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Herdswoman
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After reading about the many folks here who have celiac, I decided to do a "little light reading" on the 'net. Came across this statistic after about three hours and it was a genuine eye opener:

This is taken from the University of Chicago Celiac Disease Program Fact Sheet:

"The incidence of autoimmune diseases in the general US population is 3.5%. In a 1999 study, Ventura, et.al. found that those diagnosed with celiac disease between the ages of 2-4 years of age had a 10.5% chance of developing an autoimmune disorder.

Duration of exposure to gluten and risk for autoimmune disorders in patients with celiac disease. SIGEP Study Group for Autoimmune Disorders in Celiac Disease.

Additional findings are outlined below:

Age of Diagnosis/ Chance of developing autoimmune condition

Age 2-4........ 10.5%

Age 4-12....... 16.7%

Age 12-20..... 27%

over 20........ 34%

rest of the article is here:

http://brain.hastypastry.net/forums/showth...read.php?t=2228

and then there's:

http://www.allergyimmunolinx.com/thearts.c...pecid=21&ok=yes

and more stuff in the bibliography:

http://brain.hastypastry.net/forums/showth...read.php?t=2132

I need to get a new inkjet cartridge and start printing this stuff! Gawd, I love science!

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Thats pretty interesting.

I found this article earlier this year when I finally accepted my daughter's diagnosis of Irritable Bowel Syndrome and asked her to be considered for Celiac Sprue.

How common is celiac disease?

Celiac disease is the most common genetic disease in Europe. In Italy about 1 in 250 people and in Ireland about 1 in 300 people have celiac disease. Recent studies have shown that it may be more common in Africa, South America, and Asia than previously believed.

Until recently, celiac disease was thought to be uncommon in the United States. However, studies have shown that celiac disease occurs in an estimated 1 in 133 Americans. Among people who have a first-degree relative diagnosed with celiac, as many as 1 in 22 people may have the disease. A recent study in which random blood samples from the Red Cross were tested for celiac disease suggests that as many as 1 in every 250 Americans may have it. Celiac disease could be underdiagnosed in the United States for a number of reasons:

Diseases Linked to Celiac Disease

People with celiac disease tend to have other autoimmune diseases as well, including

dermatitis herpetiformis

thyroid disease

systemic lupus erythematosus

type 1 diabetes

liver disease

collagen vascular disease

rheumatoid arthritis

Sj?gren's syndrome

The connection between celiac and these diseases may be genetic

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Hi Katherine,

Yes, there's a simple blood test you can request your doctor to order. However, in order for it to be most reliable you must have been ingesting gluten regularly, i believe for at least 8 weeks prior to the test. So if you've been gluten free, the test may come back negative for gliadin antibodies. If the test is positive many doctors like to scope the small intestine and take a small biospsy to confirm the damage to the lining. This step is just a confirmation of the blood test.

Hope this helps.

Gena

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This is good stuff, especially if you like science.

It's really good stuff if you don't like science and can't sleep at night. :D

Note that this research is barely a year old. Information in boldface was inserted by me, otherwise this is the full, unedited transcript. Read it slowly, think about it, come back to it later and re-read. There's a lot of implications here. I forwarded this to my co-workers in GI Unit and am awaiting their critical review.

Early Diagnosis Of Gluten Sensitivity: Before the Villi are Gone

Transcript of a talk given by Kenneth Fine, M.D. to the Greater Louisville Celiac Sprue Support Group, June 2003.

"Gluten sensitivity" is the process by which the immune system reacts to gluten contained in wheat, bar ley, 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 antitissue 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 antitissue 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, antitissue 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 antitissue 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 antitissue 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 8 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 sensitivity 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 2 to almost 35% by age 20. This is a big deal if you think how much more complicated one's life is being gluten sensitive AND having an 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 test used for primary (before symptoms develop) and secondary (after symptoms develop) screening for celiac disease, blood tests for antigliadin and antiendomysial/antitissue transglutaminase antibodies, are only routinely positive after damage to intestinal villi is extensive. 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, is 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%. 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 facts 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 syndrome 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 from the 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 5 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 antitissue 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. Combining this stool testing with HLA gene testing, which we do with a cotton-tipped swab rubbed inside the mouth, is the best diagnostic approach available.

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 to be gluten sensitive: 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 respects 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 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 1970s and 80s (and improved upon in the 1990s) that blood tests for antigliadin and antiendomysial/antitissue 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, 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.

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OMG what have I started?? :D

Science geeks unite! :) For those who didn't know this--I'm one of them. Probably why I like behavior analysis which uses the scientific method to develop intervention instead of more general psychology which is based on other theories.

But I digress...

Interesting article. As mentioned earlier by me, I tested negative for gliadin antiboties, but I'd also been strictly gluten free for many years and could never get past about 2 weeks of reintroducing gluten. Also, we didn't do the sigmoid biopsy because, again, one needs exposure in order to see the physiological changes in the intestinal (sigmoidal) cells.

Nina

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amy,

i haven't read everything yet. (aaahhh, my stomach is calling out for food...), but i am so glad that you posted all of this. i have really been wondering about the link and why so many of us either have celiac or benefit from a gluten-free diet.

i just had GI appt. this week and was so furious. one of the things he wouldn't believe me on was the gluten-free diet i am on. anyway, i won't go in to it...it's jus that your post was perfect timing.

nina...i guess i am the opposite...i'm the psychology nerd...i like all that stuff better than the more scientific approach...hmmmmm....the mind is such a cool think. although, i do like the science and did a lot of pre-med classes and lots of psych classes with stats, research methods, etc...so i guess i'm just a big nerd too. no, i KNOW i am a big nerd. :D

emily

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Herdswoman, the information is very interesting. Thanks for posting. The connection with autoimmune illness is interesting/alarming.

In Feb a nutritionist suggested that I go on a gluten free diet and I found some relief to GI complaints within a month. I am still learning what "hidden" factors to look for when I go to the store and read labels, but I think I am doing pretty well.

When I saw a GI doc a few weeks ago and told him I had gone gluten free he said if it made any positive improvement, stick with it. He said that there would be no point in testing me since gluten wouldn't be present and he didn't suggest eating it just for the purpose of another test...thankfully!

NOW, Emily...... WHAT..... did your GI doc have to say? Sounds like you may be looking for a new doc soon???? Sorry, it sounds like you did get any help. I am puzzled why he wouldn't believe you about being gluten free...

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aaack! geneva! i am glad your doc said that to you about the gluten-free diet. that makes me feel better! to know there are docs who take it seriously.

i agree with his attitude...if it helps, go with it. and why put yourself through adding it back in for the test. especially since we all know that you can ahve gluten intolerance and not celiac.

anyway, no, i had an awful visit with this doc and i am so frustrated...what does a woman have to do to be taken seriously these days?

anyway, i wanted to let you know that i will post in a separate post about my appt. and i would love your feedback. i may not get to it right away, but i will get to it...b/c i really am so keyed up about it!!! well, maybe livid would be a better word! (okay, breathing, calming down now....i maybe should wait to post til i am not so cranky!)

emily

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My doc didn't believe me at first either... He said "I doubt that you've eliminated it all--no bagles, toast, pasta, cookies?" And then I told him I didn't have ANY gluten in my diet except by accident. For example, I didn't realize that Twizlers liccorice is made with wheat gluten. Other things that are accidental include barley malt. I told him I couldn't even eat Rice Krispies or Cheerios because they have barley malt in them. I've accidentally ingested texurized vegetable protien (ie. 100% gluten) at a dinner party where the hostess was a vegetarian and had fake chicken made from tvp... and became exceptionally ill. I explained that I eat brown rice pasta, rice based bread, I use oat flour to make stuff at home, I bought all my major cooking supplies via mail order including gluten free soy sauce and tamari and I occasionally cheated with pizza because it's so hard to find a close substiute for a wheat based crust.

After that, he was impressed. Em, I think many people believe they are gluten free, but have many sources that are not as obvious. Big boo boo items are things like beer, certain other distilled beverages like whiskey, malt beverages like hard lemonade, hard cider and hard iced tea, certain unfiltered saki that has barley remenants in it (while made from rice, the fermenting agent is cultured on barley).

Take a look at the forbidden foods list I posted the link to on the other thread on celiac. Also, look at the related link on maintaining a fully gluten free diet--there are some folks who are exceptionally sensitive to crosscontamination, such as oat flour that was milled near wheat flour.

Nina :D

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nina,

no, i REALLY am gluten-free...i cannot cheat AT all without consequences. i am also Casein-free, egg-free, nut-free and on and on. i am aware of the hidden sources of gluten...but am still working on it. still, i only really eat like a cave woman...meat, fish, veggies and fruit, rice, potatoes.

it wasn't that the doctor didn't believe that i was gluten-free...it was that he thought it was a lot of work to do it and not worth it if i wasn't "really celiac". it was a nuisance as a diet he said. well, yes, but it WORKS.

also, i had the genetic test for celiac as well as the ANA done, but since i had already been gluten-free for soooo long it was negative.

sorry if i wasn't clear on my level of strictness on this diet. i am truly gluten-free...

and, tinkyada is my favorite rice pasta too...we are having it tonight for dinner.

thanks for the tips. i appreciate it. those sites are helpful and i want to print the forbidden foods list once and for all.

emily

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it wasn't that the doctor didn't believe that i was gluten-free...it was that he thought it was a lot of work to do it and not worth it if i wasn't "really celiac". it was a nuisance as a diet he said.

Ohhhhh-KAY. I guess we know who hasn't been keeping up with his professional journals. Hah!

Ladies! The Blue Light is Flashing in the Dumb Department....We are running a special on physicians who would rather spout off than be accurate. Our featured items are brought to you by Emily's Gastroenterologist, top producer of inadequate and opinionated information.....

Gee, I just realized that most of you are too young to remember the blue light flashing in Kmart. Tough. Google it if you want to know more :D

Feel better, Em?

I'd love to see a separate thread with the DO's and DON'Ts, forbidden sins and hidden dangers of the gluten free diet.

What's casein, anyway?

Edited by Michelle Sawicki
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The only question my doctor asked about gluten free diet is whether I include

MALT VINEGAR.....Nina or anyone do you know what foods/drinks have?? I told him I go by the list (from the link Nina gave me earlier) and if it is on the forbidden list I don't eat it. I thought alcohol or something????

Herdswoman, I am young enough to remember the blue light specials!!

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malt vinegar is on the forbidden list--but distilled vinegar is typically okay.

Yep, I'm old enough to have personally experienced blue light specials too :D

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herdswoman....

thank you for making me LAUGH OUT LOUD!!!! that was so funny.

and yes, just to set the record straight...i still remember the blue light specials at kmart! (i am 29)....

my dad's FAVORITE store is kmart---he and my stepmom drive OUT OF TOWN to shop at a kmart! i am not kidding! yeah, he's a little nutty.

this post on gluten-intolerance is just at the perfect time to affirm my choice to stay gluten-free.

also, as for casein...that is one of the proteins in milk. my doctor at hopkins does not want milk products in ANYTHING...and i mean ANYTHING...he wants even my meds to be lactose-free...and lactose in a binder in almost everything...

so, as for being super-careful about food...that's me...it is actually a bit stressful sometimes trying to find stuff to eat! seeing as i am hungry all of the time!

i am going to turn in to a grain of rice i think...all i eat is stuff made with rice (who knew that could come up with rice-everything...cookies, milk, frozen treats...whew!)

goodnight...and thanks for the laughs. i needed it.

later alligator!

love, emily

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hi

I tested positive to all the blood tests for celiac and have that and other autoimmune diseases in my family. I had a colonoscopy and they said that there was only a 10% chance that I actually have celiac. My doctor decided no. I am on a wheat, barley, and rye free diet. I eat organic oats and spelt due to research I have done, the fact that I have no obvious symptoms from these and because my doctor said that I was just wheat intolerant like lactose intolerant. i think she might be full of it. She is supposed to be one of the best in the country and is at Cornell. however, I think she messed up on this one. I have iron deficiency, low B12, magnesium, and vitamin K levels even though I consume large amounts of these things. These all started in the last year and my blood test was for celiac two years ago. I have had bad GI problems since early childhood and am now 23. I don't know if and when I developed it. Your research is immensely helpful. Thank you. I would love advice. Would you really say no false positives, because my docs think I might have been one and I don't think so. I am very curious.

Thanks.

Leah

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I have iron deficiency, low B12, magnesium, and vitamin K levels even though I consume large amounts of these things. These all started in the last year and my blood test was for celiac two years ago. I have had bad GI problems since early childhood and am now 23. I don't know if and when I developed it. Your research is immensely helpful. Thank you. I would love advice. Would you really say no false positives, because my docs think I might have been one and I don't think so. I am very curious.

Leah, I don't mean to bail here, but this is not my research. This is Dr. Fine's research and all I did was post it. Read the article carefully. I am reading the article for the fifth time today.....each time I go over it, my understanding deepens. I print it out, highlight it, make notes in the margins, the whole geeky thing.

To look at other member's physical conditions from a purely scientific perspective is difficult in a forum such as this. I won't do it. Whether or not I would say 'no false positives' doesn't mean a hill of beans. I am not a doctor, nor do I play one on TV.

My best advice is to do what I do:

1. Read the article, think about it, re-read it and look for the answers to your questions. Go over the third paragraph very carefully. Be clear about specificity and sensitivity as they are not the same things.

2. Go to the link I provided and print out the article in it's original form. (DINET tends to make 'accent marks' and apostrophes into question marks when cutting and pasting - I tried to fix this.) You'll want to take a clean copy, as professional as it can be, to your doctor if you think she's missed something.

FWIW: I'd be really careful about challenging a senior staff member at Cornell based on my feelings and one research article whose implications are more applicable for gluten sensitivity than celiac disease. Be very careful....how you ask is more important than what you ask. I don't take that cat to the vet unless I have to.

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  • 1 year later...

My daughter has POTS. Her Gastro sent us to this web site to order stool and DNA tests to check for Gluten Sensitivity. http://www.enterolab.com/

The Dr at the lab has a theory that stool tests show Sensitivity much sooner than bllod tests because the antibodies first develop in the intestine and only later show up in blood. The stool tests will see it first.

They also provide DNA testing to determine if the person is predisposed to developing immunologic sensitivity to gluten or celiac sprue.

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Guest Julia59

This is an interesting post. I'm also one that is a science nerd. I comprehend medical literature fairly well----and the autoimmune material is particularly interesting.

I have hashemotos thyroid disease---autoimmune, and also have digestive problems----always have.

However, I rarely get nauseated or vomit----I am always constipated, bloated, gassy---and I also deal with indigestion. Only recently I feel a little nauseated in the evening.

I am diagnosed with IBS---but I don't know if it is really true as this was diagnosed by many physicians who continued to blow me off when I was deealing with the first of my POTS symptoms.

Only one gastroenterologist took my digestive troubles seriously. I saw him when I was in my late 20s. He ran an upper GI and told me I have a diverticuli in my small intestine----THE SIZE OF A QUARTER. I don't know about you, but to me this was big. Isn't that about the diameter of your small intestine? I don't know, all I do know is that I can't eat anything too rough---nuts, things with seeds, thick skinned fruit----yada-yada-yada.

Later in the course of my POTS crash, but still not diagnosed with POTS---I saw another GI doc. He confirmed the diverticuli----he told me he saw it on my endoscopy report. He said it was in the small intestine near the jejunim. He said it was a bad place to be as it was near the bile ducts. He said if I ever needed surgery on it that it would be a difficult surgery. That was the last time it was addressed. Nothing was ever mentioned about celiac. I have not seen a GI Doc since that time.

Just a couple of weeks ago I found that I am severely deficient of vitamin D----<7-----when it should be something like 25--55..... I have been put on high doses of vitamin D---and calcium.........I don't know if this is connected to any malabsorbtion issue.

I also read something about EDS---where this type of diverticuli could be a feature of EDS---it's in my saved archives. Sorry---slid off the celiac subject. But I can't help but think that all this is interrelated.

Thanks---Herdswoman.............

Julie :0)

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safe and forbidden foods lists are from Celiac.com

http://www.celiac.com/st_main.html?p_catid...-50105313921.2f

Nina

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Julia,

I would definitley check into the possibility of celiac with your doctor. You can at least rule it in or out with a simle blood test as long as you've been eating gluten in your diet regularly. They sometimes want to scope your small intestine to look for inflammation and do a biopsy as well if they suspect celiac.

Are you deficient in any other vitamins like Bs or iron? Deficiencies in these are often associated with celiac or malabsorption as well. Wouldn't hurt to look into it more. I had numerous docs tell me I had IBS for months until I was finally dx'd with celiac.

Good luck!

Gena

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Guest Julia59

Gena,

I don't think the B12 is low----but the Doc did tell me to take that too---along with folic acid.

I'll bring it up to my PCP. My diet is full of Glutin----no doubt to that----a blood test can't hurt. I have had a scope before , but no biopsy was taken----that is when they confirmed the diverticuli, and the GI Doc said avoid anything that can get into that pocket. I'm bloated 80 % of the time. the digestive issues have gone on the back burner for me as I have so much going on righ now. As long as i'm not vomiting all the time---I don't worry about it-------BUT i'm glad this was brought up as I need to start thinking about my constant gastric discomfort.

Julie :0)

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