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    Celiac Presentations at the National Digestive Disease Conference: May 19-22, 2002 - Summary by Laura Yick


    Scott Adams

    Dr. Kelly, who is a refractory sprue specialist, had interesting insights into Celiac Disease. He first described once having a patient say to him that eating at a restaurant or food take out is the gastronomic equivalent of promiscuous and unprotected sex because (you) dont know where food has been, who else its been with, and what you might get from it. Dr. Kelly explained that his job when seeing a patient with possible Refractory Sprue is to first confirm that the patient really has Celiac Disease and is adhering to a gluten-free (gluten-free) diet. He explained that some patients would rather prefer an iron shot than adhere to a gluten-free diet and that sensitivities vary which removes another drive to say gluten-free; however, if symptomatic, he has found that the patient has the motivation to adhere. Hes even had to recruit and train dieticians to take an interest in Celiac Disease. He said that Celiac Disease or Gluten Sensitive Enteropathy is driven by activated lamina propria T-cells to whom gliadin is being presented through their T-cell receptors. In Refractory Sprue, he said that the cells are evident at intraepithelial lymphocytes rather than lamina propria lymphocytes and they no longer require gluten in order to be driven. So, theyre on auto-pilot. He emphasized that this is a rare disease and advised that doctors get a competent dietician to help patient adhere to diet.


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    If the concern is that the patient is adhering but is not responding, Dr. Kelly advised doctors to think of other disorders masquerading as Celiac Disease, especially if patient is IgA, EmA (anti-endomysial) negative or if not HLA DQ2 or DQ8 (common Celiac genes) positive. He added that not every flat mucosa consistent with Celiac Sprue is Gluten Sensitive Enteropathy but that there can be a differential diagnosis such as cow protein intolerance. He said that there are unusual immunologic disorders that can be mistaken for sprue or refractory sprue. He said that doctors should consider these if the patient was not IgA endomysial or human tTg (transglutaminase) antibody positive at diagnosis. He explained that the positive predictive value of those tests are so strong that really its in some ways has a higher positive predictive value than even biopsy that you dont get very, very if any false positives at least by the immunofluorescence assay. So, if theyre negative at diagnosis considering other possibilities and this is one instance where HLA typing actually may be clinically useful if you have a patient you think has Celiac Sprue but isnt behaving or responding as you would expect with a gluten free diet and you ask do they really have Sprue. If they are HLA DQ2/DQ8 negative, then the likelihood of them having gluten sensitive disease is much, much lower. He said that serology (blood tests) were helpful but not be relied upon. He said that IG antibody levels against gliadin, or tissue transglutaminase tend to drop fairly quickly usually within 2 to 3 months provided they (patient) were positive to begin with. ...The IgG takes much longer so it tends to be less useful and of course, if they are IgA deficient, they wont be IgA positive to begin with and you cant use then. Even if their antibody levels are high to begin with, and remain high, that to me means that theyre still exposed to the antigen and they still have T-cells. Their lamina propia T-cells are still being driven by the antigen. But if theyre negative, Im afraid that its not particularly sensitive and low levels of gluten exposure may result in symptoms and poor response would not necessarily be identifiable by antibody.... Dr. Kelly said that patients with subtle manifestations of Celiac Sprue who have been previously diagnosed with irritable bowel or host of other disorders are now being more frequently seen. He said that there has been a lot of discussion in the past year about Celiac Sprue being misdiagnosed as Irritable Bowel Syndrome.

    Dr. Kelly also described the circumstance that patients with Celiac Sprue show improvement both serologically (blood) and histologically (biopsy) but their symptoms persist. He said that doctors need to be aware that just because a patient has gluten sensitive enteropathy doesnt mean they cant get another gastrointestinal disorder. He gave examples such as microscopic colitis and what he called a classical association, hyperthyroidism, or something else which could also cause diarrhea and weight loss.

    Dr. MacDonald, a celiac specialist, discussed new insights into the pathogenesis of Celiac Disease. Dr. MacDonald discussed primarily the role that other factors besides the DQ2 (gene) molecule, control the T-cells in the gut mucosa which produce the lesion or flat mucosa. In the genesis of the lesion, he explained how the T-cell immune response in the gut wall results in a gut shape of tall villi and short crypts which results in an increase in mucosa volume with flat mucosa and an increase in mucosa thickness. My husband, a PhD immunologist, interpreted this for me; He said that imagine the villi are the hill and the crypts are the valley. The valley is where things grow. The oldest cells are at the tip of the hill and as cells mature, they get transported up the hill. As damage occurs, the hill gets chopped down, valleys get deeper making more area for cells to replicate. Dr. MacDonald assumed that because the epithelium is turning over so fast in Celiac Disease that the lamina propria, the shape of the gut itself would be turning over, but actually the data says otherwise. The flat mucosa isnt turning over at all, ... a rather stable shape, its not really dynamic, its remodeled. He said that putting Celiacs on a gluten free diet may take them a long time to get better, because it takes a long time for this to go back because this is actually stable, its remodeled....

    Dr. MacDonald explained that gliadin peptides associate with DQ2 and DQ8 molecules putting themselves into the grooves to be seen by T cells. However, he gave an instance where a particular gliadin peptide doesnt fit well into the pockets of DQ2 to be seen by T cells. Tissue Transglutaminase or Ttg deamidates (removes chemical groups on certain amino acids and allows peptide to bind to DQ2) this peptide in terms of glutamine into glutamic acid, gives a negative charge, fits very well into pocket, and binding increases 100 fold. Tightness of the binding ... controls the specificity and strength of the T-cell response.

    Dr. MacDonald also described the case of a woman with cancer who was treated with interferon. He said that she had the endomysial antibodies, was DQ2 positive, and had Celiac Disease; however, he cited that the reason why the Celiac Disease was not found earlier was that interferon alpha/gamma used to treat the cancer may have precipitated clinical Celiac Disease. He added that her son was later diagnosed with Celiac Disease as well. It was also eluded to that a viral infection like a gastrointestinal flu would stimulate or produce interferon alpha.

    Dr. Alessio Fasano from the Center for Celiac Research at the Univ. of Maryland also explained that its not just the gluten antigen and genes (i.e., HLA DQ2 or DQ8) but an added element like that alluded to by Dr. MacDonald such as a viral infection which can result in Celiac Disease. Dr. Fasano described a study performed on North African children who were thought to have symptoms resembling infectious disease with symptoms like anemia and diarrhea were found to have Celiac Disease at the rate of 1 in 18. He said because they have a high consumption of grains and seem to carry a high frequency of the genetic elements, he felt that non-profit organizations may intervene to help institute a gluten-free diet in this Celiac population. Dr. Fasano mentioned a study performed in Southern California which found Celiac Disease in 2 to 4% of people with symptoms or associated diseases and 5% in family members of Celiacs. Dr. Fasano stated that the overall prevalence is 1 in 266 which he said on a global scale, by far this is the most frequently genetic disease of human kind. Fasano said that in the 1970s, it was thought Celiac Disease was confined to the pediatric population but that since 1998 there has been a surge in adult versus child cases. He believes that the disease may have been overlooked in adults because adults have more atypical symptoms like anemia, osteoporosis, abortion that would NOT see a Gastroenterologist but would see an internist, reproductive OBGyn, endocrinologist, etc.

    Dr. Fasano said that if the iceberg idea is diarrhea, weight loss, abdominal symptoms, you will surely crash into the iceberg, but he proposed, what about the people who have joint pain, constipation, fatigue, and so on. He said that if you are willing to see the monument of the problems, you have to get down under the water because in the vast majority of cases, Celiacs will not see a Gastroenterologist and that doctors must be aware of those under the water. Dr. Fasano during the question and answer session listened to a doctor in the audience describe a patient with diarrhea and schizophrenia whose diarrhea and schizophrenia resolved when put on a gluten-free diet. The doctor didnt know what to do with the patient but explained that the patients background, being of Irish descent, gave him a red flag into the possibility of Celiac Disease. Dr. Fasano in response described how there can be a change in behavior such as attention deficit disorder, depression, and schizophrenia. He described a theory that the epitopes of gluten could cross the intestinal barrier, cut into the bloodstream, and cross the blood brain barrier. He believes that there is a clear association between Celiac Disease and change in behavior.

     

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    In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease. In 1998 I founded The Gluten-Free Mall, Your Special Diet Superstore!, and I am the co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.

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  • Related Articles

    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
     
     
     
     

    Miranda Jade
    This article originally appeared in the Spring 2013 edition of Celiac.com's Journal of Gluten-Sensitivity.
    Celiac.com 01/29/2014 - Anyone diagnosed with celiac disease knows that it is almost impossible not to slip up here and there. Whether you mistakenly eat something with gluten, cross contamination or your waiter forgets to inform you that your burger is marinated with gluten, we have all been there. It usually takes me two or three days to feel better and another two or three days following that to get back to my routine after consuming a small amount of gluten. For others this process varies. Some worse, some better.
    A diagnosed celiac friend of mine recently finally got pregnant. She and her husband had been trying for quite some time. This sparked a question for me. What would consuming gluten would do to her unborn child, if anything?
    According to Amy O'Connell ( a researcher and writer with a Ph.D. and medical degree) gluten can cause problems in your unborn child. When a pregnant woman with celiac disease eats gluten the mothers villi are damaged which leads to poor nutrition and weight loss. This results in an inability to absorb calories and vitamins from food and may explain why mothers with untreated celiac disease are more likely to have a baby with a low birth weight.
    A report in the journal "Canadian Family Physician" explained that babies of untreated mothers with celiac disease could also be at risk for spina bifida or other neural tube defects, because the mother may have poor folic acid absorption in the gut.
    This isn't even taking into account the emotional effects gluten has on a mother with celiac disease. The energy loss and depression that can result from gluten consumption can be harmful to the mother and child's ability to bond which creates unneeded stress. As a new mother you have enough to worry about. There is no need to complicate things with more stress and less energy.
    If you are an expecting mother with celiac disease, now more than ever, watch what you eat. Make sure you don't slip up no matter how much you want that Cinnabon!
    Reference:
    http://www.livestrong.com/article/543324-can-gluten-hurt-an-unborn-baby-with-a-celiac-mother/ This article originally appeared in the Autumn 2003 edition of Celiac.com's Journal of Gluten-Sensitivity.

    Gryphon Myers
    Celiac.com 03/18/2013 - People are wary (for good reason) of products that are derived from gluten-containing ingredients, and few products have received quite as much heat as beer. Gluten-removed beers are almost always tested to under 20ppm gluten to allay the concerns of celiacs, but the reliability of such tests is often challenged. Can we really trust the results of gluten tests performed on beer?
    As Tricia Thompson, MS, RD writes on her blog, Gluten-Free Dietitian, the current standard for testing gluten content in foods is a sandwich ELISA test. The R5 and omega-gliadin versions of the test are the most widely used, and both have been validated in collaborative trials.
    While sandwich ELISA tests are reliable for detecting gluten in heated and non-heated food items, they are notoriously unreliable for detecting hydrolyzed gluten. Many see this as reason not to trust gluten-removed beers: the fermentation process hydrolyzes gluten in beer, so sandwich ELISA tests cannot accurately quantify their gluten content. If the test is unreliable, it's hard to believe that a once gluten-containing substance is safe for consumption by celiacs.
    However, the sandwich R5 ELISA's weaknesses are well documented and widely known. Most of these brewers are using an entirely different test that was specifically designed to detect partial gluten fragments (peptides) that may still be harmful to the gluten-sensitive. The competitive R5 ELISA is the standard test used to detect these peptides, and although it has not been validated yet, many published studies have found the competitive R5 ELISA to be a reliable indicator of hydrolyzed gluten.
    A recent article published on Medical Daily titled “Gluten-Free Beer? Common Gluten Detection Method is Inaccurate” addresses the issue of ELISA testing on beer, and claims that current testing procedures are inaccurate. This is only half true, and unfortunately, articles like these only serve to confuse the public about an already confusing issue.
    The article seems well-meaning enough; after all, there's nothing wrong with taking a precautionary stance when one's health is on the line. However, the cited study clearly states that they are using the sandwich R5 ELISA. It has already been established that the sandwich R5 ELISA is unreliable for testing beer, and for this reason, most companies do not use it when testing for hydrolyzed gluten. This makes the article's title highly misleading, as the inaccuracy of the sandwich R5 ELISA for detecting gluten in beer is, in most cases, irrelevant.
    Another point that the article fails to address is that it is not entirely clear just how toxic these gluten peptides are for gluten-sensitive individuals. The toxicity of the 33 mer peptide and numerous others have been demonstrated, but aside from that, it's possible that at least some of the peptides detected by the Competitive R5 ELISA are not toxic to celiacs.
    One should always err on the side of safety, but it is important to be as precise as possible with the scientific terminology to avoid needless (perhaps inadvertent) fear mongering, as that is one thing the celiac community does not need more of.
    Parts of this article appeared in “Common Misunderstandings of Gluten-Free Alcoholic Beverages,” from the Winter 2012 issue of The Journal of Gluten Sensitivity.
    Sources:
    http://www.glutenfreedietitian.com/newsletter/2012/08/06/standards-for-testing-food-for-gluten-issues-that-need-addressing/ http://www.glutenfreedietitian.com/newsletter/2012/07/24/beer-why-it-is-so-hard-to-assess-fermented-and-hydrolyzed-products-for-gluten/ http://www.ncbi.nlm.nih.gov/pubmed/19763549 http://www.ncbi.nlm.nih.gov/pubmed/22649922 http://www.medicaldaily.com/articles/14181/20130301/gluten-free-beer-common-detection-method-inaccurate.htm

    Jefferson Adams
    Celiac.com 06/12/2013 - Pregnant women with higher levels of issue transglutaminase (anti-tTG), an antibody common in people with celiac disease, at risk for low fetal and birth weight in their babies, according to a new study in Gastroenterology.
    A number of studies before this one have confirmed an association between celiac disease and poor growth fetus growth, but very little study had been done as to how the level of celiac disease might affect fetal growth, birth weight or birth outcome.
    In an effort to better understand how the level of celiac disease affects fetal growth, birth weight, and birth outcome, a team of researchers set out to assess the associations between levels of antibodies against tissue transglutaminase (anti-tTG, a celiac disease marker) and fetal growth and birth outcomes for pregnant women.
    The research team included J.C. Kiefte-de Jong, V.W. Jaddoe, A.G. Uitterlinden, E. A. Steegers, S.P. Willemsen, A. Hofman, H.Hooijkaas, and H.A. Moll of the Generation R Study Group at Erasmus University Medical Center in Rotterdam, The Netherlands.
    They conducted a population-based prospective birth cohort study of 7046 pregnant women. Serum samples were collected during the second trimester of pregnancy and analyzed for levels of anti-tTG.
    Based on these levels, they grouped each woman into groups of negative anti-tTG (≤0.79 U/mL; n = 6702), intermediate anti-tTG (0.8 to ≤6 U/mL; n = 308), or high anti-tTG individuals (over 6 U/mL; n = 36). They then collected data for fetal growth and birth outcomes from ultrasound measurements and medical records.
    The fetal growth data showed that, on average, fetuses of women in the positive anti-tTG group were 16 g lighter than those of women in the negative anti-tTG group (95% confidence interval [CI], -32 to -1 g) during the second trimester and weighed 74 g less (95% CI, -140 to -8 g) during the third trimester.
    The birth outcome data revealed that newborns of women in the intermediate and positive anti-tTG groups weighed 53 g (95% CI, -106 to -1 g) and 159 g (95% CI, -316 to -1 g) less at birth, respectively, than those of women in the negative anti-tTG group. Of mothers in the intermediate anti-tTG group, those with HLA-DQ2 or -DQ8 had reduced birth weights that were double those of mothers without HLA-DQ2 or -DQ8.
    This study led the researchers to conclude that levels of anti-tTG in pregnant women are inversely associated with fetal growth. The higher the anti-tTG in women, the lower the birth weights of their babies. So, women with the highest levels of anti-tTG (over 6 U/mL) saw the greatest reduction in birth weight of their babies.
    Also, women with intermediate levels of anti-tTG (0.8 to ≤6 U/mL) saw lower birth weights that were even further reduced if they carried the HLA-DQ2 and -DQ8 gene markers.
    Source:
    Gastroenterology. 2013 Apr;144(4):726-735.e2. doi: 10.1053/j.gastro.2013.01.003.

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/21/2018 - Would you buy a house advertised as ‘gluten-free’? Yes, there really is such a house for sale. 
    It seems a Phoenix realtor Mike D’Elena is hoping that his trendy claim will catch the eye of a buyer hungry to avoid gluten, or, at least one with a sense of humor. D’Elena said he crafted the ads as a way to “be funny and to draw attention.” The idea, D’Elena said, is to “make it memorable.” 
    Though D’Elena’s marketing seeks to capitalizes on the gluten-free trend, he knows Celiac disease is a serious health issue for some people. “[W]e’re not here to offend anybody….this is just something we're just trying to do to draw attention and do what's best for our clients," he said. 
    Still, the signs seem to be working. D'elena had fielded six offers within a few days of listing the west Phoenix home.
    "Buying can sometimes be the most stressful thing you do in your entire life so why not have some fun with it," he said. 
    What do you think? Clever? Funny?
    Read more at Arizonafamily.com.

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    Bakery On Main started in the small bakery of a natural foods market on Main Street in Glastonbury, Connecticut. Founder Michael Smulders listened when his customers with Celiac Disease would mention the lack of good tasting, gluten-free options available to them. Upon learning this, he believed that nobody should have to suffer due to any kind of food allergy or dietary need. From then on, his mission became creating delicious and fearlessly unique gluten-free products that were clean and great tasting, while still being safe for his Celiac customers!
    Premium ingredients, bakeshop delicious recipes, and happy customers were our inspiration from the beginning— and are still the cornerstones of Bakery On Main today. We are a fiercely ethical company that believes in integrity and feels that happiness and wholesome, great tasting food should be harmonious. We strive for that in everything we bake in our dedicated gluten-free facility that is GFCO Certified and SQF Level 3 Certified. We use only natural, NON-GMO Project Verified ingredients and all of our products are certified Kosher Parve, dairy and casein free, and we have recently introduced certified Organic items as well! 
    Our passion is to bake the very best products while bringing happiness to our customers, each other, and all those we meet!
    We are available during normal business hours at: 1-888-533-8118 EST.
    To learn more about us at: visit our site.

    Jefferson Adams
    Celiac.com 06/20/2018 - Currently, the only way to manage celiac disease is to eliminate gluten from the diet. That could be set to change as clinical trials begin in Australia for a new vaccine that aims to switch off the immune response to gluten. 
    The trials are set to begin at Australia’s University of the Sunshine Coast Clinical Trials Centre. The vaccine is designed to allow people with celiac disease to consume gluten with no adverse effects. A successful vaccine could be the beginning of the end for the gluten-free diet as the only currently viable treatment for celiac disease. That could be a massive breakthrough for people with celiac disease.
    USC’s Clinical Trials Centre Director Lucas Litewka said trial participants would receive an injection of the vaccine twice a week for seven weeks. The trials will be conducted alongside gastroenterologist Dr. James Daveson, who called the vaccine “a very exciting potential new therapy that has been undergoing clinical trials for several years now.”
    Dr. Daveson said the investigational vaccine might potentially restore gluten tolerance to people with celiac disease.The trial is open to adults between the ages of 18 and 70 who have clinically diagnosed celiac disease, and have followed a strict gluten-free diet for at least 12 months. Anyone interested in participating can go to www.joinourtrials.com.
    Read more at the website for Australia’s University of the Sunshine Coast Clinical Trials Centre.

    Source:
    FoodProcessing.com.au

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

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