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Found 25 results

  1. I have inflammation as well as Hashimoto’s thyroid disorder and my doctor encourages a gluten free diet. I have been tested and do not have Celiac like my husband. I have pretty much eliminated gluten but wondered if a very occasional meal with gluten is harmful to me? We are 100% gluten free at home and generally when dining out.
  2. Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease. Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease. A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed. The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response. "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author. That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists. In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood." O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease." The research was funded by the National Institutes of Health. Read more at: Sciencedaily.com
  3. Summary:History of gluten intolerance, symptoms have returned despite no change in diet after 5 years of the same gluten sensitivity, I now seemingly react to the smallest cross-contamination and am not getting symptom relief. Do I need to worry about refractory sprue? I posted this on the celiac sub-reddit about two weeks ago but now I thought I could get more input here. A little background. When I was 14 years old, I started having strange joint pains in my wrists, persistent neuropathies and tingling in my hands, and other strange symptoms. Pains were seemingly inflammation of the tendons, made worse by exercise, and the inflammation responded well to NSAIDs. Went to a ton of doctors, tested for RA, MS, and anything else under the sun, but everything came back negative. "We don't know." My digestive health wasn't too bad or too good: I got constipated and got diarrhea from time to time, but not too often. I didn't really experience severe abdominal pains on a consistent basis so I didn't think anything of my digestive symptoms. As a result, no one checked anything digestive. The inflammation went away with NSAIDS. The only lasting effect after was that I absolutely couldn't exercise without developing terrible tendonitis and Joint pain within a few days, which caused a lot of depression. The disease remained stable in nature for a while until when I turned 21 or so. The chronic tendinitis spread to my ankles in addition to my wrists. The inflammation began to happen without any exercise, just from me existing. I also began having some more severe digestive problems, loose stools, poorly-formed stools, stomach pains, and felt like I was in a fog all the time. I tested negative for everything rheumatological. During a late-night research session, I googled a bunch of my symptoms and found out that a lot of people with gluten intolerance experience these same symptoms. I immediately went gluten-free. Over the course of the next two weeks, my digestive health was completely restored, and my joint pains were decreased by about 80% after about 1-2 months. I had an enormous amount of energy. I felt like a new person. I went to the doctor and got tested for Celiac, but the antibody test came up negative. I was already on a gluten-free diet, so I know that probably meant little. I know that my symptoms are not reflective of traditional Celiac and I apologize for self-diagnosing (no positive test). All I know is that going gluten-free absolutely changed my life and restored my health. Over the past five years, I've had absolutely no baseline changes in my gluten sensitivity. I cook most of my food, and eat at places like Chipotle and occasionally eat at restaurants and make sure not to order anything with wheat, rye, or barley. I get "gluten-fee" pizza at pizza places knowing that it's cooked in the same ovens with bread and do fine. I avoid beer and am careful with my alcohol selection, but basically, I was always able to tolerate cross-contamination. On the one occasion when I did eat bread, I had diarrhea for a week or two and then was back to normal. I was still tremendously prone to repetitive strain injuries and inflammation, but not to the same degree I had been before and ONLY after exercise. I was living my life. ... Fast forward to about 2-3 months ago. I have been going through a very stressful period in my life, and I think the stress triggered something. Simultaneously, I have a "glutening:" for a period of a couple of weeks, on 3 or 4 occasions, I eat sushi with imitation crab meat and rice binder that has wheat in it. I start having the pains in my ankles again. X-rays have shown that my ankles are swollen, and I haven't done anything but stayed on my feet and walked. Start developing tendonitis in my wrists again. The loose stools and indigestion are back and I feel like my brain is in a fog. I only get a little bit of symptom improvement if I eat the food I cook for myself. . I now respond to foods I wasn't responding to before. Eating at the same cafeteria I was eating at 5 months ago without a problem now causes a reaction. I have seemingly become very sensitive to ANY cross-contamination whereas just half-a year ago I could tolerate it without a problem. This is after five years of absolutely no change in my baseline reactivity. What the hell is going on? I've HAD glutenings before years back, and they never caused my symptoms to return and persist as they have now! And they NEVER changed my baseline sensitivity to gluten. All of my rheumatological tests have come up negative. I finally spoke to gastroenterolist yesterday and he agreed that this could be Celiac's disease, but had no answer for me on whether my baseline sensitivity would improve. I'm not willing to gluten myself for 6 weeks to get a positive blood test. The symptoms are too much to bare and I am trying to finish graduate school. My question is... if I do have Celiac... Has it suddenly gotten worse? Is it normal to have a sudden worsening of this condition, after 5 years at steady-state? I feel like I'm losing my mind, and have no idea what to do. I'm in constant pain and it's miserable. Whatever this is, it has taken such a huge toll on my life now.
  4. I was diagnosed with Celiac disease in September when liver phosphate levels were high in annual blood work. Right after that IgA and endoscopy was performed which confirmed villi damage and high inflammation. Since Sep 2017, I have been on SGF diet. The reason I went for check up in first place was low iron, Vitamin A deficiency and abrupt weight gain. In last 2 years I have gained 20 lbs which is strangely high for active life style. Since last 6 months,being on gluten free and lactose free diet but my weight is increasing and swelling on face, feet is constantly there. Some days I wake up and weight 5 lbs less and other days I am swollen and weigh much more than my normal weight. It’s surprising to doctor about why weight and inflammation can’t be controlled even though I have been working with nutritionist and following strict diet. She put me on low FODMAP diet to address intestine inflammation. It seems like now even after introducing slowly, I can’t take any lentils or other grains which used to be main source of proteins for me. Any thing else than rice gives me stomach ache though it’s bought from gluten-free source. Being vegetarian whole my life and now gluten, lactose free, I am wondering if how can I control on weight and swelling issue. I have no thyroid issues but I am failing to control my weight even after eating control diet which is mainly Hemp protein, pumpkin seeds, other nuts, rice, potato, green vegetables, bell peppers squash. Anything else will make me highly bloated , painful stomach. Family thinks that I am paranoid and have psychological issues now. Any suggestions on reason for weight gain and uncontrollable swelling and how to take care of those. Appreciate help and thanks in advance!!
  5. Lori HC

    Anger?

    Hello everyone, I am new to join this forum, though I have been look at your posts since I was diagnosed in September (it's now end of October). Just wanted to introduce myself. My name is Lori. I'm 43, female, and have had stomach issues for my whole life. As a child, I was ALWAYS tired. My doctor couldn't figure out what was wrong with me and just told my mom to get me into sports to help tire me out at night. I missed a lot of school because I was sick quite a bit, but got good grades so no one seemed to be bothered by it. Over the past 2 years my symptoms were consistently getting worse. Just before I had my gallbladder removed (gall bladder attacks that were getting longer), I started vomiting on a regular basis. Didn't seem to matter if I had an empty or full stomach or if I felt okay. I would be vomiting at least 2 times a week and chewing on ginger tablets constantly. Diarrhea also got worse but I didn't think much of it because I had been diagnosed with IBS when I was 20 and the celiac biopsies came back negative. I was taking 2 to 4 Immodium gel pills every day just to get through work. My doctor did numerous tests to find out why I was so sick all the time but no positive results for anything. She decided to send me for another gastroscopy and colonoscopy since it had been over 20 years since my last one. There, the doctor found out that I have a sliding hiatus hernia, ulcers, and bile reflux. He also did some biopsies which came back "blunted villi" so he recommended that my doctor send me for celiac blood tests. Sure enough, they both came back positive. This after a psychiatrist told me I should be tested again - years ago when the depression medication didn't work and my inflammation levels were through the roof. Today I also found out I have osteopenia. I thought I had worked through the anger that I hadn't been diagnosed years ago (when it wasn't too late to prevent a lot of the issues I have now), but it has raised it's ugly head again. My question to all of you is, how did you get past the anger at all the missed/wrong diagnoses over the years? I would have gone back and insisted on the doctor doing something if I hadn't assumed I had IBS for over 20 years. Maybe I could have had children. Maybe I could have prevented the bone loss and hair loss. Also, did anyone find that their hair grew back? How long did it take? Happy to have found all of you! Lori Here are my symptoms/related illnesses: Depression (diagnosed at 19 with intermittent success with medication combinations) Chronic inflammation Joint pain Skin rashes Chronic fatigue B12 and Iron deficiency anemia for years - I have had to take strong supplements for over 20 years. Hair loss PCOS (but I still ovulate so I'm wondering if this is true) Insulin resistant/pre-diabetic Very overweight beginning in 20s with difficulty losing weight for years (except the time I eliminated ALL grains)
  6. Hi everyone, Is there documented link between celiac disease and gym/sport-related injuries? I'm a recently diagnosed celiac and I'm wondering if the reason I have so many injuries (which won't go away even after months of rehab) is the celiac disease. Basically, I have ongoing pain in a number of areas in my body (left shoulder, right hamstring, left Achilles). The specialist and physio I've seen both think it is tendinitis, but I've been doing the recommended rehab and stretches for it for about 10 months and it's not going away. The injuries started around August 2016. Around March 2017 (so, well after the injuries), I started getting really sick and I was diagnosed with celiac disease. I've been gluten free since April (4 months) and the 'sickness' symptoms are gone but my injuries are still here. It kind of feels like every time I do exercise, something new goes off in my body. And I'm not training like an idiot or anything - before this I was training for 10 years without any injuries. At this point I am kindof hoping to god it's because of the celiac disease and that the injuries will sort themselves out once I finish healing (which I understand takes over 6 months?). Otherwise I have no idea what to do because I've been to the sports-doctor and physio a trillion times, I've spent a million hours doing rehab and there's basically no improvement. I just wanted to know whether anyone else has experienced the same thing and if you have any advice
  7. Celiac.com 02/01/2017 - More and more evidence shows a connection between gut inflammation and type 1 diabetes (T1D). A team of researchers recently set out to assess gut inflammatory profiles and microbiota in patients with T1D, and to compare them with healthy controls (CTRL) and with celiac disease patients as gut inflammatory disease controls. The research team included Silvia Pellegrini, Valeria Sordi, Andrea Mario Bolla, Diego Saita Roberto Ferrarese, Filippo Canducci, Massimo Clementi, Francesca Invernizzi, Alberto Mariani, Riccardo Bonfanti, Graziano Barera, Pier Alberto Testoni, Claudio Doglioni, Emanuele Bosi, and Lorenzo Piemonti. They are affiliated with the Diabetes Research Institute at the IRCCS San Raffaele Scientific Institute in Milan, Italy. The team evaluated inflammatory status and microbiome composition in biopsies of the duodenal mucosa from 19 patients with T1D, 19 with celiac disease, and 16 healthy control subjects, recruited at San Raffaele Scientific Institute, in Milan, Italy, between 2009 and 2015. They assessed inflammation by gene expression study and immunohistochemistry and used 16S rRNA gene sequencing to analyze microbiome composition. Compared to CTRL and celiac disease patients, the team found an increased expression of CCL13, CCL19, CCL22, CCR2, COX2, IL4R, CD68, PTX3, TNFα and VEGFA genes in T1D patients. The immunohistochemical analysis confirmed T1D specific inflammatory status was mainly marked by increased monocyte/macrophage lineage infiltration, compared to healthy and celiac disease control tissues. The T1D duodenal mucosal microbiome also proved to be different from the control groups. This was mainly marked by increased Firmicutes, and Firmicutes/Bacteroidetes ratio and a reduction in Proteobacteria and Bacteroidetes. The expression of genes specific for T1D inflammation was associated with the excess of specific bacteria in duodenum. This study shows that patients with T1D show specific abnormalities in gut inflammation and microbiota. Greater knowledge of the complex pathogenesis of T1D will likely provide new directions for therapies targeting the gut. Look for more studies in this area in the near future, as scientists look to nail down specific treatments to prevent gut inflammation. Source: The Journal of Clinical Endocrinology & Metabolism. DOI: https://doi.org/10.1210/jc.2016-3222
  8. Celiac.com 01/02/2017 - New research shows that a group of proteins in wheat, called ATIs, may be responsible for activating inflammation in such disorders as celiac disease, multiple sclerosis, asthma, and rheumatoid arthritis. Scientists also believe that the proteins may promote the development of non-celiac gluten sensitivity. The findings were presented at UEG Week 2016 in Vienna in Vienna, Austria, a meeting organized by United European Gastroenterology for specialists to communicate the latest research in digestive and liver diseases. One group of proteins found in wheat - amylase-trypsin inhibitors (ATIs) - has been shown to trigger an immune response in the gut that can spread to other tissues in the body. ATIs are plant-derived proteins that inhibit enzymes of common parasites - such as mealworms and mealybugs - in wheat. Interestingly, ATIs also have an important role in metabolic processes that occur during seed development. The finding that ATIs may promote inflammation in the and beyond the gut, is a major step forward in understanding the mechanics of celiac disease and/or gluten-intolerance. Stay tuned for more news on this and other breaking stories in celiac disease research. Read more at MedicalNewsToday.com.
  9. Celiac.com 11/04/2016 - Patients in the earliest stages of celiac disease have TG2-autoantibodies present in serum and small-intestinal mucosa. Many suffer abdominal symptoms long before the development of villus atrophy. The classic small-bowel mucosal damage that marks celiac disease develops over time and in stages; from normal villi to inflammation and finally to villus atrophy with crypt hyperplasia. Previously, researchers have shown that intraperitoneal injections of sera from celiac patients or of purified immunoglobulin fraction into mice trigger a condition mimics early-stage celiac disease. Those same researchers recently set out to show whether re-combinantly produced, patient-derived TG2-targeted autoantibodies are alone sufficient to trigger such condition in immune-compromised mice. The research team included Suvi Kalliokoski, Victoria Ortín Piqueras, Rafael Frías, Ana-Marija Sulic, Juha A. E. Määttä, Niklas Kähkönen, Keijo Viiri, Heini Huhtala, Arja Pasternack, Kaija Laurila, Daniele Sblattero, Ilma R. Korponay-Szabó, Markku Mäki, Sergio Caja, Katri Kaukinen, Katri Lindfors. They are various affiliated with the Tampere Center for Child Health Research, the Tampere School of Health Sciences, the Department of Internal Medicine, with BioMediTech at Tampere University Hospital and School of Medicine at the University of Tampere in Tampere, Finland, with the Department of Equine and Small Animal Medicine, Faculty of Veterinary Medicine, and Department of Bacteriology and Immunology at the University of Helsinki in Helsinki, Finland, with the Central Animal Laboratory at the University of Turku in Turku, Finland, with the Comparative Medicine Karolinska Institutet in Stockholm, Sweden, with the Department of Life Sciences at the University of Trieste in Trieste, Italy, and with the Celiac Disease Center, Medical and Health Science Center, Heim Pál Children’s Hospital and Department of Pediatrics at the University of Debrecen in Debrecen, Hungary. Interestingly, mice injected with celiac patient TG2-antibodies showed changes to small-intestinal mucosa, increased lamina propria cellular infiltration and disease-specific autoantibodies in the small bowel, but did not show any clinical signs of celiac disease. Thus, celiac patient-derived TG2-specific autoantibodies seem to be enough to trigger small-bowel mucosal changes in mice, but probably not enough to trigger clinical features on their own. Triggering clinical celiac features likely requires other factors, such as other antibody populations implicated in celiac disease. Source: Amino Acids, pp 1–12. DOI: 10.1007/s00726-016-2306-0
  10. Celiac.com 07/18/2016 - Dietary phosphorus occurs naturally in dairy foods, animal meats, and legumes but according to the Institute of Medicine, high levels of phosphorus can be a contributor to cardiovascular, kidney and osteoporosis disorders. While phosphorus is considered an essential nutrient, the increased amounts found in processed foods via additives like anti-caking agents, stabilizers and leavening agents or acidifiers does not have to be stated on the nutrition label. Individuals following a gluten-free diet need to consider the health implications of phosphates found in processed foods eaten regularly in their diet. Reducing carbonated beverages is the best way to reduce phosphorus levels in the diet. Extra attention needs to be paid to the ingredient statement on foods. Ingredient statements may include these declarations: tri-calcium phosphate, tri-magnesium phosphate, disodium phosphate, di-potassium phosphate. Just because the label states "natural" or "organic" does not mean it is a healthy food for daily consumption. Fresh is best! Here is a guide to where phosphates can be found in gluten-free processed foods: Baked goods- cake mixes, donuts, refrigerated dough (pyrophosphates are used for leavening and as a dough "improver") Beverages- phosphoric acid in colas (acidulant), pyrophosphate in chocolate milk to suspend cocoa, pyrophosphate in buttermilk for protein dispersion, tri-calcium phosphate in orange juice for fortification, tetra-sodium phosphate in strawberry flavored milk to bind iron to pink color Cereals- phosphate in dry cereals to aid flow through extruder, fortification of vitamins Cheese- phosphoric acid in cottage cheese to set acidification, phosphate in dips, sauces, cheese slices and baked chips for emulsifying action and surface agent Imitation Dairy Products (non-dairy products)- phosphate as buffer for smooth mixing into coffee and as anti-caking agent for dry powders Egg Products- phosphate for stability and color + foam improvement Ice Cream- pyrophosphate to prevent gritty texture Meat Products- tri-phosphate for injections into ham, corned beef, sausage, franks, bologna, roast beef for moisture Nutrition Bars & Meal Replacement Drinks- phosphates for fortification and microbiological stability Potatoes- phosphate in baked potato chips to create bubbles on the surface, pyrophosphate in French fries, hash browns, potato flakes to inhibit iron induced blackening Poultry- tri-phosphate for moisture and removal of salmonella and campylobacter pathogens Pudding & Cheesecakes- phosphate to develop thickened texture Seafood- tri-phosphate in shrimp for mechanical peeling, pyrophosphate in canned tuna and crab to stabilize color and crystals, surimi (crab/sea sticks) tri-phosphate and pyrophosphate as cryoprotectant to protein {surimi contains gluten and is not recommended for gluten-free diets] Hyperphosphate levels can contribute to muscle aches, calcification of coronary arteries and skeletal issues. Many food companies do not provide phosphorus analysis information because it is not required on the label but here is a representative sample of phosphorus levels in some commonly consumed on a gluten-free diet. Peanuts (1 ounce) 150 mg Yogurt (1 cup) 300 mg M&M Peanuts (1.74 oz pkg) 93 mg Rice Krispies Cereal (1 cup) 200 mg Dietary recommendations for an adult for Phosphorus is 800 to 1000 mg.
  11. Hi all, looking for guidance or information. I had the private md labs celiac panel run. Results came back negative for celiac. my symptoms are: bloating constipation aches in old injury sites sinusitis These symptoms are very reliable. I have been doing various eliminations for about 4 years. They occur after a single high dose of flour, eg a lot of pizza, or after 3 consecutive days of smaller doses. Thanks in advance. jesse
  12. A team of researchers has announced what they are calling a 'pivotal advance' regarding the differential influence of bifidobacteria and gram-negative bacteria on immune responses to inflammatory triggers in celiac disease. Their study provides strong evidence that various intestinal bacteria in celiac patients can influence inflammation, and that dietary probiotics and prebiotics can help improve the quality of life for patients with celiac and other associated diseases, such as type 1 diabetes and various autoimmune disorders. To conduct their study, they the team used cultures of human peripheral mononuclear cells (PBMCs) as in vitro models. This was possible because blood monocytes constantly replenish intestinal mucosal monocytes, and accurately represent an in vivo situation. To duplicate the intestinal environment surrounding celiac disease, researchers exposed cell cultures to Gram-negative bacteria and bifidobacteria they had isolated from celiac patients, both alone and in the presence of disease triggers. They then assessed the effects on surface marker expression and cytokine production by PBMCs. Gram-negative bacteria induced higher pro-inflammatory cytokines than did bifidobacteria. The Gram-negative bacteria also up-regulated expression of cell surface markers involved in inflammatory aspects of the disease, while bifidobacteria up-regulated the expression of anti-inflammatory cytokines. Research team still need to confirm the results in clinical trials on people, but the findings offer the first support for new treatment options that may change how celiac disease is treated and possibly prevented. In the same way the certain foods may contribute to poor health, notes Louis Montaner, D.V.M., M.Sc., D.Phil. Editor-in-Chief of the Journal of Leukocyte Biology, "others can have positive effects. For people with celiac disease, this opens a line of research into new therapies that may be as accessible as a grocer's shelf." SOURCE: Journal of Leukocyte Biology. 2010;87:765-778.
  13. Celiac.com 08/18/2014 - A team of researchers recently set out to better understand the effects of gluten-free diets on obesity. The research team included F.L. Soares, R. Matoso de Oliveira, L.G. Teixeira, Z. Menezes, S.S. Pereira, A.C. Alves, N.V. Batista, A.M. de Faria, D.C. Cara, A.V. Ferreira, and J.I. Alvarez-Leite. They are affiliated with the Departamento de Alimentos, Faculdade de Farmácia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais in Belo Horizonte, Brazil. Specifically, the team wanted to determine whether a gluten-free diet can prevent the expansion of adipose tissue, and its consequences. For their study, the team fed C57BL/6 mice a high-fat diet containing either 4.5% gluten (Control) or no gluten (gluten-free). They noted body weight and adiposity gains, leukocyte rolling and adhesion, macrophage infiltration and cytokine production in adipose tissue. The team measured blood lipid profiles, glycaemia, insulin resistance and adipokines. They also assessed the expression of the PPAR-α and γ, lipoprotein lipase (LPL), hormone sensitive lipase (HSL), carnitine palmitoyl acyltransferase-1 (CPT-1), insulin receptor, GLUT-4 and adipokines in epidydimal fat. Gluten-free animals showed less body weight and adipose gain, with no changes in food intake or lipid excretion. These results were associated with up-regulation of PPAR-α, LPL, HSL and CPT-1, which are related to lipolysis and fatty acid oxidation. The team also saw improved glucose regulation, and pro-inflammatory profile-related over-expression of PPAR-γ. Intravital microscopy revealed a lower number of adhered cells in the adipose tissue microvasculature. The over-expression of PPAR-γ is related to the increase of adiponectin and GLUT-4. The results of this study suggest that gluten-free diets can be helpful in reducing fat gain, inflammation and insulin resistance. They suggest that a gluten-free diet should be tested as a way of preventing the development of obesity and metabolic disorders. Source: J Nutr Biochem. 2013 Jun;24(6):1105-11. doi: 10.1016/j.jnutbio.2012.08.009. Epub 2012 Dec 17.
  14. Hi all, I am new to this forum and decided to post my current situation with two hopes: that others may have some acquired wisdom they can share, and to also help anyone else out there who may be struggling. I have had chronic vertigo, inability to concentrate (foggy headedness), inflammation in the glands and inner ear, and sore throat for 17 months now. The symptoms ebb and flow, with some days being more tolerable and the flare-ups making me bedridden. The symptoms began during the flu season and began with a flu-like illness that developed into the syndrome. I saw two general practitioners who were puzzled and sent me to an ENT. The ENT diagnosed the vertigo as the type that occurs when the crystals in the inner ear get shaken up and said he 'didn't care' about the chronic sore throat or swollen glands. He sent me to a physical therapist who disagreed with his diagnosis and said the vertigo was likely due to neuritis, or inflammation of the nerve in the inner ear, which is thought to be caused by a viral infection. This is much more likely, but doesn't explain why I cant shake it, and there is no accepted cure for neuritis. I have been gluten free for several years. (Prior to that, I was a vegetarian and ate massive amounts of wheat gluten daily and so developed Candidiasis (thrush), another saga that involved skeptical or hostile doctors and the necessity to do research and self-diagnosis.) In the last two weeks I've also developed joint pain in the right hand and my vision is sometimes blurry or 'off'. The evidence seems to point towards some kind of autoimmune disorder, such as lupus, rheumatoid arthritis or thyroiditis. I'm now looking into lectins in food and their apparent connection to immune suppression/disorders in some people, but the research is scant. I'm going to eliminate high-lectin foods (grains, legumes, dairy and nightshades) for a week to see if this impacts the symptoms. Has anyone ever experienced anything similar, or has any substantive information about the lectin connection? Thanks so much and so nice to see this forum! megan
  15. I was just curious whether or not anyone has used this product: (below is just information on it that I copied/pasted from the Metagenics website) http://www.metagenics.com/mp/medical-foods/ultrainflamx-plus-360 UltraInflamX® PLUS 360° is a medical food formulated to provide specialized nutritional support for patients with compromised gut function reflective of an inflammatory response as seen in ulcerative colitis and Crohn’s disease. Provided in a low-allergenic-potential rice protein base, this formula is enhanced with antioxidant nutrients, selenium, zinc, calcium, folate, and vitamin B12 to address increased nutrient needs and potential deficiencies in these patients. L-glutamine is added to support intestinal mucosal cells. This formula is acceptable for an enteral diet that excludes allergens. Enteral and exclusion diets are often necessary for extended periods for patients experiencing irritable bowel conditions. Serving Size: About 2 scoops (53 g) Ingredient Amount Daily Value Calories 210 Fat 6 g Saturated Fat† 2.5 g Trans Fat 0 g Cholesterol 0 mg Sodium 40 mg Potassium 450 mg Carbohydrate 27 g Dietary fiber 4 g Sugars 8 g Protein 15 g Vitamin A (retinyl palmitate) 2500 IU 50% Vitamin A (beta-carotene) 2500 IU 50% Vitamin C 180 mg 300% Calcium 300 mg 30% Iron 1.5 mg 8% Vitamin D 45 IU 10% Vitamin E 100 IU 330% Thiamin 2 mg 130% Riboflavin 2 mg 120% Niacin 35 mg 120% Vitamin B6 5 mg 250% Folic Acid 80 mcg 20% Vitamin B12 3 mcg 50% Biotin 150 mcg 50% Pantothenic Acid 5 mg 50% Phosphorus 400 mg 40% Magnesium 330 mg 80% Zinc 13 mg 90% Selenium 75 mcg 110% Copper 1 mg 50% Manganese 3 mg 150% Chromium 60 mcg 50% Quercetin 200 mg * L-Glutamine 750 mg * L-Threonine 290 mg * L-Lysine 770 mg * L-Alanine 240 mg * DL-Methionine 175 mg * L-Cysteine 85 mg * Turmeric (Curcuma longa) Rhizome Extract [standardized to 95% (200 mg) curcuminoids] 210 mg * Rosemary (Rosmarinus officinalis) Leaf Extract 100 mg * D-Limonene 100 mg * Ginger (Zingiber officinale) Root Extract [standardized to 5% (5 mg) total pungent compounds] 100 mg * Sulfate (as magnesium sulfate) 50 mg * Ingredients: Rice protein concentrate, rice bran, rice syrup solids, fructose, orange powder, natural flavors, magnesium citrate, medium chain triglycerides, olive oil, L-lysine HCl, calcium citrate, L-glutamine, dipotassium phosphate, magnesium salts of reduced iso-alpha-acids (from hops extract, Humulus lupulus L.), hydrogenated soybean oil encapsulate, L-threonine, silica, malic acid, L-alanine, ascorbic acid, quercetin, turmeric rhizome extract, DL-methionine, d-alpha tocopheryl acetate, guar gum, dicalcium phosphate, L-cysteine HCl, D-limonene, ginger root extract, rosemary leaf extract, magnesium sulfate, zinc gluconate, xanthan gum, niacinamide, rebaudioside A (Stevia rebaudiana leaf extract), biotin, beta-carotene, retinyl palmitate, copper gluconate, pyridoxine HCl, D-calcium pantothenate, niacin, thiamin HCl, riboflavin, chromium polynicotinate (ChromeMate® GTF), cholecalciferol, cyanocobalamin, selenomethionine, and folic acid. Directions: Blend (for no longer than 15 seconds), shake, or briskly stir about 2 level scoops (53 grams) of UltraInflamX PLUS 360° into 8 fluid ounces of chilled water, juice, or acceptable fruit as listed in the dietary guidelines. Follow recommended dosage guidelines (Program Guide) or as directed by your healthcare practitioner. Consume within 10 minutes of reconstitution. NOTICE: THIS PRODUCT IS TO BE USED UNDER THE DIRECT SUPERVISION OF A PHYSICIAN OR OTHER LICENSED HEALTHCARE PRACTITIONER. DO NOT ENGAGE IN ANY DIET SUPPLYING LESS THAN 800 CALORIES PER DAY WITHOUT MEDICAL SUPERVISION. Warning: Excess vitamin A intake may be toxic and may increase the risk of birth defects. Pregnant women and women who may become pregnant should not exceed 10,000 IU of preformed vitamin A (retinyl palmitate) per day. Caution: Do not use if pregnant or nursing or if taking anticoagulants. If taking medication, consult your healthcare practitioner before use. This product is Gluten Free. Formulated to Exclude: Wheat, gluten, soy, dairy products, egg, nuts, tree nuts, fish, crustacean shellfish, colors, artificial sweeteners, and artificial flavors. Contents sold by weight, not volume. Some settling may occur during shipping and handling. Serving size is measured by weight with a scoop included for your convenience. The amount of product contained in 2 scoops may be above or below 53 grams due to variations in handling and product density. ChromeMate® is a registered trademark of InterHealth, Inc. This product contains plant pigments that will stain clothing and surfaces. This product contains no high fructose corn syrup. TAMPER EVIDENT Do not use if safety seal is missing or broken. †Saturated fat content is contributed by a beneficial form of fat, medium chain triglycerides, which have recognized health benefits. Q. How does UltraInflamX® Plus 360º Medical Food compare to other products or approaches? A. The rice protein base has a lower allergenic potential than many common protein sources, which (along with careful formulation and manufacturing) helps make this product suitable for use with an eating plan to reduce potential GI stressors and inflammatory triggers. This product contains only natural ingredients for a safer long-term approach, and has been clinically reviewed at the FMRC. Q. How does UltraInflamX® Plus 360º Medical Food work? A. This product provides targeted, research-based nutrients to modulate inflammatory and pain processes associated with IBD—with an excellent predicted safety profile. It contains a combination of plant-based ingredients that are designed to work with your body (not against it) to inhibit triggers for inflammation and pain without interfering with health functioning. An unhealthy diet (highly processed foods, low nutrients) and common food sensitivities may also influence gastrointestinal health, inflammation, and related symptoms. This product is recommended for use with a modified elimination diet—a healthful balance that limits consumption of foods with increased allergen potential and reduces dietary chemical exposure. Q. How long is UltraInflamX® Plus 360º Medical Food typically recommended? A. A typical introductory program is 25 days (with a modified elimination diet) to evaluate progress. Some people may report positive changes in just a few weeks, but individual results may vary. This product may also be recommended for long-term support. For best results, follow your health care professional's guidelines. Q. Who would benefit from UltraInflamX® Plus 360º Medical Food? A. People whose quality of life is affected by IBD ( ulcerative colitis, Crohn's disease) and associated chronic inflammation and pain. This formula may offer an advantage for extraintestinal pain and inflammation. Q. Why is UltraInflamX® Plus 360º Medical Food safe? A. Medical foods must contain ingredients that are generally regarded as safe (GRAS) or FDA approved, and Metagenics continually evaluates formula ingredients in concert with current nutritional research for optimal safety and effectiveness. Plus, Metagenics' manufacturing facility has 3 certifications for good manufacturing practices to ensure the highest quality. Key active ingredients in this formula were developed through the ExpresSyn Process® that sets a new standard in clinical certainty for natural products via demonstrated efficacy, bioavailability, and a high level of predicted safety. (This product is not recommended for those taking anti-coagulant medications. UltraInflamX® Medical Food may be an excellent alternative. This product is suitable for those who may be sensitive to lactose or soy. See online catalog for complete allergen information.)
  16. Celiac.com 10/07/2013 - People with non-celiac gluten-sensitivity often report gut and non-gut symptoms shortly after eating gluten; symptoms disappear on gluten-free diets, although these patients have no serologic markers of celiac disease, and no intestinal damage. However, there is no evidence to suggest any changes to blood or mucosa in those individuals. To better understand non-celiac gluten sensitivity, a research team recently assessed immunologic responses of duodenal mucosa samples and peripheral blood basophils, isolated from NCGS patients, after exposure to gliadin. The research team included Cristina Bucci, Fabiana Zingone, Ilaria Russo, Ivonne Morra, Raffaella Tortora, Norberto Pogna, Giulia Scalia, Paola Iovino, and Carolina Ciacci. They are affiliated with CEINGE in Naples, Italy; the Consiglio per la Ricerca e la Sperimentazione in Agricoltura in Rome, Italy; the Gastrointestinal Unit of the Department of Medicine and Surgery at the University of Salerno in Salerno, Italy; and with the Gastrointestinal Unit at the Department of Clinical and Experimental Medicine of Federico II University of Naples. Between January 2010 and July 2011, the research team gathered mucosa samples from 34 celiac disease patients who followed gluten-free diets for at least 6 months, 35 patients with untreated celiac disease, 16 patients with non-celiac gluten sensitivity (NCGS) and 34 healthy control subjects. The team diagnosed non-celiac gluten sensitivity based on patient symptoms and current diagnositic guidelines. For each of the 119 patients, the team conducted a complete clinical evaluation to exclude celiac disease while on a gluten-containing diet, a skin prick test to exclude wheat allergy, and upper endoscopy at 2 tertiary medical centers in Italy. After incubating each biopsy sample with gliadin, the team measured inflammatory markers, including anti-phosphotyrosine-monoclonal antibody (PY99), HLA-DR, intercellular cell adhesion molecule-1 (ICAM-1), CD3, CD25 and CD69. After incubation with gliadin, mucosa samples from the 69 patients with celiac disease showed increased immunofluorescence intensity for early and delayed markers of inflammation. They also found low levels of some of these markers in three patients with non-celiac gluten sensitivity and three controls. The team found normal mucosal architecture in 56.3% of patients with non-celiac gluten sensitivity. The remaining seven patients showed increased intraepithelial infiltration, but without eosinophils. They found no villous atrophy in patients with non-celiac gluten sensitivity, and no significant increases in the levels of CD63 and CD203c. The team did find that one patient each in the NCGS and control groups, whose results indicated only weak PY99 and ICAM-1 positivity, also had Helicobacter pylori infection. Unlike mucosa from patients with celiac disease, once incubated with gliadin, mucosa from patients with NCGS does not express markers of inflammation, nor does the gliadin activate their basophils. The in vitro gliadin challenge therefore should not be used to diagnose NCGS. This study does suggest that wheat components, other than proteins, might be associated with GI symptoms in patients with IBS, and should be assessed for a possible role in the pathogenesis of NCGS. Source: Clinical Gastroenterology and Hepatology. Volume 11, Issue 10 , Pages 1294-1299.e1, October 2013
  17. Hi, I'm new here. I don't have Celiac disease but I'm pretty sure I am gluten intolerant. My stomach pains go away when I eliminate gluten. I've done some on and off gluten-free diet over the past few months. I've recently been on a strict gluten-free diet for a couple weeks now. I've been tested for arthritis which came back negative. However, I do have inflammation in the body and is slowly getting worse (I'm only 32 so my tests results shouldn't be that of a 50 year old). I have recently been experiencing acne (sometimes cystic) on the face, scalp, chest and back for many months. It seems to get worse when I eat gluten foods or it could be coincidental. Does anyone know if this is related to being gluten intolerant or something else? Or perhaps I need to give my body more time to heal?
  18. Celiac.com 04/13/2011 - When people with celiac disease consume gluten, their intraepithelial lymphocytes (IELs) wreak havoc in their guts by promoting inflammation and attacking the epithelial cells lining the intestines. This autoimmune activity is mediated by arachidonic acid (AA), a cytokine produced by the IELs. But there is data that the enterocytes "the very intestinal epithelial cells attacked by the IELs" can also produce and secrete AA in response to inflammation. Do they do so in celiac disease? A recent study reported in Clinical Nutrition set out to determine just that. Using Caco-2 cells, a human intestinal epithelial cell line commonly used as an in vitro model of celiac disease, Vincentini et al. are the first to find that when these enterocytes were exposed to gliadin peptides, they did in fact generate and release arachidonic acid. Docosahexaenoic acid (DHA) is a long chain polyunsaturated fatty acid that counteracts many of the inflammatory effects precipitated by AA. When Caco-2 cells were treated with gliadin peptides and DHA, they produced much less AA (although they still made more than untreated cells). Treatment with DHA also reduced the production of other molecules involved in inflammation that were increased by exposure to gliadin, including cyclooxygenase (COX)-2, prostaglandin E2 (PGE2), and interleukin (IL)-8. PGE2 is particularly interesting, as it can increase the intestinal paracellular permeability that has been suggested to be the initial event in the pathogenesis of celiac disease. The authors suggest that by blocking the release of AA, DHA might be a tenable therapeutic option for modulating mucosal inflammation in newly diagnosed celiac patients. Source: Vincentini O, Quaranta MG, Viora M, Agostoni C, and Silano M. Docosahexaenoic acid modulates in vitro the inflammation of celiac disease in intestinal epithelial cells via the inhibition of cPLA2. Clin Nutr. 2011 Mar 19.
  19. Celiac.com 01/18/2012 - A number of small studies have shown a connection between celiac disease and various gastrointestinal (GI) cancers, but the results haven't been corroborated by larger studies, or by blood and biopsy analysis of large populations. That means that researchers just haven't been able to say with certainty what the results of those smaller studies might mean about cancer risks for the larger population. Recently, a clinical team set out to assess GI cancer risks for a larger population. The study team included Peter Elfström, Fredrik Granath, Weimin Ye, and Jonas F. Ludvigsson. They assessed risk GI cancers by using data from large groups of patients with either celiac disease, inflammation, or latent celiac disease. They assessed data from 28,882 patients with celiac disease, all with villous atrophy, and Marsh scores of 3. They also assessed data for 12,680 patients with inflammation, all with Marsh scores of 1–2. They evaluated biopsy samples at 28 different pathology centers. They assessed a third group of 3705 patients with latent celiac disease, that is, with normal mucosa, but positive blood tests. The team then compared the results against data from an age- and sex-matched population. They found that 372 of the patients with celiac disease developed incident GI cancers, while 347 patients with inflammation, and 38 with latent celiac disease developed GI cancers. That means that the first year after diagnosis and initial biopsy, celiac disease carried a 5.95-times greater risk of incident GI cancer, with a 95% confidence interval [CI], 4.64–7.64). The hazard ratio for inflammation was 9.13 (95% CI, 7.19–11.6) and for latent celiac disease was 8.10 (95% CI, 4.69–14.0). After the first year, patients showed no significant increase in GI cancer risk. The HR for celiac disease was 1.07 (95% CI, 0.93–1.23), for inflammation it was 1.16 (95% CI, 0.98–1.37). HR for latent celiac disease it was 0.96 (95% CI, 0.56–1.66). The absolute risk for any GI cancer in people with celiac disease was 101/100,000 person-years, with an excess risk of 2/100,000 person-years. The results carried some relatively good news. That is, even though celiac disease, inflammation, and latent disease all increase a person's risk for GI cancers in the first year after diagnosis, there is no increase in risk beyond the first year. Source: Clinical Gastroenterology and Hepatology. Volume 10, Issue 1 , Pages 30-36, January 2012
  20. Celiac.com 06/06/2011 - The interplay among the different immune cells mediating intestinal inflammation in celiac disease is complicated indeed. A subset of T regulatory (Treg) cells that express the Foxp3 protein are present in higher numbers in the intestines of patients with active celiac disease than in healthy controls. Treg cells act to suppress the immune system, providing tolerance to self-antigens. A recent report in the American Journal of Gastroenterology demonstrates that these cells proliferate upon the ingestion of gluten in order to suppress an overactive inflammatory response, but that their suppression is in turn suppressed by interleukin-15. First they confirmed that there is in fact increased expression of Foxp3+ cells in the intestinal mucosa of untreated celiac patients; happily, they write that "no significant differences were noted in the number of Foxp3+ cells in biopsy samples of treated celiac disease in comparison with biopsy samples of non-celiac disease controls." Next, they used an in vitro gliadin challenge system - no celiac patients were harmed during the course of this study! - to see if the increase in this cell population was dependent on gliadin, and it was. T cells are so named because they are made in the thymus; this demonstration that they can originate in the small intestine lamina propria is interesting. Treg cells are generally immunosuppressive, and the Treg cells isolated from celiac guts demonstrated this immunosuppressive ability in vitro. So the researchers wondered: why is there still so much inflammation in untreated celiac disease patients? They found that the cytokine IL-15 could suppress the proliferation of Treg cells, and completely shut down their ability to produce interferon gamma (IFN- γ ). This is at least partially because Treg cells from celiac patients turn out to have a significantly higher surface density of receptors for IL-15 than Treg cells from healthy controls, rendering them more sensitive to IL-15's effects. Zanzi et al bolstered their findings by achieving the same results using two independent experimental methods. It is not yet clear how IL-15 impairs the suppressive activity of Treg cells. But these scientists are actively working on it. Source: Am J Gastroenterol advance online publication, 5 April 2011; doi: 10.1038/ajg.2011.80
  21. Celiac.com 06/12/2009 - In a medical first, researchers at UCLA have made a connection between intestinal inflammation and systemic chromosome damage in mice, a discovery that may pave the way for early identification and treatment of human inflammatory disorders, some of which raise the risk for various kinds of cancer, according a study published in Cancer Research. Scientists discovered that local intestinal inflammation caused DNA damage to lymphocytes of the peripheral blood circulating throughout the body. So, contrary to conventional medical wisdom, chromosome damage is not limited to the immediate intestine, but involves body tissues far away from the actual inflammation. Their results showed single- and double-strand DNA breaks in the blood, and chromosome damage in peripheral blood indicating systemic genetic damage. Inflammatory diseases have been linked to some lymphomas and abdominal, liver and colorectal cancers, said Robert Schiestl, lead author, and professor of pathology, radiation oncology and environmental health sciences and a Jonsson Cancer Center scientist. Finding inflammation early – before any symptoms surface - and treating the associated causes quickly may prevent the damage that eventually triggers these cancers, he said. Before the study, researchers had no knowledge that "intestinal inflammation causes damage that can be found throughout the body,” said Schiestl, adding that this "may help explain how inflammation leads to these cancers.” Intestinal inflammation can be caused by such maladies as Crohn’s disease, inflammatory bowel disease, ulcerative colitis and Celiac disease. Nearly 1.5 million Americans, and 2.2 million Europeans currently suffer from inflammatory bowel diseases and global incidence is on the rise, Schiestl said. The discovery opens up the possibility of using chromosome damage in the peripheral circulating blood as a biomarker to spot intestinal inflammation before any symptoms surface. Researchers were able to detect chromosome damage in the blood of specially bred mice before the onset of colitis, said Aya Westbrook, a graduate student of the UCLA Molecular Toxicology Interdepartmental Program and the paper's first author. Westbrook added that disease severity correlated directly with higher levels of chromosome damage in the blood. Chromosome damage, according to study author Dr. Jonathan Braun, professor and chairman of the Department of Pathology and Laboratory Medicine at UCLA, may be the “earliest detectable indicator” of intestinal inflammatory disease. Currently, the only way to diagnose patients with inflammatory bowel disease is through full endoscopic exam, which is both invasive and costly. In theory, Braun said, a biomarker blood test might replace the invasive endoscopic exam and allow physicians to identify early inflammatory disease before it develops fully. Spotting disease and being able to ward it off early is one of the Holy Grails of all medicine. This breakthrough could “change the natural history of these diseases,” Braun said. For the first time, doctors might have a tool that can actually help spot inflammation, the earliest precursor to multiple kinds of cancer, at its earliest stages, long before any actual disease develops. This could lead to the prevention of tens of thousands of cancers. UCLA researchers have launched a clinical trial to confirm their findings in humans, Schiestl said. They’re focusing on patients with Crohn’s disease and ulcerative colitis. They're hoping the discovery will permit them to test new strategies for treating smoldering disease, which we’ve never been able to identify before,” Schiestl said, adding that they might be able to assess new drugs for treating early inflammatory disease. The research may also show why some patients with inflammatory disease develop cancers, while others endure chronic inflammation for decades, yet remain cancer-free. Researchers suspect that some unknown molecular mechanisms might work to protect some patients and not others. Finding such mechanisms might lead to tests for predicting which patients with intestinal inflammatory diseases are predisposed to cancer. Cancer Research: June 1 2009, Volume 69, Issue 11
  22. Celiac.com 03/06/2009 - A report in the February 3rd issue of Digestive and Liver Disease highlights the present understanding of transglutaminase function in gastrointestinal and liver diseases and therapeutic strategies that target transglutaminase activities. A team of American and Italian researchers recently set out to review the current body of literature regarding transglutaminase function in gastrointestinal and liver diseases and therapeutic strategies that target transglutaminase activities. The research team was made up of doctors L. Elli, C.M. Bergamini, C.M. Bardella, and D. Schuppan. They are associated with one or more of the following: Center for Prevention and Diagnosis of Celiac Disease, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, in Milan, Italy; the Department of Biochemistry, University of Ferrara, Via Luigi Borsari, Ferrara, Italy; the Department of Medical Sciences, University of Milan, Italy; and the Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, USA. Their report in the February issue of Digestive and Liver Disease highlights the present understanding of transglutaminase function in gastrointestinal and liver diseases and therapeutic strategies that target transglutaminase activities. Transglutaminases are a group of eight presently recognized calcium-dependent enzymes that act as catalysts to cross-link or deamidate proteins. They play a role in key biological functions such as the healing of wounds, the repair of damaged tissue, fibro-genesis, apoptosis, inflammation and management of the cell cycle. Thus, they play a role in numerous key patho-mechanisms of autoimmune, inflammatory and degenerative diseases, a number of which involve the gastrointestinal system. Transglutaminase 2 is of central importance, as it is crucial to the pathogenesis of celiac disease, and influences inflammation and fibro-genesis in inflammatory bowel and chronic liver disease. The recent review has implications for celiac disease, collagen, Crohn's disease, extra-cellular matrix, gliadin, inflammatory bowel disease; NFkB, and ulcerative colitis. Dig Liver Dis. 2009 Feb 3.
  23. Celiac.com 02/17/2009 - Texas AgriLife Research scientist Dr. Nancy Turner has recently discovered that a microscopic compound commonly found in plant-based foods reduces inflammation and prevents the formation of cancerous lesions in the colon. The tiny molecule, called quercetin, is easily absorbed when people eat fruits and vegetables, and so requires no specialized supplements or drugs. Quercetin is a tiny, but powerful compound that is easily absorbed from onions, peppers, tomatoes and most other common produce. According to Turner, nearly all plant-based foods offer "some level of quercetin," including "fun things like wine." Previous laboratory research has shown quercetin to be effective in reducing rates of colon cancer, but Turner's study is the first to illuminate the mechanism by which quercetin works its magic. These results offer researchers another line of inquiry into other inflammatory bowel diseases such as Crohn's and celiac disease, as it's quite likely that quercetin can offer some measure of protection against those conditions as well. According to Turner, the levels of quercetin used in the study are comparable to those "achieved in diets around the world such as...the Mediterranean-style diets." As such, reaching such levels in American diets is "not an unachievable goal," she said. In the study, Turner's research team observed the responses of rats to quercetin-supplemented diets. Some of the rats were in the early stages of colon cancer formation, while others were cancer-free. In people, as in animal models, early colonic lesions represent some of the very first pre-cancerous changes that can be seen visually. These so called "aberrant crypts," are thought to mark or predict tumor formation. Earlier studies have shown quercetin to reduce the number of these crypts, but Turner "wanted to know how it might be protecting." Cancer is commonly understood as uncontrolled cell growth, but researchers are now realizing that the normal action of cell death, a process called "apoptosis," plays a crucial role in allowing cancer to develop. Healthy bodies generally maintain equilibrium between the generation of new cells and sloughing off cells that have completed their job. Quercetin seems to play a beneficial role in both cases. It decreases the number of cells being generated in the colon [and] increases the number of cells that were undergoing apoptosis. In all, quercetin helps to maintain a normal number of cells. The research team then turned its attention to the relatively new discovery that inflammation is one of the prime instigators of colon cancer. The team focused on two enzymes, called Cox-1 and Cox-2. Cox-1 is a standard protein that the body usually exhibits. But Cox-2 has a potential role in a number of diseases. Turner explains that Cox-2 is an "inducible protein that is expressed in the body when there is some kind of external stimulus to a cell." Scientists consider high levels of Cox-2 "as being a bad thing." Research shows that not only are elevated levels of Cox-2 present in colon cancer, but that the Cox-1 levels become elevated before Cox-2 levels rise. According to Turner, it seems that Cox-1 exerts some sort of influence over whether Cox-2 expression. Both the control groups and the carcinogen-injected groups that consumed dietary quercetin had lower levels of both Cox-1 and Cox-2, suggests that there may be chance for quercetin to prevent tumor growth. Clearly, further study is needed to better understand the links. But Turner encourages people to consume lots of fruits and vegetables. She points out that, in addition promising benefits for colon cancer, quercetin has demonstrated positive influence in fighting other chronic ailments such as cardiovascular disease. *Turner's research was funded by the U.S. Department of Agriculture . Source: http://agnews.tamu.edu/showstory.php?id=972
  24. Celiac.com 09/16/2008 - Cytokines are regulatory proteins that act as mediators in the generation of an immune response. Interleukin 21 (IL-21) is on such cytokine. A team of Italian and British researchers recently evaluated the production of IL-21 in the intestinal mucosa of patients with untreated celiac disease. Several studies have documented the ability of IL-21's to regulate cytokine production by certain T cells. Another recent study demonstrated a connection between celiac disease and what is called the susceptibility locus in the chromosome 4q27, which harbors the IL-21 gene. The researchers, led by Dr. G. Monteleone at Universita Tor Vergata in Rome, set out to examine the molecular mechanisms tying IFN-gamma with celiac disease. The team found that people with celiac disease produce excess IL-21, and that IL-21 is responsible for encouraging production of interferon-gamma (IFN-gamma). In active celiac disease, large numbers of polarized T helper Type 1 (Th1) cells accumulate in the upper intestinal tract, where they produce large amounts of IFN-gamma. The team looked at upper bowel biopsies taken from 91 people from 22 to 54 years of age. 43 had untreated celiac disease, 12 patients had treated celiac disease, and 36 served as healthy controls. The mucosa of those with untreated celiac disease showed highly elevated IL-21 levels compared with the healthy control group (P < 0.001), while those with treated celiac disease showed the same levels of IL-21. When the research team blocked endogenous IL-21 in ex vivo organ cultures from untreated celiac disease patients, they saw a reduced expression of both IFN-gamma and T-bet, a master regulator of Th1 cell response. When the research team stimulated biopsy cultures with a peptic-tryptic digest of gliadin (PT) explants, the biopsies of patients with treated celiac disease showed elevated IL-21, while the controls showed no such elevation. The team was able to use an anti-IL-21 antibody to substantially reduce the enhancement of T-bet expression by PT (P = 0.01), whereas they saw no such reduction using a control antibody. These results indicate that up-regulation of IL-21 in celiac disease depends on gluten-driven active inflammation. As such, IL-21 may have a crucial role in promoting the destructive inflammation in celiac disease. If so, neutralizing the production or presence of IL-21 might offer a promising and alternative therapeutic approach in treating celiac disease, especially in treating cases of celiac disease that are unresponsive to a gluten-free diet. In a side note, several doctors have noted that the role of IL-21 does not seem to be exclusive to celiac disease, as the biopsies of patients with Helicobacter pylori infections, and those suffering from Crohn's disease show similar increases in IL-21 synthesis. Gut 2008: 57; 879-881,887-892.
  25. Nature Immunology 2, 353 - 360 (April 2001) Celiac.com 04/12/2001 - According to an article published in the April issue of Nature Immunology, Dr. Marc Rothenberg and colleagues at the Childrens Hospital Medical Center in Cincinnati, Ohio performed a series of experiments on mice which led them to the conclusion that white blood cells called eosinophils could be the cause of many food allergies and gastrointestinal inflammation. The researchers believe that the eosinophil cells, which are present throughout the body, mistakenly identify food proteins as germs in individuals with food allergies. When the intestinal lining of an allergic person is exposed to an allergen, a substance called eotaxin is released by the cells lining the intestine, which causes the eosinophil cells and other immune cells to attack them and release powerful proteins that destroy the surrounding tissues and cause eosinophilic inflammation. The results of this study are unique because this is the first time eosinophils cells have been implicated in causing allergies, even though scientists have known for some time that they were present in great numbers at the sites of inflammation caused by reactions to food. The implication of this study is the possible development of drugs that stop this reaction from occurring, and thus prevent digestive inflammation and destruction that occurs when people with food allergies eat foods to which they are allergic. These results put scientists one step further in understanding how and why the digestive system is attacked in certain individuals, and a possible means of one day controlling the process.