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    Michael Specter's Personal Perspective on Non-Celiac Gluten Avoidance


    Dr. Ron Hoggan, Ed.D.


    • Journal of Gluten Sensitivity Winter 2015 Issue


    Celiac.com 05/01/2015 - In his article titled "Against the Grain," published in the November 3, 2014 issue of The New Yorker, Michael Specter likens the Gluten and Allergen Free Expo to "a travelling medicine show" in the first paragraph (1). Just in case a reader was half asleep and missed the bias embodied in that phrase, Specter ends the same first paragraph with: "There was even gluten-free dog food." It's hard to miss the harsh, cynical tone, and it is a shame that he usurped the name of Melissa Diane Smith's informative book to title his invective.


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    What, we must wonder, is the source of his bias? He does offer some detailed explanations of the bond between glutenin and gliadin, and how carbon dioxide from the fermentation process is trapped as bread and other pastry rises, making light, fluffy bread and pastry. He has done some detailed, even impressive investigation into cooking with gluten. However, he also asserts that wheat-breeding practices haven't induced any changes that might explain the increased incidence of celiac disease since World War II. He then goes on to say: "But something strange is clearly going on. For reasons that remain largely unexplained, the incidence of celiac disease has increased more than fourfold in the past sixty years." Mr. Specter acknowledges that celiac disease is on the rise and, according to Specter, there have not been any major changes to the genetics of wheat that might explain this increase.

    This perspective appeared in a very prestigious, highly regarded publication—The New Yorker. Many people will believe these claims just because of where they were published. And here is the problem I have with that. Mr. Specter has the genetic information all wrong: Norman Borlaug was awarded a plethora of honors for his work in developing more than 6,000 new wheat hybrids, which included several strains of disease resistant, semi-dwarf wheat that increased per-acre yields by seven to ten fold, thereby leading to wheat independence in a number of third world nations. For these scientific accomplishments he was awarded the Nobel Peace Prize, the Presidential Medal of Freedom, and a Congressional Gold Medal. Several books have been written about Dr. Borlaug and his achievements, and several foreign governments, science academies, and institutions have bestowed him with awards, honorary degrees and memberships. Borlaug has even had streets, university wings, and assorted other places and artifacts named after him and has even been mentioned in popular television shows. He has been called the father of the "green revolution" and has enjoyed very widespread recognition for having been instrumental in saving many millions of lives through increasing the world's food supply in the form of wheat. It is my belief that this venerable and compassionate man of science deserved every honor that was bestowed on him (2).

    However, I also think that it besmirches Dr. Borlaug's memory when Specter dismisses all those genetic changes to wheat as a possible factor in "the growing number of cases" of celiac disease based on the statement by Dr. Donald Kasarda that he was unable to find "evidence that a change in wheat-breeding practices might have led to an increase in the incidence of celiac disease". One person's failure to find evidence for something does not prove the absence of that phenomenon. Mr. Specter also quotes Dr. Joseph Murray, the very popular and famous (at least in the gluten sensitive community) gastroenterologist at the Mayo Clinic, as an expert in wheat genetics, and quotes Dr. Murray as asserting that wheat genetics haven't changed much over the past fifty years. I'm skeptical that Dr. Murray would profess expertise in the realm of cereal grain genetics. Regardless of whether this is Mr. Specter's construct, or Dr. Murray did actually make this claim to expertise in wheat genetics and the assertion that little has changed in wheat genetics since World War II, the statement is at least incorrect when it comes to wheat genetics.

    The conundrum Mr. Specter has created by ignoring Dr. Borlaug's work sets up an article in which he attacks what he calls "gluten anxiety". He says that "nearly twenty million people contend that they regularly experience distress after eating products that contain gluten." The implication is clear. Mr. Specter would have us believe that these people are confused about changes to how they feel, and/or whether those changes resulted from switching to a gluten-free diet—apparently all twenty million of them are so confused that they now need Mr. Specter to lead them out of the darkness of their own self-delusion, and begin to appreciate that wheat, in its present genetic form, has been consumed for at least 10,000 years and it's "a staple food that has sustained humanity for thousands of years". I'd like to point out that the Levant, where wheat was first grown, was not host to all of humanity at that, or any other time. Many humans, after leaving Africa about 85,000 years ago, evolved in a variety of environmental niches where gluten grains have not been available until quite recently.

    And there are many genetic variations of wheat. Which ones, I wonder, is Mr. Specter saying have been with us for so long? Contrary to his assertions, it is this variability that serves as one of the greatest barriers to the development of genetic strains of wheat that are "safe" for consumption by people with celiac disease. Dr. Sachin Rustgi, one of the scientists who is trying to develop such a safe wheat also said that: "Different celiac patients are sensitive to different 'gluten' proteins (prolamins). If one feeds peripheral blood cells sampled from a patient or a small group of patients (from a specific geographical location) with gluten proteins derived from a wheat genotype, it is expected either to see a reaction (monitored by the production of interferon gamma) or no apparent effect. But in the latter case it does not mean that the wheat genotype is non-toxic to all celiac patients" (3). Since different proteins or protein fractions (peptides) are recognized by different celiac patients' immune systems, there is an enormous number of peptides and proteins that are potentially toxic to at least some people with celiac disease. Extrapolating from that point, people with non celiac gluten sensitivity may well be reacting to any of the proteins or derivative peptides from any of the multitudinous variants of wheat.

    Mr. Specter also makes the claim that: "Humans have been eating wheat, and the gluten in it, for at least ten thousand years." Yet the geneticist, Dr. Martin Richards, and his colleagues report that about three quarters of Europeans are descendants of hunter-gatherers, rather than the early farmers from the Levant (4). So a large majority of people of European descent have not been eating cereal grains for more than 10,000 years. Just how long they have been consuming them depends on where they lived in Europe, which may explain the variability in the frequency of celiac disease across Europe. It is worthy of note that incidence of celiac disease is particularly increased in Scandanavia, Scotland, and Ireland, where climate and topography combined to make cereal grain cultivation more difficult. Thus, one might reasonably interpret this to suggest that these populations experienced limited past exposure to these grains. It is only with modern transportation systems, combined with the abundant excesses of wheat made possible by the work of Dr. Norman Borlaug and many others, in addition to the erroneous belief that wheat is a healthy food, that we now have almost worldwide over-consumption of gluten grains. Increased consumption has led to the increased frequency of celiac disease in these relatively grain-naive populations.

    Much of the rest of the world's populations have only recently begun to eat these grains. Even in the lowlands of England, where grain cultivation is relatively easy and successful, these grains have only been there for the about the last 5,000 years. Worldwide exposure to these grains varies somewhere between several thousands of years to less than 100 years. And what data supports the notion that even 10,000 years is sufficient time for humans to make the complex adaptation to eating them? Dr. Marlene Zuk has implicitly made such a claim, through reporting on much more rapid adaptations to adult consumption of dairy products (5). However, since we are mammals, and are almost universally able to consume human milk as infants, the adaptation required for the digestion of lactose into adulthood is, comparatively speaking, quite minor. Still, more than two thirds of the world's populations are unable to do so. Mr. Specter's resistance to recognizing gluten as a dietary hazard appears to be rooted in bias, rather than a thoughtful examination of the relevant data.

    It also appears that Mr. Specter either failed to learn, or failed to mention, that humans do not have the necessary complement of digestive enzymes needed to break some of the bonds between amino acids in the storage proteins of gluten grains, so we can fully digest them (6). Surely, if we were fully adapted to eating them, we should be able to digest these proteins.

    Nonetheless, Mr. Specter repeatedly disparages and dismisses the disease entity of non-celiac gluten sensitivity, and goes on to say: "The most obvious question is also the most difficult to answer: How could gluten, present in a staple food that has sustained humanity for thousands of years, have suddenly become so threatening?" Of course, this question is only difficult to answer if one ignores the many genetic manipulations of gluten grains and a substantial body of medical research into a variety of human ailments.

    For instance, Dr. Curtis Dohan and his colleagues were the first to publish a report on the connection between some cases of schizophrenia and gluten grains titled "Relapsed schizophrenics: more rapid improvement on a milk- and cereal-free diet" in 1969 (7). This research was conducted in a locked psychiatric ward. Similarly, seven years later, Singh and Kay followed with publication of an affirming research report that, using a different study design, identified wheat as a pathogenic factor in some cases of schizophrenia (8). This work was also conducted in a locked ward where total control of the patients' food intake could be controlled. Further, neither of these reports asserted a connection between celiac disease and schizophrenia. Over the following two decades, several reports, based on sloppy, poorly designed research, were published in the medical literature, and the notion that gluten grains could be a factor in schizophrenia was quickly forgotten. Mr. Specter would have been pleased with these latter reports. Another critic of Dr. Dohan's work, Dr. Donald Kasarda, a cereal scientist at the USDA, was quite happy to make statements such as: "Dohan wasn't much of a scientist" (9). Yet it was this same individual, Don Kasarda, whose name appeared as one of the authors of a report that asserted that a subset of schizophrenic patients mount a novel immune reaction against gluten (10). Dr. Dohan and his colleagues discovered a disease process, and an effective treatment for it, forty years ahead of the group that Dr. Kasarda worked with. Yet the earlier work was unscientific—until the publication of the work led by Dr. Samaroo, with contributions from Dr. Kasarda. Did Dr. Dohan suddenly become competent? Or is there another, more reasonable explanation? I don't understand the contradictions here.

    I'm also struggling to understand Mr. Specter's quoting Dr. Kasarda in his attack on non celiac gluten sensitivity. After all, Dr. Kasarda was one of the authors who published the report of non celiac gluten sensitivity in a subset of schizophrenic patients.

    On another front, Dr. Marios Hadjivassiliou and colleagues have been reporting, over the last twenty years, on celiac disease and non-celiac gluten sensitivity in connection with a variety of neurological diseases. These include depression, cerebral palsy, neurological dysfunction, alcohol induced cerebellar degeneration that results in gluten sensitivity, ataxia, ganglionopathy, a gluten induced condition that mimicks amyotrophic lateral sclerosis, inflammatory myopathy, chorea, headaches, balance disturbances, and neuromuscular disorders. They have also reported that antibodies against one of the protein families in gluten are found in the brain (IgG class anti-gliadin antibodies) and they also attack brain tissues (11). Others have reported connections between gluten and seizure disorders in non-celiac gluten sensitivity (12), and cerebral calcifications with seizures (13). Further, several forms of gluten induced brain damage have been reported in the context of celiac disease, which suggests a similar dynamic for those with non-celiac gluten sensitivity and brain damage. Gluten induced brain disorders include headache/migraine, attention-deficit/hyperactivity disorder, epileptic seizures, mental retardation, cerebellar ataxia and behavior disorders (14) in the context of celiac disease. Any and all of these may also suggest a similar dynamic for those with NCGS.

    I have worked with learning disabled students who have shown remarkable recoveries on a gluten-free diet, similar to those described by Alexandra Blair, in her 2003 Times article about dyslexic children who improved enormously on a gluten-free diet (15). Unfortunately, these data were not published in the peer reviewed literature, so they are unlikely to persuade researchers to investigate this matter further. Nonetheless, given the data on gluten's impact on neurological and brain tissues, it does seem very possible that many learning disabilities are, at least partly, the result of non-celiac gluten sensitivity, and that they may benefit from gluten avoidance. Time and space limitations prevent me from exploring the research that identifies the psychoactive properties of protein fractions in wheat, first identified by Christine Zioudrou et al, in her 1979 publication (16), or the Hudson and colleagues' report in 1976 showing that a single subgroup of gluten proteins, called gliadins, are toxic to any of a wide variety of human cells (17). Yet Mr. Specter, calling it "gluten anxiety" would have us dismiss all of this and much, much, more peer reviewed research that identifies gluten as toxic to many people who do not have celiac disease.

    It has never been clear to me why people such as Mr. Specter are quite willing to attack new ideas and discoveries that others have made on their quest for improved health. The attackers seem to want to mock those of us who have found an answer for ourselves. He interviewed several people, whom he quoted in his article, who were just convinced that they felt better when avoiding gluten. Mr. Specter derides those gluten sensitive individuals who were generous enough with their time to allow him to interview them, apparently at the Gluten Free Expo he attended, then compared with "a travelling medicine show". It is difficult to tell whether Mr. Specter was making news or reporting it when he interviewed these people.

    Please recall the fall issue of the Journal of Gluten Sensitivity, in which I explored the flaws of the research by Dr. Biesiekierski and colleagues in Australia (18). Mr. Specter cites Professor Gibson, one of the authors of the same study, as one of his sources for discrediting the notion of non-celiac gluten sensitivity. Mr. Specter goes on to present himself as having a superior insight into the issue of non-celiac gluten sensitivity, attacking Dr. William Davis, cardiologist and author of the popular book, Wheat Belly (19), and Dr. David Perlmutter, a neurologist and author of the similarly popular book, Grain Brain (20). Are we to ignore the now thousands of researchers whose peer reviewed reports are now characterizing non-celiac gluten sensitivity as a disease entity? And should we ignore the scores of popular books asserting the same thing? Or should we ignore Mr. Specter and the flawed research from Australia? I know what I'm going to do.

    Sources:

    1. Specter M. Against the Grain. The New Yorker. Nov 3, 2014.
    2. http://en.wikipedia.org/wiki/Norman_Borlaug
    3. Adams S. Discussion with Assistant Research Professor Sachin Rustgi on the genetic modification of wheat to make it safe for celiacs. Journal of Gluten Sensitivity. 2014; 13(2): L11-14.
    4. Richards M, Macaulay V, Hickey1 E, Vega1 E, Sykes B, Guida V, Rengo C, Sellitto D, Cruciani F, Kivisild T, Villems R, Thomas M, Rychkov S, Rychkov O, Rychkov Y, Gölge M, Dimitro D, Hill E, Bradley D, Romano V, Calì F, Vona G, Demaine S, Papiha S, Triantaphyllidis C, Stefanescu G, Hatina J, Belledi M, Di Rienzo A, Novelletto A, Oppenheim A. Tracing European Founder Lineages in the Near Eastern mtDNA Pool. American Journal of Human Genetics, 2000; 67; 5: 1251–1276.
    5. Zuk M. Paleofantasy. Norton, NY: 2013.
    6. Kagnoff M. Diagnosing Celiac Disease. CSA/USA, Seattle, WA., Oct. 3-5, 1997.
    7. Dohan F, Grassberger J, Lowell F, Johnson H, Arbegast A. "Relapsed schizophrenics: more rapid improvement on a milk- and cereal-free diet" British Journalof Psychiatry. 1969; 115: 595-596.
    8. Singh M & Kay S.: 1976, "Wheat gluten as a Pathogenic factor in Schizophrenia" Science. 1976: 191; 401-402.
    9. Kasarda, D. private communication.
    10. Samaroo D, Dickerson F, Kasarda DD, Green PH, Briani C, Yolken RH, Alaedini A. Novel immune response to gluten in individuals with schizophrenia. Schizophr Res. 2010, May;118(1-3):248-55.
    11. Hadjivassiliou M1, Mäki M, Sanders DS, Williamson CA, Grünewald RA, Woodroofe NM, Korponay-Szabó IR.Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia.Neurology. 2006 Feb 14;66(3):373-7.
    12. Bruni O, Dosi C, Luchetti A, Della Corte M, Riccioni A, Battaglia D, Ferri R. An unusual case of drug-resistant epilepsy in a child with non-celiac gluten sensitivity.Seizure. 2014 Sep;23(8):674-6.
    13. Calvani M Jr1, Parisi P, Guaitolini C, Parisi G, Paolone G.Latent coeliac disease in a child with epilepsy, cerebral calcifications, drug-induced systemic lupus erythematosus and intestinal folic acid malabsorption associated with impairment of folic acid transport across the blood-brain barrier.Eur J Pediatr. 2001 May;160(5):288-92.
    14. Diaconu G, Burlea M, Grigore I, Anton DT, Trandafir LM Celiac disease with neurologic manifestations in children. Rev Med Chir Soc Med Nat Iasi. 2013 Jan-Mar;117(1):88-94.)
    15. Blair A. Wheat-free diet gives food for thought. The Times. (of London) June 12, 2004.
    16. Zioudrou C, Streaty RA, Klee WA. Opioid peptides derived from food proteins. The exorphins. J Biol Chem. 1979 Apr 10;254(7):2446-9.
    17. Hudson, D., Purdham, D., Cornell, H., Rolles, C. Non-specific cytotoxicity of wheat gliadin towards cultured human cells. The Lancet February 14, 1976. 339-341.
    18. Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology. 2013 Aug;145(2):320-8.e1-3.
    19. Davis W. Wheat Belly. Rodale Inc. NY, 2011.
    20. Perlmutter D. Grain Brain. Little, Brown & co. NY, 2013.
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    Guest linda lavine

    Posted

    I think Dr. Kasarda mentioned an isolated gluten byproduct that is often added to processed foods, and could account for some of the rise in gluten problems. This byproduct had clearly increased during the relevant time frame.

    Do you know anything about this? I wish I recalled the name.

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    Guest Carol Sidofsky

    Posted

    I always suspect an unholy connection between wheat, rye, and barley farmers and others ($$$), and so-called "scientific" nonsense so-called evidence, that it's just a gluten phobia, causing folks to want to avoid eating glutenous foods.

     

    Intelligent gluten-sensitive people (both celiacs and non-celiac gluten sensitive folks) are smart enough to AVOID gluten, and they should be PRAISED, not ridiculed!!!

     

    See Dr. Kenneth Fine (MD), Dallas, TX gastroenterologist's

    "EnteroLab" website, that goes deeply below the surface, regarding all types of gluten sensitivity. Here are 2 helpful links:

    www.finerhealth.com AND www.enterolab.com

     

    I was also told by a nice lady working at EnteroLab, that if a person suspects that he or she (or their child, etc.) might get "false negative" results from EnteroLab's stool sample testing,

    because the child (for example) might have an "IgA deficiency", that there is a blood test that can tell a person if he or she DOES have an "IgA deficiency". If a person DOES have an IgA deficiency, that person could easily come out "false negative" on the stool sample testing, even if she or he really IS gluten sensitive!

     

    That blood test, is called "Total Secretory IgA" blood test.

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    Guest C J Russell

    Posted

    More and more people are being diagnosed as celiac sufferers or as having a sensitivity to gluten. That's a fact. But is that because of recently developed strains of wheat? I seriously doubt it. I find it more likely that more people are being diagnosed because these diseases, allergies, sensitivities are more well known. Per an article by Stefano Guandalini, M.D and published by The University of Chicago Celiac Disease Center, although the symptoms have been known for thousands of years, it is only recently that a definite cause was found. Previous generations knew that the symptoms could be avoided by changing the diet, but they didn't have a clear understanding of why changing the diet helped. You can read the article at cure celiac disease dot org, A Brief History of Celiac Disease. I believe that there are more cases of celiac identified because we now have a name and a way to test for it.

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    Dr. Ron Hoggan, Ed.D.
    Celiac.com 07/30/2009 - Here is Dr. Ron Hoggan's response to Slate's unfortunate article "Throwing Out the Wheat" which was written by Daniel Engber:
    Dear Mr. Engber,
    You represented Dr. Fasano as saying:
    “For every patient whose intestinal biopsy turns up positive, he says, nine or 10 more test clean but commit to going gluten-free all the same.”
    This ratio is well established in the medical and scientific literature. The rate of gluten sensitivity, as measured by IgA and IgG antibodies against gliadin, (a protein family that is a sub-group of gluten) constitutes about 10% to 12% of the general population.  That is about ten times the rate of celiac disease found in the general population.
    These anti-gliadin antibodies (AGA) clearly demonstrate that gliadin proteins or derivative peptides are reaching the bloodstream and sensitizing the immune system to this foreign (non-self) protein.  Many of these gluten sensitive individuals experience all of the same signs and symptoms as celiac patients.
    Similarly, you state: “Since there's no way to "prove" a case of gluten-intolerance in the lab...”
    This is grossly inaccurate. Although many practitioners will state that AGA are non-specific, I doubt that any of them would argue against the statement that the presence of AGA clearly indicates that gliadin or its fractions have managed to get into the bloodstream. When they say AGA are non-specific, they simply mean that these antibodies are not associated with any specific disease. They seem to be found in a wide range of autoimmune diseases, cancers, and behavioral/psychiatric disorders.
    You also say: “If you're paying more attention to what you eat, there's a good chance your symptoms will lessen. That's not because gluten or red meat or another food is damaging your small intestine; it's because eating less makes it easier for your gut to recover.”
    This assertion is based on a flawed assumption. Gluten-free foods are much more calorie-dense than those made with gluten. Thus, a common mistake made by those beginning a gluten-free diet is to eat about the same quantities they are used to eating. For instance, if one is in the habit of taking two sandwiches in their lunch, they are likely to pack two gluten free sandwiches. Since the gluten-free bread is much more nutrient dense. Increased nutrient densities apply to pasta, baked goods, and almost all gluten-free substitutes. Thus, the switch to eating a gluten-free diet usually leads to eating less, not more, as you claim in the above statement.
    Later you state: “Chances are you'll have reduced your total intake of carbs, and thus the amount of α-amylase in your gut.”  For the reasons stated above, this is also inaccurate.
    You go on to say: “In other words, the mere fact of being on a gluten-free diet could make you more sensitive to grains and cereals—which would only reinforce your conviction that you're gluten-intolerant.”
    I am not aware of any data indicating a reduction of alpha almylase in the context of a gluten free diet. I would be amazed if you can find any such data. It reflects an assumption about the production and function of amylase that appears indefensible to me.
    The low carb craze has followed a very different path to the media, and began with a fellow named Banting in the 1800s whose doctors suggested a low carb diet to him as a means of losing weight. It worked, and he published a pamphlet about it. It saw a resurgence in the form of a ketogenic diet in the 1920s, at Johns Hopkins, as a treatment for epilepsy. Subsequent development of anti-seizure medications during the 1930s left the treatment without any patients, so it was abandoned until 1997 with the airing of First Do No Harm, a movie about one child’s plight and his parents’ struggle to find a treatment for his life threatening seizures.
    Meanwhile, research suggested that the growth of insulin sensitive tumors might be stalled by a ketogenic diet, and various case reports and subsequent clinical trials both support that perspective and indicate that most folks won’t maintain such a boring diet.
    The gluten-free diet was suggested by a concerned mom in 1932 and it was fully 18 years before Dr. Willem Karel Dickie’s doctoral thesis would be accepted and the world would begin to treat celiac disease with a gluten free diet.
    I won’t bore you with the details of this evolution but there are many twists and turns to the story of gaining acceptance of a gluten-free diet for the effective treatment of celiac disease.
    Both of these developments occurred quite separately. The two things they have in common are:
       1. They both gained popular notice and support through the Internet, and;
       2. They both defied conventional medical wisdom when they were first considered.
    Your graph simply identifies the impact that the Internet has had on democratizing health care.
    Your ill-informed attack on a gluten free diet is regrettable because it suggests it is a fad diet rather than a therapeutic one. At best, that will make it more difficult for people to get cooperation when trying to look after their own health by avoiding gluten. At worst, it will dissuade people from sticking to their diets if they believe your false assertion that gluten sensitivity cannot be identified in a lab. It can be, and is, on a very regular basis. 
    Your information on celiac disease was mostly well researched and solid, but you clearly did not put any thought or effort into finding out about gluten sensitivity (often called gluten intolerance). I wish you would correct some of this misinformation, as it is really misleading and potentially harmful.

    Daniel Engber responded to the above email insisting that “it's impossible to prove gluten intolerance in the lab.” And that “Many of the strongest advocates for those with this condition describe it as one that can only be diagnosed by process of elimination.  Or, to be more specific, by an elimination/reintroduction test.”
    He also challenged me asking if
    “All those who have AGA are gluten-intolerant?”

    Then he said that he just doesn’t believe it. 

    Here is my reply:
    July  31, 2009
    Hi Daniel,
    Thanks for your response.
    I don't know who these "strongest advocates" are, but your information about elimination/reintroduction testing being the only way gluten sensitivity is absolutely inaccurate. Check with any reputable blood testing lab that does IgA and/or IgG anti-gliadin antibody testing. They will set you right on this score.
    The presence of AGA in the bloodstream is clear, incontrovertible evidence that the body is mounting an immune response against gluten. This antibody reflects a delayed-type food sensitivity that is sometimes erroneously called an allergy.  This is gluten sensitivity. It may be transient, chronic, or permanent, but there can be no doubt that it reflects the condition that is referred to as gluten intolerance. Not everyone who is gluten sensitive will show these antibodies but, yes, everyone who shows these antibodies is gluten sensitive. It is a basic principle of immunology that elevated selective antibodies reflect prior or current exposure of these antigens to the bloodstream.
    You must have spoken with Alessio Fasano to get that quote. Just ask him about AGA testing. He will tell you the same thing I'm telling you. I have discussed these and related matters with him at some length.
    I think you are mistaken in your claim that you linked to anything that Joe Murray said. I'll be very surprised if he has said anywhere that a gluten-free diet leads to eating less (although he has repeatedly said it can cause weight loss in the context of celiac disease). Could you tell me where this link appears?
    Nonetheless, even if the volume of food consumed is less (more on that in a moment) the increased caloric density would very likely be offset by the significant increase in caloric density of gluten-free foods. While Dr. Murray has treated and spoken with many more celiac than I have, I'd be willing to wager that I have observed many more of them while eating. :-)
     
    Apparently I misunderstood your thesis. I took you to say that public awareness of low-carb/Atkin's dieting and gluten sensitivity followed a largely parallel path because they are both pop culture trends that reflect a kind of hysteria about nutrition that is not based on science. Thus, I offered some data showing that the rise in public awareness of these two nutritional perspectives are based on scientific insights and the rapid increase of public awareness of these issues in 2004 and 2006-2008 was probably the result of improved access to information on the Internet in combination with scientific discoveries during those periods. I should have detailed the discovery and development of serological tests for celiac disease and gluten sensitivity as well as the research that began to reverse the vilification of saturated fats at about the same time.
    (snip)
    The vast majority of those eating a gluten-free are eating a very high carb diet. On this issue your article is quite misled and misleading. Please take the time to respond again, as I am most interested in that link to Joe Murray's comments. I also urge you to look at the significance and nature of AGA serum antibodies. Gluten sensitivity is readily demonstrated by these simple blood tests.
    Best Wishes,    
    Ron
     

    Monday, August 03, 2009 4:50 PM
    Dan replied admitting that he had not, after all, linked to an article by Joe Murray. The link he apparently intended to put in was the following: http://www.montanaceliacsociety.com/physiciansmanual.htm
    I responded with the following message:
    Mon 8/3/2009 9:02 PM
         
    Hi Dan,
    I gave you the wrong url. Please try this one:
    https://www.celiac.com/gluten-free/index.php?showtopic=60511
    I'm wondering how you can continue to assert "it's impossible to prove gluten intolerance in the lab" when I have given you ample information to the contrary as well as directing you to blood testing labs (Great Smokies, Immuo, Imco Diagnostics, etc. etc.) that will verify my assertion. There is also a wealth of information in the peer reviewed medical literature supporting what I'm saying. I'd be happy to provide a list of relevant research reports if you are interested.  
    You don't mean to suggest that this quote from Joe Murray somehow justifies your above assertion do you? Just pick up a telephone and give him a call. I'm very confident that he will not support your notion that gluten sensitivity cannot be identified in the lab. Do remember that Dr. Murray is a sub-specialist in celiac disease. He may not be a big fan of assertions of non-celiac gluten sensitivity, but he won't deny that the AGA blood tests establish immune sensitization and hence, gluten sensitivity. Rodney Ford and Marios Hadjivassiliou are a couple of other world renowned researchers who are reporting AGA as a significant marker of serious disease in the absence of celiac disease.
    Your assertion that "it's impossible to prove gluten intolerance in the lab" was the lynchpin of your entire article. Without it, you may have to acknowledge that you have just discredited a group of people who, on the basis of solid science, are trying to improve their health. Yet you have set back their relationships with skeptical family members and friends based on your inadequate research.
    I really do think that you owe these people a retraction or at least a statement that mitigates some of the damage your article is doing. 
    Sincerely,
    Ron

    Tuesday, August 04, 2009 3:14 AM
    Dan responded saying that  he thought we were having a semantic argument.  It became clear to me that he was confusing gluten sensitivity with gluten sensitive enteropathy – which is another name for celiac disease. He thought I was talking about latent  celiac disease.

    He insisted again that gluten intolerance is not defined by any standard such as celiac disease is. He went on to say: 
    “If you want to define "gluten intolerance" and/or "gluten sensitivity" so it applies to some subgroup of those who suffer from symptoms related to gluten, that's fine with me.  I'm using the phrase "gluten intolerance" to describe all those who experience relief from the gluten-free diet without having been diagnosed with celiac.”
    I responded with the following:
    From: Ron Hoggan, Ed. D.
    Tue 8/4/2009 11:01 AM
    To: Daniel Engber
    Subject: RE: Throwing Out the Wheat
    Hi Dan,
    It sounds like you may be confusing gluten sensitive enteropathy with gluten sensitivity. The former is a descriptive name for celiac disease, while the latter indicates an immune system sensitized to gliadin.
    Selective antibodies are produced in response to foreign proteins or peptides that have breached a barrier (skin or mucosal) and are now present in the bloodstream or imbedded in self tissues. The immune system reacts as if these foreign proteins were bacterial invaders. (In fact, they are cytotoxic and neurotoxic but that is not at issue here (1, 2). If there was only one event during which gliadin proteins or peptides reached the circulation, as might be the case during a bout of flu, for instance, AGA levels usually diminish quite quickly. Thus, when a person shows elevated levels of AGA, the condition is usually chronic. It indicates that they are leaking gliadin proteins and/or peptides into the bloodstream. Celiac disease only afflicts between 10% and 15% of these people with elevated AGA. Serological tests for celiac disease identify endomysium antibodies (EMA) and tissue transglutaminase (tTG). There is no debate about the foregoing. It is common knowledge and is accepted by the vast majority of researchers and practitioners working in this area.
    The controversy comes in when we ask what elevated AGAs mean. Many claim that it is a non-specific finding. That is, AGAs are not diagnostic for celiac disease or any other currently recognized disease. They are much more common among those with autoimmune diseases, AIDS, and several other groups, but they do not provide any clues that will help diagnose a particular illness. AGAs are also found in some apparently healthy individuals. The only condition for which they fairly specific is what is often called a "leaky gut". However, most practitioners do not recognize increased intestinal permeability as a disease entity. There is no debate regarding the connection between elevated AGAs and leakage of gliadin into the body. In the past, the debate has been about whether AGAs are diagnostic for any disease and whether a leaky gut is an issue of any real concern.
    However, in the late 90s, researchers at U. Maryland, working to develop a cholera vaccine, found a protein messenger called zonulin. As its presence increases in the intestinal lumen, it relaxes the tight junctions between gut epithelial cells (3). Zonulin is overproduced by some individuals in response to gluten ingestion. It turns out that those with celiac disease, type 1 diabetes, and a variety of autoimmune diseases are particularly inclined to produce excessive quantities of zonulin in response to gluten ingestion (4).      
    Similarly, Marios Hadjivassiliou and his neurological research group at the Royal Hallamshire Hospital in Sheffield have found that AGA are elevated in more than half of all patients with neurological disease of unknown origin and only about a third of those have celiac disease. The remaining two thirds are simply gluten sensitive, as identified by AGA (5). 
    Variation in zonulin production, from one individual to another, is likely the factor that determines gluten sensitivity.
    Gluten sensitivity does not identify celiac disease, latent celiac disease, or any other enteropathy that I'm familiar with. It identifies an immune system sensitized to gluten. Avoidance of gluten in such cases can help to avoid developing additional autoimmunity, just as it sometimes does in celiac disease, but current evidence suggests that it will usually not reverse it once that autoimmunity has begun.   
    The use of Rodney Ford's term "gluten syndrome"(2) might well have saved us considerable cyber ink, as we might have been able to begin by disagreeing about the value of a gluten free diet across the gluten syndrom spectrum, rather than taking several emails to determine that you were equating gluten sensitivity with celiac disease.
    Best Wishes,
    Ron
    Sources:
    Paganuzzi AS, Zucco F, Cardelli M, de Angelis I, Mattei R, Pino A, Rocca E, Zampaglioni F.Cytotoxic effects of wheat gliadin-derived peptides.Toxicology. 1985 Dec;37(3-4):225-32. Ford RP.The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29. 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. Visser J, Rozing J, Sapone A, Lammers K, Fasano A.  Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Ann N Y Acad Sci. 2009 May;1165:195-205. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A.  Does cryptic gluten sensitivity play a part in neurological illness?  Lancet. 1996 Feb 10;347(8998):369-71. Clemente MG, De Virgiliis S, Kang JS, Macatagney R, Musu MP, Di Pierro MR, Drago S, Congia M, Fasano A. Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function.Gut. 2003 Feb;52(2):218-23.  
    Note:
    I should have added that since Dan was using the phrase gluten intolerance “to describe all those who experience relief from the gluten-free diet without having been diagnosed with celiac,”  he has defeated his own argument. If a person has symptoms and they get relief from a gluten free diet, they would have to be pretty self destructive, foolish, or self-indulgent to go back to eating gluten.

    In a private email I received from another person, he said: “After reading his original article I had the distinct feeling that a girlfriend of his (or friend/relative) had gone on a gluten-free diet and had recently dumped him--maybe because he wasn't so supportive of this change...but I don't have any proof... ”

    I am most inclined to agree with this poster’s suspicions.

    Finally, I forwarded a copy of the letter titled: “Is gliadin really safe for non-coeliac individuals? Production of interleukin 15 in biopsy culture from non-coeliac individuals challenged with gliadin peptides” by D Bernardo1, J A Garrote2, L Fernández-Salazar3, S Riestra4, E Arranz5 from  Gut 2007;56:889-890; doi:10.1136/gut.2006

    These investigators report that “gluten elicits its harmful effect” on all the individuals they studied, not just those with celiac disease. I believe that Jefferson Adams has written a detailed account of this research that appears elsewhere on celiac.com. 

    Although Mr. Engber declined to give me permission to publicly post his emails, and hence, his side of this discussion, I have invited Dan to respond to the above on celiac.com, as I would like to give him every opportunity to either provide some evidence to support his unfortunate claims about non-celiac gluten sensitivity, or to retract his damaging comments in the original article he penned. Although I have been a little rough on him, I do hope he will present his side of this debate, as it is of great importance to many individuals who must negotiate with friends and relatives to safeguard their health.

    These people would not dream of casually scattering rat poison on food to be served to a loved one. However, they seem to feel imposed upon by those who are gluten sensitive, because they do not want gluten scattered on their food. This attitude is just as inappropriate and sometimes, just as dangerous as scattering rat poison on food. 

    Sincerely,
    Ron Hoggan
     
     
     
     

    Scott Adams
    Celiac.com 05/17/2010 - Scott Adams and Ron Hoggan went on live radio last Saturday on the Love By Intuition Show with host Deborah Beauvais (Dreamvisions 7 Radio Network) in support of Celiac Disease Awareness Month. The show is broadcast live from Boston, MA on 1510 AM Revolution Boston, a progressive 50,000-watt station reaching 5 states locally, and on Energy Talk Radio in San Francisco, and it reaches over 1,000,000 listeners. The show will be re-broadcast several times and will hopefully reach many more listeners. The podcast is attached and can be downloaded or listened to from our server.
    Dreamvisions 7 Radio Network is holistic healing radio network with an eclectic group of radio hosts all with the common goal to help humankind by offering different modalities or programs combined with tools to bring awareness, joy and love to their listeners. Their vision is to continue to syndicate the Network of shows by having additional affiliates both terrestrial and Internet.



    Jefferson Adams
    Celiac.com 03/21/2012 - What do Zooey Deschanel, Keith Olbermann and Billy Bob Thornton have in common with tennis stars Novak Djokovic and Andy Murray? They are all eating gluten-free.
    Cases of celiac disease have quadrupled in the past 60 years, according to recent research. As the number of people diagnosed with celiac disease and gluten sensitivity continues to rise, so, too, does the of celebrities who avoid gluten due to celiac disease or gluten-sensitivity.
    It's not just major athletes, like tennis stars Novak Djokovic and Andy Murray, for whom sporting success requires peak conditioning and efficient nutritional uptake.
    The number Hollywood A-listers and other celebrities who have hoisted the gluten-free flag is rising, as well, and many are singing the praises of their gluten-free diet. Novak Djokovic, for example, credits his switch to a gluten-free diet to his rise to the top of his game, and near dominance in pro tennis events over the last year.
    A partial list of some noteworthy celebrities and athletes who reportedly follow a gluten-free diet due to celiac disease, gluten-intolerance, or other reasons include:
    pro quarterback Drew Brees, news anchor Heidi Collins, Katherine, Dutchess of Kent, news host Keith Olbermann, actor and writer Billie Bob Thornton, author Sarah Vowell, and actresses Zooey Deschanel, Susie Essman, Jennifer Esposito, Goldie Hahn, Gwyneth Paltrow, Emily Rossum, and Rachel Weisz.
    Let's not forget that first-daughter emeritus Chelsea Clinton's gluten-free wedding cake made quite a splash.
    So, with the growing awareness of celiac disease, and a rising interest in all things gluten-free, count on seeing more gluten-free celebrities and athletes in the news.
    And, before you roll your eyes, remember that increased awareness of celiac disease and the gluten-free diet are both upsides of high-profile athletes and celebrities touting a gluten-free diet.


    Jefferson Adams
    Celiac.com 02/27/2013 - Although about 1% of the US population, most of whom are undiagnosed, likely have celiac disease, people who have been officially diagnosed with celiac disease make up less than 0.1% of the population.
    However, 6-7% of the population have a wheat/gluten intolerance (confirmed or not) and buy gluten-free products, while a whopping 18% of shoppers surveyed said they buy gluten-free, for whatever reason, according to Packaged Facts.
    These higher percentages are part of what is driving the astronomical growth of the market for gluten-free products.
    In fact, according to the latest survey information by Packaged facts, the market for gluten-free products is growing even faster than anticipated, and is set to reach $6.5 billion in 2017. The question of when this growth will level out, and how strong the market will remain for gluten-free products once that happens remain to be answered.
    Answers to these questions will depend at least in part on the ability of product manufacturers to associate gluten-free products with healthier lifestyles and healthier eating. Meanwhile, manufacturers of gluten-free products are working hard to broaden the appeal of their products, in an effort to expand the gluten-free market even further.
    Until just a few years ago, most gluten-free products were sold by health food retailers, and even as gluten-free products expanded into conventional retailers, they tended to appear in the natural foods sections of those retailers. In fact, says Packaged Facts, mainstream retailers now account for about 79% of gluten-free sales, while the compound annual growth rate for gluten free products in the US retail market 2008-2012 is approaching 28%.
    According to SPINS, sales of gluten-free products were up 19% in the year to September 2012 in natural and conventional channels combined, while Mintel data shows that launches of new gluten-free products rose from 600 in 2007 to more than 1,600 in 2011.
    Meanwhile, Packaged Facts estimates that North America’s share of global gluten-free new product introductions has grown significantly in the past five years, and now stands at over 60%, ahead of Europe, which accounted for about one quarter of introductions. Packaged Facts' August 2012 survey of consumers who buy gluten-free products show that 35% feel that gluten-free products are "generally healthier," 27% bought gluten-free products to "manage weight," 21% said that gluten-free products are "generally low-carb," 15% bought for a member of the household with gluten or wheat sensitivity, while just 7% said they bought gluten-free products for a household member has celiac disease.
    According to Packaged Facts, the conviction that gluten-free is healthier is the top motivation for purchase. Why do consumers think gluten-free is healthier? In some respects, this should not come as a great surprise, given that many gluten-free products also happen to be all-natural, organic, and free from GMOs, artificial preservatives and other things many consumers are trying to avoid, says Packaged Facts.
    In fact, a number of food manufacturers work hard to create foods that can be marketed as healthy, with such tags as these from Ian's products: No Artificial Flavors, Colors, or Preservatives... EVER! No Hydrogenated Oil. No Trans Fats. No Refined Sugars. No Antibiotics. No Hormones. No Bleached Flours. No Tripolyphosphates.
    Jayne Minigell, director of marketing at Elevation Brands, which owns Ian’s, says that this approach is helping to create consistent double-digit growth, driving revenues to more than $30 million annually.
    At Udi’s, America's #1 gluten free bread and baked goods company wants people with celiac disease to feel like they are eating regular food, and to make everyone else feel like eating gluten-free foods is normal, according to marketing manager Regan Han.
    Do you eat gluten-free foods as part of a gluten-free diet? Do you regard gluten-free products as healthier than their gluten-containing counterparts? Do you think this growth is a good thing? Will it last?
    Sources:
    http://www.foodnavigator-usa.com/Market/The-rise-and-rise-of-gluten-free-But-can-the-meteoric-growth-continue http://www.pizzamarketplace.com/article/202685/Gluten-free-market-jumps-28-percent-in-four-years

    Sheila Hughes
    Celiac.com 05/22/2013 - Tragedy has struck the celiac community when an established author's life was taken while crossing a street in Calgary, Canada. She was a popular published author by the name of Wendy Turnball. She was made famous by her first book, Canadian Bestseller "Gems of Gluten-Free Baking."
    Wendy was diagnosed with celiac as an infant and was immediately put on a gluten-free diet. Physicians told her parents it was a childhood disease which she would outgrow. In her thirties infection reactivated her celiac symptoms.
    Wendy was passionate about baking gluten-free foods that could stand up to regular foods. She developed her very own whole-grain flours, which she called GEMS flour. She's left behind a gluten-free baking staple for celiacs everywhere to enjoy.
    Source:
    http://blogs.edmontonjournal.com/2013/04/30/best-selling-calgary-author-of-gluten-free-cookbook-dies-in-car-accident/

    Jefferson Adams
    Celiac.com 03/07/2014 - Our latest gluten-free celebrity news comes with word from eon line.com that actress Jennifer Esposito has sparked a bit of a dustup with Rachael Ray over an episode of Ray's 3 in the Bag that aired earlier this month on Food Network, in which Ray shared some favorite gluten-free recipes.
    Actress-turned-activist Jennifer Esposito called Ray out for failing to make any mention of celiac disease, and dubbed Ray's efforts a "wasted opportunity," for failing to mention celiac disease, gluten sensitivity or cross-contamination, adding: "Why be responsible?"
    Esposito also tweeted, "That would mean @rachaelray would have to understand what she is actually speaking about."
    Esposito also tweeted a link to a post in Gluten Dude's blog which slammed Ray.
    VIDEO: Get Jennifer Esposito's gluten-free pizza recipe!
    The former Blue Bloods star ended by tweeting: It's a shame that their r so many suffering at the hands of ignorance such as this."
    Esposito claims her doctor-advised 2012 medical leave from the show for celiac disease led to her suspension from the CBS series.
    Source:
    eonline

    Jefferson Adams
    Celiac.com 05/02/2014 - Depending on who is making the calculations, the market for gluten-free foods has either peaked, or will continue to rise over the next five years.
    According to Packaged Facts, the gluten-free (gluten-free) market has peaked. And in the past two years, it has failed to attract new users.
    Symphony IRI reports that growth rates of key label claims — organic, natural, and gluten-free — are leveling off.
    In the Executive briefing "What's In Store for Health & Wellness?" sales growth rates of products featuring several high-profile claims slowed in 2012.
    NPD reports that gluten free growth remains small. About 28 percent of adults 18 and older reported they are avoiding gluten, a scant one-percent increase since 2010.
    Some other interesting data that indicate that gluten-free food trends may be about to level include Hartman's report that 95 percent of consumers who followed a gluten-free diet admit they did not suffer from celiac disease or gluten intolerance.
    According to Mintel, 65 percent of gluten-free consumer think those foods are healthier, while 27 percent eat them because they believe they promote weight loss.
    The report notes that gluten-free sales levels will level and recede as this misinformation is corrected, and more consumers abandon their gluten-free diets.
    Read more at:
    Source:
    QSRWeb.com.

    Jefferson Adams
    Celiac.com 07/08/2014 - Gluten-free tennis superstar Novak Djokovic won his second Wimbledon title by outlasting the Swiss player, and seven-time champion, Roger Federer in five sets last Sunday.
    Up 5-2 in the fourth set, Djokovic was unable to capitalize at match point, but held on for a 6-7 (7), 6-4, 7-6 (4), 5-7, 6-4 victory at Centre Court.
    The championship returns the 27-year-old Serb to the world’s No. 1 ranking. Djokovic has seen his fortune improve since moving to a gluten-free diet, and credits his subsequent successes on court to his diet and to his mental conditioning.
    The rivalry between Djokovic and Federer has remained evenly balanced over the years. The two have faced each other 35 times, with Federer leading 18–17.
    They have faced off in a record 12 Grand Slam matches, including two finals, and a record nine semifinals.
    The win marked Djokovic's seventh Grand Slam title, ending a streak of three consecutive losses in major finals, and in five of his past six.
    Stay tuned for news on Djokovic’s progress, and on his gluten-free diet.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 07/07/2016 - Norelle R. Reilly, M.D., has offered several of her opinions regarding gluten-free diets in a commentary published in The Journal of Pediatrics, earlier this year (1). It is important to recognize the difference between this publication and a report of findings arising from a study. She didn't conduct a study. No ethical approval was cited or needed. Despite the inclusion of several tables and one graph, Dr. Reilly was only charting changes in the popular use of search terms between 2004 and 2015, on a single search engine, at Google.com. Her tables simply provide explanations of several acronyms and a structure for her opinions, which may suggest more substance than her beliefs warrant. She simply formed a set of opinions that may or may not be supported by the research and other reports she cited. After all, Dr. Reilly had to interpret those studies so we aren't hearing from the investigators who actually conducted that research. We are just learning her interpretations of that research. Her clinical experience may or may not have factored into the opinions she offers, but since she failed to cite any such experience it seems most unlikely. She has also lumped all gluten-free diets into a single entity, which she labels GFD and which also poses several problems as you will see shortly.
    Dr. Reilly has warned about the multiple hazards of the gluten free diet, especially for children. These hazards include its potential to cause harm due to its higher fat content, deficiencies in B vitamins and iron, as well as the increased costs of gluten-free food. She also points to social isolation and inconvenience as hazards of the gluten free diet, which would appear to include what she calls "a deterioration of their quality of life while on a GFD". She goes from there to say that the claim that "gluten is toxic" is a fiction for which there is no supporting evidence (1). She also says that those following a gluten free diet may be at greater risk from inorganic arsenic and/or mercury poisoning (1). She admonishes those who are at risk of developing celiac disease not to undertake a gluten-free diet "without first testing for celiac disease" and Dr. Reilly advises her readers that "there is no role for a GFD for children outside of treatment of celiac disease and wheat allergy" based on what she calls the "hazards" of this diet. She won't soon be going on my Christmas card list.
    As many Journal of Gluten Sensitivity readers have heard before (from me), our pre-human line of primates split from our common primate ancestor with the bonobo chimpanzee sometime between 5 and 14 million years ago, depending on what source you read. Unlike our omnivorous, primate cousins, we humans have thrived in a wide range of habitats and have populated almost every part of our planet.
    Some of us may have genes from ancestors who were cultivating and eating significant quantities of gluten grains as long as 10,000 to 15,000 years ago, in the Fertile Crescent of the Levant. Perhaps some human genes have been exposed to these grains for an even longer period. We really don't know. We can only judge based on the evidence we have. However, the evidence we have shows that most of the world's populations have had considerably less time to adapt to consuming these foods. Indigenous peoples of the Americas, Australia, as well as island dwellers from much of the Pacific Ocean, and even isolated groups of people in Europe and Asia have only consumed these foods for somewhere between 500 and about 5,000 years. A few of these populations, such as some groups of Canadian Inuit, some Pacific Islanders, etc. have only consumed gluten grains for less than 100 years. Yet Dr. Reilly would have us believe that the foods on which our forefathers thrived, while populating almost every habitable niche on earth, are somehow harmful. That seems a distinctly questionable perspective. She says that "The health and social consequences worthy of consideration in advance of starting a child on a GFD are not described adequately online or in books promoting an empiric GFD trial." Perhaps. That may simply result from the common awareness of the relatively short duration during which so many humans have consumed gluten-containing foods.
    Further, Dr. Reilly's assertion that "This Commentary [sic] will provide an update on the current GFD fad ....." (1) suggests more than a small bias on her part. Has she undertaken to guide us through the facts, fiction, and fad of the GFD, while suffering the delusions of yet another fad herself? Is it possible that Dr. Reilly, in addition to eschewing some principles of natural selection and adaptation, is tending toward a paradigm that only counts gluten-induced disease when that ailment falls within her purview? This may be a trap set by today's trend toward the increasingly specialized study and practice of Medicine. Or it may reflect a less thoughtful resistance among these professionals, reminiscent of the 80 years' resistance to the germ theory.
    Many neurologists, for instance, have been exploring a range of neurological ailments that are either triggered by gluten or are characterized by antigliadin antibodies found in the brain fluids of individuals afflicted by these neurological ailments (2). Some of these patients do have celiac disease but a majority do not(3). Yet their neurological ailments will often respond to a gluten free diet that must be more strict than is usually required to control celiac disease (4). In their work, Dr. Hadjivassiliou and colleagues have stated that "the neurological manifestations of celiac disease and NCGS are similar and equally responsive to a GFD suggestive of common pathophysiological mechanisms" (5). Thus, although Dr. Reilly is correct when she says that non-celiac gluten sensitivity (NCGS) is not yet well understood, it is quite clear that there is more information on the connection between gluten consumption and at least some cases of a wide range of neurological diseases (6, 7) than Dr. Reilly would like to credit. And these findings don't seem to be having much impact on many gastrointestinal researchers or practitioners. What is going on there?
    Further, regardless of the state of the intestinal mucosa, dermatitis herpetiformis (which Dr. Reilly did mention) is yet another form of NCGS in which it is clear that gluten exposure triggers the onset of this malady and a gluten free diet controls it. Yet she fails to mention that a subset of schizophrenia patients also experience symptom remission on a gluten-free diet, even among pre-pubescent children (8) and the association between schizophrenia and gluten has been repeatedly reported in the literature over the last half century (9 -19). The immune reaction to gluten is usually not the same as that seen in celiac disease (17). Nonetheless, for this group, the underlying trigger is gluten and its dietary restriction can produce startlingly positive results (18, 19). These psychiatric ailments can have a devastating impact on the victims' lives and their families when a simple diet can sometimes provide an effective treatment.
    While there is still some debate about whether gluten is the trigger in some cases of intestinal NCGS ailments, considerable evidence has also accrued showing that gluten is the trigger in a wide range of conditions both in association with untreated celiac disease and in the absence of celiac disease . The added problem is that Dr. Reilly has lumped all gluten free diets into a single entity. Yet many of us who avoid eating gluten also avoid other Neolithic foods, believing them to drive much of the current increases in autoimmunity, cancer, obesity, diabetes, and a host of other modern diseases. Dr. Loren Cordain's books have given rise to a large number of adherents to the "Paleo-Diet" that Cordain advocates (20). Other gluten avoiders find themselves developing symptoms when consuming "replacement" grains such as rice, corn, or millet, and choose to avoid those grains as well. Still other gluten avoiders subscribe to vegetarian diets, while others eat only organically produced meats and/or vegetables. These dietary practices also vary according to geographic location, all while avoiding gluten consumption. For instance, these variations might include increased fish consumption near the seashore and increased beef consumption inland, increased yak milk consumption in the Himalayas and increased millet consumption in West Africa. Thus, it seems questionable to lump all gluten avoiders into a single group, then suggest that they are suffering social isolation, lower quality of life, arsenic and/or mercury poisoning, and a host of other hazards.
    Dr. Reilly has argued that "The gluten-free diet (GFD) is a critical medical treatment for the millions of individuals worldwide with celiac disease (celiac disease), an autoimmune condition for which no other therapy is currently available" (1). That part is true. However, she then cites a study in which patients with celiac disease followed a gluten-free diet for an average of between 0 and 8.2 years and showed higher serum levels of mercury than either healthy controls eating a regular diet, or patients with celiac disease who were not following a gluten-free diet (21). There are several important things wrong here. The first is that Dr. Reilly has assumed that what is happening with the treated celiac patients may reasonably be assumed to be happening to those with NCGS who choose to follow a gluten-free diet. However, as she has so adroitly pointed out, people with celiac disease are different from those with NCGS. Thus, as was stated in the study of mercury and celiac disease that she cited (21), a person with celiac disease might have a genetic propensity for increased mercury absorption. Or they might experience a resurgence of those portions of the intestinal villi that are more likely to offer the primary point at which mercury is absorbed, or they might be more inclined to have mercury amalgam fillings that are degraded and absorbed due to grinding one's teeth, or chewing gum (21) or perhaps gastro-esophageal reflux is a factor in the degradation of mercury amalgam fillings. The authors of this study of mercury and celiac disease also acknowledge that their report is limited by the small number of participants. Dr. Reilly, on the other hand, fails to mention that only a small number of treated celiac patients participated in this study - only twenty of them. Neither does she seem to recognize that the study's results cannot legitimately be generalized from celiac patients on a gluten-free diet, to the non-celiac gluten sensitive population who may choose to avoid gluten. Further research might bridge that gap, but the study she cited does not (21) and such results should not be used to suggest a generalized risk that may be exclusive to those with celiac disease.
    The same study also seems to include treated celiac patients who are very new to the diet but have shown diminished tissue transglutaminase antibody levels (21). The average duration of the gluten free diet is 8.2 years, but with a deviation of up to 8.2 years. It is difficult to understand how this could mean anything else. I have contacted the lead author for clarification and have not yet received a response.
    With respect to high levels of inorganic arsenic in rice pablum, the celiac and gluten sensitive community has been aware of this problem since the 2009 publication of several articles, both in the popular and peer-reviewed scientific literature, arising out of studies conducted by professor Andy Meharg and his students the previous year (22). They found that samples of several brands of rice pablum purchased at supermarkets, commonly fed to babies, contained high levels of arsenic. Here in the Journal of Gluten Sensitivity, we also published a warning article (23). Some members of the same research group that exposed this problem with rice pablum have also published data showing that phosphorus fertilizer can mitigate uptake of arsenic in wheat (24). We continue to hope that rice farming practices will be similarly investigated and best practices will soon be prescribed for rice farmers, but Dr. Reilly has raised an important point here. Rice consumption should be limited by everyone, including those following a gluten-free diet.
    Reilly has also asserted that "there are no data supporting the presumed health benefits of a GFD" (1). This bold statement is followed by a heading that reads "Fiction: Gluten is toxic", then " There are no data to support the theory of an intrinsically toxic property of gluten" (1). Yet gliadins have also been demonstrated to damage a variety of tissue cells. In an experiment conducted by Hudson and colleagues, simple exposure to this sub-group of proteins from wheat gluten resulted in damage to several lines of embryonic cells (25). Similarly, Doherty and colleagues showed that many persons who are fed large amounts of gluten will develop villous damage or other intestinal damage, even in the absence of celiac disease (26). Some gluten proteins will cause damage to a variety of cell lines, and people fed large amounts of gluten will experience intestinal damage, yet Dr. Reilly claims that there are no data to support what she calls the "fiction" that gluten is toxic (1).
    Reilly also decries the higher fat content of the gluten-free diet. But dietary fats combine to make up a huge topic. Some promote inflammation. Others have anti-inflammatory properties. Some must be used as energy or they will prompt the liver to produce ketone bodies. These latter offer alternative fuels for the brain in the context of insulin resistance (27). Condemning its high fat content is a little like lumping all gluten-free diets into one group. It is a gross over-simplification that draws into question the writer's competence in the realm of Dietetics.
    The same can be said about Reilly's identification of iron deficiency as the result of avoiding gluten grains. Until we have a better understanding of the proportions of the various minerals that are irreversibly bound by phytates and phenols in the human gastrointestinal tract, blaming gluten grain avoidance for iron deficiency in humans is, at best, inaccurate. While she does mention that many of these nutrients we will fail to get from gluten free foods are simply fortifications that have been added to processed, gluten-containing foods, she has failed to recognize or discuss the mineral binding and wasting that ensues from eating these foods and additives together.
    Similarly, while some B vitamins are plentiful in processed, gluten-containing grains, others are not. However, the same B vitamins are abundantly available in other common food sources that do not contain the anti-nutrients common to cereal grains. Such deficiencies are not the result of a gluten free diet so much as they are the result of a poorly balanced diet, which can happen regardless of gluten exclusion.
    Reilly goes on to admonish those who are at risk of developing celiac disease not to undertake a gluten-free diet "without first testing for celiac disease" (1). This is spoken like a person who is intimately familiar with the medical system and would have little or no difficulty getting adequate testing to rule out celiac disease on request. She has probably not spent much of the previous decade or so repeatedly undergoing repeated rounds of the same useless tests, such as barium swallow X-rays, barium enema X-rays along with repeated, often unnecessary, courses of various antibiotics, multiple courses of drugs to treat ulcers that fail to show up on the aforementioned tests, and taking supplements or drugs to correct blood test abnormalities, without considering the potential underlying causes. And none of the above strategies are likely to ever suggest celiac disease. Yet these are the stock-in -trade of the general practitioner who is often reluctant to refer to gastrointestinal specialists. This reluctance frequently escalates when the above symptoms are accompanied by psychiatric and/or neurological complaints, although such symptoms are reported in between 51% and 73% of newly diagnosed celiac patients (7, 8) and some cases of psychosis can be attributed to gluten intake alone (18, 19, 28). In the face of such evidence, the claim that gluten fractions are not toxic seems almost laughable. Yet her polemic "commentary" has spawned quite a number of spin-off articles that condemn the gluten-free diet as a fad or a hoax, and many innocent victims and their families continue to suffer from the psychiatric, neurological, and other extra-intestinal manifestations of non-celiac gluten sensitivity or celiac disease. I frequently observe school children with diagnosed learning disabilities who make huge strides forward when on a gluten free diet. And the explanation is really quite simple (29). And I am saddened by the certitude with which this diet is condemned by otherwise reasonable people.
    Historically, the GFD has been contentious since it was introduced in 1937, when Dr. W.K. Dicke first began to treat his celiac patients with it. One may wonder why it has stirred so much controversy. I continue to be shocked when I read opinion articles such as Dr. Reilly's when they are included in peer-reviewed publications. I am not surprised by the many follow-up articles in the popular press that condemn the gluten free diet. This is the same resistance that I witnessed almost a quarter of a century ago, when I was diagnosed with celiac disease. I'm left wondering why so many supposedly objective professionals are so quick to oppose a diet that offers benefits to people with a wide range of maladies, many of which are, otherwise untreatable. What could motivate these vehement critics? I just don't understand.
    Sources:
    1. Reilly NR. The Gluten-Free Diet: Recognizing Fact, Fiction, and Fad. J Pediatr. 2016 May 10. pii: S0022-3476(16)30062-2.
    2. Stenberg R, Hadjivassiliou M, Aeschlimann P, Hoggard N, Aeschlimann D. Anti-transglutaminase 6 antibodies in children and young adults with cerebral palsy. Autoimmune Dis. 2014;2014:237107.
    3. Hadjivassiliou, M., Gibson, A., Davis-Jones, G., Lobo, A., Stephenson, T.,Milford-Ward, A. (1996). Does cryptic gluten sensitivity play a part in neurological illness? Lancet 347, 369-371.
    4. 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.
    5. Hadjivassiliou M, Rao DG, Grìnewald RA, Aeschlimann DP, Sarrigiannis PG, Hoggard N, Aeschlimann P, Mooney PD, Sanders DS. Neurological Dysfunction in Coeliac Disease and Non-Coeliac Gluten Sensitivity. Am J Gastroenterol. 2016 Apr;111(4):561-7.
    6. Hadjivassiliou M, The Neuroimmunology of Gluten Intolerance. Textbook chapter. in press.
    7. Zelnik N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2004 Jun;113(6):1672-6.
    8. Lionetti E, Leonardi S, Franzonello C, Mancardi M, Ruggieri M, Catassi C. Gluten Psychosis: Confirmation of a New Clinical Entity. Nutrients. 2015 Jul 8;7(7):5532-9.
    9. Dohan C. "Cereals and schizophrenia: data and hypothesis" Acta Psychiat Scand 1966; 42: 125-152
    10. Dohan FC, Grasberger JC, Lowell FM, Johnston HT Jr, Arbegast AW. Relapsed Schizophrenics: More Rapid Improvement on a Milk-and Cereal-free Diet" Brit J Psychiat 1969; 115: 595-596
    11. Singh MM, Kay SR. Wheat gluten as a pathogenic factor in schizophrenia. Science. 1976 Jan 30;191(4225):401-2.
    12. Zioudrou et. al. "Opioid peptides derived from food proteins. The exorphins" J Biol Chem 1979; 254:2446-2449
    13. Mycroft et. al. "MIF-like sequences in milk and wheat proteins" NEJM 1982; 307: 895
    14. Dohan et. al. "Is Schizophrenia Rare if Grain is Rare?" Biol Psychiat 1984; 19(3): 385-399
    15. Dohan "Is celiac disease a clue to pathogenesis of schizophrenia?" Mental Hyg 1969; 53: 525-529
    16. Ashkenazi et. al. "Immunologic reaction of psychotic patients to fractions of gluten" Am J Psychiat 1979; 136: 1306-1309
    17. Samaroo D, Dickerson F, Kasarda DD, Green PH, Briani C, Yolken RH, Alaedini A. Novel immune response to gluten in individuals with schizophrenia. Schizophr Res. 2010 May;118(1-3):248-55.
    18. Kraft BD, Westman EC. Schizophrenia, gluten, and low-carbohydrate, ketogenic diets: a case report and review of the literature. Nutr Metab (Lond). 2009 Feb 26;6:10. doi: 10.1186/1743-7075-6-10.
    19. De Santis A, Addolorato G, Romito A, Caputo S, Giordano A, Gambassi G, Taranto C, Manna R, Gasbarrini G. Schizophrenic symptoms and SPECT Abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3.
    20. Cordain L. The Paleo Diet. John Wiley & Sons. NY, 2002.
    21. Elli L, Rossi V, Conte D, Ronchi A, Tomba C, Passoni M, Bardella MT, Roncoroni L, Guzzi G. Increased Mercury Levels in Patients with Celiac Disease following a Gluten-Free Regimen. Gastroenterol Res Pract. 2015;2015:953042
    22. Meharg, A. A., Sun, G., Williams, P. N., Adomako, E., Deacon, C., Zhu, Y-G., Feldmann, J. & Raab, A. Inorganic arsenic levels in baby rice are of concern. Apr 2008 In : Environmental Pollution . 152, 3, p. 746-749.
    23. Hoggan R. How do you like your arsenic? Journal of Gluten Sensitivity, Spring 2009.
    24. Pigna, M., Cozzolino, V., Violante, A. & Meharg, A. A. Influence of phosphate on the arsenic uptake by wheat (Triticum durum L.) irrigated with arsenic solutions at three different concentrations Feb 2009 In : Water, Air, and Soil Pollution. 197, 1-4, p. 371-380.
    25. Hudson DA, Cornell HJ, Purdham DR, Rolles CJ. Non-specific cytotoxicity of wheat gliadin components towards cultured human cells. Lancet. 1976 Feb.
    26. Doherty, M., & Barry, R.(1981). Gluten-induced mucosal changes in subjects without overt small-bowel disease. The Lancet March 7, 517-520.
    27. de la Monte SM, Wands JR. Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed. J Diabetes Sci Technol. 2008 November; 2(6): 1101–1113.
    28. Jackson J, Eaton W, Cascella N, Fasano A, Santora D, Sullivan K, Feldman S, Raley H, McMahon RP, Carpenter WT Jr, Demyanovich H, Kelly DL. Gluten sensitivity and relationship to psychiatric symptoms in people with schizophrenia. Schizophr Res. 2014 Nov;159(2-3):539-42.
    29. Addolorato G, Di Giuda D, De Rossi G, Valenza V, Domenicali M, Caputo F, Gasbarrini A, Capristo E, Gasbarrini G. Regional cerebral hypoperfusion in patients with celiac disease. Am J Med. 2004 Mar 1;116(5):312-7.

    Miranda Jade
    Celiac.com 08/16/2016 - The short answer, yes! Although some women, due to certain complications are told not to exercise, for the most part exercise is totally fine while pregnant and actually quite a valid implementation to a healthy pregnancy.
    There used to be this myth that women had to be extremely careful with physical activity while pregnant due to the risk of possible miscarriage. Now we see pregnant women doing CrossFit, running, lifting weights, etc., as well as all sorts of beautiful yoga poses. This doesn't mean that if you haven’t worked out in 5 years and are pregnant you should suddenly start running 12 hours a day. No, not at all. On the other hand, if you have kept up a normal exercise routine it is totally fine to keep it up.
    Listen to your own body and understand things may feel different so don’t push yourself too much. I worked out plenty before getting pregnant and continued my many normal activities up until around 7 months. At that point I was very round and more tired than usual and going for regular walks, swimming and yoga was plenty enough "exercise" for me.
    I am celiac and I maintained my gluten-free diet during my pregnancy. I felt it was extremely important for me to be as healthy as I could so my body would feel good and therefore make my pregnancy that much easier. I have read that exercising throughout one's pregnancy can possibly shorten the labor too. Now this is a win-win in my eyes!
    The benefits of exercising while pregnant also include a lower risk of getting sick, lower risk of gestational diabetes, lower risk of depression and the list goes on. Plus, you can work on that lower core and strengthen your pelvis which will help a lot with back pains and hip issues that are all too familiar to pregnant women.
    Ask your OB-GYN or midwife for approval and once you get the green light go have some fun. You are more than likely to meet some other wonderful "future" moms, many of which are also looking to connect up and make friends.
    This is also a perfect opportunity to help other moms who may have some "odd symptoms", and if you are well-versed in the gluten-free diet and the symptoms of gluten sensitivity or intolerance, you can help another woman in need, hence her future baby. Moms uniting and sharing their tested knowledge is a lovely aspect of pregnancy these days.
    I hope this has inspired you and please feel free to contact me at any time with any questions. I focus on the gluten-free diet as well as the grain free diet, celiac disease, motherhood, and children issues. These are all subjects that I'm very passionate about.

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

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics

    Jefferson Adams
    Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
    A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.
    For their study, the team collected urine samples from 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIPs and an LFT reader. 
    They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage.
    The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
    Source:
    Gut. 2017 Feb;66(2):250-257.  doi: 10.1136/gutjnl-2015-310148.