one at 8,100 B.C.E., lasting about 500 years, and another at 5,000 B.C.E. These periods when agriculture at this locale was abandoned are "thought to be related to climatic change that became less and less conducive to agriculture" (10).

    Lewin also harkens to Mark Nathan Cohen's collation of "physical anthropological data that appear to show increasingly poor nutritional status coincident with the beginnings of agriculture.... " (10) suggesting, again, that grains were a starvation food.

    Eaton et al also approach grain cultivation from an anthropological perspective, suggesting that increased dietary protein and fats from animal/meat sources likely gave rise to increased stature of earlier humans, along with providing the necessary fatty acids for building larger brains, and allowing smaller gut sizes over the past 2.5 million years. It seems reasonable to assume that if it took our pre-historic ancestors that long to adapt to eating meats and animal fats, the very irregular adaptation period of between less than one hundred years and about 10,000 years that various world populations have been cultivating and consuming wheat, rye, barley and oats would be insufficient to allow full adaptation to eating these immune sensitizing cereal grains.

    Dr. Zuk's perspective might be tempered a bit if she considers that Europeans and their descendants do not comprise the entirety of the world's populations. There are several Asian populations that are not insignificant when compared with European populations and their progeny, including the residents of China, India, Pakistan, and South-East Asia. Even among those of us who appear quite European, there may be a mixture of genes derived from peoples of any of the other five populated continents. The approximately 10,000 year maximum period since humans began to cultivate cereal grains would have little adaptive impact on populations that have only been exposed to these grains for a period of somewhere between four or five centuries and seven or eight decades, as is the case among the indigenous people of the Americas, Australia, New Zealand, and much of Asia (6).

    Even if all humans had been cultivating and consuming cereal grains for the 10,000 years since this practice was first begun in the Middle East, the high frequency of intestinal, autoimmune, and other diseases that can be mitigated by a gluten free diet, even among descendants of Europeans, leaves little room to doubt that Dr. Zuk's projected adaptation simply has not occurred. The current prevalence of celiac disease and non-celiac gluten sensitivity identifies, at a bare minimum, between 7% and 12% of the American population that has not adapted to cereal grain consumption. While a few research projects suggest that molecular mimicry and the opioids from cereal grains contribute to autoimmunity, obesity, type 2 diabetes and cardio-vascular disease, current research does not provide any clear sense of how many cases or to what degree these health conditions are driven by gluten consumption. We know that foods derived from cereal grains are often laced with refined sugar, but the insulin stimulating properties of gluten alone are such that their role in these conditions cannot, reasonably, be denied. I feel vindicated by these many experts who decry the folly in humanity's embrace of the European grains. I wonder how long it will take for this information to filter into, and be acknowledged by, those who claim that science has led them to advocate cereal grain consumption for everyone without celiac disease and, more recently, non celiac gluten sensitivity?

    Sources:

    1. Cordain, Loren. Simopoulos AP (ed): Evolutionary Aspects of Nutrition and Health. Diet, Exercise, Genetics and Chronic Disease. World Rev Nutr Diet. Basel, Karger, 1999, vol 84, pp 19–73 http://thepaleodiet.com/wp-content/uploads/2012/08/Cerealgrainhumanitydoublesword.pdf
    2. Jared Diamond, "The Worst Mistake in the History of the Human Race," Discover Magazine, May 1987, pp. 64-66. http://www.ditext.com/diamond/mistake.html
    3. Eaton SB, Konner M, Shostak M. Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective. Am J Med. 1988 Apr;84(4):739-49.
    4. Voegtlin, Walter L. (1975). The stone age diet: Based on in-depth studies of human ecology and the diet of man. Vantage Press. ISBN 0-533-01314-3
    5. George, A. " The Paleo Diet Is a Paleo Fantasy" New Scientist. April 7, 2013. http://www.slate.com/articles/health_and_science/new_scientist/2013/04/marlene_zuk_s_paleofantasy_book_diets_and_exercise_based_on_ancient_humans.single.html
    6. Oppenheimer, Stephen. The Real Eve: Modern Man's Journey Out of Africa. Basic Books, NY, NY. 2004
    7. Fagan, Brian. Cro-Magnon: How the Ice Age Gave Birth to the First Modern Humans. Bloomsbury Press, New York. 2011
    8. http://www.utep.edu/leb/Pleistnm/sites/pendejocave.htm
    9. Brody, Hugh. The Other Side of Eden: Hunters, Farmers and the Shaping of the World. Douglas 7 McIntyre Ltd., Vancouver, B.C., Canada. 2000
    10. Lewin, Roger. A Revolution of Ideas in Agricultural Origins. Science. vol 240, May 20, 1988

    Image Caption: A paleo diet was the norm for the vast majority of human history. Image: CC--snowpea&bokchoi
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    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 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).
    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$#@@#$$". It is also difficult to see such reports being published when a retrospective study I was involved in remains unpublished. Perhaps that is due to the finding that the gluten free diet had a very positive impact on the behavior and scholastic performance of many children.
    The gluten sensitive community has come a long way, but many biased journalists, physicians, and researchers continue to resist the notion that gluten is a food that harms many people.
    Sources:
    Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology. 2013 Aug;145(2):320-8.e1-3. https://ca.shine.yahoo.com/gluten-intolerance-is-fake-093131285.html http://kitchenette.jezebel.com/gluten-sensitivity-is-apparently-b$#@@#$$-1577905069 http://stanfordhospital.org/digestivehealth/nutrition/DH-Low-FODMAP-Diet-Handout.pdf 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. 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. 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. 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.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 11/10/2016 - So far, 2014 has been a challenging new year for me. I was reminded of some events that happened almost fifty years ago. Based on that reminder, I resolved to contact a former girlfriend, both to suggest that she get testing for celiac disease, and to apologize for some insensitive things I said and did when I was 17. She was a year younger than me and one grade behind me in school. She was very slender and exceedingly self-conscious about having what she called "a chest like a boy". (She may have been experiencing delayed development, as is sometimes seen in celiac disease.) Every new place we visited, she went looking for the washroom as soon as she could. Movie theatres, restaurants, libraries, everywhere we went, she found the washroom first. She even did that the first time she was at my mother's house, which occasioned an uncharitable comment from my mom.
    Pat was also troubled by some microscopic hair that was growing on her upper lip. It sounds silly now, but these things were important to her at the time. I remember telling her that nobody could see her "moustache" without a magnifying glass. Nonetheless, she put Nair on it and, for at least one day, had the brightest red upper lip I have ever seen. She said it was too sore to put makeup on, so it really drew a lot of unwanted attention. Until meeting my wife, I never knew anyone who was as honest about who she was. I regret that I didn't appreciate her as much as I should have, but that was partly due to my age.
    Time passed, way led onto way, and life happened. Forty nine years later, there I was, looking for her on Facebook and other social media. I tracked her through old phone numbers, family members, and I even searched the title on her parents' home. I was full of excitement about re-connecting with my old friend, a person with whom I had shared those last innocent days of adolescence. Our friendship had been cut short because her dad was transferred to a city more than 600 miles away, and she was annoyed with me because I had said and done some insensitive things. We never even wrote to each other. I used to talk about her with my students, explaining our mutual fascination with literature. I thought about her often, but never, until this year, considered contacting her.
    After about a month of searching, I eventually found her. Much to my dismay, I was almost a year too late. She had passed away on March 10th of 2013, at the age of 64. At the time of her death, she was in the process of being evaluated for Parkinson's disease. She was at home when she experienced her last, massive seizure, which resulted in brain death. Both of her daughters are heartbroken over Pat's sudden, unexpected passing. Already a widow, Pat had left this world before I took the time and made the effort to be in touch with her again. I was filled with sadness, disappointment, and regret when I first reached one of her daughters and confirmed that she was the person I had known. I still wonder, if I had gotten in touch a decade earlier, would she still be alive? Would a gluten-free diet have helped her? I'll never know, but the relevant literature does seem to suggest that a gluten-free diet may have helped (1, 2).
    Then, a week or so ago, I received an email from a concerned mom. Her athletic, teen-aged son was recovering from a brain concussion he had sustained. His friends who had sustained similar concussions, at other times, reported having recovered more quickly. His mom began to wonder if her son's slow recovery could be the result of his celiac disease, despite more than a decade of strict compliance with the diet. I didn't know. I could only offer the suggestions that he try daily supplementation with medium chain triglycerides, and a ketogenic diet, as they seem to have stopped my life-long tremors. I also suggested that he try avoiding dairy and soy as well, based on research I did 14 years ago for my grandson.
    This concerned mom also mentioned, "I generally find doctors are dismissive of the idea that celiac is linked to any issues outside the digestive tract, unless it's malnutrition-related, and they tend to think everything should be hunky-dory if you just follow the gluten-free diet." She went on to say that "It gets kind of old being thought of as the silly, overprotective mom."
    Neurological researchers have long known about a correlation between a variety of neurological ailments and gluten sensitivity, with or without celiac disease (3). We also know that neurological symptoms are commonly found among more than half of patients with celiac disease (4). Also, despite modern diagnostic protocols and technology, we are still seeing some overlap between celiac disease and both amyotrophic lateral sclerosis (5) and multiple sclerosis (6) as well as other neurological illnesses. For instance, the increased presence of the gene named Parkinson's disease 7 (PARK7) has been found in the duodenal mucosa of untreated children with celiac disease and may be implicated in the alteration of the permeability of their intestinal barriers (7). This further suggests an important link between gluten sensitivity and Parkinson's disease. This gene may predispose to the appearance of this most distressing disease later in life.
    Many people with celiac disease continue to experience neurological symptoms, despite compliance with a gluten-free diet. This may suggest that the neurodegenerative dynamics, once initiated by gluten ingestion, may continue, either in the absence of gluten or in response to trace amounts of gluten (10). I also started to wonder if the cellular and immune system clean-up processes that follow brain injuries might initiate some of the same damaging autoimmune processes in the brain? They might also occur in response to other dietary factors which may trigger autoimmune dynamics that mimic reactions to gluten, or maybe there is some other, unknown factor that triggers the brain damage.
    One research group on the leading edge of the investigation of gluten sensitivity in relation to neurological illnesses reports that, "Incomplete elimination of gluten from the diet may be enough to abolish gastrointestinal symptoms with recovery of the small bowel mucosa but is insufficient to arrest the state of heightened immunological responsiveness resulting in neuronal injury" (10). So, when it comes to even tiny amounts of gluten, they may be enough to perpetuate gluten induced neurological illnesses. There may also an agent in the environment that is causing a cross reaction. This area really needs more investigation, as baby boomers threaten alarmingly increased rates of all forms of dementia.
    We already know that people with celiac disease are at much greater risk of developing neurological diseases than the general population (13). These ailments range from headaches to learning disabilities to movement disorders to tic disorders, to seizures, to sensory disorders (4) and many who have non-celiac gluten sensitivity also experience a high rate of neurological disease (3). Does that also mean that young athletes with celiac disease will take longer to recover from head injuries?
    Does it also mean, given the slow acceptance of gluten as a factor in many common neurological illnesses (11) that people like my former high school flame will never be told about the neuro-protective benefits of a gluten-free diet or a ketogenic diet? Surely, resistance to the well established data showing neurological manifestations of gluten sensitivity as a scientific fact (12) is more emotional than rational. A gluten-free diet and/or a ketogenic diet should be offered to those people regardless of whether their neurologist is either resistant to, or not staying current with, his/her professional literature. But they cannot offer what they do not know or have developed some bias against. Dr. David Perlmutter has done an excellent job of getting the word out to the general public, with his recent book titled Grain Brain, but there is much more work to do.
    People who are gluten sensitive, and are therefore at greater risk of developing neurological disease, might be well advised to look carefully at the benefits of a high fat, ketogenic diet, and the benefits of supplementing with medium chain triglycerides and Omega 3 fatty acids (14). Equally, they might be well advised to avoid the pro-inflammatory omega 6 and omega 9 fatty acids, as well as limiting the amounts of polyunsaturated fats they eat, which are also pro-inflammatory 14). I find that I feel my best when I am in mild, diet-induced ketosis (about 15 mg/dl as measured in morning urine, with Ketostix, which are inexpensive and available at most drug stores). There are a number of good books that explore the fine points of a high fat, ketogenic diet. These include The Art and Science of Low Carbohydrate Living by Volek and Phinney, The Ketogenic Diet by Lyle McDonald, and many others.
    Finally, when considering a gluten-free diet for neurological ailments, it is important to recognize that 20 parts per million may be far too much gluten to consume. The maximum threshold to qualify as gluten-free under the United Nations Codex Alimentarius Commission and many other regulatory agencies, including the FDA, is 20 parts per million. Without further research, especially in the field of neurology and gluten sensitivity, we will never know what, if any, levels of gluten are safe to consume.
    Regardless of the nature of your neurological ailment, whether it is Parkinson's disease, or seizures, or multiple sclerosis, or amyotrophic lateral sclerosis, or brain cancer, or almost any other kind of cancer (15), or even if you are just slow recovering from a neurological injury, the positive results of dietary interventions might offer you a whole new lease on life.
    Sources:
    http://www.medscape.com/viewarticle/770593 Currie S, Hadjivassiliou M, Clark MJ, Sanders DS, Wilkinson ID, Griffiths PD, Hoggard N. Should we be ‘nervous' about coeliac disease? Brain abnormalities in patients with coeliac disease referred for neurological opinion. J Neurol Neurosurg Psychiatry. 2012 Dec;83(12):1216-21. Matheson NA. Letter: Food faddism. Am J Clin Nutr. 1975 Oct;28(10):1083. Zelnik N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2004 Jun;113(6):1672-6. 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 Batur-Caglayan HZ, Irkec C, Yildirim-Capraz I, Atalay-Akyurek N, Dumlu S. A case of multiple sclerosis and celiac disease. Case Rep Neurol Med. 2013;2013:576921. Vörös P, Sziksz E, Himer L, Onody A, Pap D, Frivolt K, Szebeni B, Lippai R, GyÅ‘rffy H, Fekete A, Brandt F, Molnár K, Veres G, Arató A, Tulassay T, Vannay A. Expression of PARK7 is increased in celiac disease. Virchows Arch. 2013 Sep;463(3):401-8. Hadjivassiliou M, Grünewald RA, Lawden M, Davies-Jones GA, Powell T, Smith CM. Headache and CNS white matter abnormalities associated with gluten sensitivity. Neurology. 2001 Feb 13;56(3):385-8. Hadjivassiliou M, Sanders DS, Grünewald RA, Woodroofe N, Boscolo S, Aeschlimann D. Gluten sensitivity: from gut to brain. Lancet Neurol. 2010 Mar;9(3):318-30 Hadjivassiliou M, Grünewald RA, Davies-Jones GA. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. Tengah P, AJ Wills. Questions and Answers About the Neurology of Gluten Sensitivity. Pract Neurol 2003;3:354-357 Hadjivassiliou M, Grünewald R. The Neurology of Gluten Sensitivity: science Vs conviction. Pract Neurol 2004;3:4, 124-126. Hadjivassiliou M, Grünewald R. Gluten sensitivity as a neurological illness. Neurol Neurosurg Psychiatry. May 2002; 72(5): 560–563. http://www.omegascience.org/product_ingredients/coconut_oil.aspx Paoli A, Rubini A, Volek JS, Grimaldi KA. Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. Eur J Clin Nutr. 2013 Aug;67(8):789-96

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 12/21/2016 - I have previously criticized the use of a single blind test protocol for a gluten-free diet. In past issues of The Journal of Gluten Sensitivity I have also been critical of some double blind research protocols for investigating dietary variables for a variety of reasons not relevant to the current topic. However, there are good reasons that the double blind protocol continues to be favored, especially among medical researchers. Single blind testing is where the research subjects are not aware of the intervention being used whereas, in a double blind test, both the subjects and the researchers are kept in the dark about the intervention until the end of the trial. Sometimes that requires the use of placebos. In other protocols, it involves masking the intervention.
    The primary merit of double blind, over single blind tests is that the former eliminates something called "confirmation bias". Single blind testing was first developed because patients' and other experimental subjects' expectations were thought to skew results. Under some circumstances, this problem is called a placebo effect. We can see the placebo effect in action when research subjects are split into two groups. One group is given the medical treatment or drug being investigated, while the other group is given a placebo. This placebo may be a sugar pill or some other substance or treatment that should have no significant or measurable medical impact on the subject. The placebo is given to subjects/patients as if it could provide medicinal properties. Because the patient expects to feel better with this placebo intervention, some subjects do start feeling better. That's the placebo effect. Single blind testing does reduce this problem.
    Especially for drug treatments, blinding subjects does make sense. However, another confounding variable was soon recognized as arising from single blind tests. It turns out that, in addition to patients' reporting health benefits from sugar pills and other placebos, the physicians and other scientists were skewing the results in another fashion. This is where confirmation bias comes in. The term identifies a situation where researchers miss signs of a problem with gluten. (A fascinating book titled The Structure of Scientific Revolutions (1962), by Thomas Kuhn provides detailed explanations of this phenomenon in his descriptions of several experiments that clearly show this tendency.) To some extent we all have a tendency to confirm our expectations in what we see. This confirmation bias can have an impact on research results in two ways. First, it can lead researchers who are interacting with the test subjects to communicate, either through body language, or verbal "slips" to indicate that they expect a given patient to improve following the intervention or drug being investigated, leading to more of the placebo effect. It can also lead researchers to interpret their results in ways that confirm what they expected to see, rather than in a more objective light.
    Placebo effect and confirmation bias can be nullified in a double blind study when researchers subtract the portion of the placebo group who are feeling better on the placebo from the number who report feeling better in the experimental group. (The experimental group is the group that was given the actual drug or medical treatment under investigation.) This simple arithmetic eliminates the number of people in the experimental group who were likely to report feeling better even though they were only given the placebo. The remaining number of experimental subjects who report feeling better after the medical intervention are thought to reflect the number of people who actually experience a benefit induced by the treatment.
    My concern with physicians running single blind tests on patients who believe that they feel healthier on a gluten-free diet is that the physician is likely to see what she/he expects to see (confirmation bias). So skeptical physicians who would request that their patients do a gluten challenge in the form of a single blind test are most likely to see what they expect to see. This may be why more than 95% of people with celiac disease remain undiagnosed in the USA. Confirmation bias seems to afflict many physicians practicing in the USA. Judging from my years of exchanging correspondence with gluten sensitive people from all over the world, similar dynamics seem to be at work, to varying degrees, in many other countries as well.
    A protocol that requires the patient to undergo a gluten challenge in a single blind test format is offensive in its implications. It denies the limitations of the very physicians who would be charged with conducting these tests, making observations, and treating patients accordingly. I sincerely believe that physicians are intelligent, hard-working individuals who have pursued a career that is dedicated to helping people. I also believe that they are equally fallible in their judgments and pre-conceived notions about others, especially when it comes to dietary interventions. If physicians cannot accept the observations of their patients, why should their patients be willing to accept their physicians' observations and conclusions? Who has more at stake in this relationship? And who is in a better position to observe even very subtle responses to gluten ingestion?
    As a culture, we seem to have lost track of why we consult physicians. Although we are all subject to confirmation bias, most of us are not seeking insulting instructions that disparage our honesty, integrity and reliability. When I visit my family physician, I want her to act as my guide to the science she is familiar with, and render the best guidance she can offer based on her expertise and paying careful attention to what I report. If my problem is beyond her knowledge or experience, I expect to be referred to a specialist in my area of concern.
    I usually consult her, on a collaborative level, when she has some relevant expertise that will compliment my own expertise. I can not foresee a set of circumstances in which I would allow her to conduct a single blind trial on me. I do not accept the premise that she is less susceptible to her confirmation bias than I am to the placebo effect. Thus, my expectation of my physician is that we work together to solve any health problems that arise. I must say that both my current physician, whom I have been seeing for the last five years, and my previous physician who worked with me for the previous eleven years, have consistently exceeded my expectations. In both cases, they seem very happy that I am trying to take responsibility for my own health care and that I consider their advice to be a resource rather than the final word in the matter. I'm very grateful for these relationships, as they, and the gluten-free, dairy-free, diet, along with reduced soy and refined sugar consumption, have helped me achieve a much better state of health than I previously considered possible.

  • 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