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    Does Obesity Play a Major Role in Triggering Autoimmune Diseases?


    Jefferson Adams
    Image Caption: Image: Wikimedia Commons--Victovoi

    Celiac.com 11/28/2014 - According to a new study, obesity plays a major part in triggering and prolonging autoimmune diseases, such as celiac disease, Crohn's disease and multiple sclerosis.


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    Image: Wikimedia Commons--VictovoiThe study appeared recently in Autoimmunity Reviews by Prof. Yehuda Shoenfeld, the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases at Tel Aviv University's Sackler Faculty of Medicine and Head of Zabludowicz Center for Autoimmune Diseases at Chaim Sheba Medical Center, Tel Hashomer.

    According to the research, obesity erodes the body's ability to protect itself, triggering a pro-inflammatory environment that promotes the development of autoimmune diseases, hastens their progression, and impairs their treatment.

    For some time now, says Professor Shoenfeld, researchers have been aware of the “negative impact of contributing disease factors, such as infections, smoking, pesticide exposure, lack of vitamins, and the like. But in last five years, a new factor has emerged that cannot be ignored: obesity.”

    According to the World Health Organization, about one-third of the global population is overweight or obese, nearly a dozen autoimmune diseases are now associated with excess weight, which now impact nearly 5-20% of the global population. That is why, according to Shownfeld, it is “critical to investigate obesity's involvement in the pathology of such diseases."

    The main culprit is not fat itself, but adipokines, compounds secreted by fat tissue, which impact numerous physiological functions, including the immune response.

    In tandem with their own study, Shoenfeld and his colleagues reviewed 329 studies from across the globe that focused on the connections between obesity, adipokines, and immune-related conditions like rheumatoid arthritis, multiple sclerosis, type-1 diabetes, psoriasis, inflammatory bowel disease, psoriatic arthritis, and Hashimoto thyroiditis.

    "According to our study and the clinical and experimental data reviewed, the involvement of adipokines in the pathogenesis of these autoimmune diseases is clear," says Shoenfeld. "We were able to detail the metabolic and immunological activities of the main adipokines featured in the development and prognosis of several immune-related conditions."

    One of the team’s more interesting findings was that obesity also promotes vitamin D deficiency, which, “once corrected, alleviated paralysis and kidney deterioration associated with the disorder… [and] improved the prognosis and survival of the mice.”

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    Interesting article. For quite awhile I thought that celiac disease caused obesity. I thought that a person with celiac disease ate more because they weren't absorbing the nutrients from their food and their bodies were trying to get more nutrients. Until now, I never considered that it was the other way around, that it was obesity that was causing their disease.

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    Guest J. Hergott

    Posted

    That is infuriating, we are born genetically predisposed to celiac disease, we become obese trying to get nutrients our villi can't absorb.

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    Autoimmune diseases run in my family, on both sides. Many of us have always been thin, others were slightly overweight or became overweight when they became older. In our family trees, weight doesn't seem to be a factor in autoimmune diseases, including celiac and Hasimoto's.

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    Guest CanadaCeliac

    Posted

    That is infuriating, we are born genetically predisposed to celiac disease, we become obese trying to get nutrients our villi can't absorb.

    I agree, J. I haven't always been obese, but did gain 100 pounds in the year prior to diagnosis, and was still hungry all the time. Since then, I've lost more than half the weight and am no longer so hungry.

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    Guest Kristin

    Posted

    Complete nonsense! Before being diagnosed with celiac, I was unable to keep weight on me no matter how much I consumed. Even while eating over 20,000 calories a day! gluten-free diets have very high GI levels and often celiac patients develop diabites 2 as well as many other auto immune illnesses.

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    My son was diagnosed with celiac disease last summer at 19 years of age. He is too thin -- has always been too thin -- and struggles to gain weight. While I can accept that obesity might exacerbate an autoimmune condition because of inflammation, it is genetic susceptibility that puts people at risk. If you don't have the genes, you don't get the disorder. What about all the obese people who do not have autoimmune diseases? Autoimmune thyroid disease wreaks havoc on metabolism which can lead to weight gain. Many celiacs also have thyroiditis. Many others also have Type 1 Diabetes.

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    Obesity does not play a "major" role in triggering an autoimmunity, nor can anything prolong an autoimmunity because once you have developed an autoimmunity you have that for life. Period. It does not just go away if you stop being obese. When I was diagnosed with an autoimmune disease I had never been considered even overweight ever in my life much less obese. I would personally need a much more realistic explanation for me to ever pay that price to read the actual medical paper.

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    Guest Jefferson

    Posted

    Complete nonsense! Before being diagnosed with celiac, I was unable to keep weight on me no matter how much I consumed. Even while eating over 20,000 calories a day! gluten-free diets have very high GI levels and often celiac patients develop diabites 2 as well as many other auto immune illnesses.

    That may be true in your case, but you are not "most people." The science is pretty clear that large numbers of people diagnosed with celiac disease are either overweight, or obese. Regarding this article, the science says that obesity is a major factor in the development and prolonging of autoimmune diseases. It does not say that thin, or non-obese people can't develop these diseases.

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    Guest Jefferson

    Posted

    Obesity does not play a "major" role in triggering an autoimmunity, nor can anything prolong an autoimmunity because once you have developed an autoimmunity you have that for life. Period. It does not just go away if you stop being obese. When I was diagnosed with an autoimmune disease I had never been considered even overweight ever in my life much less obese. I would personally need a much more realistic explanation for me to ever pay that price to read the actual medical paper.

    Read my response above. That may be true in your case, but you are not "most people." The science is pretty clear that large numbers of people diagnosed with celiac disease are either overweight, or obese. Regarding this article, the science says that obesity is a major factor in the development and prolonging of autoimmune diseases. It does not say that thin, or non-obese people can't develop these diseases.

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    Guest Jefferson

    Posted

    That is infuriating, we are born genetically predisposed to celiac disease, we become obese trying to get nutrients our villi can't absorb.

    The study says that obesity is a major factor in the development and prolonging of autoimmune diseases. It does not say that thin, or non-obese people can't develop these diseases. Basically, according to this study, if an otherwise healthy, thin person became obese, they would face in increased risk of developing autoimmune conditions, and that those conditions would be harder to control than if that person were thin. I hope that helps.

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  • Related Articles

    Scott Adams
    This article appeared in the Winter 2006 edition of Celiac.coms Scott-Free Newsletter.
    Celiac.com 07/10/2006 - Three years ago my father was diagnosed with celiac disease and I was told by my mother that it is hereditary and that I too should get screened for it. I did some research and immediately knew that I had this disease. I wouldn't admit it to anyone at the time because how on earth could I possibly live without pasta and fresh-baked bread for the rest of my life?! You should know that I have been sick for my entire life—I had colic until I was six, got ulcers when I was eight, appendicitis at 14, calcium bone spurs at 17, 19, 24 and 36, infertility at 24, gall stones at 37—just to mention a few of the conditions Ive had that were likely related to my untreated celiac disease.
    About six months later I decided to go see my doctor—I was in a severe state of depression, and I had lost the ability to think—much less talk. Carrying on a full conversation was nearly impossible because of my inability to speak in full sentences. I was extremely sick with a severe cold, and I had an infection or the flu at least once each month for the preceding two to three years. I told my doctor that I thought that he should test me for celiac disease. Since I weighed in at over 300 pounds he literally laughed at this idea. According to him there was absolutely no way that I could have celiac disease—because I was fat!
    Shortly after that my parents came to visit and tried to talk me into eating gluten-free—at least during the time that they were here. I agreed because I had to cook gluten-free for them anyway. Within three days of starting a gluten-free diet I felt like a million bucks. My depression lifted and within a month I was losing weight and my brain started working again. I have been gluten-free for three years now—not only do I feel like a million bucks, but I have lost over 100 pounds. I shudder at the idea that I was literally eating myself to death—and it was not because I didn't have any will power or that I was eating bad food—it was because my body couldnt process and absorb the food that I was eating. My personal experience, combined with my research, has left me completely convinced that celiac disease is (and will continue to be) a significant cause of obesity—and that this will continue to be the case until there is a better understanding of the disease and its relationship to obesity.
    What is Celiac Disease?
    Celiac disease is a permanent intolerance to gluten1, which is a protein found in, wheat, rye, and barley. When gluten is ingested the digestive system is unable to properly break it down, and an autoimmune response is triggered in the gut that causes the villi of the small intestine to become damaged—leading to malabsorption of crucial nutrients. There is no cure, and the only way to control it is through a 100% gluten-free diet.
    The disease has a vast array of symptoms, and it is rare that two people will exhibit the same ones. Some will have diarrhea while others will have constipation, and some will not have either but instead may have osteoporosis, diabetes, headaches, fatigue, autoimmune thyroid disorder or any number of other conditions and symptoms found to be associated with it. In many cases these symptoms are associated with the inability to gain weight—children with celiac disease are often small and fail to thrive 1.
    Nearly every source that I consulted for this paper referred to malabsorption and how most people with celiac disease lost weight or couldn't gain weight. Only a few sources even mentioned obesity—and when they did it was only in passing. As celiac disease awareness steadily increases and more research is done on it hopefully it will become apparent that many cases of obesity are also related to it.
    The Common Thread
    Autoimmune thyroid disease has recently been linked to celiac disease. Recent research has demonstrated that 3.4% of patients with autoimmune thyroid disease also have celiac disease2. The thyroid gland secretes hormones to control the body's metabolic rate3, and to accomplish this it must have iodine. When celiac disease is present along with autoimmune thyroid disorder, the body does not have the ability to absorb the iodine to produce the necessary hormones. Additionally there are many different disorders such as obesity, diabetes, allergies, weight-loss, gastrointestinal problems, etc., that can be caused by having a damaged or compromised thyroid gland3 (all of these disorders, by the way, can be related to celiac disease). It has been known for years that obesity has been linked to thyroid problems, and that the thyroid produces 5-monodeiodinase, the bodys natural method of conserving fuel during shortage," and the body "elicits the same physical reaction as famine," which can then cause the affected person to gain weight3.
    Another disorder commonly associated with celiac disease is malabsorption, which can also lead to malnutrition. When someone with celiac disease eats foods that contain gluten it results in damage to the surface of the small intestine and destruction of their nutrient-absorbing villi. This can lead to leaky gut and an inability for them to absorb vital nutrients from their food. By continuing to eat foods containing gluten, eventually vital organs including the brain, thyroid, liver, kidneys—essentially any organ that depends heavily on nutrients—will be starved, which will leave them susceptible to other diseases and conditions. I personally experienced brain malfunctions, gall bladder problems, and was diagnosed numerous times with an under-active thyroid. Naturally treatments for this proposed thyroid condition didnt work because their true cause had not yet been found. At one point a doctor asked me to consider the idea that my obesity was the result of my bodys attempt to cope with malnourishment4. This phenomenon is similar to yo-yo dieting, where dieters who have deprived themselves or proper nutrition for too long gain weight at faster rates than non-dieters after they resume eating normally. I always thought that I had fallen victim to yo-yo dieting, and that I had dieted myself into a permanent state of obesity. I now understand that it was because I had undiagnosed celiac disease, and my body was actually malnourished.
    Under normal nutritional conditions humans only absorb about 80 percent of the nutrients from the food they eat, and the rest of the nutrients pass through the body4. With celiac disease, however, the body is unable to absorb the necessary nutrients, which causes some peoples bodies to become a super-efficient machine that begins storing as much fat as possible in order to survive. This nutrient deficiency convinces the body that it is starving to death, which sends it into starvation-mode. Since humans need a certain percentage of body fat reserves to stay alive—and because it takes more work for the body to burn fats than carbohydrates—a body that is in starvation mode tends to crave carbohydrates and more efficiently convert them to fat for later use4.
    There has been much research that links celiac disease to diabetes. Diabetes occurs when the bodys cells are unable to absorb enough blood sugar5. Although the cause is different, the resulting malabsorption is similar to that seem in celiac disease—although in the latter the malabsorption is not just limited to sugar. The connection between diabetes and celiac disease as described by Marschilok:
    Both diseases have genetic and environmental origins. This means an individual is more at risk of developing either problem when a close relative also has it. On the genetic side, development of one reveals the pre-existing and larger risk that the genes for the other may be present. At least two genes and gene locations are connected with each disease. One gene for each disease is near one gene for the other on the same chromosome. Nearby genes are more likely to pass together to offspring.
    However, while the genes are necessary, they are not sufficient to produce the diseases. On the environmental side, researchers know gluten is needed to produce celiac disease, but they also know its not the only environmental cause. With diabetes, the environmental causes are being extensively studied for prevention and cure. Roughly ten percent of celiacs either have Type I diabetes or might develop Type II diabetes6 .
    An astonishing 40% of people with diabetes are also obese—even though there was not very much in the way of medical research to indicate why this is so. Diabetes is described as your cells inability to produce or absorb insulin, which leads to an excess of sugar in the blood stream7. If a person injects or produces too much insulin it will increase the level of hunger and cause obesity. I personally find this information disturbing as there are some in the medical community who still blame obesity on character flaws—I cant begin to tell you how many times I have been told: if you just didn't eat so much you wouldn't be fat.
    A number of overweight and obese acquaintances of mine have asked me how I managed to lose over 100 pounds and look so healthy while doing it. I explained my celiac disease diagnosis and gluten-free diet to them, and how the diet has made me not feel hungry for the first time in my life—due to the fact that I am now absorbing nutrients properly. Six of these extremely obese people have actually gone to their physicians to get tested for celiac disease—and each was met with the same skepticism as me. They persisted and finally got their doctors to perform the necessary tests—and to the surprise of all each were diagnosed with celiac disease! Immediately after going on the gluten-free diet they all experienced a decrease in hunger and massive weight-loss. For the first time they were eating only when their bodies were truly hungry, instead of eating too much due to starvation signals caused by malabsorption.
    This could also be part of the reason that high protein, low carbohydrate diets work so well for many people. By removing the carbohydrates from ones diet you generally remove a large portion of the gluten as well, which can cause those with celiac disease who are obese to lose weight quickly—at least for a month or so. However, on the high protein diet you are still not removing all gluten which will eventually cause them to gain the weight back—even though they are still on the diet. This was my experience with the low carbohydrate diet, and I suspect that a lot of others who are obese and have undiagnosed celiac disease had or will have the same experience.
    Conclusion
    I once had a family member literally yell at me about my weight and ask me why I was being so selfish and not thinking about my husband and daughter—they told me that I should just lose the weight. I was devastated, I truly had tried every diet on the face of the earth and each and every time I would loose 20-30 pounds quickly (regardless of the type of diet), only to gain it back (while still following the program)—sometimes as much as two fold! Since being diagnosed with celiac disease three years ago I have not only lost the weight but I have also kept it off, and each week a little bit more comes off. I am completely convinced that celiac disease does and will continue to be a common cause of obesity until the medical community—through scientific research—realizes that there is a connection.
    Many obese people might not be overweight if they were just properly diagnosed and treated. Certainly it is not the case that all obese people are that way because they just plain eat too much and do not have any will power. I suspect that there are better medical reasons to explain most cases of obesity, and celiac disease is just one of them. Not too long ago it was estimated that celiac disease only affected 1 in 10,000 Americans8. That figure was then revised to 1 in 5,000, and now, after much research, it is at least 1 in 133. The actual diagnosis rate, however, is only about 1 in 5,000, which is only a small fraction of those who have it. Similarly, the causes of obesity in America are not fully understood, and more research needs to be done to determine just how many cases of obesity are caused by untreated celiac disease. I believe that a significant percentage of obese people have undiagnosed celiac disease, and that celiac disease screening should be part of ordinary blood workups for all obese people.
    References:
    Adams, S. (May 2005). A Celiac Disease and Gluten-Free Resource since 1995. Retrieved May 18, 2005, from www.celiac.com. Collin, Kaukinen, Valimaki & Salmi, (2002). Endocinological Disorders and Celiac Disease, Endocrine Reviews (pp 1-38).
    3. Life Extension, Thyroid Deficiency, Online reference for Health Concerns. Retrieved May 26, 2005 from www.lef.org/protocols/prtcls-txt/t-prtcl-104.html. Balley, L. (June 2004) Obesity in Developing Countries Compares to U.S. Yo-Yo Dieting. Retrieved June 16, 2005 from: http://www.eurekalert.org/pub_releases/2004-06/uom-oid060804.php. Katz H., (2005). Hope for Obesity and Diabetes. Retrieved June 19, 2005 from http://www.reporter-archive.mcgill.ca/Rep/r3112/mice.html. Marschilok, K., (1997). Diabetes and celiac Disease. Gluten-free Living. Hoover, J., (2001). Obesity Causes Diabetes–Fat Chance! Diabetes Health Magazine. Retrieved June 19, 2005 from http://www.diabeteshealth.com/read,1009,2168.html Vogren, C.L., (September 15, 2003). Awareness Can Be Best Medicine: Parents who lost son to celiac disease want to shed light on often-overlooked ailment. The Gazette. Retrieved June 19, 2005 from http://www.csaceliacs.org/CDintheNews/COSpringsGazette091503.php

    Jefferson Adams
    Celiac.com 12/19/2011 - Very little data has been collected about how body mass relates to celiac disease in children in the United States. Recently, a team of researchers sought to document the way celiac disease presents in children with normal and with elevated body mass index (BMI) for age, and to study BMI changes in those kids following a gluten-free diet.
    The research team included Norelle Rizkalla Reilly, Kathleen Aguilar, Benjamin G. Hassid, Jianfeng Cheng, Amy R. DeFelice, Philip Kazlow, Govind Bhagat, and Peter H. Green. They are variously affiliate with Columbia University School of Medicine.
    The team reviewed data from patients treated at their specialty clinic from 2000 to 2008, for whom follow-up growth data available. In all, they evaluated 142 children from 13 months to 19 years in age, all with biopsy-proven celiac disease.
    To compare the results, they assessed patient height, weight, and BMI by age (z score), and grouped results by BMI as underweight, normal, or overweight.
    To be certain which of the patients were following a gluten-free diet, the team used results of serological assays, and data of noncompliant patients, which they assessed separately.
    Their analysis included only data gathered during the observation period, which they then expressed as change in height, weight, and BMI z score per month of dietary treatment.
    They found that almost 1 in 5 (19%) of patients showed an elevated BMI at diagnosis (12.6% were overweight, while 6% obese). Nearly 3 out of 4 patients (74.5%) showed normal BMI.
    The team followed each patient for an average of 35.6 months. Three out of four patients (75%) with an elevated BMI at diagnosis showed a substantial decrease in BMI z scores after following a gluten-free diet. Nearly half (44%) of those patients showed a normalized BMI after following a gluten-free diet.
    North American children with celiac disease frequently present as either normal weight or overweight. Patients with normal BMI at diagnosis showed sharply higher weight z scores after following a gluten-free diet, and 13% became overweight. This means that normal weight individuals will likely gain weight on a gluten-free diet, and that just over one in ten will become overweight.
    However, for overweight and obese children with celiac disease, the results indicate that a gluten-free diet may be helpful in lowering BMI.
    Source:

    JPGN 2011;53: 528–531

    Jefferson Adams
    Celiac.com 08/27/2012 - Because so many patients are now overweight upon diagnosis for celiac disease, and so fee present as classically underweight, doctors are revising the clinical presentation guidelines for celiac disease diagnosis.
    That being said, some researchers have voiced concern that some patients might gain further weight while on a gluten-free diet.
    Recently, a team of researchers conducted a study to assess the impact of a gluten-free diet on body mass index (BMI) in a nationwide group of celiac patients and to isolate any variables that might help to predict favorable or unfavorable BMI changes.
    The research team included Anniina Ukkola, Markku Mäki, Kalle Kurppa, Pekka Collin, Heini Huhtala, Leila Kekkonen, and Katri Kaukinen. They are affiliated variously with the School of Medicine, University of Tampere, and the Department of Gastroenterology and Alimentary Tract Surgery at Tampere University Hospital, both in Tampere, Finland.
    To assess weight and disease-related issues, the researchers looked at 698 newly detected adults who were diagnosed with celiac disease by classical or extra-intestinal symptoms or by screening.
    The researchers measured BMI upon celiac diagnosis and after one year on a gluten-free diet. They then compared the results against data for the general population.
    Study data showed that 4% of patients were underweight at celiac diagnosis, 57% were normal weight, 28% were overweight and 11% were obese.
    On a gluten-free diet, 69% of underweight patients gained weight, while 18% of overweight and 42% of obese patients lost weight. BMI remained stable for the other patients.
    Both symptom- and screen-detected celiac patients showed similar results. The patients with celiac disease showed a more favorable BMI pattern than the general population.
    The most favorable BMI changes were seen in patients with self-rated gluten-free diet expertise, along with those who were younger upon diagnosis. Dietary counseling did not seem to impact .
    The initial method of detection does not seem to matter for people with celiac disease who are following a gluten-free diet. Both screen-detected and symptom-detected celiac disease patients who followed a gluten-free diet showed similar improvements in body mass index (BMI).
    Source:
    European Journal of Internal Medicine Volume 23, Issue 4, Pages 384-388, June 2012

    Jefferson Adams
    Celiac.com 04/06/2015 - Several studies have shown that many patients with celiac disease experience changes in body weight after starting a gluten-free diet, but researchers still don't have much data on rates of metabolic syndrome in this population.
    A team of researchers recently set out to assess rates of metabolic syndrome in patients with celiac at diagnosis, and at one year after starting gluten-free diet. The research team included R. Tortora, P. Capone, G. De Stefano, N. Imperatore, N. Gerbino, S. Donetto, V. Monaco, N. Caporaso, and A. Rispo. They are affiliated with the Department of Clinical Medicine and Surgery, University Federico II of Naples, Naples, Italy, or with the Department of Education and Professional Studies, King's College London, London, UK.
    For their study, the team enrolled all consecutive patients with newly diagnosed celiac disease who were referred to their third-level celiac disease unit. For all patients the team collected data on waist circumference, BMI, blood pressure, HDL cholesterol, triglycerides, and blood sugar levels.
    The team diagnosed metabolic syndrome according to the International Diabetes Federation (IDF) criteria for European countries. They reassessed rates of metabolic syndrome in patients after 12 months of gluten-free diet.
    The team assessed ninety-eight patients with celiac disease, two (2%) who fulfilled the diagnostic criteria for metabolic syndrome at diagnosis, and 29 patients (29.5%) after 12 months of gluten-free diet (P < 0.01; OR: 20).
    After 1 year on a gluten-free diet, the team compared the patient data to baseline, with respect to metabolic syndrome sub-categories. They found 72 vs. 48 patients exceeded waist circumference cut-off (P < 0.01; OR: 2.8); 18 vs. 4 patients had high blood pressure (P < 0.01; OR: 5.2); 25 vs. 7 patients exceeded glycemic threshold (P = 0.01; OR: 4.4); 34 vs. 32 patients with celiac disease had reduced levels of HDL cholesterol (P = 0.7); and 16 vs. 7 patients had high levels of triglycerides (P = 0.05).
    The results of this study show that celiac disease patients have a high risk of developing metabolic syndrome 1 year after starting a gluten-free diet.
    To address this, the research team recommends an in-depth nutritional assessment for all patients with celiac disease.
    Source: 
    Aliment Pharmacol Ther. 2015;41(4):352-359.

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    Jefferson Adams
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    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. 
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    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