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      Frequently Asked Questions About Celiac Disease   04/07/2018

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


    Dr. Rodney Ford M.D.


    • Journal of Gluten Sensitivity Summer 2015 Issue - Originally published July 16, 2015


    Celiac.com 10/27/2015 - In 2006, I presented a research paper called "Who warrants a gluten-free diet?". At that time I was thinking about the sick children who were coming through my clinic with skin, gut and brain symptoms: that is they had eczema and itchy skin; sore tummies and constipation; and behaviour disturbances. It turned out that most of this group of children had high levels of Anti-Gliadin-Antibodies (AGA), of whom 80% got completely better when they went on a gluten-free diet. This was a landmark paper for me, and it led me to describe "The Gluten Syndrome".


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    However, that was nearly 10 years ago! and a lot has happened since then. Perhaps most notable the publication of the consensus paper on the Spectrum of Gluten-Related-Disorders. The algorithm developed to diagnose gluten sensitivity/ intolerance relies on the elimination and challenge of gluten, rather than immunologic blood tests. I have been using the AGA test in my clinic since 1989 (that is for 25 years!) and I have found it extremely useful as a diagnostic test, when it is positive. But, many people react to gluten and have negative AGA results. So I agree with the authors of the "Spectrum" paper. The basis of a gluten-sensitivity/intolerance diagnosis should be based on elimination and challenge. Importantly, prior to removing gluten from your diet, please ensure that you get the appropriate tests for celiac disease (see this link for a gluten-blood-test discussion).

    So who in the year 2015 should be suspected of having a gluten-related-illness? Well anyone who has chronic symptoms. Even if they have a diagnostic label - because they might have the wrong diagnosis. so here are the 3 steps in my gluten-free logic:

    Step ONE - the premise IF:

    • a) Gluten sensitivity is common: estimates show it affects over 10% of the population;
    • B) Gluten-related illnesses are varied and have multiple symptoms: a quote from the consensus paper on the Spectrum of Gluten-Related-Disorders emphasizes this. The symptoms in gluten sensitivity may resemble those associated with celiac disease but with a prevalence of extra-intestinal symptoms, such as behavioral changes, bone or joint pain, muscle cramps, leg numbness, weight loss and chronic fatigue. Their symptoms include abdominal pain (68%); eczema and/or rash (40%); headache (35%); "foggy mind" (34%); fatigue (33%); diarrhea (33%); depression (22%); anemia (20%); numbness in the legs, arms or fingers 20%; and joint pain (11%);
    • c) There is no definitive diagnostic test for gluten sensitivity: the Consensus paper goes on to say "However, currently there are no laboratory biomarkers specific for gluten sensitivity. Usually the diagnosis is based on exclusion criteria; an elimination diet of gluten-containing foods followed by an open challenge is most often used to evaluate whether health improves with the elimination or reduction of gluten from the patient’s diet";
    • d) There is no harm from going on a gluten-free diet; in other words a gluten-free is healthy.

    Step TWO - The logical THEN:
    Then the logical conclusion is that "anyone", with "any symptoms" that are "chronic and unexplained" (that is they do not have a definite diagnosis) and "at any time" (people can develop gluten-illness at any time in their life) should be put onto a gluten-free diet for a clinical trial for three months or more.

    Step THREE - The CONCLUSION:
    The logical conclusion is that whatever the blood-test results, and whatever the endoscopy results, and whatever the symptoms, a beneficial response to a gluten-free diet suggests that their illness is gluten-related (some people might demand a double blind food challenge).

    Comment
    Up until now, most gluten/celiac doctors have dismissed the idea that their patients might be suffering from "non-celiac gluten-sensitivity" (NCGS). They have attributed their patients beneficial response to a gluten-free diet as a placebo response (all in their head!). This is clearly not the case. There is mounting evidence for this: see this research paper - Small Amounts of Gluten in Subjects with Suspected Nonceliac Gluten Sensitivity: a Randomized, Double-Blind, Placebo-Controlled, Cross-Over Trial. In this paper the authors conclude: "In a cross-over trial of subjects with suspected NCGS, the severity of overall symptoms increased significantly during 1 week of intake of small amounts of gluten, compared with placebo".

    The above logic means that ALL people, with ANY undiagnosed illnesses, at any TIME in their life, should be given a gluten-free trial. This is likely to have huge health benefits and wide ramifications on the management and burden of ill health on the community. Already 10% of Australians and Canadian are adopting a gluten-free diet, and 30% percent of adults in the USA are interested in avoiding or cutting down on gluten in their diets, says a survey from the NPD Group, a consumer research firm. NDP has been following gluten-free issues since 2009 and its January 2013 survey revealed the highest interest in gluten-free diets yet (reported in HuffPost - 26 Feb 2015).

    It is my prediction that in another generation most people who wish to stay healthy, will choose to adopt a gluten-free diet, before they get harmed by gluten.


    Image Caption: Image: CC--Anders Sandberg
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    Guest Bea Hord

    Posted

    I have been on a gluten-free diet for 30 years and am now 84 years old, and will be glad to share.

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    Guest Katrina

    Posted

    Completely agree with Dr Rodney, I have celiac 6 years diagnosed but primarily nerve-related symptoms.

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    Guest Mary Thorpe

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    Thank you for your voice of logic, Dr. Ford. I have thought for a long time that anyone who has chronic, unexplained symptoms should try the gluten free diet, after, as you mentioned, first getting tested for celiac disease. I had two big symptoms but also many minor symptoms I never would have suspected to be from gluten that all disappeared after adopting a gluten-free diet that has led to a far superior quality of life. Even today, after 17 years, something will pop into my mind that makes me realize "that doesn't happen to me anymore." For instance, I no longer routinely get bronchitis after a cold (and, in fact, rarely even get colds). No more recurrent strep throat, canker sores, muscle spasms and subluxions, esophageal spasms, white spots on my finger nails or heart palpitations, besides the biggies of chronic migraine and diarrhea. I am not diagnosed celiac because I tried the gluten-free diet on my own and didn't have the testing first. But I know I never looked back.

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    Guest Mary Thorpe

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    P.S. I am glad to hear that you find the AGA to be very useful. When I worked for the Center for Celiac Research (15 years ago), the tTg test was on the verge of making the AGA obsolete and I argued strongly for keeping it in the arsenal which caused a bit of conflict there! I tried to improve the sensitivity of the assay by expanding the ELISA target to other gliadin molecules besides alpha but don't think I knew to include deamidated gliadin. But I felt strongly in my gut that there was more to gluten sensitivity than celiac disease and it's nice to feel vindicated.

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    Guest Janet Newman

    Posted

    Love to hear that gluten sensitivity is being treated as real. I went gluten free 4 years ago because of sinus allergies. 3 doctors were not helping me. I went gluten free on my own. At first I could fudge a little. Then I realized that I had stomach pain and diarrhea every time that I ate gluten. I have had stomach problems for over 20 years that the doctor could not figure out what was the cause. I might add that I have suffered with eczema most of my life. I became more diligent at staying off the gluten. Over time I realized that my restless leg problem is severe when I get a hold of something with gluten. This usually is from cross contamination at a restaurant. It is like my body was fighting a war inside while the outside of me just wants to go to sleep. Gluten free is my normal life now. I will never go back.

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    This article originally appeared in the Winter 2004 edition of Celiac.com's Scott-Free Newsletter. Transcript of a talk given by Kenneth Fine, M.D. to the Greater Louisville Celiac Sprue Support Group––transcribed by Marge Johannemann; Edited by Kelly Vogt.
    Celiac.com 03/04/2004 - Gluten sensitivity is the process by which the immune system reacts to gluten contained in wheat, barley, rye, and oats. The reaction begins in the intestine because that is where the inciting antigen, gluten, is present (from food). When this immunologic reaction damages the finger-like surface projections, the villi, in the small intestine (a process called villous atrophy), it is called celiac disease (or sometimes celiac sprue or gluten-sensitive enteropathy). The clinical focus of gluten-induced disease has always been on the intestine because that is the only way the syndrome was recognized before screening tests were developed. The intestinal syndrome consists mainly of diarrhea, gas, bloating, nausea, vomiting, fat in the stool, nutrient malabsorption, and even constipation. Although the small intestine is always the portal of the immune response to dietary gluten, it is not always affected in a way that results in villous atrophy. Even though recent research has shown that celiac disease is much more common than previously suspected, affecting 1 in 100-200 Americans and Europeans, past and emerging evidence indicates that it accounts for only a small portion of the broader gluten sensitive clinical spectrum (often referred to as the “Tip of the Gluten Sensitive Iceberg”). With better understanding of how gluten triggers immune and autoimmune reactions in the body under the control of various genes, and advancing techniques of detecting these reactions, it is becoming apparent that the majority of the gluten sensitive population (the submerged “mass of the iceberg”) do not manifest villous atrophy in its classic, complete form and therefore do not have celiac disease. In these non-celiac, gluten sensitive individuals, the brunt of the immune reaction either affects the function of the intestine, causing symptoms without structural damage, affects other tissues of the body (and virtually all tissues have been affected in different individuals), or both. This is important because the commonly used diagnostic tests of clinically important gluten sensitivity (blood tests for certain antibodies and intestinal biopsies) are only positive when villous atrophy of the small intestine is present. But if only a small minority of gluten sensitive individuals actually develop celiac disease, the majority, who have not yet or may never develop villous atrophy, with or without symptoms, can remain undiagnosed and untreated for years. This can result in significant immune and nutritional consequences, many of which are irreversible even after treatment with a gluten-free diet. Some of these disorders include loss of hormone secretion by glands (hypothyroidism, diabetes, pancreatic insufficiency, etc), osteoporosis, short stature, cognitive impairment, and other inflammatory bowel, liver, and skin diseases, among others. Only with early diagnosis, can these problems be prevented or reversed.
    I am here to report on a scientific paradigm shift regarding early diagnosis of gluten sensitivity based on about 30 years of medical research by myself and others. My message is that earlier and more inclusive diagnosis of gluten sensitivity than has been allowed by blood tests and intestinal biopsies must be developed to prevent the nutritional and immune consequences of long-standing gluten sensitivity. Imagine going to a cardiologist because your blood pressure is high or you're having chest pain, and the doctor says he is going to do a biopsy of your heart to see what is wrong. If it ‘looks' O.K., you are told you have no problem and no treatment is prescribed because you have not yet had a heart attack showing on the biopsy. You would not think very highly of the doctor utilizing this approach because, after all, isn't it damage to the heart that you would want to prevent? But for the intestine and gluten sensitivity, current practice embraces this fallacious idea that until an intestinal biopsy shows structural damage, no diagnosis or therapeutic intervention is offered. This has to change now because with newly developed diagnostic tests, we can diagnose the problem before the end stage tissue damage has occurred, that is “before the villi are gone,” with the idea of preventing all the nutritional and immune consequences that go with it.
    There are many misconceptions regarding the clinical presentation of gluten sensitivity or celiac disease: For example, that you cannot be gluten sensitive if you have not lost weight, are obese, have no intestinal symptoms, or are an adult or elderly. However, the most widely held and clinically troublesome misconception is that a negative screening blood test, or one only showing antigliadin antibodies (without the autoimmune antiendomysial or anti-tissue transglutaminase antibody) rules out any problem caused by gluten at that time or permanently. For some reason, the high “specificity” of these blood tests has been tightly embraced. Specificity means if the test is positive, you surely have the disease being tested for with little chance that the positive is a “false positive.” But sadly, a negative test does not mean you do not have the problem. This is the biggest pitfall of all because the only thing a very specific test, like blood testing for celiac disease, can do is “rule in” the disease; it can not “rule it out.” If you've got very far advanced and/or long-standing celiac disease, it is likely that the test will be positive. However, several studies have now revealed that it is only those with significant villous atrophy of the small intestine who regularly show a positive antiendomysial or anti-tissue transglutaminase antibody, the specific tests relied upon most heavily for diagnosis of gluten-induced disease. When there was only partial villous atrophy, only 30% had a positive test. More disturbing perhaps, were the results with respect to screening first degree relatives of celiacs with blood tests. Despite some biopsy-proven early inflammatory changes in the small intestine but without villi damage, all blood tests were negative.
    For some reason, it's been perfectly acceptable to celiac diagnosticians that a patient must have far advanced intestinal gluten sensitivity, i.e., villous atrophy, to be diagnosed and a candidate for treatment with a gluten-free diet. That means from the specific testing standpoint, there's never (or rarely) a false positive. But what about the larger majority of gluten-affected people who do not presently have or may never get this end stage, villous atrophic presentation? They are out of luck as far as blood testing is concerned. So the fact is that we have erroneously relied on specificity (always picks up gluten sensitivity after it has caused villous atrophy, never having a false positive) instead of sensitivity (doesn't miss gluten sensitive people even though they might be picked up early, even before full-blown celiac disease develops). Would a test relying on specificity rather than sensitivity be good enough for you, or your children? Consider the risk of not getting an early diagnosis versus going on a gluten free diet a few months or years prematurely. While I do not recommend anyone to have a biopsy (especially children) for diagnosis because of the shortcomings and invasive nature of this technique, I particularly do not want someone to have a biopsy showing villous atrophy, since by that time, associated bone, brain, growth, and/or gland problems are all but guaranteed. And here is another related problem: You have a positive blood test, but, if a small bowel biopsy comes back normal or nearly normal, you are told that the blood test must have been a “false positive” and that gluten is not your problem. Would you believe that, especially in light of the fact that most such people would have gotten the blood test in the first place because of a specific symptom or problem? Let's hope not. All that means (positive blood test, negative biopsy) is that the gluten sensitivity (evidenced by antibodies to gliadin in the blood) has not yet damaged your intestines severely.
    Evidence of this comes from a study that I performed. We tested 227 normal volunteers with blood tests for celiac disease. Twenty-five of these people (11%) had either antigliadin IgG or IgA in their blood versus only one (0.4%) that had antiendomysial, anti-tissue transglutaminase, and antigliadin IgA in the blood. So for every one person in a population that has the antibodies that have 100% specificity for celiac disease of the intestine (antiendomysial and anti-tissue transglutaminase), there are 24 that have antibodies to gliadin that may not have celiac disease. So what is going on with the 11% with antigliadin antibodies in blood? Are these false positives (rhetorically)? You're telling me that there is a disease called celiac disease and it is associated with antibodies to gliadin in the blood and sometimes it damages the intestine? But people with antigliadin antibody in their blood but no other antibodies do not have a clinically significant immunologic reaction to gluten? Do you see the problem? How can 11% be false positives? What about the 89% with none of these antibodies? You cannot equate having no antibodies at all (a negative test) with having antigliadin antibodies alone. If you have antibodies to gliadin, something is going on here. Where there's smoke there's fire. The purpose of this study was to test this hypothesis: That an antigliadin antibody alone does indicate the presence of an immune reaction to gluten that may be clinically important. Using tests for intestinal malabsorption and abnormal permeability (i.e., tests of small bowel function, unlike a biopsy which says nothing about function), we found that 45% of people with only an antigliadin IgG or IgA antibody in blood (without either antiendomysial or anti-tissue transglutaminase antibody) already had measurable intestinal dysfunction, compared to only 5% of people with no antibodies to gliadin in their blood. When we did biopsies of these people's intestines, none had villous atrophy with only a few showing some early inflammation. Thus, having an antigliadin antibody in your blood does mean something: That there is nearly a 1 in 2 chance that functional intestinal damage is already present even though it may not be visible structurally at the resolution attained by a light microscope assessment of a biopsy.
    As mentioned at the outset, not all gluten sensitive individuals develop villous atrophy. Evidence for this has been around for a long time. In 1980, a medical publication titled “Gluten-Sensitive Diarrhea” reported that eight people with chronic diarrhea, sometimes for as long as 20 years, that resolved completely when treated with a gluten-free diet, had mild small bowel inflammation but no villous atrophy. In 1996 in a paper called “Gluten Sensitivity with Mild Enteropathy,” ten patients, who were thought to have celiac disease because of a positive antiendomysial antibody blood test, had small bowel biopsies showing no villous atrophy. But amazingly, these biopsies were shown to react to gluten when put in a Petri dish, proving the tissue immunologically reacted to gluten (which was likely anyway from their positive blood tests). Two other reports from Europe published in 2001 showed gluten sensitivity without villous atrophy (and hence without celiac disease). In one of these studies, 30% of patients with abdominal symptoms suggestive of irritable bowel syndrome having the celiac-like HLA-DQ2 gene but no antibodies to gliadin in their blood, had these antibodies detected in intestinal fluid (obtained by placing a tube down into the small intestine). Thus, in these people with intestinal symptoms, but normal blood tests and biopsies, the antigliadin antibodies were only inside the intestine (where they belong if you consider that the immune stimulating gluten also is inside the intestine), not in the blood. This is the theme we have followed in my research, as we are about to see.
    More proof that patients in these studies were gluten sensitive came from the fact that they all got better on a gluten-free diet, and developed recurrent symptoms when “challenged” with gluten. Although the gluten-sensitive patients in these studies did not have the villous atrophy that would yield a diagnosis of celiac disease, small bowel biopsies in many of them showed some, albeit minimal, inflammatory abnormalities. Yet, when a symptomatic patient in clinical practice is biopsied and found to have only minimal abnormalities on small bowel biopsy, clinicians do not put any stock in the possibility of their having gluten sensitivity. As much as I would like to take credit for the concept, you can see from these studies that I did not invent the idea that not all gluten sensitive patients have villous atrophy. It has been around for at least 23 years, and reported from different parts of the world.
    For many years there has also been proof that the intestine is not the only tissue targeted by the immune reaction to gluten. The prime example of this a disease called dermatitis herpetiformis where the gluten sensitivity manifests primarily in skin, with only mild or no intestinal involvement. Now from more recent research it seems that the almost endless number of autoimmune diseases of various tissues of the body also may have the immune response to dietary gluten and its consequent autoimmune reaction to tissue transglutaminase as the main immunologic cause. A study from Italy showed that the longer gluten sensitive people eat gluten, the more likely they are to develop autoimmune diseases. They found that in childhood celiacs, the prevalence of autoimmune disease rose from a baseline of 5% at age two to almost 35% by age 20. This is a big deal if you think of how much more complicated one's life is when one is both gluten sensitive AND has an additional autoimmune disease.
    So preventing autoimmune disease is one very important reason why early diagnosis and treatment of gluten sensitivity is important. Early diagnosis before celiac disease develops also holds the potential of preventing other clinical problems such as malnutrition, osteoporosis, infertility, neurologic and psychiatric disorders, neurotube defects (like spina bifida) in your children, and various forms of gastrointestinal cancer. Another reason for early diagnosis and treatment is very straightforward and that is because many gluten sensitive individuals, even if they have not yet developed celiac disease (villous atrophy), have symptoms that abate when gluten is removed from their diet. Furthermore, from a study done in Finland, a gluten sensitive individual who reports no symptoms at the time of diagnosis can improve both psychological and physical well-being after treatment for one year with a gluten-free diet.
    Despite the common sense and research evidence that early diagnosis of gluten sensitivity offers many health advantages over a diagnostic scheme that can only detect the minority and end-stage patients, until now, the limitation was still in the tests being employed. As mentioned above, the main tests used for primary (before symptoms develop) and secondary (after symptoms develop) screening for celiac disease, blood tests for antigliadin and antiendomysial/anti-tissue transglutaminase antibodies, are only routinely positive after extensive damage to intestinal villi. As shown in a 1990 publication, this is because unless you have full blown, untreated celiac disease, the IgA antibodies to gliadin are only INSIDE the intestine not in the blood. Measuring antigliadin antibody in blood and intestinal fluid (obtained by the laborious technique of having research subjects swallow a long tube that migrates into the upper small intestine), researchers found that in untreated celiacs, antigliadin antibody was present in the blood and inside the intestine, whereas after villous atrophy healed following a year on a gluten-free diet, the antigliadin antibody was no longer in the blood but was still measurable inside the intestine in those with ongoing mild inflammation.
    An important conclusion can be drawn from these results, as these researchers and myself have done: Gluten sensitive individuals who do not have villous atrophy (the mass of the iceberg), will only have evidence of their immunologic reaction to gluten by a test that assesses for antigliadin IgA antibodies where that foodstuff is located, inside the intestinal tract, not the blood. This makes sense anyway, because the immune system of the intestine, when fighting an antigen or infection inside the intestine, wages the fight right in that location in an attempt to neutralize the invading antigen, thereby preventing its penetration into the body. It does this with T cells on the surface of the epithelium, the intraepithelial lymphocytes, and with secretory IgA made with a special component called secretory piece that allows its secretion into the intestine.
    The excellent English researchers that made the discovery that they could detect the immunologic reaction to gluten inside the intestine before it was evident on blood tests or biopsies knew it was a breakthrough, testing it many times over in different ways, and further extending the clinical spectrum of gluten-induced disease to include a phase before the villi are damaged, so-called “latent celiac sprue”. Furthermore, they developed this technique of assessing the intestinal contents for antigliadin antibodies into what they viewed as a “noninvasive screening test for early or latent celiac sprue” (what others and I would simply call “gluten sensitivity”). However, this was not exactly noninvasive, nor was it simple. It still required the patient to swallow a tube, followed by a complete lavage of all their gastrointestinal contents with many gallons of nonabsorbable fluid that had to be passed by rectum and collected into a large vat to be analyzed for the presence of antigliadin antibodies.
    While this was indeed a conceptual breakthrough, it practically went unnoticed by the medical community because the cumbersome procedure of washing out the intestine just could not be done in a normal clinical setting. To this day, I am not sure how many people even know that it was not me, but rather this well known celiac research group, led by the late Dr. Anne Ferguson, who pioneered the assessment of the intestinal contents as a viable and more sensitive source of testing material for the early reactions of the immune system to gluten. What we did in my research was to refine and simplify the method of collecting and measuring these intestinal IgA antigliadin antibodies before they can be detected in blood. That is, instead of washing out the antibodies from the intestine, we allow them to be excreted naturally in the stool (feces). And so with that idea, and our ability to measure these antibodies in stool, as others before us had done for fecal IgE antibodies directed to food antigens, our new gluten (and other food) sensitivity stool testing method was born.
    It was actually my research of microscopic colitis that led me to discover that stool analysis was the best way of assessing for gluten sensitivity before celiac disease develops. Microscopic colitis is a very common chronic diarrheal syndrome, accounting for 10% of all causes of chronic diarrhea in all patients, and is the most common cause of ongoing chronic diarrhea in a treated celiac, affecting 4% of all celiac patients. However, from my published research, despite the presence of the celiac HLA-DQ2 gene in 64% of patients with microscopic colitis, very few get positive blood tests or biopsies consistent with celiac disease. Yet, small bowel biopsies revealed some degree of inflammation sometimes with mild villous blunting in 70% of cases. According to the facts and previously discussed shortcomings of celiac blood tests, antibodies to gliadin are unlikely to be detected in the blood in these patients because they lack villous atrophy. So negative blood tests for antigliadin antibodies per se did not, in my mind, rule out the possibility that these patients with microscopic colitis, a disease that under the microscope looks like celiac disease (but of the colon), and that affects many celiac patients, were not gluten sensitive themselves. But as Dr. Ferguson's research revealed, these antibodies might be detectable inside the intestine. And since we surely were not going to perform that cumbersome intestinal lavage test in my patients, we decided to see if we could find these antibodies in the stool as a reflection of what is coming through the intestine.
    Here's the first set of data that we found showing the superior sensitivity of stool testing versus blood tests for antigliadin IgA antibodies. In untreated celiac disease patients, we found a 100% positivity in the stool versus only 76% in blood. In hundreds of microscopic colitis patients since tested, only 9% have antigliadin antibody in blood but 76% have it in stool. And the same is true of 79% of family members of patients with celiac disease; 77% of patients with any autoimmune disease; 57% of people with irritable bowel syndrome-like abdominal symptoms; and 50% of people with chronic diarrhea of unknown origin, all of whom have only about a 10-12% positivity rate for blood tests (like normal volunteers). Thus, when you go to the source of production of these antibodies for testing, the intestine, the percentage of any population at a higher than normal genetic and/or clinical risk of gluten sensitivity showing a positive antigliadin stool test is 5 to 7.5 times higher than would be detected using blood tests. In normal people without specific symptoms or syndromes, the stool test is just under 3 times more likely to be positive than blood (29% vs. 11%, respectively). That's a lot more people reacting to gluten than 1 in 150 who have celiac disease. 29% of the normal population of this country, almost all of whom eat gluten, showing an intestinal immunologic reaction to the most immune-stimulating of dietary proteins really is not so high or far fetched a percentage, especially in light of the fact that 11% of them display this reaction in blood, and 42% carry the HLA-DQ2 or DQ8 celiac genes.
    Why is this so important? Because some people with microscopic colitis never get better when they're treated, and most autoimmune syndromes only progress with time, requiring harsh and sometimes dangerous immunosuppressive drugs just for disease control. If the immune reaction to gluten is in any way at the cause of these diseases as research suggests, and if we had at our disposal a sensitive test that can diagnose this gluten sensitivity without having to wait for the intestinal villi to be damaged, then treatment with a gluten free diet might allow the affected tissues to return to normal or at least prevent progression. We now have that test in fecal antigliadin antibody. Just a few weeks ago we completed the first follow-up phase of our study: What happens when a gluten sensitive person without villous atrophy goes on a gluten-free diet for one or two years. While I am still gathering and analyzing the data, most of the subjects reported a much improved clinical status (utilizing an objective measure of symptoms and well being). Not everybody gets well, because sadly not everyone stays on a gluten-free diet (as they sometimes admit on the surveys). Some people have the misconception that if they don't have celiac disease, but “I just have gluten sensitivity” then maybe they do not have to be strict with their gluten elimination diet. I do not think that is the case. Although a gluten free diet is like anything: Less gluten is not as damaging as more gluten, but certainly no gluten is optimal if a gluten sensitive person desires optimal health.
    Of the first 25 people with refractory or relapsing microscopic colitis treated with a gluten-free diet, 19 resolved diarrhea completely, and another five were notably improved. Thus, a gluten-free diet helped these patients with a chronic immune disease of a tissue other than small bowel (in this case the colon), who have been shown to be gluten sensitive by a positive stool test in my lab. The same may be true of patients with chronic autoimmune diseases of any other tissue, but who do not have full-blown celiac disease. Gluten-free dietary treatment, sometimes combined with dairy-free diet as well, has been shown to help diabetes, psoriasis, inflammatory bowel disease, eczema, autism, and others.
    Thus, my approach (and I believe the most sensitive and most complete approach) for screening for early diagnosis and preventive diagnosis for clinically important gluten sensitivity is a stool test for antigliadin and anti-tissue transglutaminase IgA antibodies (IgG is not detectable in the intestine) and a malabsorption test. The malabsorption test we developed is special, because you no longer have to collect your stool for three days; we can find the same information with just one stool specimen. Stool testing in combination with HLA gene testing, which we do with a cotton-tipped swab rubbed inside the mouth, is the best diagnostic approach available for gluten sensitivity.
    Who should be screened for gluten sensitivity? Certainly family members of celiacs or gluten sensitive people being at the highest genetic risk. For the most part, all of the following patient groups have been shown to be at higher risk than normal for gluten sensitivity: Chronic diarrhea; microscopic colitis; dermatitis herpetiformis; diabetes mellitus; any autoimmune syndrome (of which there is an almost end-less number like rheumatoid arthritis, multiple sclerosis, lupus, dermatomyositis, psoriasis, thyroiditis, alopecia areata, hepatitis, etc.); Hepatitis C; asthma; chronic liver disease; osteoporosis; iron deficiency anemia; short stature in children; Down's syndrome; female infertility; peripheral neuropathy, seizures, and other neurologic syndromes; depression and other psychiatric syndromes; irritable bowel syndrome; Crohn's Disease; and people with severe gastroesophageal reflux (GERD). Autism and possibly the attention deficit disorders are emerging as syndromes that may improve with a gluten- free (and additionally casein-free) diet. A diagnosed celiac might be interested in our testing to know (after some treatment period no shorter than a year) that there is no on-going damage from malabsorption, for which we have a test. If a celiac is having ongoing symptoms or other problems, a follow-up test should be done just to be sure there's no hidden gluten in the diet, or something else that could be present, like pancreatic enzyme deficiency which often accompanies celiac disease, especially in its early stages of treatment.
    Historically, with respect to diagnostic methods for celiac disease, from 100 A.D., when celiac disease was first described as an emaciating, incapacitating, intestinal symptom-causing syndrome, to 1950, we had just one diagnostic test: Clinical observation for development of the end stage of the disease. Then in 1940 to 1960, when the discovery of gluten as the cause of celiac disease occurred, the best diagnostic test was removing gluten from the diet and watching for clinical improvement. It was during this period that the 72-hour fecal fat and D-xylose absorption tests were developed as measures of gluten-induced intestinal dysfunction/damage. In the mid- to late1950's, various intestinal biopsy methods were pioneered and utilized, showing total villous atrophy as the diagnostic hallmark of celiac disease. You've heard the intestinal biopsy called the “gold standard”; well as you can see, it is a 50 year-old test, and thus, the “old” standard. It was not until the 1970's and 80's (and improved upon in the 1990's) that blood tests for antigliadin and antiendomysial/anti-tissue transglutaminase were developed, but again these tests like all methods before, can reliably reveal only the “heart attack” equivalent of the intestinal celiac syndrome: Significant villous atrophy or bad celiac disease.
    We are in a new century, a new millennium, and I have built upon what my research predecessors have started; mostly on the work of researchers who laboriously put down tubes and sucked out intestinal fluid for testing for antigliadin antibody when it was not present in blood. We now know that a stool test for antigliadin antibody is just as good and much simpler. The wide-reaching ramifications of knowing that so many more people and patients are gluten sensitive than have ever been previously known has led me to assume a professional life of medical public service. To do so, I started a 501©3 not-for-profit institute called the Intestinal Health Institute, have brought these new diagnostic tests to the public on the internet (at http://www.enterolab.com), and volunteer my time helping people with health problems by email and by lecturing. With greater awareness and education of both the public and medical community that early diagnosis of gluten sensitivity can be achieved before the villi are gone, more of the gluten sensitive iceberg will be diagnosed and treated early, leading to far fewer gluten-related symptoms and diseases than has ever been experienced before.
    Dr. Fine has been an intestinal researcher and an academic and clinical gastroenterologist for 15 years. He is the Director of The Intestinal Health Institute and The www.EnteroLab.com Clinical Laboratory in Dallas Texas.

    Dr. Ron Hoggan, Ed.D.

    This article appeared in the Spring 2005 edition of Celiac.coms Scott-Free Newsletter.
    Celiac.com 04/10/2005 - Celiac disease is, by definition, a condition in which the intestinal wall is damaged as a result of eating gluten. It is a chronic illness in which the symptoms wax and wane1 for reasons that are not yet understood. Celiac disease is the result of genetic and environmental factors. We now know two HLA markers (DQ2 and DQ8) for the predisposition for celiac disease2. One environmental factor is, of course, the consumption of gluten, but there may be other environmental contributors. Recent research reveals that about 1% of the population suffers from this condition3 although most remain undiagnosed.
    On the other hand, gluten sensitivity is characterized by antigliadin antibodies. This condition afflicts at least 12% of the general population4 and is found in patients with a wide variety of autoimmune diseases. In some studies of neurological diseases of unknown origin, a majority of patients show signs of gluten sensitivity4. These patients are mounting an immune response to the most common food in the western diet, yet many practitioners consider gluten sensitivity to be a non-specific finding, frequently counseling patients to ignore these test results. This is particularly unfortunate since a strict gluten-free diet has repeatedly proven helpful to patients who are fortunate enough to consult a practitioner who is versed in gluten sensitivity and its connection with autoimmunity.
    Untreated celiac disease carries an added risk for a wide variety of additional autoimmune diseases. The most likely cause of this predisposition to additional autoimmune disease is a condition sometimes referred to as leaky gut syndrome. We know that gluten causes intestinal damage. We also know that this damage allows large undigested and partly digested proteins to leak into the bloodstream through the damaged intestinal wall. This leakage results in immune system production of antibodies to attack these foreign proteins as if they were invading microbes. The result is the production of a huge variety of selective antibodies, and each type recognizes a particular short chain of amino acids located somewhere in the proteins structure. Unfortunately, our own tissues can contain very similar or identical sequences of amino acids. Hence, by a process called molecular mimicry, we are producing antibodies that attack both the foreign food proteins that are leaked into our blood through the damaged intestinal wall, and similar amino acid sequences in our own tissues, often resulting in an autoimmune disease5.
    The supposedly non-specific antigliadin antibodies in gluten sensitivity provide two important pieces of information: 1) That the intestinal wall has been damaged and is permitting leakage of food proteins into the bloodstream, and; 2) That the dynamic contributing to increased autoimmunity in celiac disease may well be an important contributing factor in gluten sensitivity5. The currently common view that celiac disease is a serious illness, while disregarding gluten sensitivity, is dangerous to gluten sensitive patients.
    This bias is also a divisive element in the gluten-sensitive/celiac community. Whether a person has "biopsy proven" damage to the intestinal wall, if this person gets sick from eating gluten, or mounts an immune response to gluten, we are all in the same leaky boat (please pardon the pun). We need to work together to get a better understanding of gluten sensitivity in all its forms (including celiac disease). As a community, we need to discourage any kind of dismissal of illnesses that are partly or wholly mediated by gluten.
    If we can stand together in our quest for widespread recognition of the damaging impact of gluten consumption, we can all enjoy a healthier life. Our descendants will also inherit a more gluten-savvy world.
    Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be ordered at Celiac.com. Rons Web page is: www.DangerousGrains.com
    Sources:
    Cooke W, Holmes G. Coeliac Disease. Churchill Livingstone, New York, N.Y. 1984. Fasano A. Celiac disease--how to handle a clinical chameleon.
    N Engl J Med. 2003 Jun 19;348(25):2568-70. Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago S, Elitsur Y, Green PH, Guandalini S, Hill ID, Pietzak M, Ventura A, Thorpe M, Kryszak D, Fornaroli F, Wasserman SS, Murray JA, Horvath K. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study. Arch Intern Med. 2003 Feb 10;163(3):286-92. Hadjivassiliou M, Grunewald RA, Davies-Jones GA. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. Braly J, Hoggan R.. Dangerous Grains, Penguin-Putnam-Avery, New York, N.Y., 2002.

    Dr. Rodney Ford M.D.
    This article appeared in the Autumn 2006 edition of Celiac.coms Scott-Free Newsletter.
    Celiac.com 12/11/2006 - Yes, thats what I think. Gluten-sensitivity is a disease of your brain and nerves.
    The gluten puzzle
    I have come to this conclusion after studying the effects of gluten on my patients for over a decade. I am a pediatric gastroenterologist and allergist. I run a busy clinic for children and their parents. I have been increasingly concerned by the large numbers of my patients who are affected by gluten. I was perplexed by their wide-ranging symptoms. The puzzle was to explain how gluten could cause so much ill health to so many people in so many different ways, including celiac disease.
    Faulty brain control
    Eureka! The solution came when deep in discussion with my friend and colleague, Ron Harper, Professor of Neurobiology, UCLA. We were both struggling with the concept of multiple symptoms that needed to be explained. The answer appeared absurdly simple: disturbed "brain control". It suddenly seemed obvious—gluten could disturb the neural pathways of the body. Gluten was gradually damaging the brain and the nerves of susceptible people. It was the brain that was the common pathway for the manifestations of all of the gluten symptoms. So I set out to research what the world medical literature had to say.
    Is gluten a neurotoxin?
    I felt excited. I reviewed my patients in this new light—I began looking for a brain-grain connection. I began to see gluten as a neurotoxin—this could provide a universal model of gluten-sensitivity. This toxicity might act through inflammatory mechanisms or cross-reactivity with neurons. I began accumulating the evidence for my proposal that gluten-sensitivity is a brain and nerve disease.
    "Full Of It!"
    The concept of "Full of it" developed from the stories from my patients. I wrote my hypothesis down in a book now called Full of it! It refers to our diets being full of gluten; to the world being full of gluten-sensitive people; to the medical practitioners who are so skeptical of adverse reactions to gluten; to the enthusiasm of people who are feeling vibrant again on a gluten-free diet; and to those who are brimming with hope that the problem of gluten has now been recognized.
    Food allergy skeptics
    As a junior doctor I decided to formally research the food allergy phenomenon. I was awarded a research post and carried out the first comprehensive food allergy studies in New Zealand. I triumphantly demonstrated that food allergy was both a real entity and that it was common. But, to my disappointment, my colleagues were reluctant to believe me or my data. They professed a "disbelief" in food allergy. This surprised me as I had the research data.
    My next step was to conduct four more years of investigation of food allergy in Australia (at the Royal Childrens Hospital, Melbourne). This was a bigger and more elaborate study. My Doctoral Thesis (1982) based on this work is called: Food hypersensitivity in children: diagnostic approaches to milk and egg hypersensitivity. Since then I have continued my investigations into food allergy—but still today (25 years later) medical skepticism abounds. This "disbelief" is held despite the vast body of research describing food allergy. There seems to be an underlying unwillingness for doctors to consider food allergy as a possibility. Unfortunately, this also applies to gluten reactions.
    The shocking truth
    The shocking truth about gluten is that gluten foods are causing tremendous damage—but currently this is going mostly unrecognized. Unfortunately, gluten grains have become our staple diet. The quantity of gluten in our food supply has been steadily increasing. Yet worse, official Health Policies endorse gluten grains as the foundation of our food pyramid.
    Medics turn a blind eye
    Gluten is sapping the energy and wellbeing of countless millions. To date, the medical profession has turned a blind eye to glutens wider problems whilst focusing all of their attention on the narrow problem of celiac disease.
    A typical story
    I received emails like this every day:

    "Dr Ford, I have emailed you a number of times regarding our two children.
    I thought I should let you know that since going gluten free for the last three months, at last our son and daughter have put on some weight.
    If I had kept them on a normal gluten diet (which they recommended at the hospital) we would be still be having the headaches and sore tummies as well as the bad moods which our son would have. People just thought he was a naughty child, but now he is so different - we can talk to him without getting into any fights.
    I congratulate you for all your efforts on bringing gluten intolerance to the media and medical profession. More children and their families may find long awaited help. We have had to put up with this for seven years! At long last there is light at the end of the tunnel. Kind regards, Sue and Garry."
    Can gluten damage your brain?
    I believe that gluten was actually causing these two children to be sick. That is the explanation for their "naughty" behavior, their moods and their headaches.
    I postulate that gluten can damage your brain. I have come to this conclusion by the abundant circumstantial evidence from my observations of my patients who are gluten-sensitive. I have pondered the next questions: "Why do they have such an array of symptoms from gluten?" "Why do they recover so quickly when gluten is removed?" And "Why do they deteriorate so rapidly when only tiny amounts of gluten are eaten?" The concept of a brain/nerve disease can explain everything.
    The brain/nerve hypothesis
    "The symptoms from gluten occur through its action on the nervous system".
    I propose that gluten-sensitivity is a brain condition. Each and every organ in your body has some form of brain/nerve control. I propose that gluten can injure the delicate nervous networks that control your guts functions. A malfunction will subsequently lead to all of the gut symptoms that have so well been described. In addition, gluten can also directly affect brain function, which leads to the primary neurological symptoms that are so commonly seen with gluten-sensitivity.
    What is new?
    There are a number of new ideas that I put forward. These are based on circumstantial evidence. They produce a unifying theory of the symptoms that are attributed to gluten toxicity.
    A brain disease
    I consider that gluten-sensitivity is mostly a neurological problem. A major contribution to this debate is the realization that the brain has a central role in the expression of the symptoms that have, until now, been attributed to the local toxicity of gluten in the gut. A nerve disease
    I propose that gluten-sensitivity is a nerve disease. There is a gigantic network of nerves that controls every function that your gut is programmed to do. There are as many nerve cells in your gut as there are in your head! (about 25 billion nerve cells). I call it your tummy brain (or gut brain). Your tummy brain can be directly damaged by gluten reactions. This is the cause of so many sore tummies and bowel troubles. A wide spectrum of neurological manifestations
    For decades, there have been reports of unexplained brain and nerve symptoms which are associated with celiac disease. Although these associations have been described, there has been no universal mechanism proposed. However, if gluten is seen as a neurotoxin, then the explanation has been found. A very common disease
    Reactions to gluten have recently been documented to be extremely common. About one-in-ten people (as ascertained by blood donor studies) have high levels of gluten antibodies in their blood. My clinical studies have arrived at this same high number of gluten-sensitive people. Others have data to show that it is even more prevalent. Am I full if it?
    You might ask, "Is he full of it?" Yes, I am full of excitement and hope for the future. So many people can now be helped, if only this information can be widely distributed. I am full of ideas and full of enthusiasm. I hope that you are full of hope for your healthy and vibrant future.
    Tariq's story:

    "Dear Rodney,

    Thank you for your care and support of my family in regard to our allergies, gluten sensitivity and celiac disease that exists within that framework.

    My son Tariq, who is nearly 12 years old, has been a patient of yours over a number of years for his multiple food allergies. Tariq also suffers from dyslexia. Over the last several years Tariq has been becoming increasingly tired, lacking in energy and motivation, struggling with school work and constantly scratching due to his eczema and rashes covering all of his body.
    During this time, even though he has attended soccer training up to four times a week he somehow gained a lot of weight. Tariq was constantly grumpy and had low mood levels.

    Two months ago you diagnosed Tariq with gluten-sensitivity (his tTG 4; IgG-gliadin 86; IgA-gliadin 9).
    Tariq was extremely reluctant to go on a gluten free diet. But as the rest of the family had gone gluten-free—so he was forced also to become gluten-free.
    The changes that a gluten-free diet has evoked in Tariq have been astounding. His energy levels have increased, his skin has vastly improved, he has lost a lot of his excess weight (even though his appetite has increased) and he has shown improvement in his dyslexia.
    Tariq is not as grumpy as he was and his mood levels have improved. Tariq is now vigilant about gluten and can see the differences it has made to his life and the quality of it.
    Also, the other soccer parents have noticed a vast improvement in Tariqs energy levels and speed. His teacher has also noticed a big difference.
    Thanks again.
    Regards, Rosemary"
    Are you affected?
    The shocking truth is that gluten can damage your brain and that so many people are being encouraged to eat gluten-foods that might be steadily eroding their health and energy. If you have any lingering doubt about your own health, then I suggest that you check out the possibility of gluten-sensitivity.
    If you have any comments or questions we would love to hear from you.
    Dr Rodney Ford is a Pediatric Gastroenterologist, Allergist and Nutrition Consultant. He has been Associate Professor of Pediatrics at the Christchurch School of Medicine, University of Otago. He runs a busy Childrens Gastroenterology and Allergy Clinic in Christchurch, New Zealand. He has written over a hundred scientific papers including book chapters and books. www.doctorgluten.com
    This includes a series of five books on gluten: why it can make you ill and how to go gluten-free.
    Are You Gluten-Sensitive? Your Questions Answered Going Gluten-Free: How to Get Started The Gluten-Free lunch book The book for the Sick, Tired and Grumpy (Gluten-Free kids) Full of it! The shocking truth about gluten (The brain-grain connection - ISBN 978-0-473-10407-8)

    Dr. Scot Lewey

    This article appeared in the Winter 2007 edition of Celiac.coms Scott-Free Newsletter.
    Celiac.com 01/30/2007 - Gluten intolerance resulting in symptoms and illness similar to celiac disease without meeting diagnostic criteria for celiac disease is a new concept. This concept of non-celiac gluten sensitivity (NCGS) or gluten related disease (GRD) may be a new paradigm that is hard for some people to swallow, especially when I suggest that it affects as much as 10% to 30% of the population.
    Gluten ingestion is an avoidable, treatable, and reversible cause of illness in many people. It is contributing to the rising epidemic of autoimmune diseases. Many resist these concepts finding them either unbelievable, unacceptable or both. I believe that their rejection is neither rational nor helpful. It may be reasonable to reject them for cultural or financial reasons though I don’t believe they can legitimately be rejected based on scientific grounds or experience.
    Celiac disease is not rare. Celiac disease affects 1 in 100 people in the world. Yet the diagnosis of celiac disease is still frequently missed and/or delayed.
    It is a common disease that is often undiagnosed or misdiagnosed. It may even be the most common autoimmune disorder. Though the risk is largely genetic, it is preventable by simply avoiding gluten. Autoimmune diseases associated with celiac disease may also be preventable by avoiding gluten.
    When I was in medical school over twenty-five years ago, I was taught that celiac disease was rare. In residency we were shown photos of short, emaciated children with skinny limbs and pot-bellies. We were told that their medical history included symptoms of profuse, watery, floating, foul-smelling diarrhea, and iron deficiency anemia. The picture and story was burned into the hard drive of our brains, not necessarily because anyone believed we would see someone with celiac disease in our practice, but because celiac disease was considered rare and odd enough that it was a favorite board examination question. That image and story remains in the mind of most physicians, preventing them from seeing celiac disease in a much broader light.
    When I entered subspecialty training in gastroenterology, 13 years ago, specific blood tests for celiac disease were available but still new. We were beginning to order the blood test when classic symptoms of celiac disease were seen without an identifiable cause, or if we happened to sample the small intestine during endoscopy and classic Sprue changes were seen in the intestinal biopsy. celiac disease was still considered somewhat rare. We did not routinely biopsy the small intestine to screen for celiac disease, and genetic tests were not yet available.
    It wasn’t until 2003 that Fasano’s landmark article reported Celiac disease affected 1 in 133 people in the U.S. Only recently has it been accepted that family members of people with celiac disease, those with digestive symptoms, osteoporosis, anemia, and certain neurological, skin or autoimmune disorders constitute high risk groups for celiac disease. They have an even higher risk of between 2% to 5%, though most physicians are unaware of these statistics. Every week, using the strict diagnostic criteria, I confirm 2-3 new cases of celiac disease. I also see 5-10 established celiac disease patients. However, for every identified celiac disease patient there are 3-10 who have clinical histories consistent with celiac disease, but who fail to meet the diagnostic criteria. Yet they respond to a gluten-free diet. Many have suggestive blood test results, biopsies and or gene patterns but some do not.
    More than 90% of people proven to have celiac disease carry one or both of two white blood cell protein patterns or human leukocyte antigen (HLA) patterns HLA DQ2 and/or DQ8. However, so do 35-45% of the general U.S. population, especially those of Northern European ancestry. Yet celiac disease is present in only 1% of the same population. DQ2 or DQ8 are considered by some experts to be necessary though not sufficient to develop celiac disease. However, celiac disease without those two genes has been reported.
    Other gluten related diseases including dermatitis herpetiformis, the neurological conditions of ataxia and peripheral neuropathy, and microscopic colitis have been described in DQ2 and DQ8 negative individuals. The DQ genetic patterns found in other gluten related diseases and associated with elevated stool antibody tests indicate that many more people are genetically at risk for gluten sensitivity. Furthermore, the response of numerous symptoms to gluten-free diet is not limited to people who are DQ2 or DQ8 positive.
    Most celiac experts agree upon and feel comfortable advising people who meet the strict criteria for the diagnosis of celiac disease: they need to follow a life-long gluten-free diet. Controversy and confusion arises when the strict criteria are not met, yet either patient and/or doctor believe that gluten is the cause of their symptoms and illness.
    Many alternative practitioners advise wheat-free, yeast-free diets, which are frequently met with favorable response to what is really a form of gluten-free diet. Similarly, the popularity and successes of low carbohydrate diets require adherence to a diet that has been credited with improvement of headaches, fatigue, bloating, musculoskeletal aches, and an increased general sense of well-being that is self-reported by many dieters. I believe this is because of the low gluten content. Gluten avoidance is clearly associated with improvement of many intestinal and extra-intestinal symptoms such as those listed above.
    Many also stumble onto this association after initiating a gluten-free diet or wheat-free diet on the advice of friends or family members; dieticians, nutritionists, alternative or complementary practitioners; or after reading an article on the Internet.
    Within the medical community, there seems to be an irrational resistance to a more widespread recommendation for gluten avoidance. Physicians who maintain that those who fail to meet strict criteria for diagnosis of celiac disease should not be told they have to follow a gluten-free diet will often acknowledge that many of these patients respond favorably to a gluten-free diet. Some, however, continue to insist that a gluten-free diet trial is unnecessary, unduly burdensome, or not scientifically proven to benefit those who do not have celiac disease. This position is taken despite the absence of evidence that a gluten-free diet is unhealthy or dangerous and much evidence supporting it as a healthy diet.
    Those of us who have observed dramatic improvements, both personally and professionally, find such resistance to recommending a gluten-free diet to a broader group of people difficult to understand. Considering the potential dangers and limited benefits of the medications that we, as doctors, prescribe to patients for various symptoms, it really seems absurd to reject dietary treatments. Yet, it does not seem to cross most doctors’ minds to suggest something as safe and healthy as a gluten-free diet, let alone to, at least, test for celiac disease.
    My personal journey into gluten related illness began when my physician wife was diagnosed with celiac disease. I had mentioned to her numerous times over several years that I thought she should be tested for celiac disease. After her second pregnancy she became progressively more ill experiencing, for the first time in her life, diarrhea, fatigue, and chronic neuropathy. An upper endoscopy revealed classic endoscopic findings. Celiac disease blood tests were elevated, and genetic testing confirmed she was DQ2 positive. This forever changed our lives and my practice. But the story doesn’t end there.
    Having diagnosed myself with irritable bowel syndrome (IBS) and lactose intolerance in medical school, I had not considered gluten as a possible cause of my symptoms until my wife turned the table on me and said I should also be tested for celiac disease. My blood tests were not elevated but I was confirmed to also be DQ2 positive.
    Having observed a good response to gluten-free diet in a few of my patients who had elevated stool gliadin antibody levels, I looked critically at the research behind this testing and spoke with Dr. Ken Fine before paying to have my entire family tested through Enterolab. Both my gliadin and tTG antibodies were elevated and I responded well to a gluten-free diet. I began recommending stool antibody and DQ genetic screening to patients who did not meet the strict criteria for celiac disease but appeared to have symptoms suggestive of gluten sensitivity. Contrary to some critics’ claims about the stool antibody tests, there are many people who do not have elevated levels. Almost everyone I have seen with elevated levels has noted improvement with gluten-free diet, including myself.
    Not only did my “IBS” symptoms resolve and lactose tolerance dramatically improve, but my eyes were further opened to the spectrum of gluten related illness or symptoms. I was already aggressively looking for celiac disease in my patients but I began considering non-celiac gluten sensitivity (NCGS) or gluten related diseases (GRD) in all my patients. What I have found is that gluten is an extremely common but frequently missed cause of intestinal and non-intestinal symptoms. Dramatic improvements in symptoms and health can be observed in patients who try a gluten-free diet.
    Since only a fraction of DQ2 or DQ8 positive individuals have or will eventually get celiac disease, does that mean gluten is safe to eat if you have those gene patterns? Even if you do not get celiac disease, does continuing to eat gluten put you at risk for other autoimmune diseases, especially ones linked to the high risk gene patterns? Why do some people with these patterns get celiac disease but most do not? Do some who do not have celiac disease experience symptoms from gluten that would improve with gluten-free diet? These questions need to be answered so that people can decide whether they want to risk that gluten is causing them to be ill, or is increasing their risk of celiac disease or other autoimmune diseases.
    Added to my gluten-free diet, a daily diet of scientific articles on celiac and gluten related disease has revealed that there are many clues in the literature and research indicating the existence of non-celiac gluten sensitivity or a need to broaden our definition of celiac disease. Dr. Hadjivassiliou has called for a new paradigm. He advocates that we start thinking of gluten sensitivity not as an intestinal disease but a spectrum of multiple organ, gluten-related diseases. Mary Schluckebier, director of CSA, asks that physicians interested in this area work on forming and agreeing on new definitions for gluten related illness while pushing for more research and cooperation between medical researchers, food and agricultural scientists, dieticians, and food manufacturers.
    Only those who look for NCGS and advise a gluten-free diet to those not meeting the strict criteria for celiac disease, are going to see the larger group of people who have a favorable response to a broader application of the gluten-free diet without further research. Those of us who are personally affected by gluten sensitivity or professionally involved in treating individuals with adverse reactions to gluten (or both) should support the research into the broader problem of gluten related illness. I believe that NCGS is real and will be validated in studies. Are you open to this concept and are you willing support more research in this area?
    Dr. Scot Lewey is a physician who is specialty trained and board certified in the field of gastroenterology (diseases of the digestive system) who practices his specialty in Colorado. He is the physician advisor to the local celiac Sprue support group and is a published author and researcher who is developing a web based educational program for people suffering from food intolerances, www.thefooddoc.com
    Copyright 2006 The Food Doc, LLC. All Rights Reserved.

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

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

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

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

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

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

    Dr. Rodney Ford M.D.
    Celiac.com 03/15/2016 - "Creating health comes down to the food we eat and how we choose to live our lives." – Dr. Terry Wahls
    Lots of people find it hard to believe that such a common food as wheat/gluten could possibly be implicated in causing skin diseases. They say something like this: "Everyone eats wheat, but not everyone gets skin troubles—so it can't be wheat!" This logic is flawed. I have written this book so that you can read all of the evidence about gluten-related skin disease in one place. "Cutaneous gluten sensitivity" is one of the new terms applied to the group of gluten-related skin diseases.
    Max belongs to this leg in the photo. He is very itchy and sore. He is 18-years old and not getting any better—in fact he has been getting worse. He came to me seeking help. Mum wrote,
    "Max has been suffering from debilitating dermatitis over his whole body for the last 3 years. He is withdrawn, self-conscious, covered with sores, and feels he will never get better. Unfortunately, the creams he is putting on just seem to irritate him."
    So, I am investigating him for gluten-related eczema. It will be a relief for him if the tests come out positive for gluten. What should be the strategy to get him better?
    I don't want him to go through the rest of his life like Elizabeth Whitesell, from the Gluten Zero Facebook page, who explains:
    "I was frantic with itching before my celiac diagnosis. The dermatologists never addressed the possibility of celiac, just gave me new treatments for my itching. I cannot name all of the creams, oils, pills and ointments I used, along with a blue-light treatment. Steroid shots, creams and pills were a major part of my treatment." "I received some temporary relief and never traveled without my creams. Itching on my hands was so fierce that I carried a frozen ice block (the kind used in coolers) in my purse. When we were at a public event, I gripped my hands around the ice to ward off a noisy itching attack. Ice was my godsend to keep the itching from following its neurological path. All of my blouses had blood dot stains from clawing my upper arms like I was an ape when into full-time mode." "My best treatment was freezing 2-liter bottles of water and holding them between my knees as I laid down to go to sleep. If I could fall asleep before the freaking stage began, I was on a roll. More frozen bottles were kept in a cooler by my bed for when the thaw came and I was too tired to walk downstairs to replace them." "What a saint of a husband I had. Once I went gluten-free, so many changes came for the better. I did not suddenly notice the absence of itching but, one day, looked back and realized I was not traveling and sleeping with frozen bottles anymore. I hope dermatologists are more informed now." Skin Diseases Associated with Celiac Disease
    Gluten is known to cause skin disease. Gluten can definitely cause itchy skin. Collectively, these skin-diseases provoked/triggered/caused by gluten can be called "cutaneous gluten sensitivity". This is an umbrella term which includes:
    Dermatitis Herpetiformis (DH); Celiac associated skin diseases; Non-celiac associated skin diseases. So what is the evidence?
    1) Dermatitis Herpetiformis: To summarise the previous chapter, the classic skin complaint is dermatitis herpetiformis. It usually affects the elbows, knees, buttocks, scalp, and back. It begins as little bumps that then change into little blisters. People say that they are driven mad by the itching. It is caused by an immune reaction to gluten in the skin. Microscopic clumps of immune-complexes get deposited just under the skin. This creates the very itchy rash. These tiny particles of immunoglobulins can take years to clear up once you start on a gluten-free diet. It is reported that it can take up to ten years before you make a full recovery.
    2) Celiac Associated Skin Diseases: Marzia Caproni and co-workers have detailed the skin diseases that have so far been associated with celiac disease (and perhaps by implication, with gluten).
    In their paper, "Celiac Disease and Dermatologic Manifestations: Many Skin Clues to Unfold Gluten-Sensitive Enteropathy" they include common skin complaints that most people do not associate with gluten-illness:
    Dermatitis Herpetiformis Psoriasis Alopecia Areata Chronic Urticaria Hereditary Angioneurotic Edema Cutaneous Vasculitis Atopic Dermatitis Eczema Vitiligo They also remind us that enamel defects, delayed eruption, recurrent aphthous ulcers, cheilitis, and atrophic glossitis are gluten-associate conditions and that "the diagnosis of celiac disease can sometimes be made from a smile!"
    Their important message is that anyone with any of these conditions should be investigated for celiac disease.
    3) Non-celiac Associated Skin Diseases
    The skin is a frequent target organ in gluten-sensitivity. The skin, hair and teeth can all be disturbed by gluten. However, eczema is a much more common manifestation of gluten-sensitivity.
    Humbert and his dermatology colleagues (Gluten intolerance and skin diseases, 2006) wrote this about gluten and skin disease:
    "Gluten sensitivity, with or without celiac disease symptoms and intestinal pathology, has been suggested as a potentially treatable cause of various diseases. There have been numerous reports linking celiac disease with several skin conditions. Dermatitis herpetiformis is actually a skin manifestation of celiac disease. Autoimmune diseases, allergic diseases, psoriasis and miscellaneous diseases have also been described with gluten intolerance." "Dermatologists should be familiar with the appraisal of gluten sensitive enteropathy and should be able to search for an underlying gluten intolerance. Serological screening by means of anti-gliadin, anti-endomysial and tissue-transglutaminase antibodies should be performed. Gluten intolerance gives rise to a variety of dermatological manifestations which may benefit from a gluten-free diet." This is an important statement.
    In 2010, Korossy reported a skin eruption that he called "gluten-sensitive dermatitis" which he says is clinically indistinguishable from dermatitis herpetiformis but lacks the IgA connection. (Non-dermatitis herpetiformis gluten-sensitive dermatitis: a personal account of an unrecognized entity, Korossy, 2010).
    Cutaneous Gluten Sensitivity
    Bonciolini et al (2015) have made a study of the skin manifestations of people with Non-Celiac Gluten Sensitivity (NCGS) Cutaneous Manifestations of Non-Celiac Gluten Sensitivity: Clinical Histological and Immuno-pathological Features, Bonciolini et al 2015
    They have adopted the term 'cutaneous gluten sensitivity'. They describe 17 consecutive patients affected by NCGS. They had excluded celiac disease and wheat allergy. They said:
    "The skin lesions observed were similar both to eczema and psoriasis and did not show a specific histological pattern. Furthermore, no serological marker was useful to identify these patients. The only data common to most of these patients affected by NCGS associated to non-specific skin manifestations are: the itching; the presence of C3 at the dermoepidermal junction; a rapid resolution of lesions when adopting the gluten free diet. Therefore, dermatologists must be familiar with the cutaneous manifestations and symptoms of gastrointestinal disorders. An appropriate understanding, work-up, consultation and management will help to identify the important cutaneous–gastrointestinal connection and ensuring that this important gastroenterological disease in patients with skin manifestations is not ignored.
    Finally, we suggest an accurate follow-up of all patients who report intense itching and gastrointestinal disorders, even when histology and morphology of the skin lesions do not identify a specific skin disease.
    We also suggest the adoption of gluten-free diet for at least three months assessing any positive effects."
    A Family Affected by Cutaneous Gluten Sensitivity
    Katrina Ojakaar writes this about the severe skin problems in her family that were eventually shown to be related to gluten-harm: "I had terrible eczema on my legs as a child. As an adult I had recurrent eczema on my eyelids and hands in addition to severe dry, itchy skin on my scalp, back, and legs. I also developed rosacea on my face that was treated unsuccessfully with antibiotics and topical ointments. At the age of 44, I had a lab test that showed gluten was making me sick. I immediately stopped eating food that contained gluten and within weeks watched my skin transform. I no longer have raw eczema patches or dry skin; and my rosacea has disappeared." "My daughter, Lila, had horrific diaper rash as an infant and nothing seemed to heal her sore bottom. Even as she grew out of diapers, her bottom was always irritated. Lila's skin was also very dry and irritated. Lotions and even plain bath water caused a sting. But when Lila stopped eating gluten, her skin simply healed. She now has smooth, soft, and moist skin without irritation and enjoys a relaxing bath." "My mother suffered from psoriasis on her legs and scalp until she stopped eating gluten at the age of 72. She is now 75, and the psoriasis has disappeared. Her skin is healthy, and she doesn't eat gluten, dairy, or oats." My father had rosacea on his face and was diagnosed with the autoimmune disease called lichen planus about 12 years ago. He had raw, bleeding sores on his scalp. And his fingernails and toenails disintegrated where he was left with only tender skin. Three years ago my dad stopped eating gluten, and two months later, his fingernails started to grow back. He now has a thin narrow layer of nail at the age of 80. The lesions related to his lichen planus disease on his scalp are gone. And, my father's rosacea, like mine, also healed when he stopped eating gluten." Keratosis Pilaris
    Keratosis pilaris, or sometimes called 'chicken skin' is blamed on gluten by many people. It is very common, occurring in about 10% of people, and there seems to be a hereditary nature to it. It tends to lessen with age, being prominent in toddlers. Any gluten connection remains speculative.
    Anne Luther writes:
    "One of the many pleasant surprises I had when I stopped eating gluten was the disappearance of three different skin rashes. There were non-itchy bumps on my back and arms, non-itchy red bumps on the soles of my feet and a very itchy rash on my legs behind my knees. None of these were ever diagnosed by a doctor but they all disappeared after I had totally eliminated gluten from my life." Keratosis pilaris is skin condition characterized by rough patches of skin caused by small, acne-like bumps. It is found mostly on the upper arms, upper thighs, and cheeks. It can feel a bit like sandpaper or goose-flesh. These little bumps are usually white, but can be red. They do not hurt. Sometimes they can feel a bit itchy.
    Keratosis pilaris seems to be caused by a build-up of keratin, the protein that helps create the protective skin barrier. Once keratin has formed into a hard plug at the opening of the hair follicle, this can block the oil and sweat glands. Consequently, these substances cannot escape out onto the skin, and results in these patches of rough, bumpy skin.
    I see a lot of keratosis pilaris in my Clinic. The gluten connection not clear, but many parents report its disappearance on a gluten-free diet.
    What happened to Max?
    Remember Max's legs at the beginning of this Chapter? Well it turned out that Max had two copies of the HLA gene DQ2 which gives him a 1-in-7 chance of developing celiac disease. It also increases his likelihood of having gluten sensitivity. However his blood tests for gluten (AGA) and celiac disease (tTG) were negative. But he did have evidence of a wheat allergy from his EAST tests. His total IgE levels were extremely high as well (over 4000), showing his heightened allergic status.
    So he has now embarked on a trial of a gluten-free diet. Mum says, "I feel that we are starting to get to the bottom of it now." It will be another 6 months before we know his results of his gluten-free diet. It can take a long time to heal.
    This was an excerpt from Dr Rodney Ford's latest eBook: "Dermatitis Eczema: Gluten Wheat – Solving the Eczema Puzzle." Available at: http://www.GlutenEczema.com

    Curtiss Ann Matlock
    Celiac.com 03/30/2016 - The woman's voice, polite but firm came over the line: "We cannot accommodate your mother."
    "You can't accommodate her?" I wondered if I'd heard wrong.
    "No. We just had a team meeting and it was decided we cannot accommodate your mother because of her diet."
    "Oh." The line hummed as I took in both the news and the woman's frosty tone. The previous week the woman, the admissions coordinator of the nursing home, had been all warm and inviting, even eager to have my mother.
    Finally I came out with, "Well…thank you for letting me know," and the line clicked dead as the woman hung up.
    I had not seen this coming. I hadn't realized that a nursing home would, or could, turn down a patient based on the need for a therapeutic diet. I thought the reason for a nursing home was to care for ill people.
    When I toured the nursing home, the woman proudly proclaimed the facility as being on Newsweek's top recommended list, and gave the appearance of understanding my mother's gluten-free diet, saying, "My niece has told me of it. She's convinced me to eat more gluten-free." The woman went so far as to take notes on my mother's preferences, her love of sleeping in and drinking coffee, and then plopped in my arms a thick packet of Medicare forms. In all ways she had been exceedingly pleasant. Indeed everyone I met at the facility had been pleasant. Purring cats roamed the facility's hallways, birds sang from cages, and they even had a pot-bellied pig in the shade of a tree that could be seen through a window, all for the comfort of the patients. It struck me that they could do these many things for their patients, but feeding one small woman with celiac disease a gluten-free diet was beyond them.
    My mother is eighty-eight years old, a pixie with a contagious smile and genteel Southern manner. She was diagnosed with celiac disease at the age of seventy-five. At that time she was on daily use of a nebulizer, sleeping half days and could not leave home and the bathroom unless she took Imodium. The diagnosis and strict adherence to the gluten-free diet returned her to an active life. She took up painting and driving her aging neighbors out to enjoy shopping.
    A year ago, in rapid succession, a mass was found in one of her lungs, glaucoma took her sight and a stroke impaired her right hand and memory. For months, she required caregivers around the clock. Today she is mobile with the aid of a walker and can manage nights on her own. She can do one thing for herself, and that is get herself to and from the bathroom. Everything else must be done for her—bathing and dressing and maintaining clothes, medications, food preparation, working the television and her bedside radio. On occasion she will get confused and afraid, so I try not to leave her alone for more than an hour. With the aid of private caregivers and hospice assistance, I have been able to keep her in my home, where she has lived for the past six years. However, her funds are depleting for private care, and there is no one to help me care for her.
    After the disappointing phone call from the nursing home admissions coordinator, I sat thinking over all the above facts and allowing myself a sizable hissy fit. Then I gathered myself together and took another look at the nursing home facilities in my area.
    For the next two weeks, I sought more information and made lists. My plan was to be better prepared in knowledge and approach. Running on the theory that it is lack of knowledge that causes the fear of a situation, I put together information on my mother: a list of her conditions, needs and food preferences. Because of no longer having teeth, nor wearing dentures, and her advanced age, she needs soft foods, her favorites being eggs and Vienna sausage, puddings, bananas. At the time she would eat mashed chicken and some vegetables, all simple things. I wanted to reassure the admissions director and staff of the nursing facilities that my mother was easily cared for, and that I was willing to help with her food. I also had two brochures from Gluten Intolerance Group: a single sheet on celiac disease itself, and a color glossy brochure, put together in cooperation with the National Foundation for Celiac Awareness, entitled Celiac Disease in the Older Adult. I hoped to engage the interest of people whose primary aim and business is providing healthcare to the elderly.
    What I discovered is a general lack of any interest in the welfare of the elderly.
    The young woman admissions coordinator of my second choice of facilities, a modern, airy facility, answered my question about their kitchen and possible meeting with the dietary manager, with, more or less, "I've shown you around the building. I don't know what else you want to know." Then she added, "And right now we don't have any female beds available."
    At another facility, the admissions coordinator brushed aside any idea of speaking with the dietician. She did not know what celiac disease was, but assured me they could, "probably handle it."
    The best facility that I found had a waiting list of at least forty names. They stayed so full that they did not provide temporary respite care. Even so, the admissions coordinator showed me around the building, which was very old, and the sight of an elderly blind woman slumped uncomfortably in a wheelchair in the hallway haunted me. Yet their menu posted on the bulletin board seemed promising. "We do home-cooking," the coordinator said proudly. Then she glossed over my request to see their kitchen and meet the dietician. She admitted to never having heard of celiac disease, but said, "We've had many people with uncommon conditions," and put my mother's name on the waiting list. My eye followed her fingers working the pen far down the yellow legal pad. When I offered to leave the brochures about celiac disease with her, she did not even glance at them, but dismissed them with a sweeping wave, saying, "Oh, there's no need."
    Weeks passed. My mother's hospice social worker joined in on the search. She found a facility willing to give the respite stay a chance. "They've had a previous celiac patient," she said.
    By now I was quite skeptical, but also curious with this news. The facility she suggested was the closest near my home, and I could easily visit each day. I agreed to meet with the admissions coordinator.
    The woman said that, yes, the facility had had a previous patient with celiac disease. It was the experience with this patient, who had been uncooperative and would steal food off other patients' trays, that caused the hesitation on their part. "But we're told your mother wouldn't do that," she said.
    Upon studying the fact that my mother was quite incapable of snatching food anywhere, the admissions coordinator said they were willing to offer respite care. I was impressed (surprised is the better word) when the coordinator called the dietary manager to meet me. He read the diet listing I had made up for my mother and said they would have no trouble in providing for her. I volunteered to bring her favorites of chocolate pudding and canned peaches and Vienna sausage for times they might have things she could not eat, and of course any homemade gluten-free cakes.
    We packed my mother up, and she went for her week respite at the facility. Her long-time caregivers went as well to provide support in the strange environment, help her learn her way to the bathroom, and to circumvent the inevitable glitches.
    The first day for lunch in the dining room, my mother was brought Vienna sausages (which I had provided), nothing else. My mother's caregiver went to the kitchen and inquired of the cooks, surveyed the kitchen and the menu of baked chicken and broccoli and how it was cooked and said, "She can have that." We began to wonder how the previous patient had been fed. I also began to wonder if anyone even glanced at the diet I had printed for my mother.
    However, the glitches that week were small. My mother ate well, enjoying their broccoli and branching out to embrace canned spinach. We learned the main reason the facility could and did for that week, succeed in feeding my mother quite well was that they had a full working kitchen and did not rely on food service, where all the meals come prepackaged.
    The respite week also worked because of my mother's private caregivers. They monitored the food and educated the kitchen staff. The dietary manager went so far as to voice his gratitude to one of the caregivers for helping them learn what my mother and could not eat.
    While it appeared no one read any of the dietary information, over all the stay went well enough that a month later, I decided to try it for long term care. The plan was to have her private caregivers ease my mother through the transition for approximately a month, and then gradually reduce their hours, as the nursing home staff learned my mother's needs. We believed it possible to educate the staff.
    The first week went fairly smooth, with a few expected glitches. After that, things went downhill. A semi-soft diet had been requested; this never materialized. My mother's food would be placed on her tray in her room, and left, covered. Either my mother's private caregivers or I had to come in and help my mother eat. Mom's private caregivers continued to mash any meat and large chunks of vegetables, such as sweet potato served still in the skin. They continued to intercept sandwiches on bread and dishes of cake and snack cookies left on her tray. Throughout all of this, my mother's caregivers or I consulted with the dietary manager and the kitchen staff. We thanked them for the good food when it came. We explained again what she could and could not have. We formed the habit of checking each day's menu and writing out foods from that menu that my mother could eat. The kitchen staff accepted these menus and taped them near the stoves. When there was nothing on the menu that my mother could or would eat, we suggested easy canned substitutions. Sometimes she got these substitutions, sometimes not.
    Then came the day when I was told that for the evening meal my mother had been served a hotdog and fries of some sort, both too hard for her, or anyone, to eat. (Keep in mind we are paying for this food.) My mother's caregiver took her back to the room and served my mother her snack cakes and pudding I had provided. Her roommate shared in the cakes, because she had come in too late from her dialysis treatment to get dinner. Why her tray had not been saved for her, I have no idea. I had never seen this woman provided any sort of special diet, and she was both diabetic and had kidney disease.
    The following morning I also I learned one of the kitchen staff responsible for following the therapeutic diet said to my mother's caregiver: "Oh, she doesn't need that diet. That's all made up."
    I faced the fact that providing for my mother was too much trouble for the staff, and they were simply unwilling. My mother was never going to get the food nor the care in eating that she would require at this facility.
    As of this writing, my mother is back home. Private caregiver hours have been drastically reduced. I am able to do this, for now.
    Here are some chilling facts: Studies indicate that today in our country not only are the incidents of celiac on the rise in all age groups, but the median age for celiac diagnosis is just under 50 years of age, with one-third of newly diagnosed patients being over the age of 65.* (Celiac Disease in the Elderly, Shadi Rashtak, MD and Joseph A. Murray, MD)
    This is the age group who are the primary caregivers for themselves and their parents. This is the age group who more often must undergo surgeries and stays in rehabilitation nursing facilities.
    Couple the above figures with the fact that we are an aging population. At the current rate, the number of people age 65 and older is projected to double between now and 2050. The baby boomers, responsible for the great population growth, now average over the age of 65.* (An Aging Nation: The Older Population in the United States, by Jennifer M. Ortman, Victoria A. Velkoff, and Howard Hogan, U.S. Department of Commerce, Economics and Statistics Administration, U.S. Census Bureau.)
    These simple facts paint a picture of a growing challenge. We must be able to provide short and long term nursing home care for the many celiac patients around us today—my mother, myself, the number of over-60 celiacs I've talked to—as well as the tidal wave looming on the horizon.
    In addition, we have other food intolerances on the rise, and we have the needs of those with diabetes and kidney disease and other conditions requiring dietary restrictions. At present, all of these people, not only those with celiac, are being overlooked and discounted.
    I have no solid answers to this immense problem. I do have suggestions on things that can be started.
    The celiac community must recognize and begin to talk seriously about the problem of dietary care in nursing homes. Printing up a glossy brochure with the advice to have the doctor write an order for a therapeutic diet is a start. We have to step out more aggressively with ways to educate and implement therapeutic diets in a real way. We have programs in place educating restaurants and the food industry. Let's get aggressive with the health industry.
    Of course, my experience is that these facilities do not want to be educated. This is where legislation is required. We need to lobby for legislation that requires compliance in the nursing facility industry, in the same way that food labeling compliance was attained.
    Further, we need to support the push for legislation for a required number of CNAs per patient in nursing home facilities. At present, there are laws only governing the minimum number of RNs required per patient in nursing facilities. * (Minimum Nurse Staffing Ratios for Nursing Homes, Ning Jackie Zhang; Lynn Unruh; Rong Liu; Thomas T.H. Wan, Nurs Econ. 2006;24(2):78-85, 93.) There are no mandatory minimums for the number of CNAs, the people who actually do the bulk of the patient care—those who would monitor a person's diet and help that person to eat. At present the nursing home facility is allowed to choose for themselves the number of CNAs they need.
    I remarked to a friend that there were a number of camps for children with celiac disease, places the child could get away and enjoy and eat safely.
    "Well, what about for the elderly?" my friend said. "It seems if they can do it for kids, they could do it for the elderly."
    What about the elderly? This is our new challenge—to make certain those elderly people with food sensitivity needs are well cared for.

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

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

    Dr. Rodney Ford M.D.
    Celiac.com 07/15/2016 - This week I have noticed many blogs/articles claiming that the only illness that can be caused by gluten is celiac disease. Yes, they state that celiac disease alone needs a gluten-free diet. I totally disagree with this distorted out-of-date viewpoint. There are tens of millions of non-celiac people who testify that gluten causes them significant harm. It is my suspicion that the wheat lobby is cranking up these anti-gluten-free messages as a way of stopping wheat sales from slumping. Why else promote such a barrage of misinformation?
    As if to counter such negative press, I got this email last week:
    "Dear Dr Ford, since we had our appointment I have taken George off gluten and have noticed a huge difference in his behaviour. George is now a much more sociable and loveable little boy. He has manners, he shares and he will say sorry if he has done something wrong. Obviously he is still a 4 year old boy so I have to expect some behaviour issues and sibling rivalry. Thank you so much for giving me my little boy back." By way of explanation, George was aggressive and having difficulty learning, he was easily distractible and he was always fighting with his sister. His parents saw him as being a naughty boy, however he was displaying severe ADHD behaviours. They wondered if he might need some medication and were exploring psychological help for their family.
    However, as I have seen a lot of behaviour-disturbed children get completely better off gluten. So I tested him for celiac disease (this was negative), I then recommended a strict gluten-free trial for three months. As you have read, his parents say that there has been a dramatic change, and now see him as a "sociable and loveable little boy" – in just a few weeks!
    To me this is clear evidence that gluten can cause significant inflammatory damage to our nerves and brains. George was displaying ADHD behaviours, triggered by gluten. It is a pity that those who are ridiculing the gluten-free diet movement are attempting to deny children like George the knowledge of healing on a gluten free diet.
    Evidence points to the nervous system as the prime site of gluten damage. This theory is attractive because it gives a unifying answer that explains the following conundrums:
    a mechanism of the non-gut symptoms of celiac disease; the behaviour disturbances caused by gluten reactions; the psychiatric and personality disorders provoked by gluten; the multitude of neurological symptoms; the autonomic nervous system disturbances (often seen in people with celiac disease); why such small amounts of gluten can cause such major reactions by the amplification effect of the nervous system (not dependent on any gut damage); why gluten can create such a diverse range of symptoms. Because any agent that causes widespread neurological harm (think of multiple sclerosis and Syphilis) can generate almost any array of symptoms. Nerve and brain damage from gluten can also explain why celiac patients with extensive gut damage can be asymptomatic. The histological gut damage in celiac disease is not mediated through this neurologic system: it is caused by local toxicity to the bowel in susceptible people. If these people are not highly sensitized to gluten, then they may not experience any symptoms mediated through neural networks.
    I got mad and grumpy
    I would also like to tell you about Nick. When he was 8 years old he wrote his story down for me:
    "My name is Nick and I am eight and a half years old. I had a problem when I had gluten, so my mum found Doctor Ford to help me. He helped me get off gluten. When I tasted the first chocolate biscuit it tasted weird but now I'm getting used to it. I had troubles when I was on gluten. Every day I got mad with myself and sometimes with others. I didn't want to be mad. I was grumpy." I had dizzy spells
    I also had dizzy spells every day and I didn't feel well. They thought that I had a heart problem when I was 8. I went to the doctor and to the hospital lots and lots as they were trying to figure out what was wrong with me. I wasn't very well. When I was on gluten I had sore tummies at least twice a week.
    I am off gluten and I have more energy
    Now I am on a gluten-free diet. When I'm off gluten, I still sometimes have dizzy spells – but not usually. You might lose weight when you first start go gluten-free because you are getting used to it.
    At school I found I had to get off gluten, as I couldn't sit still on the mat. I now have got more energy to run. I can sprint now. I can sleep better too. I used to not have enough energy but now I have enough energy to sprint around the cross-country. I've achieved in my spelling now and I'm much better at school. My Doctor Ford is a nice man because he talks nicely. Tons of people need to go and see him.
    Gluten-free helps your attitude
    Please come to our diet because it helps you breath better, it helps your attitude change. It makes you be stronger. Me and my brother used to fight a lot when I was on gluten but we like one another now. I liked gluten foods but I can't have it as it's not good for me.
    In my family we have got a dog and four humans – Jordan, Dad, Mum and me. We are all gluten-free but my dad doesn't have to be gluten-free. It's unfair when my dad eats gluten and it makes me feel hungry.
    The food can be nice
    Our gingerbread bakery bakes us nice food. When I found out I was allowed to have a gluten-free birthday cake I was very happy. We go to Gingerbreads once a week. I buy chocolate chip biscuits they taste delicious. World come and be gluten-free as it makes me delighted! I love people that make yummy gluten-free foods.
    My brother says that being on a gluten-free diet is like being in China with no noodles. He finds it hard and says he just wants to be normal. I say he will get used to it.
    Nick
    Nick's mum adds:
    Prior to going gluten-free Nick had the following list of symptoms:
    Rashes Sore tummy and runny poos Very irritable Very tired – slept more than 12 hours Poor memory and learning hard work Behaviour problems – got very angry with others Bad hay fever and asthma Intolerant to dairy Dizzy spells for 6 months and not feeling well Very fussy eater. The good news is that of today (six months later), he is not having a lot of these symptoms and he is a much nicer person all around. He can now have dairy products again."
    Mum
    The implication of gluten causing neurologic network damage is immense. With estimates that at least one in 10 people are affected by gluten, the health impact in enormous. Understanding the components of the gluten syndrome is important for the health of the global community.
    Written in the spirit of cooperation and knowledge sharing. You can read many more patient stories in my book "Gluten-Related Disorder: Sick? Tired? Grumpy?" http://www.GlutenRelatedDisorder.com 

    Dr. Rodney Ford M.D.
    Celiac.com 10/12/2016 - How early can you diagnose celiac disease? This is a most challenging question for everyone: children, parents, pediatricians, gastroenterologists and many other health professionals. This is because, like so many other diseases, celiac disease is a progressive condition that slowly creeps up on you. In addition, there is disagreement about what constitutes a definitive diagnosis of celiac disease. What if the small bowel biopsy result is at odds to the blood test results?
    It is my opinion that the fundamental diagnostic requirements for celiac disease remain unresolved. This makes early diagnosis problematic!
    Do you keep waiting (whilst suffering from symptoms) for classic gut damage to be visible in a bowel biopsy before adopting a gluten-free diet? Or do you recognize the early onset of celiac disease and go gluten-free prior to this gut damage occurring? Will you be accused of "masking" celiac disease if you are an early gluten-free adopter?
    Currently, most guideline protocols require a definitive diagnosis of celiac disease by demonstrating small bowel tissue damage. This is achieved by performing and upper gastrointestinal endoscopy, taking a tissue biopsy of the mucous lining of the small bowel, and then showing specific tissue damage (villus atrophy) under the microscope: this is the small bowel biopsy procedure.
    However there is significant controversy about the accuracy and necessity of a small bowel biopsy test. We will have a close look at the difficulties and shortcomings of these tests. But first, let's look at these diagnostic problems in relation to Francesca.
    Meet Francesca who is highly at risk of celiac disease
    So how early could we diagnose Francesca's celiac disease? She has just turned 3-years-old. Her mother has celiac disease, diagnosed over 10 years ago. So mum bought Francesca for my opinion because she had started to have some loose bowel motions (runny poops), although sometimes she did have hard bowel motions, which were difficult to pass. She also had a big distended tummy, was getting more cranky, and a bit more tired. Because of mother's celiac disease, Francesca was already consuming a smaller amount of gluten, although she was eating at least one slice of normal wheat gluten bread each day. Her mother's question was: "Has Francesca now developed celiac disease?" This problem confronts me most days in the Clinic.
    How should I investigate and manage her illness?
    What blood tests should I request? How do I interpret her results? Should I organize a small bowel biopsy? Do we look for early evidence of gluten problems, or do we wait for end stage celiac damage? Should she go on a gluten-free diet now? Should we be concerned about "masking" celiac disease? Francesca's blood tests show:
    She does carry the HLA gene DQ2: this makes her a likely candidate for developing celiac disease. The tissue-damage antibodies were normal: the tTG (tissue Trans-Glutaminase) levels were low normal, but the IgG-DGP (Diamidated Gliadin Peptide) levels were borderline (18 units, with a normal range 0-20). Her EMA (Endomesial Antibody) was negative: the borderline DGP is very suspicious and evidence of early celiac disease. IgG-AGA (Anti-Gliadin-Antibody) level was moderately raised: showing that she has developed an immune response to gluten. She has not had an endoscopy: with her tissue damage antibodies at low levels, the likelihood of abnormal tissue histology is very low. My opinion
    In my opinion, this child is at extreme risk of developing celiac disease. I would like to see her on a strict gluten zero. However, it is now up to her parents to decide whether they will wait until she actually develops gut damage, or do something now to prevent her getting a serious disease.
    What would you do if she were your child? Well her parents decided to place her gluten-free and they saw a big change for the better in just a few weeks. Her bowels become normal, her energy levels improved and she is now a happy girl.
    So what is her diagnosis? I call her early celiac disease. Others would say she has non-celiac gluten-sensitivity. Some would claim that I am unwarranted to suggest a gluten-free diet until she has a positive biopsy and they accuse me of "masking" celiac disease by treating her symptoms.
    Why let Francesca unnecessarily suffer whilst waiting for her to get progressively sicker until we can get a tissue diagnosis?
    Written in the spirit of cooperation and knowledge sharing. You can read many more patient stories in my book "Gluten-Related Disorder: Sick? Tired? Grumpy?" (www.GlutenRelatedDisorder.com).

    Dr. Rodney Ford M.D.
    Celiac.com 04/26/2017 - "The universe is made of stories, not atoms" — Muriel Rukeyser
    Helen, a woman with severe lifelong eczema/dermatitis, wrote to me a few weeks ago, saying "I have taken your advice and been strictly gluten free for five months now. The eczema inflammation is 99% gone and my skin quality has significantly improved. I do still get a bit itchy around my neck area and elbow creases, more so at night when it is warm.
    I have noticed a significant improvement in my asthma also. I still use antihistamines perhaps once or twice a week for runny nose. Does this mean I will need to be gluten free for life? Which of your books would you say would be the most relevant for someone in my position? Thank you for your assistance, regards, Helen.
    I recommended eBook: "Dermatitis Eczema: Gluten Wheat – Solving the eczema puzzle." Available at: http://www.GlutenEczema.com
    This is an excerpt from the chapter: "Children better off gluten/wheat".
    To help you get a better idea of how gluten can trigger eczema, here are narratives of some children whose eczema got better when their gluten sensitivity was recognised and treated. Most had good remission of their eczema on a gluten-free diet. Their stories told by their parents.
    To give context to the blood test values, the normal reference ranges were:
    AGA: 0–15 tTG: 0–20 Celiac disease with bad eczema
    Lily at five years old was diagnosed by me with celiac disease. Symptoms: eczema. Run down, pot tummy and slow growth. Tests: All of her blood tests were positive for celiac disease (tTG 120) and she had an abnormal intestinal biopsy which confirmed the bowel damage of celiac disease. AGA very high (115).
    Her mum said:

    "Lily has now been gluten-free for the last year. She came to see Dr. Ford to investigate her allergies. She had a blocked nose and troublesome eczema. She also had quite a pot tummy and Dr Ford said that her growth was slow (she was thin and short). Dr Ford said that she needed blood tests for gluten and celiac disease: these were both positive. So she had an endoscopy, which was abnormal, showing the villus blunting of celiac disease. Therefore, she had to go on a gluten-free diet."
    "Since she has been gluten-free over the last year, she has gotten better and better. She no longer has lots of infections, she has more energy, and interestingly, her allergies have nearly gone away. Her skin used to give her a lot of trouble – she had a lot of bad eczema. Her eczema now is very much better and she only has small amounts left in her creases. And if she has any gluten errors it flares up."
    Recovering from gluten-eczema
    Isabella, at two years old, was recovering from her eczema. I asked her mother what happens if Isabella has any gluten. Her mum said:

    "Isabella had eczema all over her body. She was on strong steroid creams. She had the positive blood tests for gluten antibodies (AGA of 66), so it was suggested I take her off the gluten. I did this."
    "I took her off gluten and it has cleared her eczema up. Now, when she does eat anything with gluten in it she gets little patches of eczema on her legs. I just can't believe it!"
    Blood all over her sheets
    Emily was three years old. She had a high anti-gliadin antibodies (AGA 48) but she did not have celiac disease (normal tTG). Her mother told me:

    "Initially her skin was really sore, dry and scratchy. She would have blood all over her sheets in the morning from scratching while she was asleep. Her poos were really sloppy and nasty."
    "But after taking gluten out of her diet her skin cleared up within days, and the itchiness of her skin settled. She was just so much happier."
    Dry skin and worsening eczema
    Breanna and Alyssa, twins aged 3 years. Symptoms: eczema and poor sleeping. Both had high AGA levels (60 & 68) and normal tTG levels (5 & 3). They did not warrant an endoscopy.
    Mum writes:

    "My twins were born at 26 weeks. During our stay in NICU they developed very dry skin, at times you felt like you wanted to peel the dry skin off. The word eczema was mentioned on more than one occasion. There is a history of eczema and asthma in our family, so at the time I tried to deny all knowledge of that word."
    Dry skin and worsening eczema
    "Eleven weeks later we took our twins home. Their skin was still dry and we were given a moisturiser to use as required. As time went on their skin didn't improve and eventually at around the age of one year they showed real signs of eczema. We started to use steroid creams: 1% Hydrocortisone to start with, then onto a much stronger steroid cream. Soon, this stronger cream was used all the time to control their eczema as the other creams were of no real help."
    "At around 2 years old, while at a playgroup session one of the mothers was talking about her daughter's eczema and how she had gone to see Dr Ford and now there were no signs of it there today. Of course my ears pricked up. I was interested to hear how her diet affected her skin and the word gluten was mentioned."
    At the time it didn't mean a lot to me. Therefore, I made an appointment and I was excited to think that we might be able to change the girls' diet and their skin condition may improve.
    They had positive gluten blood tests
    "The day arrived and we had our first visit. He talked to us about this gluten thing and that if we could avoid it then their skin might make a dramatic improvement. I was keen to try anything. Firstly, they had to have some skin prick allergy tests – it showed a reaction to wheat among a few other things. Next, the girls had a blood test confirming that they definitely had an allergy to gluten, and their iron levels were also very low. The final step was to set about changing their diet. I can honestly say that this was daunting to start with but once we got our heads around the issues, it became second nature."
    Sleeping at last!
    "One of the biggest changes we have noticed is that they are now sleeping so much better. I was constantly up and down to them all night and was getting so worn out now we can almost guarantee a full nights sleep, Yahoo!! The other major issue was the steroid cream use: we haven't used the strong steroid cream for 12 months. So for me, going gluten-free was a huge step in the right direction."
    Gluten-free gets easier
    "There are heaps of products that we can use and the staff in shops were very helpful with information and getting stock in. I have since brought a number of cook books all with sections on gluten-free that have been helpful. When baking or cooking, I now just do it the gluten-free way and everyone in our family eats it with no complaints. We have all adjusted accordingly."
    "Our thanks goes out to Dr Ford for all his help. I also send good luck to all of you who are about to embark on a gluten-free diet – the rewards will be well worth the sacrifice."
    Sharon
    Losing her hair – alopecia
    Ella, age 6 years. Symptoms: eczema, alopecia, moody, abdominal pain, multiple food allergy. AGA high (49), tTG normal (3), EMA negative, Small bowel biopsy, normal.
    Mum writes:

    "Ella is now age 6 years. At age 3 years Ella started to lose her hair. After a year of scalp treatment, by the time she turned 5 years old, all but one small patch had regrown."
    Losing her hair
    "About 4 months later a small patch of alopecia reappeared and her hair loss rapidly progressed from there. At this time her eczema, always present in a mild form, worsened and became almost impossible to control. Many forms of treatment were tried and all failed. Within the year Ella had lost all her hair and was constantly itching. Over this time Ella also complained of tummy pains and weight loss."
    Diagnosed as gluten-sensitive
    "As her father has celiac disease, we decided to get Ella checked. Her blood test was positive but the biopsy was negative for celiac disease. In discussion with the GP and some unanswered questions we eventually had an appointment with Dr Ford. After this appointment, Ella started on a strict gluten-free diet and has remained on it for the past 4 months."
    Amazing results
    "The results are amazing. Ella has stopped most of her scratching and she is far more comfortable. Ella's mood has changed and she is now a very happy little girl. Best news of all is that she has started to have a small amount of hair growth."
    "At no time, despite the variety of people seen and the fact that they were aware of family history, did anyone suggest getting Ella tested for celiac disease. It was purely parents at the end of their tether, pushing."
    Sue
    She was getting worse eczema
    Tessa, age 2 years. Symptoms: eczema, poor growth, multiple food allergy. Tests: AGA high (51), tTG normal (7), Biopsy not done.
    Mum writes:

    "Tessa was our first-born baby. She weighed a healthy 8lb and was breastfed until 6 months. I introduced solids at 5 months. Having given a bottle of expressed milk every night since she was 10 weeks, I found that she preferred this and weaned herself."
    Eczema at the time of solids
    "Tessa had eczema from the time she commenced solids, but it was manageable with mild steroid ointments. However, at six months her eczema became more distressing for her. She had her first course of antibiotics at this age."
    "We felt that we were using more and more topical steroids, oral antibiotics, and even a course of oral prednisone. None of these treatments felt satisfactory to her family. We needed a solution to prevent the problem. Not only was her skin getting worse but also she was quietly losing weight. A friend suggested visiting Dr Rodney Ford."
    Allergies to egg, dairy and peanuts
    "Our first visit involved an extensive medical history and allergy testing. Tessa was found to be allergic to egg, dairy, peanut, grass, and cats. We excluded the food allergens from her diet. But, over the next four months Tessa had a dramatic weight loss, going from the 50 percentile to falling off the Child Health nurse growth graph. She required more steroids, and antibiotics."
    Waking screaming
    "My angel baby, who had slept through the night from age 6 weeks, was now 16 months and woke every night screaming inconsolably. We were getting desperate, putting in an awful lot of work by eliminating dairy and egg with no rewards. With a new baby due to be born Tessa's exhausted parents needed answers. Back to Dr Ford we went. He suggested running some blood tests to check her gluten markers. It came back that her Anti-Gliadin Antibody was 51, suggesting that she was gluten-sensitive."
    Gluten-free as well!
    "We trailed a gluten-free, egg-free, and dairy-free diet. This was a totally overwhelming prospect for our family, as at that time we were introducing a two-week-old baby to the world! Luckily, Tessa's father, who too is an adult sufferer of eczema, was able to take all this on board and went off grocery shopping, bringing back lots of acceptable goodies. It was also at this time that I learnt of the real benefits of living in a small town."
    We had a gluten-free buddy
    "We were very fortunate that another mother of gluten-sensitive children took me by the hand grocery shopping, showing me how easy it is! Also, the church where we regularly attend made a whole week's worth of meals for the freezer which all fitted the requirements for Tessa's diet. All this really just through word of mouth!"
    At last she is better
    "We are so excited to see such an improvement. She has just been allergy tested again and we are able to introduce egg and dairy again. I had been giving small amounts of dairy already, hoping that she would have grown out of this. At one point all she would eat was cheese, so to get some calories into her that is what we fed her. Having Tessa on a gluten-free diet requires us to be organized and creative. It is especially difficult when you spontaneously decide to go out for the day: there are no guarantees that we will find appropriate food for Tessa, so usually we pack a lunch."
    Gluten-free is expensive
    "The food that is gluten-free is also usually twice the price of other foods. We have had to learn to bake, which is something I still struggle with. We have had some major disasters, especially baking cakes. Whenever it seems too difficult, and we are out of ideas, it is not too hard to find a reason to keep trying."
    Improved gluten free
    "Our little girl has significantly improved since becoming gluten-free. She has not required antibiotics or oral steroids for eczema since commencing the diet. We can now apply the topical steroid ointments as prescribed "sparingly". She no longer gets up in the morning, her pyjamas and sheets covered in blood, and forehead weeping. She can play in sandpits without fear that the sand will get into her sores, and once again they will be infected."
    "We are so lucky that something so simple as changing Tessa's diet has had such a dramatic affect on her life."
    Mum
    Think about the gluten-eczema link
    As you have been told by these families, gluten has been found to be an important trigger for eczema in these children.
    My research findings show that the majority of people over three years of age, who have ongoing and troublesome eczema, have gluten-sensitivity. When gluten is removed from their diets, they get better.
    Advice about blood testing for gluten and for information on a gluten-free diet can be found on our webpage: http://www.DrRodneyFord.com and in the previous chapters.
    This is an excerpt from Dr Rodney Ford's eBook, "Dermatitis Eczema: Gluten Wheat – Solving the eczema puzzle" Available at: http://www.GlutenEczema.com
    Written in the spirit of cooperation and knowledge sharing.

  • Recent Articles

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

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

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

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

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

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

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

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

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

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

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

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

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

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

    Jefferson Adams
    Celiac.com 04/17/2018 - Could the holy grail of gluten-free food lie in special strains of wheat that lack “bad glutens” that trigger the celiac disease, but include the “good glutens” that make bread and other products chewy, spongey and delicious? Such products would include all of the good things about wheat, but none of the bad things that might trigger celiac disease.
    A team of researchers in Spain is creating strains of wheat that lack the “bad glutens” that trigger the autoimmune disorder celiac disease. The team, based at the Institute for Sustainable Agriculture in Cordoba, Spain, is making use of the new and highly effective CRISPR gene editing to eliminate the majority of the gliadins in wheat.
    Gliadins are the gluten proteins that trigger the majority of symptoms for people with celiac disease.
    As part of their efforts, the team has conducted a small study on 20 people with “gluten sensitivity.” That study showed that test subjects can tolerate bread made with this special wheat, says team member Francisco Barro. However, the team has yet to publish the results.
    Clearly, more comprehensive testing would be needed to determine if such a product is safely tolerated by people with celiac disease. Still, with these efforts, along with efforts to develop vaccines, enzymes, and other treatments making steady progress, we are living in exciting times for people with celiac disease.
    It is entirely conceivable that in the not-so-distant future we will see safe, viable treatments for celiac disease that do not require a strict gluten-free diet.
    Read more at Digitaltrends.com , and at Newscientist.com