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    Food Allergies and Sensitivities: Is Gluten an Underlying Factor?


    Dr. Ron Hoggan, Ed.D.
    • Journal of Gluten Sensitivity Spring 2015 Issue - Originally published April 8, 2015

    Food Allergies and Sensitivities: Is Gluten an Underlying Factor?
    Image Caption: Photo: CC--dan4th nicholas

    Celiac.com 12/08/2015 - Is the rate of food sensitivity and allergy growing? Or are we just more concerned about it because children experience anaphylactic crisis, sometimes even dying from exposure to peanuts, strawberries, and all the other foods that most of us think of as harmless? Even if the rates are growing, what is the cause? And should we, in the gluten sensitive community, be concerned about developing such allergies? After all, celiac patients were often told that there was no greater risk of developing IgE food allergies among those with celiac disease than is experienced by the general population (1, 2). I was certainly told this, on more than one occasion, by apparently well qualified medical practitioners. Yet, more recent research is showing that those with any autoimmune disease, including celiac disease, have a much greater risk of developing such allergies (3). Unfortunately, we still have more questions than answers. Nonetheless, the issue really does warrant exploration, especially among those who are gluten sensitive. Further, since the numbers of those with non-celiac gluten sensitivity remain controversial, we can also look at the issue from another perspective.

    For instance, a study of childhood IgE allergy frequency, at a center in Texas devoted to treating allergies and similar ailments, the investigators looked at antibody reactions to cow's milk, eggs, fish, peanuts, sesame, shellfish, soy, tree nuts, and wheat. They reported that the rate of all of these allergies combined had almost tripled (from 3% to 8%) in only five years (4). That is a startling rate of increase. If this finding can be applied more broadly, it should be alarming.

    However, another research group at Cornell University in Ithaca, New York, reported that childhood emergency department visits for food allergy reactions remained stable over a nine year period, while adult visits for food allergy reactions declined over this same time period (5). The central thrust of their report appears to be that we have an improving understanding of how to manage our own and our children's allergic reactions, so emergency room visits are becoming, relatively less frequent. This may simply signal that allergies are becoming so common that, as a culture, we are becoming better versed in how to avoid or manage mild allergic manifestations.

    Yet another group of investigators in Australia state that there has been a "dramatic rise in the prevalence of IgE-mediated food allergy over recent decades, particularly among infants and young children " (6). They go on to suggest that this increase may be due to "the composition, richness and balance of the microbiota that colonize the human gut during early infancy" (6). They further assert that IgE food allergies are connected to an impaired barrier function of epithelial cells that line the intestinal wall, in combination with immune dysregulation (6).

    Still others assert that the increase in allergies may be tied to climate change via several factors including "variability of aeroallergens, food allergens and insect-based allergic venoms" (7).

    Martin Blazer, M.D., in his book titled Missing Microbes argues that overuse of antibiotics may be at the root of both the increase in food allergies, as well as the increasing prevalence of celiac disease, through disrupting the gut microbiome and selection for antibiotic-resistant strains of microbes (8).

    Some or all of the foregoing theories may well have a legitimate influence on our growing rates of allergies. As I see it, however, the various theories postulated to explain these increasing rates have left out one powerful dietary trend that has also accompanied these increases in IgE food allergy prevalence. For instance, compromised intestinal barrier function is a well documented feature of gluten grain consumption, although it is greatest in the context of celiac disease. The increased release of zonulin, triggered by eating gluten grains, may also be a critical factor in the development and persistence of the disease process, especially in cases of celiac disease, type 1 diabetes, rheumatoid arthritis, ankylosing spondylitis, Crohn's disease, systemic lupus erythematosus, and about one quarter of cases of multiple sclerosis (9, 10).

    In the gut, gluten triggers increased release of zonulin, which weakens the junction between the epithelial cells that form the intestinal walls, and usually provide a protective barrier where these cells connect (11). The "gap" between these cells, caused by increased zonulin release, allows undigested proteins and peptides to bypass the cells that usually transport digested particles from the intestine to the bloodstream. Partly digested proteins, small peptides, also move through these epithelial cells, following the same path that fully digested food particles follow. However, according to Dr. Fasano, those are usually so degraded that they don't trigger antibody production (9). Thus, the leaky gut that has long been associated with celiac disease, and is often seen as a characteristic of, but not restricted to this ailment, is a critical stage in the development of this illness. This leakiness is, as most readers will know, reversed by a gluten-free diet.

    We are now seeing, in the peer reviewed medical literature, a wide range of ailments being identified as manifestations of undigested food proteins being "leaked" into the circulatory system. Further, there is a dose-dependent relationship between increasing gut permeability and increased gluten consumption, both in celiac disease and in other forms of autoimmunity (12). If this dose-dependent relationship also applies to many of those with other sensitivities, at admittedly lower levels of permeability (13), and if that is the dynamic that underlies much of the increasing trend of IgE food allergies, we should be seeing the rates of these allergies continue to rise in the general population. And, if we continue with our gluten gluttony, who can say how many ailments are associated with gluten consumption and increased zonulin release?

    It is also possible, perhaps even probable, that some of us experience increased zonulin release into the bloodstream, rather than into the intestinal lumen. If so, those peoples' epithelial linings of lungs, nasal passages, and blood brain barriers, may be more compromised than those individuals who primarily experience a leaky gut. By weakening these other barriers, they may invite other ailments that are less obviously triggered by gluten and other food proteins.

    Dr. Alessio Fasano has stated that new understandings of zonulin's role in autoimmunity, inflammation, and some cancers, "suggests that the autoimmune process can be arrested if the interplay between genes and environmental triggers is prevented by reestablishing [sic] the intestinal barrier function" (9). An animal study showed that AT1001, an experimental drug that blocks the action of zonulin, protected against autoimmune attack on pancreatic islet cells (9) which produce insulin. A human study of twenty-one subjects, reported similar findings (14).

    While it is true that intestinal infections have also been shown to induce zonulin release in the gut, the issue of microbes may not be as large a factor as it at first appears. When bacteria colonize our intestines, there are three possible outcomes: First, the infection may run rampant and kill us, thus solving the problem in a most undesirable manner. Second, and much more likely, we may take antibiotics and deplete or eliminate these infectious agents in our intestines. Third, and most likely, a combination of our immune systems, other microbes resident in our gut, antibiotics, and other, possibly unknown factors, may quickly or slowly bring the infectious agent under control. By reducing its numbers sufficiently that it won't pose a serious threat to our well being, and the harmful impact of these microbes has been muted.

    The second and third possibilities will be both the most common and most desirable. Also, as soon as the microbe in question is under control, zonulin release should be diminished to a point where it is either a minor factor in triggering continued zonulin release or, because it has been eradicated, the microbe will become irrelevant to zonulin release. On the other hand, for as long as we consume gluten, zonulin continues to be released, thus disrupting tight junctions in the intestinal, pulmonary, sinus, and other mucosal membranes, permitting allergens to reach our circulatory systems, ultimately giving rise to the growing prevalence of dangerous allergies that may sometimes manifest in anaphylactic reactions.

    The most important issue here seems to be the impact of gluten consumption on zonulin release, along with its impact on several protective barriers in the body, weakening them at the previously tight junctions between their cells. These include the blood brain barrier, which usually protects the brain from impurities and antibodies in the blood. It also includes the mucosa that line the lungs and nasal passages that protect us from airborne toxins and microbes. When that barrier is compromised, small particles from the air that we breathe will reach our circulation and trigger immune reactions...also known as allergies.

    Perhaps the most important barrier is in the digestive tract. It is made up of several variants of mucosa that protect the tissues of the gastrointestinal tract from toxins and the unwanted particles in our foods and beverages (well, most of them anyway). This, it seems to me, is the crux of our growing crisis with environmental allergies and the elevated zonulin levels that sometimes accompany them. And we can't even begin to combat this dynamic without first understanding it better.

    In the meantime, adding AT1001 to gluten-containing flours might be useful. Conversely, the media voices that are selling the idea that a gluten-free diet is an expensive fad might soon see research that reveals the gluten-free diet as an excellent prophylactic against developing IgE allergies, a variety of cancers, autoimmunity, some psychiatric illnesses, and many neurological diseases. In the interim, we can only use our own best judgement and decide for ourselves. Would the dietary products of gluten grains really be that great a loss to the palate? Is it a reasonable trade-off to risk falling prey to all of the potential consequences that come to us through elevated release of zonulin?

    More compellingly, perhaps, Professor Loren Cordain's assertion that humans have not had enough time to become fully adapted to eating cereal grains, especially as a dominant portion of our diet (15), appears to gain considerable support from the discovery and characterization of zonulin. Further, although some European, Asian, and northern African genes may have had as much as 15,000 years to adapt to this food source, most of the world's inhabitants have had a much shorter time to adapt. These are periods that are most appropriately measured in centuries and decades. The assumption that gluten grains can be safely consumed by all humans, because we have been eating them for "thousands of years" is unlikely to be true for most of the world's current population, and may represent a Eurocentric perspective.

    Sources:

    1. Csorba S, Jezerniczky J, Ilyés I, Nagy B, Dvorácsek E, Szabó B. Immunoglobulin E in the sera of infants and children. Acta Paediatr Acad Sci Hung. 1976;17(3):207-14.
    2. Greco L, De Seta L, D'Adamo G, Baldassarre C, Mayer M, Siani P, Lojodice D. Atopy and coeliac disease: bias or true relation? Acta Paediatr Scand. 1990 Jun-Jul;79(6-7):670-4.
    3. Fraser K, Robertson L. Chronic urticaria and autoimmunity. Skin Therapy Lett. 2013 Nov-Dec;18(7):5-9.
    4. Amin AJ, Davis CM. Changes in prevalence and characteristics of IgE-mediated food allergies in children referred to a tertiary care center in 2003 and 2008. Allergy Asthma Proc. 2012 Jan-Feb;33(1):95-101.
    5. Clark S, Espinola JA, Rudders SA, Banerji A, Camargo CA. Favorable trends in the frequency of U.S. emergency department visits for food allergy, 2001-2009. Allergy Asthma Proc. 2013 Sep-Oct;34(5):439-45.
    6. Molloy J, Allen K, Collier F, Tang ML, Ward AC, Vuillermin P. The potential link between gut microbiota and IgE-mediated food allergy in early life. Int J Environ Res Public Health. 2013 Dec 16;10(12):7235-56.
    7. Bielory L(1), Lyons K, Goldberg R. Climate change and allergic disease. Curr Allergy Asthma Rep. 2012 Dec;12(6):485-94.
    8. Blazer M. Missing Microbes. Harper Collins, Toronto, Canada, 2014.
    9. Fasano A. Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev. 2011 Jan;91(1):151-75.
    10. Yacyshyn B, Meddings J, Sadowski D, Bowen-Yacyshyn MB. Multiple sclerosis patients have peripheral blood CD45RO+ B cells and increased intestinal permeability. Dig Dis Sci. 1996 Dec;41(12):2493-8.
    11. Tripathi A, Lammers KM, Goldblum S, Shea-Donohue T, Netzel-Arnett S, Buzza MS, Antalis TM, Vogel SN, Zhao A, Yang S, Arrietta MC, Meddings JB, Fasano A. Identification of human zonulin, a physiological modulator of tight junctions, as prehaptoglobin-2. Proc Natl Acad Sci U S A. 2009 Sep 29;106(39):16799-804.
    12. Fasano A. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol. 2012 Feb;42(1):71-8.
    13. Drago S, El Asmar R, Di Pierro M, Grazia Clemente M, Tripathi A, Sapone A,Thakar M, Iacono G, Carroccio A, D'Agate C, Not T, Zampini L, Catassi C, Fasano A. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol. 2006 Apr;41(4):408-19.
    14. Paterson BM, Lammers KM, Arrieta MC, Fasano A, Meddings JB. The safety, tolerance, pharmacokinetic and pharmacodynamic effects of single doses of AT-1001 in coeliac disease subjects: a proof of concept study. Aliment Pharmacol Ther. 2007 Sep 1;26(5):757-66.
    15. Cordain L. Cereal Grains: Humanity's Double-Edged Sword. in Simopoulos AP (ed): Evolutionary Aspects of Nutrition and Health. Diet, Exercise, Genetics and Chronic Disease.
    16. World Rev Nutr Diet. Basel, Karger, 1999, vol 84, pp 19–73
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    Guest Shauna Lula

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    Great article. Has Adrenal fatigue been researched with response to gluten issues? I am finding that trying to help that issue has allowed me to be less sensitive to my allergies.

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  • About Me

    As co-author of "Dangerous Grains" and "Cereal Killers", the study of the impact of gluten continues to be a driving passion in my life. I am fascinated by the way that gluten induces illness and impedes learning while it alters mood, behavior, and a host of other facets of our existence. Sure, the impact of gluten on health is an important issue, but that is only the most obvious area of impact. Mood disturbances, learning disabilities, and the loss of quality of life due to psychiatric and neurological illness are even more tragic than the plethora of physical ailments that are caused or worsened by gluten. The further I go down this rabbit hole, the more I realize that grains are a good food for ruminants - not people. I am a retired school teacher. Over the last decade, I have done some college and university level teaching, but the bulk of my teaching career was spent working with high school students. My Web page is: www.DangerousGrains.com

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    Dr. Ron Hoggan, Ed.D.
    Beware the Gluten-Free Diet
    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. Rodney Ford M.D.
    Gluten-Free Logic: The Three Steps
    Celiac.com 10/27/2015 - In 2006, I presented a research paper called "Who warrants a gluten-free diet?". At that time I was thinking about the sick children who were coming through my clinic with skin, gut and brain symptoms: that is they had eczema and itchy skin; sore tummies and constipation; and behaviour disturbances. It turned out that most of this group of children had high levels of Anti-Gliadin-Antibodies (AGA), of whom 80% got completely better when they went on a gluten-free diet. This was a landmark paper for me, and it led me to describe "The Gluten Syndrome".
    However, that was nearly 10 years ago! and a lot has happened since then. Perhaps most notable the publication of the consensus paper on the Spectrum of Gluten-Related-Disorders. The algorithm developed to diagnose gluten sensitivity/ intolerance relies on the elimination and challenge of gluten, rather than immunologic blood tests. I have been using the AGA test in my clinic since 1989 (that is for 25 years!) and I have found it extremely useful as a diagnostic test, when it is positive. But, many people react to gluten and have negative AGA results. So I agree with the authors of the "Spectrum" paper. The basis of a gluten-sensitivity/intolerance diagnosis should be based on elimination and challenge. Importantly, prior to removing gluten from your diet, please ensure that you get the appropriate tests for celiac disease (see this link for a gluten-blood-test discussion).
    So who in the year 2015 should be suspected of having a gluten-related-illness? Well anyone who has chronic symptoms. Even if they have a diagnostic label - because they might have the wrong diagnosis. so here are the 3 steps in my gluten-free logic:
    Step ONE - the premise IF:
    a) Gluten sensitivity is common: estimates show it affects over 10% of the population; Gluten-related illnesses are varied and have multiple symptoms: a quote from the consensus paper on the Spectrum of Gluten-Related-Disorders emphasizes this. The symptoms in gluten sensitivity may resemble those associated with celiac disease but with a prevalence of extra-intestinal symptoms, such as behavioral changes, bone or joint pain, muscle cramps, leg numbness, weight loss and chronic fatigue. Their symptoms include abdominal pain (68%); eczema and/or rash (40%); headache (35%); "foggy mind" (34%); fatigue (33%); diarrhea (33%); depression (22%); anemia (20%); numbness in the legs, arms or fingers 20%; and joint pain (11%); c) There is no definitive diagnostic test for gluten sensitivity: the Consensus paper goes on to say "However, currently there are no laboratory biomarkers specific for gluten sensitivity. Usually the diagnosis is based on exclusion criteria; an elimination diet of gluten-containing foods followed by an open challenge is most often used to evaluate whether health improves with the elimination or reduction of gluten from the patient’s diet"; d) There is no harm from going on a gluten-free diet; in other words a gluten-free is healthy. Step TWO - The logical THEN:
    Then the logical conclusion is that "anyone", with "any symptoms" that are "chronic and unexplained" (that is they do not have a definite diagnosis) and "at any time" (people can develop gluten-illness at any time in their life) should be put onto a gluten-free diet for a clinical trial for three months or more.
    Step THREE - The CONCLUSION:
    The logical conclusion is that whatever the blood-test results, and whatever the endoscopy results, and whatever the symptoms, a beneficial response to a gluten-free diet suggests that their illness is gluten-related (some people might demand a double blind food challenge).
    Comment
    Up until now, most gluten/celiac doctors have dismissed the idea that their patients might be suffering from "non-celiac gluten-sensitivity" (NCGS). They have attributed their patients beneficial response to a gluten-free diet as a placebo response (all in their head!). This is clearly not the case. There is mounting evidence for this: see this research paper - Small Amounts of Gluten in Subjects with Suspected Nonceliac Gluten Sensitivity: a Randomized, Double-Blind, Placebo-Controlled, Cross-Over Trial. In this paper the authors conclude: "In a cross-over trial of subjects with suspected NCGS, the severity of overall symptoms increased significantly during 1 week of intake of small amounts of gluten, compared with placebo".
    The above logic means that ALL people, with ANY undiagnosed illnesses, at any TIME in their life, should be given a gluten-free trial. This is likely to have huge health benefits and wide ramifications on the management and burden of ill health on the community. Already 10% of Australians and Canadian are adopting a gluten-free diet, and 30% percent of adults in the USA are interested in avoiding or cutting down on gluten in their diets, says a survey from the NPD Group, a consumer research firm. NDP has been following gluten-free issues since 2009 and its January 2013 survey revealed the highest interest in gluten-free diets yet (reported in HuffPost - 26 Feb 2015).
    It is my prediction that in another generation most people who wish to stay healthy, will choose to adopt a gluten-free diet, before they get harmed by gluten.

    Monique Attinger
    How to Succeed At Reducing Oxalate on a Gluten-free Diet
    Celiac.com 11/03/2015 - Many people today are dealing with the need to be gluten-free, whether from allergies, intolerance or celiac disease. Being gluten-free can be the difference between being healthy and having chronic, potentially debilitating, symptoms.
    However, sometimes being gluten-free is not enough.
    The challenge with a gluten-free diet is that many of the most popular gluten-free flours are actually high in oxalate! Oxalate is a toxin that occurs naturally in most plant foods, but at very different levels, some relatively safe, and some not. Oxalate can even kill at high enough doses. The scientific challenges in the oxalate field, as well as oxalate's potential relationship to celiac sprue, were discussed in the feature article by Susan Costen Owens which appeared in the Spring issue of this journal. In this follow up article, you'll find the practical advice on how you can reduce the level of oxalate in your gluten-free diet.
    A great example of a popular high oxalate gluten-free flour is almond flour. Almonds are one of the very highest oxalate foods, with about 300 mg of oxalate for one half cup of whole nuts. Given that you will actually have more nuts in a half cup of flour than you will in a half cup of whole nuts, you could have 400 or more milligrams of oxalate in that single half cup of flour.
    So, your daily morning muffin made with almond flour could be 200-250 mg of oxalate. This means that you may not feel as good on your gluten-free diet as you might expect because your digestive tract can be suffering with ongoing inflammation from a new source – oxalate.
    Now 250 mg of oxalate might not seem so bad – unless you consider that a low oxalate diet is defined as 40-60 mg of oxalate per day! That makes your morning muffin the equivalent of 4-5 days worth of oxalate, for someone who is eating a typical low-oxalate eating plan.
    If you've been eating a lot of nut flours, you might be wondering what you can substitute instead? The one nut flour that is low oxalate is coconut flour. This can be a great option, if you like the density of nut flours, and want a flour with higher nutrition. All other nut flours are high; most seed flours are high too. Nuts themselves are some of the highest oxalate foods in nature. Baked products made with nut flours will be particularly high in oxalate – and if you add chocolate, you compound the problem.
    Unfortunately, this is more bad news for lovers of chocolate baked goods. Chocolate is another extremely high oxalate ingredient: cocoa has more than 35 mg of oxalate per tablespoon and the substitute carob, is no better! Given that many baked goods could easily have 1-2 tablespoons of chocolate or carob per serving, you can see how your oxalate intake could really add up. Of course, this doesn't include the fact that many baked goods – like brownies – will combine both cocoa and nuts, for a double hit of oxalate.
    The same problem arises with many of our common gluten-free baking flours and spices. They can often add an overload of oxalate to each serving, with the potential for problems later as oxalate accumulates in the body. So, how can you avoid gluten, and not introduce more of a known toxin into your body?
    The trick is knowing enough about oxalate to avoid it effectively.
    The first thing to learn is how to get flavor in your food without the oxalate. Oils and extracts are typically much lower in oxalate than the whole herb or spice, and yet retain the flavor for baking and cooking purposes. The process by which oils are pressed and extracts are made appears to leave the oxalate behind.
    This rule of thumb gives us a way to get the taste we want, and avoid oxalate. For instance, to get a chocolate taste without too much cocoa, you can carefully craft a recipe that balances the use of cocoa with chocolate extract, chocolate flavoring and even a bit of coffee. Using food grade cocoa butter, which has zero oxalate, in place of butter or oil, is another way to boost that chocolate flavor. If you use the lowest oxalate flours as well, you leave some room for a bit more cocoa because you are not adding a lot of oxalate in the flour. By doing this, you can get the flavor you want while avoiding the oxalate.
    Another example of baking smart is an almond flavored cookie. You can actually make a cookie with almond oil as well as almond extract for extra taste – while almonds themselves are extremely high, both the oil and the extract have almost no oxalate at all!
    This concept of using oils and extracts is particularly important if you like the sweet taste of cinnamon. Cinnamon is a very high oxalate spice with over 38 mg of oxalate for just one teaspoon! Choose instead cinnamon oil or cinnamon extract. Cinnamon oil is available from various outlets that sell culinary oils. You can get cinnamon extract in the supplement section of your grocery or health food store – generally, it is sold in capsules. When cooking with it, you simply open the capsules and put the powdered extract into your dish. Substitute about the equivalent amount of dry extract for ground cinnamon.
    The second thing to learn is how to pick low oxalate flours. While many of the gluten-free flours are high in oxalate, the process of picking appropriate flours may not be as hard as it first appears.
    Oxalate is often present in the "bran" of a grain. As a result, most whole grain flours are actually high in oxalate. This seems strange to us because we are told to get more fiber and eat whole grain. But the truth is that not all whole grains are good for us and we can get our fiber in other ways not so tied to oxalate.
    Interestingly, most starches are low oxalate (even if they come from high oxalate whole foods), in the same way that oils are low oxalate. This means that starches are our friends when we want to cook! Most starches (including potato, corn, green bean and sweet potato) are low in oxalate, and can be used as part of the flour combination in a baked good to get a lighter, fluffier result.
    Again, the explanation is similar to the explanation regarding oils and extracts: when we remove the starch from even a high oxalate food, we appear to leave the majority of the oxalate behind. But be careful to get starches and not flours when you are dealing with high oxalate whole foods – items like potato flour or sweet potato flour are extremely high in oxalate, and should be avoided. Only the starches are safe on a low-oxalate eating plan.
    You can consume some medium oxalate foods, and still remain low oxalate overall. This expands the possible flours that you can use. Good options include white masa (which is a corn flour), green pea, lupin, sorghum, and sweet rice flours. While buckwheat and quinoa are also common in gluten-free foods, these grains are very high in oxalate. You should ideally avoid them.
    So what do you do if you are used to baking with nut flours? If you want high nutrition flours that are much lower in oxalate than nut flours, look to legume flours. Consider black-eyed pea flour (also called cowpea bean flour), garbanzo bean flour, or yellow pea flour. All of these legume flours are low in oxalate. However, because legume flours can be heavy, combine them with low oxalate starches, like corn, rice, green bean, potato or sweet potato starch to get the right texture in your baked goods.
    When we combine the lowest oxalate flours with others that are medium (and sometimes small amounts of higher oxalate flours), we can get the right kind of flavor and texture, yet remain low in oxalate per serving. A great example is a flour mix that contains a variety of flours. One easy combination of flours is ½ cup of sweet rice flour (medium oxalate), with ½ cup of coconut flour (medium oxalate), ½ cup of potato starch (low oxalate) and ½ cup of cornstarch (low oxalate). This particular flour combination can be used in crepes, and results in a crepe that has the same kind of stretch that you have with gluten flours, because of the properties of the various flours used in the combination.
    While some of us will be experimental and will like the idea of playing with flours and starches to develop our own recipes, others will not. If you are looking for a good quality gluten-free flour mix that you can use at home, consider Orgran. Another great option for baking (as well as pancakes) is gluten-free Bisquick.
    So far we've presumed that you are baking or making your own gluten-free items. But what if you are buying packaged gluten-free foods?
    When looking at baked goods, look for starches in the first five ingredients. So, you should see low oxalate flours early in the ingredients, because these will be the largest components of your baked good. Avoid items with buckwheat flour, hemp, quinoa, sesame seeds, and teff in general. All of these ingredients are so high in oxalate, that even small amounts would be a problem. While tapioca starch and white rice flour are high in oxalate, in smaller amounts, they should be fine.
    If you are considering reducing oxalate in your diet, the best way to do that is slowly! When you reduce oxalate too quickly, you can experience stressful symptoms as the oxalate that is stored in your body leaves too quickly. The process of oxalate moving out of your tissues and into your blood, seeking then a site of secretion, is called "dumping" by our project since it is a very common experience. This can be the culprit behind digestive symptoms, fatigue, brain fog, rashes and other symptoms.
    Ideally, you would slowly phase high oxalate foods out of your diet. So rather than completely abandoning your morning muffin made with almond flour, you would slowly reduce your portion by ¼ of a muffin per week, until you were no longer eating an almond flour muffin after 4 weeks. During those 4 weeks, you slowly introduce your new morning muffin, ¼ at a time, which is now made with coconut flour.
    You would also want to remove only one food at a time in this way – so that oxalate is very slowly phased out, and you can also use up some of the high oxalate foods that you have in your home. It's not only easier on your body to do this change slowly, but it's also easier on your pocket book!
    Oxalate is not just an issue with grains and flours – it can also be an issue with other foods. So while this article has focused more on the specific issues with gluten-free baking and cooking, there are other high oxalate foods that you need to be aware of if you want to reduce oxalate in your overall diet.
    You may have heard or seen information that points at leafy greens as high oxalate foods. While such common staples as spinach, beets and Swiss chard are extremely high in oxalate, you can enjoy other greens in a healthy diet. Consider other leafy greens like arugula, turnip greens, mustard greens or certain varieties of kale, like dino / lacinto or purple, to get leafy veggies in your diet. Most lettuces are low in oxalate and high in nutrition, including romaine and leaf lettuce. Eating low oxalate does not have to mean removing whole food groups from your diet, nor losing all your high nutrition options!
    Many of the common fruits are lower in oxalate and can be incorporated in your diet – including berries. Many people have mistakenly heard that all berries are high oxalate. Testing done by Dr. Michael Liebman of the University of Wyoming shows this is not true! According to test results from his lab, both blueberries and strawberries are low oxalate, and raspberries are medium oxalate. So while you might want to avoid blackberries (which are very high in oxalate), you can safely eat other healthy berries.
    However, other fruit can be extremely high in oxalate. Citrus can be tricky because it's important to know not just which fruit you are eating, but which parts. Many citrus juices, like grapefruit, orange, lemon and lime, are low oxalate per serving, so you can still get the taste of these items when cooking with the juice. But don't eat a lot of grapefruit – the whole fruit is high oxalate. Similarly, if you use citrus zest for extra flavor, you'll find that it's a problem: the oxalate levels are too high.
    Sometimes you need to know the variety of a food, or need to watch your serving size. Pears are a great example. Some varieties of pears have tested low; others have tested high. When choosing pears, go for Bartlett (also called Williams pear).
    Many exotic and tropical fruits are high, including kiwi, figs, papaya, gauva, and pomegranate. Some are so high that they could be dangerous to consume in a single serving! Star fruit has this dubious distinction: it is so high that people have had seizures and even died from eating star fruit when their kidneys were in trouble.
    It is important to recognize that many of the foods that we think of as being the healthiest may also contain a lot of oxalate. Vegans can be particularly susceptible to eating a very high oxalate diet, as they may be getting their protein primarily from high oxalate legumes, including soybeans. If you want to include legumes in your diet for the fiber and nutritional benefits, focus on the low and medium oxalate legumes. That list includes red, green, brown and yellow lentils, green peas, red kidney beans, tofu, garbanzo beans, yellow and green split peas, lima beans and black-eyed peas.
    Note that tofu is okay – but whole soybeans are not. This is one of the most challenging aspects of the diet. Some foods are okay in the right form, or with the proper processing. So much as extracts, oils and starches are lower in oxalate than the whole foods they come from, some processed forms of foods are lower than the whole, unprocessed food. So you can eat tofu – but don't eat edamame.
    A last point that can help you to reduce oxalate in your diet is to consider how a food is cooked. When a food is boiled, you may actually reduce the amount of oxalate in the food. Oxalate can be soluble, and so it will leach into the cooking water, and can then be thrown away. There is no other cooking method that can reliably reduce oxalate, other than cooking or soaking in water. However, this flies in the face of current nutritional advice, which focuses on eating as many foods as possible raw. While you don't have to boil everything you eat – there are a number of very low oxalate veggies and fruits that can be eaten and enjoyed raw – boiling can be a valuable strategy to reduce this known toxin, and leave you with a more nutritious end result.
    If you have more questions about oxalate and your diet, please see the website www.lowoxalate.info. There is also an associated support group, which is currently at Yahoo, called Trying_Low_Oxalates. In addition, we have a Facebook group with the same name. On Facebook, we also have two additional recipe groups, one of which is focused specifically on vegan eating. These support groups can help you to make lower oxalate choices part of your diet and can also help you gain a perspective on how oxalate may have been affecting other issues in your health.
    Lower Oxalate Flours, Starches and Products
    Potato starch Cornstarch Green Bean starch Sweet Potato starch Flax meal / seed White masa corn flour Green pea flour Lupin flour White rice flour Sweet rice flour Coconut flour Black-eyed pea (cowpea) flour Garbanzo bean (chickpea) flour Water chestnut flour Yellow pea flour Low Oxalate per serving
    General Mills Corn Chex (1/2 cup) General Mills Rice Chex (1/2 cup) Arrowhead Mills gluten-free Popcorn (1 cup) Eden Kuzu Pasta (1/2 cup) Thai Kitchen Rice Noodles (1/2 cup) Annie's Homegrown Macaroni and Cheese, gluten-free (1/2 cup) Tinkyada White Rice Spaghetti (1/2 cup) Lotus Foods Bhutan Red Rice (1/2 cup cooked) Higher Oxalate Gluten-free Products
    Medium oxalate per serving Udi's White Sandwich Bread (1 slice) Nabisco Cream of Rice (1/4 cup dry) Envirokids Gorilla Munch (1 cup) Orville Redenbacher's Popcorn (1 cup) Mission Yellow Corn Tortillas (1) Tinkyada Brown Rice Spaghetti (1/2 cup cooked) Tolerant Foods Red Lentil Rotini (1/2 cup cooked) Lundberg Brown Jasmine Rice, boiled (1/2 cup) Extremely High Oxalate foods
    Beans (Anasazi, Black/Turtle, Cannellini, Great Northern, Navy, Pink, Pinto, Red, Soy, White) Cactus/Nopal Carob Cocoa Powder/dark and milk chocolate Fruits (Apricot, Blackberries, Figs, Guava, Kiwi, Pomegranate, Rhubarb, Star Fruit/Carambola) Grains (Amaranth, Buckwheat, Quinoa, Teff) Nuts (Almonds, Cashew, Brazil, Hazelnut/filberts, Macadamia, Peanuts/Spanish Peanuts, Pine) Seeds (Caraway, Chia, Hemp, Poppy, Sesame) Herbs/Spices (Allspice, Cinnamon, Clove, Cumin, Curry Powder, Ginger, Onion Powder, Turmeric) Potatoes (Russet, Burbank, Idaho, Fingerling) Vegetables (Artichoke, Beets, Eggplant, Hearts of Palm, Jerusalem Artichokes, Okra, Plantain, Swiss chard, Spinach, Sweet Potato/Yam)  
    Guide to Lower Oxalate Substitutions 
    (chart on substitutions is used by permission from: https://www.facebook.com/pages/Low-Ox-Coach/551330634959001/)
     
    High Oxalate Ingredient(s)
    What it's used for
    Lower Oxalate Substitution
    Spinach
    Greens in a stir fry
    Cooks down for sauces / dips
    ARUGULA. Similar flavour and consistency. Substitute one for one.
     
    Beets
    Greens in a stir fry
    Sweet root veggie
    Used for detox
    For stir-fries, try other greens, like turnip or kohl rabi. You can also use red cabbage for a red veggie (if you need something red). Try boiled carrots or parsnip for dishes that need a root veggie. If you want a gentle detox, try lemon juice in water to start your day.
     
    Swiss Chard
    Greens in a stir fry
    Steamed
    Boiled
     
    Dino / Lacinto Kale. Lowest ox when boiled. Can also try mustard greens or dandelion greens.
    Almonds
    Snack
    Baking
    Gluten free crusts
    For snacks, try pumpkin seeds. For baking, either go to coconut flour (rather than almond flour) or use a lower ox nut and smaller quantities. For bread, try pumpkin seed butter or sunflower seed butter. Pecans or walnuts are the lowest ox nuts.
     
    Almond or peanut butter
    Spread for bread
     
    Sunflower seed butter, macadamia nut butter, pumpkin seed butter, golden pea butter (golden pea is the lowest oxalate)
     
    Sesame seeds
    Used for both flavour and as the whole seed
    While sesame seeds are high, the oil is zero oxalate! So, try using either plain or toasted sesame seed oil to flavour dishes.
     
    Most dried beans, including red beans, adzuki beans, black beans, etc
    Chili
    Savory dishes
    Dips
    Try subbing lower ox legumes like black-eyes peas, red lentils, green and yellow split peas, garbanzo beans and lima beans.
     
    Brown rice
    Side dish
    Casseroles
    Stir-fries
    Sub with either brown rice that is soaked, drained and cooked like pasta (in lots of water), or use white rice. Uncle Ben's is one of the lowest rices.
     
    Chocolate / Cocoa
    Desserts of all kinds!
    Try lesser amounts of chocolate, or a combination of cocoa and chocolate flavoured stevia. Also, can sub white chocolate in many applications, like white chocolate chips for cookies. In a recipe, sub food grade cocoa butter in place of other specified oils / butter.
     
    Tomato sauce
    Sauces
    Casseroles
    Pastas
    Instead of 100% tomato sauce, sub with 1-2 tablespoons of tomato paste, ½ cup pumpkin or butternut squash puree and water to thin as required. Add appropriate spices for the dish.
     
    Black tea
    Beverages
    Decaf green tea, many herbal teas or coffee
    Nutmeg
    Spice
    Mace
     
    Black pepper
    Spice
    White pepper
     
    Sweet potatoes
    Dishes of all kinds
    Butternut squash or other suitable squash with the right texture and flavour.
     
    Onion, carrot and celery to use to start soup
    One of the most common combinations to start soup or stir fry
    Garlic, shallot and red pepper is a favourite. You can also use garlic, shallot and green cabbage.
     
    Lemon or orange rind
    Dishes of all kinds
    Lemon or orange juice, with a thickener. In some cases, lemon or orange extract.
     
    Cinnamon
    Dishes of all kinds
    Cinnamon extract (purchased in a dry capsule supplement at the health food store. Break open capsules and put contents in your dish).
     
    Regular potatoes
    Boiled, or used in dishes
    Baked
    You can boil new, red-skinned, white-fleshed potatoes and then add to dishes. You can also sub cauliflower or radishes, 1 to 1. (Radishes are great cooked!) To sub for a baked potato or for a dish that uses potato raw, try rutabaga or turnip (which can be scalloped or turned into a baked fry.)
     
    Regular pasta
    Usually for main dishes or side dishes
    Zucchini "noodles", or cornstarch noodles, or other tested and low ox pasta like Shiritaki noodles (which are also low carb and zero calories). You can get cornstarch "angel hair" pasta or Shiritaki noodles at Asian food markets.
    Oatmeal
     
    Breakfast
    Baking
     
    Sub with ½ oatmeal and ½ flax meal for cooked cereal with the same texture but lower oxalate.
    Turmeric
    Baking
    Flavor
    Sub with curcumin extract. This can be purchased as a health supplement in capsules. Capsules can be opened and the contents added to food and beverages.
    Ground ginger
    Baking
    Flavor
     
    Sub with fresh ginger or ginger root extract.
     
    From the author:
    If you have ever been diagnosed with an autoimmune disease and have been trying to lower oxalate, will you participate in the development of this science by filling out a survey?
    We would also like to find out whether reducing oxalate has affected your autoimmune condition.
    The link to our survey is here: https://www.surveymonkey.com/r/CMN5KK7

    Maria Lerario
    Gluten-Free Grocery Store Bread Reviewed
    Celiac.com 11/17/2015 - For most people, when they think of gluten, the first thing that comes to mind is bread. And for most people with celiac or a gluten sensitivity, that is what we miss most.
    While people with celiac or gluten sensitivity may never be able to experience the wide selection or soft texture that "glutenous" bread offers, there are still some tasty gluten-free bread options available at most grocery stores. In order to find the best gluten-free bread options, I went to my local Giant Eagle and tried all of the gluten-free bread available and explored four main aspects: taste, texture, price, and variety.
    The three brands of gluten-free bread offered at Giant Eagle were Schar, Udi's, and Goodbye Gluten.
    In the variety category, Udi's offered the largest selection of bread with the choice of white bread, multigrain bread, cinnamon raisin bread, and millet-chia bread and omega flax and fiber bread. Udi's also offers a large variety of other products ranging from muffins and cookies, to pizza crusts and tortillas.
    While Udi's may have the largest variety of the three brands, Schar offered a few different kinds of bread as well, with a cinnamon raisin and multigrain option along with an assortment of rolls.
    In the category of price, Goodbye Gluten came in as the most inexpensive per ounce at $0.27 per ounce. Udi's was in the middle $0.37 per oz. and Schar was the most expensive of the three, coming in at $0.40 per oz.
    Now let's get down to business. Taste and texture—the two aspects that are hardest to get right when making gluten-free bread. In my opinion, Udi's won both categories with the tastiness, most normal textured bread. My only critique was the slices of bread weren't big enough! All three brands seemed to have their slices of bread on the smaller side, but Udi's bread seemed to be especially small.
    Although Udi's took the first prize in three of the four categories, that is not to say the other two brands were not good. I was impressed with all three brands, but my main critique covers the texture category.
    The Goodbye Gluten bread seemed to be very dense, and while most gluten-free bread crumbles more than normal, I felt that the Goodbye Gluten loaf broke easier than the other two. However, it was very moist, something that is hard to come by in gluten-free bread.
    With the Schar bread, I felt that it was a little dry and grainy rather than moist and chewy like normal gluten filled bread. However, I found that when I toasted the bread, it had a texture more consistent with normal toast.
    Overall, I was satisfied with all three brands, but Udi's was the favorite. With the texture and taste being spot on, I did not need much else to convince me, but the added bonus of the reasonable price and large variety made it the most desirable gluten-free bread available.

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

    Dr. Rodney Ford M.D.
    Why Have I Got A Sore Tummy?
    Celiac.com 01/20/2016 - I've got a sore tummy! So many children say they have tummy pain. I see them every day in my clinic. Is this attention seeking or actual pain?
 They often say: "I've got a sore tummy", or "My tummy's sore", or
 "Tummy hurt", or "I've an ache in my tummy" or "Why is my tummy sore?"
    This is such a common complaint that mostly these symptoms are ignored or explained away as attention seeking. However, I have found that the majority of these children with so-called 'chronic abdominal pain' are affected by gluten sensitivity.
    I've got a sore tummy?
    Attention seeking or actual pain? In my experience, these children are in real pain. They need investigation and treatment. They need help for their tummy pains to go away. Yes, sometimes children do mix up the urge to do a poop with a pain (they feel uncomfortable before they do a poop), and it is gone when they poop. Some children mistake hunger as a pain. But most children with recurring "sore tummies" have a different pain. They are sore, in pain and really hurting. Can you imagine how they must feel when their pain is just ignored by their parents?
    Should children be expected to put up with tummy pains?
    Unfortunately, many health professionals and pediatricians are still living with teachings from the past. They refer to the writings of the 1960's. As 50 years ago it was believed that a child complaining about a tummy pain was being "bad" or "naughty". Their discomfort and pain was dismissed as "nothing serious" and told "they'll grow out of it" (the authors of these books were John Apsley "Child Development" and Professor Ronald Illingworth "The Development of the Infant and Young Child: Normal and Abnormal").
    I totally disagree with them. Long ago when they wrote their books, they did not have any blood tests available to diagnose gluten-related disorders; nor did they have any knowledge about gluten or celiac disease; nor was the role of food allergy understood. Consequently, most common symptoms, including chronic tummy pains, were simply attributed to "the state of being a child"!
    How many symptoms do you need to have? How severe do your symptoms have to be? How sick do you need to be? – before anyone will take your illness seriously? Why should we ignore a distressed child? Why should they be told "you will grow out of it"?
    These children have real pains. These children warrant serious attention. These children need help and understanding for their symptoms. Some of these children have unrecognized gastric reflux symptoms; some have celiac disease; some have Helicobacter pylori infection; some have chronic constipation; some have food intolerances; and many have gluten sensitivity/ intolerance.
    So what do I do in my clinic? Well I request gluten and celiac blood tests for ALL of these children who come and see me with tummy upset. To my surprise (I started this type of testing over 20 years ago), most of these sore-tummy-children have high levels of Anti-Gliadin-Antibody (AGA). When they strictly avoid gluten and go onto a gluten-zero diet—most get completely better. Their tummy pains go away, and often their parents report better mood and energy. Also better appetite and better eating.
    For instance:
    "Thanks for the blood results. A month ago, as soon as I got the first lot of blood results back, I took Mark off gluten all together (as you recommended). There has been a big improvement in him sleeping and he seems a lot happier. I haven't been giving him the reflux medication (Losec) for a good few weeks now: I had upped his dose to two pills a day but there was no improvement until I took him off gluten. So it must of been gluten upsetting his tummy. So at this stage we won't need a follow up appointment as with my family history we are pretty clued up with it all. Thanks for your help sorting Mark, it's greatly appreciated." Mum.
    Please don't just ignore them—please test and treat them! Please do not dismiss what your child is telling you: you may be able to help them. They might have a gluten-related disorder. They are not "attention seeking" they are in actual pain.

    See "The Gluten Syndrome" for more details. Also see Dr Rodney Ford's latest Kindle book: "Gluten-Related Disorder: Sick? Tired? Grumpy?" (www.GlutenrelatedDisorder.com).

    Dr. Ron Hoggan, Ed.D.
    Gluten Grains are a Problematic Food for Humans
    Celiac.com 01/26/2016 - One part of our natural protection from the microbes and toxins in our environment is the innate part of our immune systems. This includes everything from our skin, to the mucous we produce in various tissues which engulfs unwanted or harmful particles, isolating them and ultimately expelling them from the body in fecal matter and mucous, such as from our sinuses. While our immune systems have other components, it is the innate system that provides most of our protection from the world outside our bodies. The intestinal mucosa is very much a part of this system. Thus, since Hollon et al found that "Increased intestinal permeability after gliadin exposure occurs in all individuals" (1), there should be little doubt that humans are not well adapted to consuming these storage proteins from wheat, or gliadin's near relatives from rye and barley. Anyone eating these grains is opening a portal into their bloodstreams so toxins, microbes, along with undigested and partly digested proteins can enter their circulation. Without gliadin's impact, these various substances would probably not have entered the bloodstream and would have been wasted with feces.
    Just as few of us would ever consider putting fecal matter on an open wound, neither would we knowingly introduce this same material into the bloodstream through the intestinal wall. Yet, that is the net effect of humans consuming gluten grains. We are giving microbes access to our circulation. These harmful substances may be destroyed by other parts of our immune systems. Or perhaps we will develop episodic or chronic inflammation, leading to vascular damage where plaques can accumulate to cause atherosclerosis. Or the inflammation may use up available serotonin and its precursor, tryptophan, leading to depression. Or this they may cause one of the many other forms of damage that can be induced by inflammation. Or perhaps these infectious agents will manifest in other ailments, the causes of which will often remain obscure, as they degrade our health. Just one example of this risk can be found in a recent report in which antibiotic resistant staph infections were detected in 13% of pasteurized milk samples, and in 75% of raw milk samples (2). The acid in our stomachs, another part of the innate immune system, may provide some protection against this hazard. 

    On the other hand, microbes that have gained entrance into the circulation have also been implicated in some cases of arthritis, where the infectious agent binds to proteins in synovial fluid. Selective antibodies then target these complexes, causing damage to both the invader and the self tissues (3, 4).
    Toxins, especially those from insecticides and other chemicals likely to be found in or on our food supply are also cause for concern. Although most cases of organophosphate insecticide poisoning were the result of suicide attempts, these substances are widely used on a variety of food crops, and can be very dangerous (5). After all, both herbicides and pesticides are designed to kill small organisms. Because of our size, we may require more of these substances to get the job done but we, too, are organisms.
    One component of such substances is inorganic arsenic, which can also be found in natural rock deposits, some wood preservatives, rice, and sea foods, any or all of which can find its way to our bloodstreams (7) especially if we consume gluten grains. Of particular concern is that rice is often a staple of the gluten-free diet and it has been shown to have a strong affinity for inorganic arsenic, which "is a chronic, non-threshold carcinogen" (7). Thus, unlike smoking tobacco, even the smallest dose can result in cancer. Further, there are many areas of the United States where the groundwater is significantly contaminated with arsenic (8). Either drinking such water or excessive dietary reliance on rice grown in such a contaminated area can result in arsenic poisoning, as reported by Signes-Pastor et al (7) in a housewife in Saudi Arabia, who had celiac disease and relied heavily on rice. These authors first suspected dietary non-compliance until urine tests revealed an arsenic concentration at 46 times the highest value of the normal range (7). Her symptoms included: "progressive fatigue, profound watery diarrhea (12 times/d), palpitation, dry mouth, poor appetite, poor taste, sleeplessness, impaired concentration, and short-term memory" (7).

    Proteins from outside our bodies are eschewed by our selective immune systems, identifying them as foreign, and mount an attack against these "aliens". So any undigested proteins from the foods we eat, if they arrive in our bloodstream, are going to result in the mobilization of antibodies aimed at the destruction of these proteins. This sounds like a process for developing an allergic response against common foods.
    However, some proteins are worse than others. Gliadin, for instance, has long been recognized as harmful to many human cells (9). Humans also lack the necessary enzymes to fully digest it (10). Thus, after gliadin has caused increased zonulin production, leading to increased intestinal permeability, it can enter the bloodstream and travel to various tissues and organs where this undigested or partly digested family of proteins will induce one or more of their range of damaging impacts on the cells each molecule contacts. Dolfini et al have also reported that gliadin "induces an imbalance in the antioxidative mechanism of cells" (11) and it wreaks havoc on human cells by changing their shape, structure, and reducing their viability, as well as inhibiting enzyme production within the cell and/or inducing cell death (11).
    Since some humans have been consuming these grains for more than 10,000 years, one might expect that we would have evolved a digestive tract that could neutralize this threat to our wellness. Unfortunately, the issue isn't that simple. Only a small segment of the human population started cultivating gluten grains so long ago. The early development of this agriculture was also very localized and episodic. It would begin in one area then, for some unknown reason, the fields would be abandoned after some period of time. Then it would (excuse the pun) crop up in another, nearby area of the Fertile Crescent (what is now parts of Iraq, Iran, Kuwait, Syria, Lebanon, Jordan, Palestine, Israel, and Egypt). The net result was that it took some time before cereal agriculture was a thriving concern. This may be explained by the illnesses that are reflected in the bones of those early farmers (11). Gluten grains appear to have taken a much greater toll on their health than it does on us now, so some adaptation has probably occurred. Nonetheless, once grain cultivation got a good start, it spread fairly quickly across Europe, arriving in England by about 5,000 years ago.
    Populations living in environments that were not conducive to grain cultivation, either due to climate or soil conditions would wait much longer to incorporate gluten grains as a staple in their diets. Modern transportation systems were required to bring this crippling food to some doorsteps in Scandanavia, parts of Scotland and Ireland, and many other such environments throughout Europe. However, even in those halcyon days when the sun never set on the British Empire, Europeans really weren't the only people on the planet. They may have behaved as if they were, but that's an issue for another discussion. In the meantime, the bulk of the world's population had not eaten gluten grains until much more recently, when Europeans "shared" these grains almost everywhere they traveled. Most of the populations these Europeans met during their travels had also missed out on the many European plagues, including bubonic plague, smallpox, and typhoid fever, as well as the filthy living conditions that were common in Europe. These conditions had selected only those with the most vigorous immune systems to carry on as Europeans. When gifts such as smallpox-infected blankets were given to natives, these naive populations succumbed, in large numbers.
    Further, only a small percentage of these naive populations who were very recently introduced to gluten were developing celiac disease. For instance, only about 5.6% of Saharawi children of Northern Africa had developed celiac disease when tested by Dr. Catassi and colleagues some 50 years or so after they had begun to eat gluten (12).
    European "explorers" probably didn't really notice such illnesses among their grain-naive hosts. Nobody had the technology or the medical understanding to identify celiac disease or the many neurological ailments that gluten causes anyway. Many of us still deal with deep wells of medical ignorance, in the context of a very modern medical system, when it comes to our disease, so how could we expect anything more from those sea-faring Europeans of four or five centuries ago?
    Perhaps those gluten derived opioids probably felt pretty good to people who tried gluten. Whatever the reason, the rest of the world seems to have adopted Europe's dietary choices, pursuing the "comfort" of gluten grains while developing myriad forms of autoimmune disease, neurological dysfunction, gastrointestinal complaint, and a variety of other ailments. And most of the people I encounter would rather deny the health risks than give up donuts, cake, pie, and toast (13).
    Note: I'm proud to announce that I've been given the privilege of reviewing a new book that will be published early next year, under the Touchstone imprint, by Simon and Schuster. I will be writing about some interesting new insights this exciting book offers into the world of gluten sensitivity in the next issue of the Journal of Gluten Sensitivity.
    Sources:
    Hollon J, Puppa EL, Greenwald B, Goldberg E, Guerrerio A, Fasano A. Effect of Gliadin on Permeability of Intestinal Biopsy Explants from Celiac Disease Patients and Patients with Non-Celiac Gluten Sensitivity. Nutrients 2015, 7, 1565-1576. Akindolire MA, Babalola OO, and Ateba CN. Detection of Antibiotic Resistant Staphylococcus aureus from Milk: A Public Health Implication. Int. J. Environ. Res. Public Health 2015, 12, 10254-10275. Li S, Yu Y, Koehn celiac disease, Zhang Z, Su K. Galectins in the Pathogenesis of Rheumatoid Arthritis. J Clin Cell Immunol. 2013 Sep 30;4(5). Cordain L, Toohey L, Smith MJ, Hickey MS. Modulation of immune function by dietary lectins in rheumatoid arthritis. Br J Nutr. 2000 Mar;83(3):207-17. Coskun R, Gundogan K, Sezgin GC, Topaloglu US, Hebbar G, Guven M, Sungur M. A retrospective review of intensive care management of organophosphate insecticide poisoning: Single center experience. Niger J Clin Pract. 2015 Sep-Oct;18(5):644-50. Hasanato RM, Almomen AM. Unusual presentation of arsenic poisoning in a case of celiac disease. Ann Saudi Med. 2015 Mar-Apr;35(2):165-7. Signes-Pastor AJ, Carey M, Meharg AA. Inorganic arsenic in rice-based products for infants and young children. Food Chem. 2016 Jan 15;191:128-34. United States Geological Survey. 2005. Arsenic in ground water in the United States. http://water.usgs.gov/nawqa/trace/arsenic/ Last Modified: Thursday, 17-Nov-2011 Hudson DA, Purdham DR, Cornell HJ, Rolles CJ. Non specific cytotoxicity of wheat gliadin components towards cultured human cells. Lancet 1976; 1: 339-341. Kagnoff M. Private communication. 2005 Dolfini E, Elli L, Roncoroni L, Costa B, Colleoni MP, Lorusso V, Ramponi S,Braidotti P, Ferrero S, Falini ML, Bardella MT. Damaging effects of gliadin on three-dimensional cell culture model. World J Gastroenterol. 2005 Oct 14;11(38):5973-7. Rätsch IM, Catassi C. Coeliac disease: a potentially treatable health problem of Saharawi refugee children. Bull World Health Organ. 2001;79(6):541-5. Cordain L. Cereal grains: humanity's double-edged sword. World Rev Nutr Diet. 1999;84:19-73.

    Maria Larkin, M.Ed, RDN/LD
    Glyphosates and Gluten-Related Disorders
    Celiac.com 02/16/2016 - About two years ago, as a result of two comprehensive review articles written by research scientists, Anthony Samsel and Stephanie Seneff, the term "glyphosates" made media headlines.
    Based on more than 200 citations, their reviews concluded that long term exposure to glyphosates via ingestion (in food and water) and/or inhalation seems to parallel the incidence and clinical features of celiac disease and may contribute to a number of diseases including autism, cancer, Parkinson's Disease, Alzheimer's Disease, infertility, depression, inflammatory bowel disease, Multiple Sclerosis, cancer, allergies, eosinophilic esophagitis (EOE), obesity, and kidney disorders.
    In case you don't already know, glyphosate (an organophosphate) is the active chemical ingredient in Monsanto's trademarked herbicide called RoundUp, which in the last 15 or more years has become very popular and is used throughout the world. It is largely used in "no-till non-organic production systems" as a desiccant (drying agent) for many genetically engineered (GE) food crops, especially those considered "RoundUp Ready" such as corn, soy, canola, cotton, sugar beets and alfalfa. RoundUp Ready foods are genetically engineered to resist being killed by RoundUp.
    While wheat is not a genetically engineered food crop, RoundUP is used on all non-organic wheat crops to produce a greater yield and reduce any rye grass weeds. The glyphosates in the RoundUp kill weeds by disrupting the shikimate pathway in the plant.
    I once used RoundUp to kill some weeds in my yard thinking that it was safe and nontoxic. It was thought then that humans and animals could not be affected by this weed-killing herbicide because humans and animals don't possess the shikimate pathway, only plants and bacteria do.
    That was until Samsel and Seneff set me straight. The bacteria in the human gut, which outnumbers the cells in our body, do have shikimate pathways. Glyphosates suppress the enzyme necessary for the shikimate pathway to produce aromatic amino acids such as tyrosine, tryptophan and phenylalanine. This happens in plant cells, too, where reduced levels of other amino acids have been discovered including serine, glycine and methionine.
    What does this mean for we humans? These amino acids are precursors to neurotransmitters (found in the gut and in the brain). Tryptophan alone is necessary for the production of serotonin, "the happy hormone." An impaired supply of serotonin frequently found in celiac disease causes depression. Impaired serotonin receptors in the gut sets the stage for inflammatory bowel disease.
    So besides blocking the shikimate pathway for the production of nutrients in foods, glyphosates seem to reduce the overall bioavailability of nutrients in the foods we eat. I have been a regular advocate for taking a daily multi vitamin and mineral, contending that the food we eat may lose nutrients from farm to table. Low and behold, Samsel and Seniff's review substantiated my contention. They cite two studies, which showed multiple mineral depletions in soybean crops treated with glyphosates. The depleted nutrients in the soybeans mirrored those frequently found in celiac disease, including cobalamin (B12), iron, molybdenum, selenium and sulfur. The authors hypothesize that the association between celiac disease and autoimmune hypothyroid disease may be due to a selenium deficiency.
    Samsel and Seniff suspect that chelation in the gut due to glyphosate ingestion may further account for deficiencies in cobalt, molybdenum and iron in these foods. This confirms yet another contention of mine that a single nutrient can indeed disrupt a whole system. The chelation of cobalamin in the gut is suspected to contribute to neurodegeneration and heart disease; the synergistic dynamic of molybdenum deficiency altering the body's supply of sulfate can have the consequence of cancer, anemia and insulin resistance. The authors purport that glyphosates disruption of the sulfur transport in the body is "the most important consequence of glyphosate's insidious slow erosion of health."
    The health of the human intestinal tract is affected by glyphosate ingestion and inhalation. Citing a study on the effects of glyphosates on predatory fish, Samsel and Seneff's review showed that glyphosates cause damage to the intestinal mucosal folds and microvilli similar to what is seen in celiac disease. Beneficial gut bacteria are killed, allowing the pathogenic (disease-causing) bacteria to proliferate, producing a state of bacterial dysbiosis (microbial imbalance). With reductions in the beneficial Bifidobacteria and Lactobacillus bacteria, the breakdown of both gluten and phytase are impaired, leading to the inability to digest gluten. The pathogenic bacteria such as E. Coli and C. Difficile can lead to kidney failure and inflammation. These authors argue that other digestive pathologies, such as pancreatitis, fatty liver disease and EOE are due to impaired CYP function in the liver. Could there also be a link between the high rates of small intestinal bacterial overgrowth (SIBO) and gut dysbiosis caused by glyphosate disruption of these enzymes?
    Glyphosates disruption of CYP enzymes in the liver occurs with celiac disease. These enzymes are involved in detoxification of xenobiotics (foreign chemical substances), so theoretically a reduction of CYP enzymes slows detoxification. Vitamin D3 and cholesterol synthesis and regulation of retinoic acid are also a part of the CYP enzyme system. It has puzzled me at times, that some of my patients do not respond to high dose vitamin D supplementation. The concept that glyphosates effect on CYP enzyme inhibition results in inadequate vitamin D activation in the liver could be a mystery solved. CYP enzymes are also important in bile acid production, gallbladder and pancreatic function. Samsel and Seneff hypothesize that glyphosate "disrupts the transport of sulfate from the gut to the liver and pancreas", resulting in bile acid insufficiency and gall bladder disease. Excess retinoic acid as a result of glyphosate exposure is similarly found in celiac disease and has been linked to reproductive disorders.
    How can we avoid glyphosate exposure? The obvious answer is not to use this herbicide to kill weeds in your yard. In the best interest of health, eat organic foods as much as possible, avoid the "the dirty 15" and genetically engineered foods. Check out your local farmer's market and buy from certified organic farmers. Eat animal products fed with non- genetically engineered foods. If you eat wheat, choose organic wheat. Glyphosates cannot be washed off of food, and there is yet no known way of detoxifying glyphosates from the body. The authors suggest eat garlic or soak in an Epsom salts bath to ensure adequate sulfur intake. Sea salt is a natural way to include minerals in your diet along with eating vegetables.
    Maria Larkin, M.Ed, RDN/LD owns Better Gut Better Health, LLC, a nutrition counseling practice in Durham and Portsmouth, NH. She is a registered dietitian and functional medicine provider, specializing in gastrointestinal concerns, food allergies and sensitivities. Website: www.bettergutbetterhealth.com.
    References:
    Samsel, A. and Seneff, S. Glyphosate's Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to Modern Diseases. Entropy, 2013: 15 (4): 1416-1463. Samsel, A. and Seneff, S. Glyphosate, pathways to modern diseases II: Celiac sprue and gluten intolerance. Interdisciplinary Toxicology, 2013: 6 (4): 159-184.

    Amie  Valpone
    Lost and Found
    Celiac.com 02/23/2016 - Rather than enjoying the youth of my 20's, some of the 'best years of my life,' I suffered from over a decade of chronic illness—everything from Lyme disease to C-diff colitis to hypothyroidism and chronic systemic candida. It started with severe leg swelling and chronic pain on a daily basis. By mid-afternoon, I carried what felt like bricks of water in my legs. On top of that, I was plagued by horrible digestive issues that left me feeling sick, lethargic and just plain gross. This was what I suffered with before I started my journey of detox, which led me to feeling younger and more energetic than I had felt since I was a kid.
    During my decade of chronic illness, on a daily basis I focused on eating clean and detoxing my body by eating lots of fresh, organic foods such as fresh herbs, raw nuts, seeds and tons of veggies that helped support my thyroid, gut and liver function and to support the removal of toxins in my body. When you're trying to detox, organic salads filled with fresh, whole ingredients are always a good idea!
    'Eating Clean' is all about adding in whole, organic fresh foods to your lifestyle and feeling good about what you are putting into your body. It's not about feeling deprived or going on a diet. Wellness is more than just calories, it's nourishment for your body to keep you healthy and strong. At this point in my life, I can honestly say that after reading almost every detox and medical book, seeing over 500 doctors including an entire week at Mayo Clinic, I've learned that the answers were within me the whole time. I had to be my own doctor and put the missing pieces together. My doctors could only do so much and they didn't communicate with each other, plus they didn't understand anything outside of their specialized field, which left me feeling hopeless and lost.
    Whether you're suffering from chronic illness or just the occasional headache or bloated belly, I hope to inspire you to be your own doctor and realize that wellness starts with what's on your plate. Start tossing out the processed foods in your fridge and pantry today, add in beautiful, fresh foods and I promise you'll feel better just looking at the beautiful colors and tasting their amazing flavors. Get creative, go out and pick up a bunch of fresh herbs and start adding them to your meals—you will be amazed at how much flavor they can add to your them without having to add refined, unhealthy oils or other processed ingredients.
    This is a fun recipe to pack in a mason jar with a lid and take to work for lunch, or you can toss it all together and serve it in a big bowl for a quick weeknight for dinner. I love to cook quinoa in large batches on Sunday nights for myself and my clients, so that I always have it ready in my fridge to add to quick salads for lunch, stir-fry's for dinner, and even warmed up on the stove top for breakfast with almond milk and cinnamon.
    Simple Honey Sunflower Quinoa Bowl
    Serves 4
    Ingredients:
    ½ cup quinoa 2 medium yellow summer squash or zucchini, thinly sliced or diced 1/3 cup thinly sliced jicama or peeled apple 2 tsp. finely chopped fresh basil, plus more if desired 2 Tbsp. sunflower seeds Juice of 2 medium lemons ½ tsp. honey 2-3 Tbsp. extra-virgin olive oil Sea salt and pepper, to taste Pinch crushed red pepper flakes, optional Directions:
    Cook quinoa according to package directions. Remove from heat; fluff with a fork, cover and set aside.
    Meanwhile, steam squash in a steamer basket over medium heat for about 5-7 minutes or until tender. Add to quinoa mixture and toss to combine. Add jicama, basil and sunflower seeds; toss again.
    In a small bowl, whisk lemon juice, honey, olive oil, sea salt and pepper. Drizzle over quinoa mixture and toss to combine. Season to taste and transfer mixture to a sealed container and place in the lunchbox with a spoon and napkin.
    Amie Valpone, founder of TheHealthyApple.com, wrote her first cookbook, over 200 recipes free of gluten, dairy, soy, eggs, corn, sugar, peanuts and processed foods, Eating Clean: Detox, Fight Inflammation, Reset Your Body & Get to the Root Cause of Illness, which is available for pre-order now on Amazon.com.

    Dr. Ron Hoggan, Ed.D.
    There's a New Kid on the Block!
    Celiac.com 03/09/2016 - Many of us continue to struggle with a wide range of health concerns, digestive complaints, neurological symptoms, and/or apparently unrelated wellness issues such as low energy levels or continuing episodes of brain fog. Yet, we are gluten-free to the best of our ability. Some of us expend inordinate periods of time preparing all our own meals to ensure the strictness of our diets. Yet the symptoms persist or continue to escalate. For many of us, our health care providers are unable to help. They order more and more testing as they seek more and more obscure possible causes for our repeated visits. You may even be one of those people who simply gives up on the medical profession, and either continues to seek answers on your own, or just tries to accept your current, less than optimal state of health. Many of us continue to believe the faulty information in the "Food Pyramid" and "My Plate". These and other such guides erred with respect to our celiac disease, but we continue to accept flawed claims about the health benefits and dietary importance of grain fiber. Thus, while having eliminated gluten grains, we continue to consume other grains for these benefits. Yet, if the authors of My Plate, etc., could be so wrong about the gluten grains, surely all of their claims should be suspect. Or, if we have great faith in them, we should at least examine the evidence that supports their claims.
    We know, by virtue of the celiac's leaky gut, that additional food sensitivities are common among those who were diagnosed as adults. Similarly, those who strayed from careful gluten avoidance will also be likely to have triggered immune reactions to a variety of other food proteins and peptides. Further, Dr. Marios Hadjivassiliou and colleagues have long reported that when there are neurological symptoms that are associated with either celiac disease or non-celiac gluten sensitivity, those individuals need to be even more vigilant than most celiacs about avoiding even tiny traces of gluten. Thus, whether you are continuing to experience celiac symptoms, neurological symptoms, or other health problems that may be driven by diet, I have some good news. There is a new kid on the block.
    His name is Peter Osborne, D.C., and he has written an exciting new book about gluten sensitivity and more, much more. Titled No Grain No Pain, Osborne's book brings a breath of fresh air to the many stale controversies that hover over the health issues that are driven or aided by various grains. As the title suggests, his primary focus is on the chronic and acute pain that can be caused by eating various cereal grains. In addition to the gluten grains, he identifies several immune and hormonal pathways and dynamics by which the consumption of storage proteins from other grains can cause pain. Meanwhile, he shows that antibody delivery, via the lymph system, is reliant upon movement and muscle contractions because, unlike blood circulation, we don't have a dedicated organ for pumping lymph. Additionally, he points out that these families of storage proteins bear a striking resemblance to those found in gluten grains and sheds light on them as important forces behind many forms of chronic pain.
    Dr. Osborne's plain language explanation of the differences between selective and innate immune reactions, and how they impact on the protein and peptide sensitivities we develop is really quite impressive. I have never read a clearer, more concise explanation of these two facets of human immune systems and how they can interact when things go awry. He presents a series of compelling case histories that show the very dynamics he identifies as problematic, also explaining exactly what these individuals did to recover from their painful symptoms. And this is the most ingenious facet of his book. Osborne identifies the dynamic, then provides an illustrative case history to show both how and why the ailments developed, and how and why the patient gets well again.
    He also acknowledges that each of us is unique, making such statements as "Never make the assumption that a food is safe or healthy for everyone." That, I think, is the most telling statement in his aptly titled new book: "No Grain No Pain". His explorations touch on the bacteria that populate our intestines, for good or ill, and how grain consumption can alter those populations. He also explores the elegant interplay between various critical vitamins, minerals, bacteria, and macronutrients that is both unique to each of us, and can have a profound impact on each of our immune systems. His discussion of imbalanced intake of omega 3 and omega 6 oils is another important feature of our individuality.
    While excess omega 6 oils will induce inflammation in anyone, and adequate omega 3 oils will counter inflammation in all of us, each of us has her/his own unique capacities for emulsifying, absorbing, and metabolising these fats. Nonetheless, Osborne provides some clear guidelines for balancing our intake of these essential fats toward reducing inflammation. Most of us are currently getting more omega 6 fats than we need, and not enough of the omega 3 fats. That leads to unnecessary inflammation and pain.
    I must admit that I was initially put off by the book's central argument, especially since it was presented before the enormous body of supporting information. After all, there is a limit to how many foods I can stop eating! However, I soon warmed to the topic as I saw that it is not much of a step to eliminate the other grains he identifies as problematic. After all, that still leaves us able to eat many healthful fruits, vegetables, berries, and meats.
    I was also taken by his discussion of what he calls "grainbesity". The explanation of AGEs is, I think, critical to understanding how important these substances are to the extensive damage they can wreak on all parts of the body and brain.
    Similarly, zinc and magnesium, while very important to the proper function of our immune systems, are also critical to managing blood glucose and insulin levels. And unwanted weight gain is often accompanied by deficiencies in these minerals. As we gain weight, our joints are compressed, resulting in joint damage and pain. Weight loss, is the obvious answer, but without these critical minerals, that task may be close to impossible. Further, additional food sensitivities may also be a factor in the vicious, downward, weight-gain spiral.
    Dr. Osborne also explores the broad world of unintended consequences from a variety of over-the-counter and prescribed medications. I was aware that many NSAIDs can cause or increase gut leakage of food proteins and peptides into the bloodstream, resulting in autoimmunity and other damaging dynamics. However, I also learned that Ibuprofen can damage the stomach lining and small intestine. Since vitamin B12 deficiency is common in my family, with many members getting regular shots because their intrinsic factor appears to be compromised, it may be worthwhile looking at their ibuprofen use. Similarly, he examines a variety of dietary deficiencies that can be corrected with supplements, and he provides a host of recipes along with a dietary program that gradually weans the follower off the gluten-free, standard American diet.
    He has a revolutionary, detailed view of the whole field of gluten sensitivity and he assures the reader that if they will just follow his dietary plan for 30 days, she or he is very likely to discover a pathway that will reduce or eliminate their chronic pain.
    On a personal level, many readers are already aware of the substantial relief that my mother got just from avoiding gluten grains. She was able to stop taking morphine, go back golfing, and lose one hundred pounds. (Accumulating that much extra weight is no small feat on a woman who wasn't quite five feet tall.) She lived a much longer life than was likely more than twenty years ago. Yet, when she arrived at the first of two seniors' homes, to live in what is called "assisted living", her dietary needs were not met. In theory, a gluten-free diet was available. In reality, she watched while others consumed tasty treats for dessert, while she was given the same old fruit plate, or Jello. Predictably, she started to cheat. By six years ago, she was frequently eating gluten-laden desserts. In an attempt to "start over" and be closer to my wife and I, she and my step-father moved to another assisted living facility. I spoke with the chef before they agreed to move. He assured me that he would address my parents' needs.
    Yet after he had seen my mom cheat a few times, he stopped providing for her gluten-free diet, as he said that if she wasn't making the effort, why should he? I was sympathetic to his point of view until I discussed it with the community health nurse. She said that "We don't stop accommodating diabetics' needs just because they falter on their diet. Why should he do that with her?" Having thought about it, I returned to the chef and pressed him to provide her with gluten-free food. He promised to do so. It was not long before my mother was lapsing into more and more pain. I then spoke with the manager of the facility. She agreed to provide mom with gluten-free food.
    By two years ago, mom's mind was going, she couldn't remember what foods had gluten in them, and she forgot to ask for gluten-free alternatives. She steadily re-gained about fifty pounds. Concerned about her weight and her pain, she wanted to return to the diet, but was simply unable to do so. She would forget and eat treats with her neighbors. I watched her eyes light up when one of them brought yet another such deadly treat to share with her.
    My own experience is that pain is very forgettable. I doubt that women would give birth to a second child, in this day of available birth control, if pain weren't so easy to forget. It is only when I revisit a particular source of pain that I recall its intensity. I suspect that is true for my mom as well. If so, it is my hope that Dr. Osborne's book, and all the subsequent publications about dietary grain and the pain it causes will enlighten enough folks that cooperation at such extended care facilities will become easier to enlist.
    In the meantime, I find myself reading every book on the subject of celiac disease and/or non-celiac gluten sensitivity that comes my way, especially those that explore chronic pain and/or weight gain. In the case of No Grain No Pain, I had the privilege of reading it before its publication. A representative of Simon and Schuster contacted me with a copy of this book, asking me to write a promotional blurb for it. I was happy to read it. Then, I was very pleased to be able to give her the positive blurb she requested, in time for its release late in January 2016. Doubtless, they have contacted many others who have provided similar comments, and I hope that they found it as valuable and compelling as I did.
    My mom passed away on June 30, 2014, from a massive stroke. I authorized that she be unplugged from life support systems, as the doctors believed that she would not have any intellectual capacity in the unlikely event that she did recover. She had told me, many times, that she was tired of the pain, tired of the confusion, and tired of living. I'll miss my mom, and I have many second thoughts about how I handled or failed to handle the situations she found herself in. I'll never know, for sure, if my decisions were right or wrong. For myself, I'm pleased that she is no longer in pain, and I have re-dedicated myself to the dietary re-education of as many people as I can. And I hope that Dr. Osborne's new book will help others to avoid the "extended care" trap that my mom fell into.
    Source:
    1. Osborne P., NO GRAIN, NO PAIN. Touchstone, New York. 2016.

    Yvonne Vissing Ph.D.
    The Zen of Going Gluten-Free
    Celiac.com 03/23/2016 - Often when people hear that someone is "going gluten-free," they think that just means people are not eating wheat. This kind of thinking focuses on the obvious—since gluten is in foods it means watching what is eaten. They may associate this change in diet with some biological process or disease issue. In the world of the general public, they're not really sure what "gluten" is and they're not totally convinced that eliminating it will improve health. But for those of us who make a commitment to going gluten-free, it is far more than just eliminating certain food products. It is a personal transformation of self. What people don't often talk about is it being a psychological and social change as well.
    In many ways, making a commitment to seriously go gluten-free is an act of Zen. The Urban Dictionary defines Zen as "a state of focus that incorporates a total togetherness of body and mind. Zen is a way of being. It also is a state of mind. Zen involves dropping illusion and seeing things without distortion created by your own thoughts." What I've found is that going gluten-free requires thoughtful practice, observing the body, monitoring the mind, and seeking knowledge that one integrates into regular practice. The result is the personal expression of insight into daily life.
    Going gluten-free isn't just about eating. It is also about personal discipline. It has a lot to do about how we think and how we live. When we started going gluten-free we thought it was just going to entail a dietary switch. What we've learned over the last decade is that going gluten-free is an act of Zen. Our journey into becoming gluten-free started because health issues forced us down that path. We didn't willingly choose to go there. We would have been content with gorging on Texas toast, pasta, and Oreos for the rest of our lives. But if we did, we would have been chronically sick. The Universe pushed us onto the gluten-free road. At first, we did not go gracefully. We stumbled and fell and made a mess of going gluten-free. Going gluten-free seemed miserably hard and terribly inconvenient. We couldn't find products that tasted good, and those we found were expensive and weren't necessarily healthy (the amounts of eggs, butter or oil in many of them were mind-boggling). We spent too much money on poor-tasting products that were very difficult to find. We griped and complained. We felt alienated and imprisoned. Going out to eat was life-threatening because most restaurants didn't cook dishes that were safe, or if they did they cooked them in an environment in which they could be cross-contaminated. The idea of having to eat awful-tasting food and not being able to go out to eat for the rest of one's life was dreadful and depressing. Eating is one of the joys of life, and feeling like one was never going to be able to eat delicious food again felt like a fate worse than death. Going gluten-free seemed doomed to be an act of suffering. Sometimes, it is only through making a mess of our lives that we figure out how not to.
    Such is the case with our going gluten-free. What we didn't realize until later was that we had created this negative reality in our minds. You can go gluten-free smoothly, effortlessly, inexpensively, and easily with no disruptions in your daily lives. It need not be a big deal. This process may take a bit of time. The secret in this transformation has little to do with the gluten-free foods available. It has more to do with what is going on in our heads.
    Years of diligent practice, trial-and-error, patience and persistence, and learning have helped us to transform our perception of going gluten-free into an easy, inexpensive, and delicious way of eating. It has also fostered a different relationship with what we eat, why we eat, and how we eat. It has changed our relationship with food itself, how it is prepared, and how it is consumed.
    Thinking you can eat anything you want and not get sick is illusion for people who must go gluten-free. It requires mind-over-matter self-control when we're hungry and desire foods that may not be safe. Giving in to that longing for a certain cookie or a bite of Grandma's homemade lasagna can make a person with celiac very sick. Being mindful of why that food item creates desire in us is a useful mental exercise. Certain foods evoke memories and emotions that are more delicious than the foods themselves. We can still enjoy the memories without eating foods that aren't good for us.
    Food is very social and relational. Eating something served that isn't safe in order to please or not to appear rude, when it has a high likelihood of making us sick, isn't being kind to oneself. There have been times we've gotten annoyed when what-should-be-safe food has been contaminated. On the surface, it shouldn't be a big deal to redo the dish. But the symbolic message conveyed by serving someone with celiac glutened food is more problematic because it reflects that the server didn't really care about our needs. What happens to our relationships with family, friends, or certain establishments who go out of their way to make sure we can eat good foods, safely, in a no-big-deal manner? We care for them all the more. Frankly, we secretly want to see what goes on in the kitchen and read the ingredients on a product and not just take a waiter's declaration that "I'm sure it's gluten-free" to be an accurate reflection of reality until we are sure that what they say accurately reflects how actively sensitive they are to the needs of others who have dietary needs that are different from their own. Issues of trusting others, and trusting ourselves, is part of the gluten-free process. Helping to teach those who didn't understand the importance of being gluten-free in a constructive and thoughtful manner is much better than getting angry at them and refusing to eat with them again.
    Going gluten-free requires mindfulness. It gives us a relationship with our food as well as with others. Eating whole and healthy foods is better for us. Taking time to understand what's in our food really matters. Cooking ingredients in a thoughtful, less-hurried way creates lovelier dishes. Consuming them with gratitude and in communication with others makes them even more delicious. We want to know where the food came from, how it was cooked and what it was cooked with, and details of the dish's preparation. Were those oats grown next to a wheat field? Did these nuts get processed on machines that also processed other items that contained glutens? Were there croutons on the salad that you just picked off? Asking questions in a non-combative way is an art. Learning to read labels and knowing the list of unsafe ingredients must be transformed from being a big deal to it being just another routine step in an ordinary day. Learning how to shop, cook, clean, serve and eat are all actually complicated steps that require attention to detail. It is in the transformation of managing all these details into a smooth, seamless and calm process that going gluten-free becomes Zen.
    It took us a long time to realize that going gluten-free successfully has more to do with what's going on in our heads than what's going on in the kitchen. Look upon going gluten-free as a Zen experience, in which you have to change one pattern of behavior for a new, better one. You, like we, may find you have to change attitudes toward eating in general and eating gluten foods in particular—and you will be all the better for it.
    We'd love to help you to learn more about our approach to going gluten-free. Check out our book, Going Gluten-free, which is available from Amazon and NorLights Press, and let us know how your journey is going!

    Betty Wedman-St Louis, PhD, RD
    Vitamin B12 and Celiac Disease
    Celiac.com 04/12/2016 - Vitamin B12 is a group of cobalt containing compounds described by Alan R. Gaby, M.D. in Nutritional Medicine called cobalamins. Methylcobalamin is the coenzyme form of B12 that is critical for human health. Hydroxocobalamin is a more stable form of B12 but it first needs to be converted to an active form before use in metabolism.
    Vitamin B12 is important in DNA synthesis, red blood cell formation, homocysteine metabolism and the production of S-adenosylmethionine (SAMe). Adequate B12 is essential for proper neurological and immune function.
    The importance of Vitamin B12 in health and anemia management began during the Depression era when animal protein foods were limited in the American diet. Three physicians who reversed pernicious anemia in dogs were awarded the 1934 Nobel Prize for medicine. Dr. George Hoyt Whipple and two other physicians fed the dogs and humans 1/2 pound of fresh liver per day as a means to control anemia.
    Animal proteins—meat, poultry, fish, eggs—are the sources of Vitamin B12 for humans. Plants do not need or produce B12. How B12 gets into your blood is a complex dance of stomach acids and intrinsic factors that starts with pepsin in the stomach splitting off the B12 from the protein compound. The intrinsic factor made by the parietal cells of the stomach attaches to the B12 to be shuttled to the ileum where receptors pull it into the blood.
    Once in the blood, B12 is picked up by transcobalamin to be carried to cells throughout the body. Any excess is stored in the liver or excreted in the urine.
    If inadequate intrinsic factor is available—loss from aging or proton pump inhibitor use—B12 deficiency symptoms such as macrocytic anemia, neurological disorders and psychiatric symptoms (memory loss, depression, confusion, paranoia) may occur. Severe B12 deficiency can result in intestinal damage, hyper-pigmentation of the skin, hypotension, and immune dysfunction.
    The Institute of Medicine indicates that only 2 to 4 mcg Vitamin B12 is needed daily. The average American diet contains 5-15 mcg per day according to NHANES studies. Vegetarians and infants breastfed by vegan mothers are at greatest risk of developing B12 deficiency.
    Other factors increase the risk of developing Vitamin B12 insufficiency. Achlorydria secondary to gastritic, gastric bypass surgery, and ileal resection for Crohn’s disease need assessment due to malabsorption. Apathy abounds throughout the medical community despite the 2009 Centers for Disease Control and Prevention statistics indicating 1 out of every 31 people over 50 being B12 deficient. With increasing numbers of gastric bypass patients and Crohn’s resections, this deficiency could be significantly higher.
    Adverse symptoms can first be noted with the CBC test indicating large RBC or macrocytosis—a folate and B12 deficiency. Other symptoms may include balance problems, numb hands and feet, leg pains, early onset dementia, pre-Parkinson’s-like disease, infertility and depression.
    Many physicians are poorly educated on Vitamin B12 importance since it is a vitamin and easy to treat. Treatment with methylcobalamin injections with few definitive ways to test efficacy seems to be a primary factor. A complete medical history assessing for gut inflammation, celiac disease, GERD, recent nitric oxide use in surgery, and genetic factors like MTHFR should trigger a closer look at B12 adequacy even with a normal homocysteine (HCY) plasma test. High levels of B12 on standard blood analysis usually indicates poor absorption and not intoxification of Vitamin B12. Elevated B12 results >800pg/ml frequently indicate PPI use or low stomach acid malabsorption. Lab results <350pg/ml may still be inadequate for a patient with celiac disease, gluten enteropathy or gastric bypass surgery, so supplementation should be considered.
    Medications matter when considering Vitamin B12 status. Below are common drugs that impair absorption:
    Antacids- maalox, MOM, Mylanta, Tums Histamine blockers- Zantac, Tagamet, Axid, Pepcid Proton Pump Inhibitors- Prevacid, Prilosec, Nexium,. Omeprazole, Acidhex Colchicine Questran Metformin, Glucophage Celexa, Effexor, Elavil, Nardil, Paxil, Prozac, Zoloft, Wellbutrin Ativan, Librium, Valium, Xanax Viagra, Cialis, Levitra Compazine, Haldol, Risperdal, Tegretal Vitamin B12 supplementation is probably the safest medical treatment available. Many people need B12 injections to show improvement in their symptoms. Effectiveness of injections depends more on frequency of administration than on amount given with each injection. Those who improve with injections rarely improve with oral or sublingual products no matter how large the dose because the routes of administration are not capable of achieving high enough absorption levels.
    Treatment with Vitamin B12 needs to be continued for life. Until more research on efficacy and safety of oral B12 is available, intramuscular daily or weekly injections should be considered a standard of care, especially in celiac disease and those with gastric bypass surgery.
    A 20 page handout on Digestive Wellness is available for $15 from Dr. Betty Wedman-St Louis, 17920 Gulf Blvd, Ste 606, St. Petersburg, FL 33708. It includes information on how GMO foods destroy health which will be covered in a future article.

    Dr. Rodney Ford M.D.
    Gluten-related Disorders: Not Black and White
    Celiac.com 04/20/2016 - I am likely to be accused of gluten heresy. That is because I propose that celiac disease and gluten sensitivity usually coexist. By this I mean that they are not mutually exclusive entities.
    In other words, most people who have celiac disease are also gluten-sensitive. Many people who are gluten-sensitive are likely to develop celiac disease with continued gluten exposure (depending on their genetic markers).
    My observations show that the distinction between celiac disease and gluten-sensitivity (the gluten syndrome) is blurred. The purpose of published algorithms and decision trees are designed to separate out celiac disease from other gluten-illnesses. I suggest that this thinking is flawed.
    For example, most flow charts go something like this: (See Flow Chart 1 at left).
    People are selected for celiac-blood-tests for a number of reasons. If your blood tests are positive (and usually if you carry a DQ2/8 gene), then you get an endoscopy to confirm/deny the diagnosis. This allows you to be categorized either Yes-celiac disease or Not-celiac disease. There is no overlap. This is an "us-and-them" scenario.
    However, isolating YES-celiac disease from every other gluten problem does not take into account that people who have gluten-gut-damage may well have other manifestations of gluten-related disorders.
    Such simplistic algorithms (decision trees) strike problems at every decision point. Such as: Who should be tested? Who should be re-tested? When should these tests be done? At what age? On how much gluten? What tests should be done? What are the cut-off levels? How important is carrying the DQ2/8 genes? What about sero-negative celiac disease? How accurate are endoscopic biopsies? Who interprets the Marsh scale? How long should a gluten challenge be?
    Such simplistic algorithms (decision trees) also do not give satisfactory answers to the following questions:
    Why do 10% of people with celiac disease have little or no symptoms, despite having severe small bowel damage (villous atrophy)? This group is called "asymptomatic" celiac disease. Villous atrophy alone cannot account for the majority of gluten-related symptoms. Why do half of the people with celiac disease have autonomic nervous system dysfunction? This is the disturbance of the automatic nerve activity of your internal organs. This cannot be directly attributed to villous atrophy. Why do most people with celiac disease have some brain/mental upset, including the pervasive brain-fog? Many people have neurological disease from gluten but do not have established celiac disease. How can so many "extra-intestinal manifestations" of celiac disease be attributed to intestinal gut damage alone? I am sure that you will have witnessed strong feelings from the defenders of 'celiac-disease-is-a-stand-alone illness'. For instance, read these two opposing comments from Facebook:
    A. "I find it hard to believe that gluten intolerant people (or gluten avoiders) are as strict as us who have celiac disease." B. "I am gluten intolerant (suspected Celiac but I refuse to eat gluten in order to be tested properly) … I am incredibly strict on what I eat." The world of gluten is not black and white! But there remains a tension between those who have "biopsy-proven" celiac disease, and those people who are "gluten-intolerant". However, there is a cross-over between gluten-sensitivity/intolerance and celiac disease. There is no sharp dividing line – there is lots of grey!
    I would like to see the support groups of both celiac disease and gluten sensitivity work together with a focus on their common ground. This is already happening in some countries. Both groups promote an accurate diagnosis and a strict gluten-free diet. But I call into question the accuracy of current diagnostic methodology.
    Another comment from Facebook is a good example of these blurred lines:
    "I had an endoscopy and I have some small intestine damage: increased intraepithelial lymphocytes, shortened villi and duodenitis. The gastroenterologist said I had gluten-sensitivity but because I was not celiac (wasn't Marsh stage 3a), he said that I didn't need to be quite as careful with gluten. But I know I am super sensitive - even a small piece of chocolate with gluten in it makes me sick for a few weeks. I suspect that I either didn't have enough gluten before the endoscopy, or I am in the early stages of developing it."
    This is what I conclude:
    Both groups (people with celiac disease, and people with gluten sensitivity/intolerance) come under the umbrella category of gluten-related disorders. The term non-celiac gluten-sensitivity (NCGS) excludes those with evidence of intestinal damage from gluten. But with time and continued gluten ingestion, some of these people will develop celiac disease. NCGS is part of the gluten-related disorders spectrum (see my book: www.glutenrelateddisorder.com). Both groups have an identical list of possible symptoms. They are both equally harmed by gluten. They are indistinguishable from each other without blood tests and/or endoscopy. For both groups, my recommendation is to be zero gluten. Avoidance of cross-contamination is crucial for everyone. Both groups can be exquisitely sensitive to gluten. Some celiacs experience no symptoms from gluten, making it more of a challenge for them to remain gluten-zero. Some gluten-sensitive people do not yet have overt symptoms but are developing an inflammatory state. Many people who are gluten-sensitive produce antibodies to gluten, AGA (anti-gliadin-antibodies). There is a large literature on this. AGA-positive people are more likely to develop gluten-illnesses. AGA tests are recommended in the Fasano paper the "spectrum of gluten related disorders", for the celiac and gluten sensitivity work-up (particularly for neurological disorders). I use them on a day-to-day basis in my Clinic, and so do many other practitioners. More wheat/gluten harmful proteins have yet to be identified. Early in the development of celiac disease, the person can have significant symptoms, and they may have elevated AGA antibodies, but they may have no evidence yet of intestinal damage. At this stage these two conditions are indistinguishable. How early can you diagnose celiac disease? Do you have to wait until there is substantial intestinal damage so that you can make the classic diagnosis with villous atrophy? Or do you keep on eating gluten until the damage has occurred? Or do you go strictly gluten zero and not know if you are gluten sensitive or have early celiac disease? The HLA gene (DQ2/DQ8) cannot be used as a casting vote. It is my recommendation to abandon gluten as early as possible and not wait until you have substantial intestinal damage, which may never heal. Not only is the gluten intolerant community (this includes celiac disease) confused about gluten-illness. Also, the medical fraternity is confused. The science and clinical issues are rapidly developing whilst most medical practitioners are still looking for the classic celiac with weight loss, malabsorption, and a bloated tummy (and are using an out-of-date simplistic algorithm). Many people request celiac tests of their GPs but are denied the test. The community is much more aware of gluten related disorder than medical practitioners. Yes, there are a lot of issues to think about. These gluten-illnesses are complicated to diagnose. My prediction is that increasing numbers of people will adopt a gluten zero diet. However, almost certainly it is much more than the substance gluten that is making us sick. It will take a long time to unravel all of these strings. Most people are after an easy answer, or a drug, or a vaccine. But I'm sure that it is going to become even more complicated as we learn more. These complexities do not show up in a simplistic algorithm.
    The way for an individual to solve this is to adopt a gluten-zero diet, lifelong.

    Yvonne Vissing Ph.D.
    Children and Gluten Freedom
    Celiac.com 05/03/2016 - How do you know when your child has gluten sensitivity, gluten intolerance, or celiac disease? If gluten issues run in your family and you know there is a predisposition to having problems with gluten in foods, then you may be alert to signs that it has been passed on to your child. But if you and your biological family members never had problems with it, then you're not expecting gluten to be an issue. Children arrive with a complicated genetic past that we may not always have the details about. We may not know the health history of the families of our child's other parent, or even sometimes our own. We may not know if anyone had reactions to gluten. Because celiac and gluten sensitivities can appear as chameleons, genes for it may be masked as other health issues. Parents may be a carrier and have no identifiable symptoms at all. People may have celiac disease without ever knowing it.
    It's complicated to raise a child. When they don't feel well, it's hard to figure out when their health problems are physical, emotional, social, or psychosomatic. When it comes to kids, having a belly ache is a common occurrence. So are a variety of symptoms that are linked to celiac disease or gluten intolerance or sensitivity, like headaches, fatigue, skin issues, depression, or GI track problems. When are signs pointing at the normal wear-and-tear of growing up—and when they are related to a syndrome like celiac disease? It takes a significant period of observation to figure this out.
    Celiac disease is regarded to be an immune-mediated enteropathy caused by a permanent sensitivity to gluten in genetically susceptible individuals. The North American Society for Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN) found that the prevalence of celiac disease in children between age two-and-a-half and age fifteen ranges from 1 in 80 to 1 in 300 children. This means that in a pediatric practice of 1,500 children there are probably between 5 and 20 children with diagnosed or undiagnosed celiac disease—and potentially a lot more if one adds in gluten intolerance or sensitivities. According to the National Foundation for Celiac Awareness, celiac disease is genetically based, so reactions to gluten are more commonly found in those who have a family history of this autoimmune condition. They collaborated on a multi-phase research project with people diagnosed with celiac disease and at-risk family members who remained untested. Celiac disease was found in 5 to 10 percent of the family members of persons who had been diagnosed with celiac disease. But people may have reactions to gluten yet not have celiac disease. Some may have gluten intolerance or be sensitive to it without being diagnosed with celiac disease, so the actual relationship of health problems potentially associated with gluten may be considerably higher. First and second-degree relatives have more of a risk of developing celiac disease than are more distant relatives. For instance, their research found that celiac disease can occur in about 1 in 22 among children and their parents or siblings. But in analyzing the child's relationship to aunts, uncles, nephews, nieces, cousins, grandparents, half-siblings who may have celiac, the number decreases to 1 in 39. Detailed results of their research can be found from the NFCA's Seriously, Celiac Disease campaign.
    In our family, Chris never knew he was predisposed to celiac disease until he hit his twenties. Celiac is sneaky—while it can occur within people at any age, sometimes it doesn't show up until people get a bit older. As a child, he grew up on sandwiches, cookies, macaroni and cheese, and Grandma's home-made bread. When he had a tummy upset, as good mom I'd bring him chicken noodle soup and saltines. I never knew about celiac disease. My family came from a long line of gluten aficionados. As he hit adolescence and his teen years, signs of gluten intolerance emerged, only we didn't know that's what they were. Few parents link together migraines, skin problems with belly upsets and food "allergies." Chris's doctor dismissed his symptoms as independent, routine growing-up conditions without putting all the pieces of the puzzle together to realize that they were actually all a part of a larger celiac syndrome. It was only when he took a road trip and visited his father's sister and his cousins that he learned about the family's predisposition to celiac. His grandma always had stomach problems, I recall. She lived at a time and place where regular folks living in small towns were simply unaware of conditions such as celiac. As the old saw goes, you can't know what you don't know. In hindsight, she clearly had gluten issues. The gene seems to have been latent in her children, but passed on to take more active forms into the next generation of Chris and his cousin. It's confusing, because one child in the family can have a severe case of celiac while a full-blood sibling may have no sign of it at all! If he hadn't taken that road trip and stopped to visit his aunt, he may never have known that he had celiac. Upon that realization, suddenly everything made sense. All of his erratic symptoms were actually a picture-perfect portrayal of someone with celiac disease!
    We learned a bit about the disease, went to the store looking for gluten-free foods and quickly began modifying his diet. Since his MD couldn't figure out what was making him feel so bad, and if cutting out gluten could make him feel better, we decided that was a course worth pursuing. He felt better immediately. He has never been officially tested for celiac disease, although that would probably have been a better course of action. At that point in time, we simply didn't know about the testing options.
    Testing options have improved significantly over the last decade. The diagnosis of celiac disease can be done with a biopsy of the small intestine mucosa. Blood or serological tests are also helpful but less definitive. The University of Chicago Celiac Disease Center finds that the serum anti-tissue transglutaminase (tTG-IgA) is a widely used antibody blood test for screening for celiac disease, as is a total serum IgA test. The total serum test bolsters the reliability of the tTG test. A newer version of an old anti-gliadin antibody test has been developed called DPG or deamidated gliadin peptides test. Tissue transglutaminase (TTG) measures, endomysial antibody (IgA antibody to endomysium EMA) are recommended by many experts, while formerly used antigliadin antibody tests (AGA) are not as widely used.
    About 95% of people with celiac disease have the HLA-DQ2 gene and most of the remaining 5% have the HLA-DQ8 gene. Genetic testing can determine if someone has one or both of these genes. If someone has the gene it means they are at risk of developing celiac disease, but it does not mean that you necessarily have it. A positive genetic test should be followed up with a celiac blood panel to determine if someone has celiac disease. Celiac disease experts recommend family member testing as a proactive approach to diagnosis and then follow up with tests every 2-3 years or if potential symptoms start to emerge. They note that it is possible for someone to initially have a negative test result, but then test positive years later. This is worthwhile to know when trying to figure out if a child has celiac disease or not. It also means that re-testing may be a necessary process, since both the child's body and the disease propensity may change over time.
    What are warning signs that a child may have celiac disease? According to the North American Society of Pediatric Gastroenterology, Hepatology and Nutrition and other celiac experts, there are both gastrointestinal and other symptoms to look for—symptoms that one may not logically associate with gluten. But remember that many of these symptoms may exist independently in children and have no relationship to having celiac disease at all! This is what makes trying to figure out whether or not a child has it extremely challenging.
    Once a determination is made that a child has celiac disease or is highly predisposed to be gluten intolerant or sensitive, changing the child's exposure to gluten in foods becomes of utmost importance. The problem is, most people aren't aware of gluten issues in general, and they particularly aren't thinking of it occurring in children. As Kay Chick (2014) describes in her article, there are many things that parents and teachers can do to proactively prevent problems in routine situations. She points out that many school cafeterias aren't equipped to safely serve children who have to go gluten-free. Most parents don't realize that making accommodations for children with celiac disease are assured under Section 504 of the Rehabilitation Act of 1973 and the Individuals with Disabilities Education Act; seventy-four percent of parents who participated in her study reported their children did not have a 504 plan or written into an Individualized Education Program (IEP) to help everyone make accommodations for their celiac disease. Children with celiac may also be eligible for services under the Individuals Disabilities Education Act (IDEA) if it has an impact on their ability to learn.
    Social events like birthday parties, camps, and field trips may expose children to gluten in foods and provide no alternatives for those who can't eat them. Sharing food is a common childhood occurrence, but an experience that leaves celiac kids out unless they are sure the food is safe. Going to another child's house to play or for a sleep-over may be an extra-big deal for a celiac kid. When the team goes out for a pizza party or ice cream cones after a game, the child with celiac has to be extremely careful. It helps enormously when adults and people in supervisory roles understand that when children need to avoid gluten, it is not because it is a choice—it is a health necessity. While a public awareness campaign to help people understand that there are children (and adults) who have to avoid gluten is underway, there's still a long way to go. Children need to learn self-advocacy skills to keep themselves healthy. This is sometimes hard to do when interacting with parents, teachers, and other adults who think that they understand the complications associated with needing to be gluten-free—and they actually don't.
    Going gluten-free doesn't have to be hard, but when it comes to children and youth, often it is. From identifying that celiac disease could be a problem, to diagnosing it, to addressing it in one's daily lifestyle, children are a special interest population. In order to help celiac children to live long and healthy lives, it begins with educating adults, most of whom will never have to personally go gluten-free. Speaking out on behalf of a celiac kid is an important thing to do. Adults in all professions need to learn what celiac is and how to institute celiac-safe strategies into their organizations. Even if they aren't affected, adults need to realize how their decisions and behavior may adversely impact children.
    Our youngest citizens count on adults to always be looking out for their best interests. Speak with your local schools, recreation groups, and youth-oriented civic organizations to make sure the leaders understand that the chances are high that they are serving children with celiac disease. Help them to understand that they should learn more about what it is, that they should make sure eating arrangements always take into consideration children with special dietary needs, and have food alternatives readily available. Every parent would expect the same concern and attentive care if their child had celiac. And as a community, aren't all children "our" children?
    For more information, see our book, Going Gluten Free (Norlights Press 2015). Yvonne Vissing has been appointed by the United Nations to be a Policy Chair for Child Rights, under the UN Convention on the Rights of the Child.
    Resources:
    Chick, Kay. The Educational, Social, and Family Challenges of Children with Celiac Disease: What Parents Should Know. 3/19/2014. Celiac.com Children's Digestive Health and Nutrition Foundation (CDHNF). www.cdhnf.org Diagnosis and Treatment of Celiac Disease in Children. Journal of Pediatric Gastroenterology and Nutrition. 2005; Volume 40, Number 1 (Jan): 1-19. National Foundation for Celiac Awareness. http://www.celiaccentral.org/ North American Society of Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN) http://www.naspghan.org//files/documents/pdfs/medical-resources/celiac/CeliacGuidelineSummary.pdf Raising Our Celiac Kids (ROCK). https://www.celiac.com/articles/563/1/ROCK-Raising-Our- celiac-Kids---National- celiac-Disease-Support-Group/Page1.html University of Maryland School of Medicine Center for Celiac Research http://glutendude.com/celiac/celiac-disease-symptoms/

    Betty Wedman-St Louis, PhD, RD
    Celiac.com 07/18/2016 - Dietary phosphorus occurs naturally in dairy foods, animal meats, and legumes but according to the Institute of Medicine, high levels of phosphorus can be a contributor to cardiovascular, kidney and osteoporosis disorders.
    While phosphorus is considered an essential nutrient, the increased amounts found in processed foods via additives like anti-caking agents, stabilizers and leavening agents or acidifiers does not have to be stated on the nutrition label. Individuals following a gluten-free diet need to consider the health implications of phosphates found in processed foods eaten regularly in their diet. Reducing carbonated beverages is the best way to reduce phosphorus levels in the diet. Extra attention needs to be paid to the ingredient statement on foods.
    Ingredient statements may include these declarations: tri-calcium phosphate, tri-magnesium phosphate, disodium phosphate, di-potassium phosphate. Just because the label states "natural" or "organic" does not mean it is a healthy food for daily consumption. Fresh is best!
    Here is a guide to where phosphates can be found in gluten-free processed foods:
    Baked goods- cake mixes, donuts, refrigerated dough (pyrophosphates are used for leavening and as a dough "improver") Beverages- phosphoric acid in colas (acidulant), pyrophosphate in chocolate milk to suspend cocoa, pyrophosphate in buttermilk for protein dispersion, tri-calcium phosphate in orange juice for fortification, tetra-sodium phosphate in strawberry flavored milk to bind iron to pink color Cereals- phosphate in dry cereals to aid flow through extruder, fortification of vitamins Cheese- phosphoric acid in cottage cheese to set acidification, phosphate in dips, sauces, cheese slices and baked chips for emulsifying action and surface agent Imitation Dairy Products (non-dairy products)- phosphate as buffer for smooth mixing into coffee and as anti-caking agent for dry powders Egg Products- phosphate for stability and color + foam improvement Ice Cream- pyrophosphate to prevent gritty texture Meat Products- tri-phosphate for injections into ham, corned beef, sausage, franks, bologna, roast beef for moisture Nutrition Bars & Meal Replacement Drinks- phosphates for fortification and microbiological stability Potatoes- phosphate in baked potato chips to create bubbles on the surface, pyrophosphate in French fries, hash browns, potato flakes to inhibit iron induced blackening Poultry- tri-phosphate for moisture and removal of salmonella and campylobacter pathogens Pudding & Cheesecakes- phosphate to develop thickened texture Seafood- tri-phosphate in shrimp for mechanical peeling, pyrophosphate in canned tuna and crab to stabilize color and crystals, surimi (crab/sea sticks) tri-phosphate and pyrophosphate as cryoprotectant to protein {surimi contains gluten and is not recommended for gluten-free diets] Hyperphosphate levels can contribute to muscle aches, calcification of coronary arteries and skeletal issues. Many food companies do not provide phosphorus analysis information because it is not required on the label but here is a representative sample of phosphorus levels in some commonly consumed on a gluten-free diet.
    Peanuts (1 ounce) 150 mg
    Yogurt (1 cup) 300 mg
    M&M Peanuts (1.74 oz pkg) 93 mg
    Rice Krispies Cereal (1 cup) 200 mg
    Dietary recommendations for an adult for Phosphorus is 800 to 1000 mg.

    Betty Wedman-St Louis, PhD, RD
    Vitamin K2 for Healthy Bones and Arteries
    Celiac.com 10/18/2016 - Vitamin K was discovered in 1929 and named for the German word koagulation with Herrick Dam and Edward A. Doisy receiving the Nobel Prize for their research in 1943. But Vitamin K is a multi-functional nutrient.
    Vitamin K1 or phyloquinone is found in green leafy vegetables like spinach and used by the liver for blood coagulation within 10 hours.
    Vitamin K2 or menaquinone (referred to as MK-4 through MK-10) comes from natto (fermented soybeans), organ meats, egg yolks, and raw milk cheeses. It circulates throughout the body over a 24 hour period and is synthesized in the human gut by microbiota according to the Annual Review of Nutrition 2009. Aging and antibiotic use weakens the body's ability to produce K2 so supplementation needs to be considered.
    The Rotterdam Study in the Journal of Nutrition 2004 brought into focus the role of K2 as an inhibitor of calcification in the arteries and the major contributor to bone rebuilding osteocalcin- NOT calcium supplementation that many health professionals had recommend. The study reports K2 resulted in 50 percent reduction in arterial calcification, 50 percent reduction in cardiovascular deaths, and 25 percent reduction in all cause mortality. K1 had no effect on cardiovascular health.
    Dennis Goodman, M.D. in Vitamin K2- The Missing Nutrient for Heart and Bone Disease describes why most western diets are deficient in K2. Dietary awareness of Vitamin K has focused on anti-clotting since warfarin was approved as a medicine (in 1948 it was launched by the Germans as rat poisoning) and President Eisenhower was administered warfarin following his heart attack. Little attention was paid to any other nutritional importance this essential fat-soluble vitamin could provide.
    Menaquinones (K2 or MK) are rapidly depleted without dietary intake of natto or animal sources needed for repletion which results in bone health issues, especially in menopause. Without it, the body does not use calcium and Vitamin D3 to activate osteoblasts to rebuild bone. Menaquinones cause cells to produce a protein called osteocalcin which incorporates the calcium into the bone. Without it, calcium moves into the artery wall and soft tissues of the body leading to hardening of the arteries and osteoporosis.
    The benefit of K2 is not new research. In 1997 Shearer presented the roles of vitamins D and K in bone health and osteoporosis prevention in the Proceedings of Nutrition Society. The Osteoporosis International meeting in New Zealand 2013 re-emphasized this nutrient's importance proclaiming the best treatment for osteoporosis is achieving a strong peak bone mass before 30 years old and increasing Vitamin K2 food sources in the diet throughout life.
    The richest food source of K2 is the Japanese fermented soybean natto, which is produced with Bacillus natto, a bacterium that converts K1 to MK-7. Fermented cheeses like Swiss and Jarlsberg contain Mk-8 and Mk-9 which can be converted to K2 at a 20 to 40 percent lower rate than from natto, but more appealing to the western taste buds. Grass-fed beef and egg yolks are the most common source of K2 in the American diet.
    For those who have not acquired a taste for fermented soybeans or natto, my nutrition mentor, Adelle Davis, had it right when she recommended eating liver once a week. Celiacs need to be sure that their diets include ample red meats, eggs and fermented cheeses or yogurt or else dietary supplementation with Vitamin K2 (MK-4) is recommended. Without it, bones can become soft tissues and arteries "turn to stone" or calcified.
    A Chart of Vitamin K levels in Foods can provide insight into food choices for menaquinone compared to Vitamin K1. It was adapted from Schurgers et al. Nutritional intake of vitamins K1 (phylloquinone) and K2 (menaquinone) in the Netherlands. J Nutr. Environ. Med. 1999.
     
    Food K1 MK-4 MK-7,8,9 Meats 0.5-5 1-30 0.1-2 Fish 0.1-1 0.1-2   Green Vegetables 100-750     Natto 20-40   900-1200 Cheese 0.5-10 0.5-10 40-80 Eggs (yolk) 0.5-2.5 10-25    
    The American Heart Association and many medical professionals who advocated no organ meats or red meat and egg yolks, deprived Americans of primary sources of Vitamin K2 which is essential for bone and cardiovascular health.

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