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    Early Diagnosis of Gluten Sensitivity: Before the Villi are Gone by By Kenneth Fine, M.D.


    Scott Adams

    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.


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    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.

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    Guest Laurie Andreoni, DC

    Posted

    Thanks for this. 'Celiac sprue' was mentioned in passing in school. After finding the majority of my patients were sensitive to wheat, and convincing them to eliminate just that grain from their diets, I've seen a multitude of symptoms resolved. I recently had a few new patients with celiac disease that were already on a gluten-free diet and still felt horrible. With appropriate nutrient supplementation, we're seeing a significant decrease in symptoms within 4-6 weeks. It's a beginning, but as they get better, the referrals increase and we can find out more. An article like yours is an enormous help to a 'newbie' like myself.

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    Guest Kamal Rastogi MD

    Posted

    Certainly, this research article is an excellent information for my practice.

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    Guest ruth Ortiz

    Posted

    I appreciate the information. Have been 'treated' for IBS for over 25 years and it just kept getting worse. A nutritionist finally came to my rescue! I am feeling much better at 80 years of age.

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    Guest Jennifer Shaft

    Posted

    My 9 year old daughter had an IgG mid to high positive but showed no intestinal damage. She has chronic constipation, is underweight and shows a number of other symptoms. Being released by the negative biopsy really bothered me because I was so sure that we had finally found our diagnosis. It's nice to know that I am not completely crazy. I am bookmarking this for my husband to read.

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    This article is very informative and helpful to me and to anyone who will read it. I was diagnosed with

    gastroparesis a year ago. I already had IBS an umbilical hernia and was told last week that I have mesentericitis. I was told in 2001 I had lupus--yuck--just shoot me. lol. Because I've suspected being gluten sensitive for over a year, but haven't been tested so I'm not sure I can handle hearing anymore. I get an endoscopy/colonoscopy every year because my Mom's sister and brother both died of colon cancer. My Dr.GI takes biopsies on both so far was told I had hemorrhoids, so had surgery last September. Very frustrating when I've always eaten so healthy I thought. I never smoked or drank and I eat fish/chicken/veggies/fruits and never coffee. I do drink hot tea. What a mess my poor digestive system is in.

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    Guest Maurice Conard

    Posted

    I have been frustrated by the M.D. Gastroenteroligists in my city of Winchester, VA. They have told two of us they can do no more for us.

     

    No stool tests were ever considered. A biopsy (colonoscopy) was taken of the colon but according to your data that means nothing.

     

    I was diagnosed with small intestinal bacterial overgrowth and treatment was antibiotic, Neomycin for 14 days. I gained weight for five days after treatment ended and then started losing weight again and have lost another 10 pounds. This is nearly 50 pounds in four years. Went on antibiotic for second time out of necessity.

     

    Assured I did not have cancer but again only blood tests were done. I get joint pains at times that swell a little and come and go. Usually, the joint pains start and hour or two after meals. Probably eating something wrong.

     

    My digestive system is also a mess with constipation, but not extremely bad most of the time. I have only had diarrhea three times since the real blitz hit in September 2007. Yet, I had a big diarrhea session back in February 2007 and that may have been viral and triggered this.

     

    Thank you very much for your work and concern for others. Most doctors today just want to give you a pill. That cures nothing and eventually does more damage than good.

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    Reading these comments lets me see that I'm not alone. I have had symptoms of C-IBS for most of my life. In 2005 it flipped to diarrhea prominent with constant flares. My GI doc noted small intestinal inflammation on a biopsy, but the blood celiac panel 'ruled' it out. I actually asked for the blood test after discovering that my 5-year-old nephew had been diagnosed with celiac sprue and our symptoms were almost identical. Three years later I am still sitting with an IBS diagnosis. I am severely malnourished...cupped fingernails, osteoporosis, joint pain, thinning hair. People who have not seen me in years are shocked at my being skin and bones and immediately assume I suffer from an eating disorder. (I eat huge amounts of food and still remain a pitiful 90 lbs at best.) I need help, but the medical community treats me as though I'm a neurotic hypochodriac because I look so great 'on paper' when they test for other diseases (thyroid, adrenal function, liver function, etc.) I'm so tired of looking like a skeleton with skin. All my muscle has wasted away. I will sometimes gain a bit of the weight back and then another flare hits and I'm back down to under 90 lbs again. I just wish someone would help me, but when I brought up this article to three different specialists they all told me it was false..if the blood tests were negative and the 'pill cam' showed nothing, then it's IBS. I hate to cut out gluten unnecessarily, but who do you believe? I either have to go with my physicians' opinions (chosen by my insurance company) that I have IBS or undergo tests that, if positive, they will refuse to recognize as valid proof of a gluten sensitivity.

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    Guest Nancy

    Posted

    Dee, # 8 My 24 year old son diagnosed himself after many years of the Md saying it's IBS and just take Imodium. He had strong urges to eat gluten products but refrained from eating , using rice potatoes, and other starches. He has been gluten free for over a year now and is gaining the weight that he never could before. All of the symptoms including bloating , gas , diarrhea, etc. have gone away. His body is much stronger now. No more dark circles and bulging under his eyes.

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    Guest Aimee

    Posted

    Just because you don't have a true diagnosis doesn't mean you can't go ahead and try living gluten free and see if it helps. That's what I'm doing while my doctors are going down every other road and I'm much better for it.

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    Excellent and very informative, please suggest appropriate tests in India for me!

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    Guest Lynda

    Posted

    I too have suffered for almost 17 years with many doctors telling me that I am just stressed out and treating me like a hypochondriac. I started out having severe stomach pains with diarrhea, fever, vomiting after meals - it felt like poison in my stomach. After I had a colonosopy and was diagnosed with IBS. Years later, after still feeling bad and going to an alternative doctor, I found out that I have several food allergies. After cutting out these foods I feel so much better. However, all the symptoms and pain have not gone away. The other symptoms, such as joint pain, mental fog, fatigue, numbness, etc. are still present and getting worse. I believe that my problem has something to do with celiac disease or some other digestive disease not diagnosed. If you have similar symptoms or believe you have IBS, Crohns, diverticulitis, etc. then you need to get a book entitled 'Breaking the Vicious Cycle' by Elaine Gottschall. The book is about eating a specific carbohydrate diet. I read it and tried the diet for 3 weeks. It was like night and day between how good I felt and the usual horrible way I have felt for years. The diet is hard, especially for someone like me that is a carbohydrate addict - sweet tea and chips and queso! I really want to get back on this diet , but at the same time I want to go to a doctor and get an accurate diagnosis. I am afraid to even try and see a doctor again because I don't want to waste the money, be insulted, or have another false label like IBS. Thanks for this website because it gives people like me hope and support.

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    Fantastic Article. I showed slightly elevated anti-gliadin to which my doctor said I was not coeliac - not even mentioning that I could still be intolerant despite several health problems. I was told I probably had IBS but there was not much else that could be done. Luckily another doctor re-reviewed the test and suggested I start a Gluten Free diet, this article has helped fill in some gaps.

    I was wondering, I also have PCOS (Poly Cystic Ovaries Sydrome) and there is a lot of cross over in the symptoms and health issues (Diabetes, irregular menstrual cycles, fatigue). Has there ever been a link between the two problems established?

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    Thank you so much for your articles. They are full of so much valuable information and give me hope. I tested positive over a year ago with the IgA antibodies but my scopes came back negative. I still decided to go on a strict gluten free which I have been on for over 8 months now. I am feeling so much better but still have very sharp pains every time I eat in my lower left side of the colon (it's been that way for over 3 years now). To read that Pancreatic enzymes might be an issue was helpful as I was wondering this myself but didn't realize there was a link with Celiacs. My Dr. is now saying that it's IBS (which was his initial diagnosis) given that I am still having pain after 8 months of a strict diet. How long does it take for the gut to heal? I don't think I was misdiagnosed given my blood test results, family history (my mom has an autoimmune disorder of Lupus) and 'stomach problems' have run in the family for years. How do you test for pancreatic enzymes (or lack of)? Many thanks again for your wonderful site. It's been tremendously valuable to me over the past 8 months.

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    Guest Pro.Dr.

    Posted

    Thank you so much for your articles. EXCELLENT ARTICLES!

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    Guest Crystal

    Posted

    My mom has been diagnosed with celiac for over 20 years now and I have just started getting really sick after a stomach flu. I've been through tons of tests including stool samples, blood samples, CT scans, endoscopy and a biopsy. the stool and the biopsy showed beginning signs of celiac disease but my doctor won't 'officially' diagnose me. Even though he has told me flat out that there is really nothing else that would explain my symptoms. (especially the history of celiac in my family) he tried to tell me yesterday that maybe I should go back onto a regular diet, just in case 'we are missing something', and I wanted to just strangle him because the day before I got incredibly ill just from a little cross contamination. I'm beyond frustrated and depressed that I can't get answers from the people that I need them from the most.

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    Thank you very much for this fantastic information. My Mom was diagnosed with celiac three years ago, has fibromyalgia, and this spring was found to have a cancerous tumor in her colon. I don't want to go down this same road. I have tested very high positive for only one of the five antibodies on the celiac sprue blood panel--a confusing result. My MD said he didn't know what to do about this because I don't have intestinal symptoms. But I am hypothyroid and have inflammation in other tissues/joints, all things that signal at least to me, the warning signs of celiac (latent celiac). Even without any kind of diagnosis or doctor telling me what to do, I am going gluten-free. What other choice is there?

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    Guest delancy

    Posted

    What an exciting journey, you sent me on reading your article. The contents has opened more doors for exploration, which I will immediately embark on.

     

    In the interim, I am clueless as to why the medical; professionals have not taken the opportunity to advance their cognitional efforts into this area. We the patients would not be held "hanging ourselves" do to our lack of knowledge provided by or personal care providers.

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    This article is very informative and helpful to me and to anyone who will read it. I was diagnosed with

    gastroparesis a year ago. I already had IBS an umbilical hernia and was told last week that I have mesentericitis. I was told in 2001 I had lupus--yuck--just shoot me. lol. Because I've suspected being gluten sensitive for over a year, but haven't been tested so I'm not sure I can handle hearing anymore. I get an endoscopy/colonoscopy every year because my Mom's sister and brother both died of colon cancer. My Dr.GI takes biopsies on both so far was told I had hemorrhoids, so had surgery last September. Very frustrating when I've always eaten so healthy I thought. I never smoked or drank and I eat fish/chicken/veggies/fruits and never coffee. I do drink hot tea. What a mess my poor digestive system is in.

    Hi I was wondering if you found any information on mesentericitis. I was just told I had this. My doctor doesn't know how to treat it. Thank you.

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    Guest Sarah K

    Posted

    Reading these comments lets me see that I'm not alone. I have had symptoms of C-IBS for most of my life. In 2005 it flipped to diarrhea prominent with constant flares. My GI doc noted small intestinal inflammation on a biopsy, but the blood celiac panel 'ruled' it out. I actually asked for the blood test after discovering that my 5-year-old nephew had been diagnosed with celiac sprue and our symptoms were almost identical. Three years later I am still sitting with an IBS diagnosis. I am severely malnourished...cupped fingernails, osteoporosis, joint pain, thinning hair. People who have not seen me in years are shocked at my being skin and bones and immediately assume I suffer from an eating disorder. (I eat huge amounts of food and still remain a pitiful 90 lbs at best.) I need help, but the medical community treats me as though I'm a neurotic hypochodriac because I look so great 'on paper' when they test for other diseases (thyroid, adrenal function, liver function, etc.) I'm so tired of looking like a skeleton with skin. All my muscle has wasted away. I will sometimes gain a bit of the weight back and then another flare hits and I'm back down to under 90 lbs again. I just wish someone would help me, but when I brought up this article to three different specialists they all told me it was false..if the blood tests were negative and the 'pill cam' showed nothing, then it's IBS. I hate to cut out gluten unnecessarily, but who do you believe? I either have to go with my physicians' opinions (chosen by my insurance company) that I have IBS or undergo tests that, if positive, they will refuse to recognize as valid proof of a gluten sensitivity.

    My recommendation is to go on a strict gluten free diet for no shorter time than 1 year like Dr. Fine in this article says, you have nothing to lose and everything to gain. Be strict about it, it's not that hard to do. That's what I am doing after 8 years with symptoms (IBS and peripheral neuropathy) I can find no other answer and am feeling a little different after 3 weeks on gluten free. Good luck.

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    Guest r. wade markham

    Posted

    I have many of the clinical findings described.

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    Guest Lorraine

    Posted

    Great article with well-reasoned arguments. I just wish the medical community would catch up. I have had symptoms for the past 10 years, but always fairly mild. Now after surgery, my symptoms have increased in severity. However, I don't expect that the doctors in my area will properly diagnose me. Since I experienced relief on a gluten-free diet a couple years ago after following it for only about a month, I am just gonna do what I know is best for my body and cut out the gluten again.

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    Guest Christina

    Posted

    Just because you don't have a true diagnosis doesn't mean you can't go ahead and try living gluten free and see if it helps. That's what I'm doing while my doctors are going down every other road and I'm much better for it.

    It really is not a good idea to go gluten free while doctors are running tests because it could indicate inaccurate results. There is no benefit to a gluten free diet unless you have a diagnosis of celiac and have the lab results and symptoms to prove true celiac.

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    Guest Sara

    Posted

    It really is not a good idea to go gluten free while doctors are running tests because it could indicate inaccurate results. There is no benefit to a gluten free diet unless you have a diagnosis of celiac and have the lab results and symptoms to prove true celiac.

    I disagree with what someone posted here: Not just celiac's need to refrain from eating gluten. I have been diagnosed as gluten sensitive which is a precursor to celiac as well as having Hahimito's Thyroiditis (an autoimmune condition). So there are many people that will benefit from following a gluten free diet. I do agree that changing the diet should wait until after testing if that is what the patient wants - a definite test result. But you don't necessarily have to wait for testing to remove gluten from your diet if you feel you will benefit from it.

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    This article is awesome! I am fairly sure that I am gluten-sensitive and that my dad had full blown celiac. He had diabetes and died from fatty liver disease & cirrhosis. I'm not going to wait for the medical community to catch up. It seems silly to waste time testing when I could potentially be solving the problem myself. I've decided to go on a gluten-free diet to see if it helps my symptoms. In addition to the standard symptoms, I also have a lot of brain fog and chronic fatigue after years of stress. I am hoping that helps.

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  • Related Articles

    Scott Adams
    Celiac.com 02/12/2007 - Before they are diagnosed, people with celiac disease often find themselves in an unenviable position. They may go out of their way to eat a wholesome, balanced diet including plenty of fruits and vegetables, a good variety of whole-grain foods, and a modest amount of meat and dairy, yet still find themselves suffering a whole range of bothersome stomach and digestive complaints including indigestion, gas, stomach cramps and diarrhea, alternating with constipation. Thats because people with celiac disease are intolerant of the protein gluten. Gluten is found in wheat, rye, and barley (oats contain a type of gluten that may be safe for most celiacs), and is found in the soft, white inside of the grain, its what makes dough, and flour and water paste, sticky and gooey.
    When people with celiac disease eat food made from these grains, even in small amounts, their immune systems seem to treat the gluten as foreign invader, and basically create a massive defensive action against what might be, for most people, part of a good healthy diet. The immune reaction that is triggered by gluten causes inflammation of the intestines, which leads to many problems that are associated with malabsorption, and ultimately to the general gastrointestinal malaise associated with undiagnosed celiac disease, or with gluten contamination in otherwise mindful celiac patients on a gluten-free diet.
    Diagnosis and Treatment of Celiac Disease are Important
    Unless celiac is treated, it becomes difficult for the digestive system to absorb enough nutrients from food to carry on proper body functions, and resulting vitamin deficiencies can cause a wide range of symptoms, including a condition known as malabsorption. Weight-loss, listlessness, feeling or looking malnourished, are all signs of the nutritional malabsorption associated with untreated celiac disease.
    Left untreated, celiac disease can become life-threatening. People can waste away. More likely though are higher instances of certain cancers, particularly of the intestines, and other diseases associated with untreated celiac disease. Thats why its advisable for people with any of these symptoms to check with their doctor to ensure a proper diagnosis, and to have follow up wellness checks.
    Even a negative blood test for celiac disease doesnt mean youre fully out of the woods. For a long time, research put the number of celiac patients at around 0.5% of the worlds population, or around 1 in 200 people. Recent studies however, have shown that to be a low estimate, and incidence is more likely around 1% of the population, or 1 in 133 people. Celiac Disease, however, is looking more and more like a very small part of the much larger Gluten sensitive picture.
    More ominous still, new evidence shows Non-Celiac Gluten intolerance to be around 30 times more prevalent than celiac disease, and if could affect up to 15% of people worldwide. 1 in 7 people are gluten-sensitive or gluten-intolerant. These people test negative or inconclusive for Celiac Disease, but suffer most of the same symptoms and long-term problems associated with celiac disease when they ingest wheat. This group of people are sometimes referred to as Non-Celiac Gluten Sensitive.
    Because the symptoms overlap with many other ailments, Gluten intolerance can easily be missed or misdiagnosed; especially in light of negative blood or biopsy tests--and this may lead many to miss out on discovering the simple and drug-free remedy of a Gluten-free diet for a dramatic recovery. If classic screening techniques for celiac disease do not identify the disease in someone who is in the Non-Celiac Gluten Sensitive category, or if the test results are borderline or inconclusive, often the only other approach to discover the problem is via the Elimination Diet.
    Once the cause is understood, and the necessary adjustments are made to the diet, celiac disease and gluten sensitivity are easily treated. A diet free of gluten usually brings both short and long-term improvement. This isnt always quite as easy as it sounds, as so many processed foods contain hidden forms of wheat that are used as binding or flavoring agents.
    Once you become aware of damaging foods and avoid them, a gluten-free diet can restore small intestine function within a few weeks to a few months. Once the mucosa of the intestine is no longer inflamed, most absorption issues will usually subside. The inflammation in the intestine will subside as gluten is eliminated.
    Echinacea and goldenseal may help to speed this process along. These two immune system boosters are often packaged together in capsule form. You may also find Echinacea and goldenseal in combination with slippery elm, marshmallow, geranium, and other herbs. This combination goes by the generic name of Roberts Formula, and is made by a number of manufacturers. Roberts formula treats the digestive tract by creating a beneficial layer of slime that is healing to digestive tissues. Check your local health food store.
    Echinacea and goldenseal are important healers because they have anti-inflammatory and antibacterial properties. One cautionary note, however: Dont take these herbs continuously. Generally, two weeks on and two weeks off for a period of up to two months.
    How to Replace Lost Nutrients Caused by Untreated Celiac Disease
    At the very least, most celiacs will benefit from a daily multivitamin/mineral supplement that includes calcium, 1,000 milligrams, along with 400 milligrams of magnesium (note that too much magnesium can cause diarrhea). Lack of vitamin B6 is partly to blame for symptoms of celiac disease, Pyridoxal-5-Phosphate (P-5-P) is often a good choice, as it requires no conversion to make vitamin B6, and can be easier on the stomach.
    Vitamins can also speed healing. Because the absorption of fats is particularly poor in celiacs, many celiac patients commonly suffer deficiencies of vitamins A, C, D, E, and benefit from taking these in supplemental form, along with a chelated form of zinc supplement. As with any supplement, read the directions and keep your doctor fully informed about what you are taking and how much.
    A typical dose, for example, is 1,000 to 2,000 international units (IU) of vitamin A in the form of fish oil (too much can have toxic effects so discuss this with your doctor), 100 to 200 IU of vitamin D also in fish oil, 500 to 1000 milligrams of vitamin C, 100 to 400 IU of vitamin E, and 15 to 30 milligrams of chelated zinc.
    Check with your doctor before taking more than 20 milligrams of zinc. Beta-carotene, 10,000 I.U. daily, can also be helpful, as can Iron, 60 mg. daily, if a blood test indicates iron deficiency.
    In addition to a good multivitamin/mineral for support, and other vitamins, digestive enzymes, which digest gluten, may also be helpful. To improve nutrient absorption and assimilation, these should be supplemented.
    Celiac patients also often suffer a deficiency of vitamin K., which can be supplemented through green foods, especially alfalfa. Green food supplements contain many essential nutrients, including trace minerals. Evening primrose oil is a good source of the omega-6 essential fatty acids that celiac patients often lack.
    Silica soothes inflammations in the gastrointestinal tract. It is available in both capsules and gel form.
    Medicinal clay is excellent in promoting healing of the walls of the colon and protecting it from irritation by toxins and dry, abrasive matter.
    Daily Dosages of Supplements for Celiacs:
    Green food supplements, 1 tbsp. Evening primrose oil, two 500 mg capsules three times daily Multivitamin supplement, as directed on the label Medicinal clay, dissolve 1 tsp. of clay in ½cup of water at room temperature and drink twice daily. Papain, 500 mg three times daily Pyridoxal-5-Phosphate, 50 mg daily Silica, 3-6 capsules; in the gel form, follow the directions on the label Vitamin B complex, 50 mg twice daily Vitamin B12, 100 mcg Vitamin C, with bioflavonoids, 5,000 mg one to three times daily Herbal Remedies in the Treatment of Celiac Disease
    Herbal remedies can help soothe intestinal irritation and inflammation and heal damaged mucous membranes.
    Roberts Formula Take 4 drops of agrimony tincture in water, three times daily. Sufficient silica in the intestines will reduce inflammation, and strengthen and rebuild connective tissue. Take 3 cups of silica-rich horsetail tea or 15 drops of tincture in liquid three times daily. A combination of burdock, slippery elm, sheep sorrel and Turkish rhubarb tea helps different types of inflammations in the gastrointestinal tract. Use dandelion, saffron and yellow dock herbal teas to that purify and nourish the blood. Pickled ginger can be eaten for anti-inflammation properties.

    Rivkah Roth D.O., D.N.M.
    Celiac.com 08/28/2012 - What's In A Name and When Does Celiac Predisposition Become A Disease?
    No doubt that global awareness about celiac disease and its possible involvement in a myriad of other (mostly autoimmune response related) conditions is growing. Growing, unfortunately, is confusion about terminologies and medical implications.


    The “Common” Understanding
    "Celiac disease" has become a generic blanket term not unlike how "Kleenex" today signifies no more than a box of tissue paper of any brand. So, in the public mind, "celiac disease" today stands for everything connected to a reaction to gluten.[1]
    Such an approach is highly imprecise and misses
    the need for distinction between non-celiac and/or celiac gluten sensitivity and the fact that a predisposition does not necessarily constitute disease.

    The 2012 Internationally Accepted Definition
    In an attempt to bring some clarity to the medical community, the world’s leading celiac minds earlier in 2012 met for an international convention in Oslo, Norway.[2]  During that convention, and after considering many of the most commonly used terms, they recognized

    …the presence of genetic, predisposing patterns…
    and called for a

    …distinction between "celiac disease" versus "gluten-related disorders"… [3]
    Let us be clear: This terminology refers solely to the underlying toxic effect of gluten rather than the possibly resulting disorders that may be based on other, additional triggers as well.


    Genotyping Tells Non-Celiac from Celiac Gluten Sensitivity
    Along with ever mounting genotype-related research, detailed HLA-DQ2/DQ8 human leukocyte antigen genotyping[4] today allows us to distinguish between predispositions to non-celiac and/or celiac gluten sensitivity (NCCGS) predisposition.
    Increasingly, research results link gluten issues to a considerable list of specific conditions and, therefore, allow for and promote a “natural” approach (i.e. gluten free diet and lifestyle) to resolve a complex panel of non-obvious signs and symptoms.
    Accordingly, "Celiac" is not (yet) a disease but a metabolic predisposition, i.e. the body’s inability to digest certain grain proteins, prolamines, etc.—much like a gasoline fueled car will sputter and eventually corrode on diesel fuel.


    Predisposition vs. Disease
    A genetic predisposition to celiac only becomes a disease (e.g. celiac disease or one of the non-celiac gluten sensitivity enabled conditions)[5] if the body’s inability to digest gluten and certain other grain proteins is ignored at the expense of the immune system.[6]
    In other words, an individual genetic predisposition to celiac only develops into full blown disease if that particular individual does not adhere to a gluten-free diet and lifestyle.
    An European Union et al commissioned research paper concluded:

    The environment clearly plays a crucial role in the development of celiac disease: No gluten, no disease!….
    …Because gluten is present in relatively large amounts in a variety of common food products, the daily gluten intake in a Western diet is high. In combination, we see that every HLA-DQ2– and/or -DQ8–positive individual is exposed to a large repertoire of immunogenic and abundant gluten peptides, and this may be an important factor determining disease development. There is, at present, no evidence linking additional environmental factors to celiac disease. [7]


    Big Business: Catering to a Gluten Free Diet
    The facts are everywhere and are illustrated further by these research abstract numbers posted on PubMed:
    18,565 on “celiac disease” (607 alone in 2012 – Jan. to Jly.) 9,689 on “gluten” (385 in 2012 – Jan. to Jly.) 3,447 on “glutenfree” (192 in 2012 – Jan. to Jly.) In addition, 38,878 abstracts deal with wheat research, whereof 1,862 in 2011, and 1,384 in 2012 to date (Jan. to Jly.).
    Clearly: $6.1bn spent 2011 on gluten-free foods in the USA—and a 30% growth from 2006 to 2010 in Canada to $2.64bn—indicate “Big Business” complete with the risk of missed, omitted, and mis-information for the goal of promoting greater consumption of gluten-free processed foods.
     
    The Challenge
    Our present naming confusion, therefore, may end up fuelling potential manipulation and mismanagement of the patient and consumer from the part of medical, pharmaceutical, supplement, and food industries.
    Even the above mentioned latest attempt at coordinating nomenclature and distinction between non-celiac and/or celiac gluten sensitivity brings with it several major flaws and challenges:
    It may take years for new naming conventions to become accepted throughout the international medical and dietary community. Recognizing a term such as "gluten-related disorders" or “non-celiac gluten sensitivity” calls for a total revamping of our medical and diagnostic systems in order for the large number (so far about 160) of autoimmune and other disorders to be recognized as gluten-related.   In addition, future questions will arise as research identifies and confirms more genetic links:
    Already, clinic practice shows that some of the "celiac" patients, previously diagnosed by positive intestinal biopsy[8] and serological findings now, on genotyping[9], turn out to carry "non-celiac" and not “celiac” gluten sensitivity alleles. Where does this leave such individuals on the traditionally used "celiac disease" versus "gluten-related disorder" specter?
    Clearly, despite good intention for a more precise naming distinction, it appears that additional work is needed in order to entrench new medical terminology and disease pictures.
     
    Conclusion
    Until then, whenever one of my patients receives a positive HLA gene test, I will adhere for clarity’s sake to the terms of “non-celiac” and/or “celiac gluten sensitivity” (NCCGS).
    This terminology refers solely to the underlying toxic effect of gluten and prevents a wrong implication of predisposition=disease diagnosis. Instead, “non-celiac and/or celiac gluten sensitivity” will simply point to the inherited underlying predisposition to specific additional triggers and complications if exposed to gluten.
    Most importantly, I will make sure to instill in my patients that disease is not the inevitable outcome of their genetic predisposition, and that a 100% gluten-free diet and lifestyle allows for avoidance, control, and perhaps even reversal of a complex web of interrelated autoimmune-based conditions and disorders, both for non-celiac and for celiac gluten sensitivity related disorders.

    [1] http://www.ncbi.nlm.nih.gov/pubmed/22351716  Ann Intern Med. 2012 Feb 21;156(4):309-11. Nonceliac gluten sensitivity: sense or sensibility?
    [2] http://www.ncbi.nlm.nih.gov/pubmed/22345659  Gut. 2012 Feb 16. [Epub ahead of print] The Oslo definitions for coeliac disease and related terms.
    [3] http://www.ncbi.nlm.nih.gov/pubmed/19940509  Int Arch Allergy Immunol. 2010;152(1):75-80. Epub 2009 Nov 24. Differential mucosal IL-17 expression in two gliadin-induced disorders: gluten sensitivity and the autoimmune enteropathy celiac disease.
    [4] http://www.ncbi.nlm.nih.gov/pubmed/22123644  Curr Opin Gastroenterol. 2012 Mar;28(2):104-12.  Advances in coeliac disease.
    [5] See future articles posted in these pages...  
    [6] http://www.ncbi.nlm.nih.gov/pubmed/21787225  Int Rev Immunol. 2011 Aug;30(4):197-206.  Important lessons derived from animal models of celiac disease.
    [7] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC209453/?tool=pmcentrez  J Clin Invest. 2001 November 1; 108(9): 1261–1266. doi:  10.1172/JCI14344  PMCID: PMC209453  Interplay between genetics and the environment in the development of celiac disease: perspectives for a healthy life.
    [8] http://www.ncbi.nlm.nih.gov/pubmed/22742547  Arch Pathol Lab Med. 2012 Jul;136(7):735-45.  An update on celiac disease histopathology and the road ahead.
    [9] http://www.ncbi.nlm.nih.gov/pubmed/21593645  J Pediatr Gastroenterol Nutr. 2011 Jun;52(6):729-33.  HLA-DQ genotyping combined with serological markers for the diagnosis of celiac disease: is intestinal biopsy still mandatory?

  • Recent Articles

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

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

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

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

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