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Celiac.com 10/23/2021 - A compelling new idea has dawned on the medical/scientific horizon. Dr. Rodney Ford, a pediatric gastroenterologist in New Zealand who calls himself "doctorgluten" on the Internet, has come up with a startling hypothesis that synthesizes and makes sense out of a wide range of otherwise confounding findings in the celiac and gluten sensitivity literature. For instance, why have Dr. Marios Hadjivassiliou and his group found that some people with neurological disease with anti-gliadin antibodies but without celiac disease, recover on a gluten-free diet? And why do other neurology patients sometimes recover from their neurological problems after treatment of their coexisting celiac disease? (Sadly, as Dr. Ford points out, by the time neurological disease develops the prognosis is often very poor.) Further, why do so many celiac patients present with such a wide range of symptoms, most of which are not obviously or usually associated with gut disease? And why are so many individuals who suffer from psychiatric, autoimmune, and even some infectious diseases, helped by a gluten-free diet? The answer to all these questions, according to Dr. Ford's hypothesis, is that the gluten-driven disease is primarily an affliction of the brain. Gluten proteins and/or derivative peptides reach the brain and cause neurological damage along with hormonal and neurotransmitter abnormalities. The nerves in the gut, about as voluminous as the brain, are also damaged by these proteins and peptides. The net result is a cacophony of signs, symptoms, and manifestations across a broad range of organs and body systems. From epilepsy to abdominal distress to schizophrenia, gluten induced damage to the brain and connected nerve fibers can and does disrupt virtually any and every part of the body. Dr. Ford marshals a large body of evidence in his new book, Full of it!, to support this radical departure from conventional wisdom in the celiac/gluten-sensitivity research field. Step by step he explains very simply how the enormous complex of nerves in the brain, spine, and abdomen interact to control all our body systems. He avoids technical terminology as much as possible by using terms such as "tummy brain" which are both clear and instructive even to those who are unfamiliar with medical terminology. The implications of this hypothesis are startling and extensive. If, as Dr. Ford suggests, gluten actually damages the brain in most of us who are gluten sensitive, then celiac disease is just one result of that damage. Instead of occupying the center of the research stage it should be viewed as just one of many gluten mediated illnesses, and that is exactly what Dr. Ford articulates. His hypothesis highlights the need to test for anti-gliadin antibodies frequently and recommend a gluten-free diet whenever these positive test results are found, whether or not celiac disease is present. Dr. Ford credits a number of research heroes of gluten-related medical research, including Dr. Curtis Dohan, Dr. Marios Hadjivassiliou, Dr. Michael N. Marsh, Dr. Alessio Fasano, Dr. W.T. Cooke, Dr. A De Sanctis, Dr. Kenneth Fine, Dr. G.K.T. Holmes, Dr. A-M Knivsberg, Dr. Kalle Reichelt, and a host of others too numerous to list. Without doubt, Dr. Ford has ‘seen further because he was standing on the shoulders of these giants,' (to paraphrase Sir Isacc Newton's famous statement). Nonetheless, Dr. Ford's novel view of this mass of research findings has led to his well supported hypothesis - one that threatens to overturn the current conception of gluten mediated disease. The symmetry and beauty of Ford's insight comes, in part, from its simplicity. It explains why there are so many and such varied manifestations of gluten sensitivity while making a minimal number of assumptions. And that, according to the long-standing principle of science called Occam's Razor, is the best possible explanation for a particular phenomenon.

Celiac.com 01/09/2021 - Ever stand on a school playground when a very loud siren would go off and feel like it was rattling your brain because it was so loud? If not from the local school ground, perhaps that siren was at the fire station, or other public building in your neighborhood? For the last 40 to 50 years, many of us remember hearing an ‘air raid siren' go off. In our area, it was on the first Tuesday of the month at 1:00PM. Air raid drills were a ‘warning system' to let us know that we had to take cover. From the days of the attack on Pearl Harbor through the dawning of the Nuclear Age, the air raid siren was designed to give us all a chance to ‘take cover' to get ourselves and our families to safety. Well as it turns out, our bodies have a similar early warning system. The National Institutes of Health tells us that Auto-Immune Diseases (the immune system attacking our own body tissue) collectively affect more than 24 million people per year in the U.S.(1) To put this in perspective, Cancer affects nearly 9 million people per year and Cardiovascular Disease affects close to 22 million people. And we know that only about 1/3rd of the people with an Auto-immune Disease are diagnosed.(2) That means about 72 million people are suffering with a self-destruction process (the immune system attacking its own body tissue). That puts Auto-Immune Diseases at the top of the list of the most common diseases in America today. But it's not screened for. To most of us, autoimmune diseases are unknown. Our medical system waits until the signs and symptoms are severe enough with organ failure and irreversible damage before we identify it. It's not screened for, it's looked at as a ‘last-resort' type of diagnosis. In general, autoimmune disorders can be classified as either organ specific or non-organ specific. In organ-specific autoimmune diseases, antibodies are specifically directed against targets localized in a particular organ and are often detected in the blood. Examples of organ-specific autoimmunity include Hashimoto's Thyroiditis (thyroid tissue), Type I Diabetes (pancreas tissue), Multiple Sclerosis (brain and nerve tissue), and Myasthenia Gravis (muscle tissue). In contrast, the non-organ-specific autoimmune disorders are characterized by the presence of antibodies directed against multiple targets (not specific to a particular organ). This results in the involvement of several organs or endocrine glands and is often characterized by the presence of specific circulating antibodies. Non-organ-specific autoimmunity includes diseases such as Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis (RA), and Scleroderma.(9) A growing number of studies have identified that the body makes these antibodies directed against itself—otherwise known as auto-antibodies—years, and sometimes for a decade before a diagnosis is made. The antibodies damage tissue slowly and steadily until finally people begin showing symptoms, and eventually receive a diagnosis. In Systemic Lupus, for example, research shows that the progression of auto-antibodies for Systemic Lupus Erythematosous (S.L.E.) begin to present five years before a diagnosis is typically made. The immune system began an ‘early-warning system' (by producing auto-antibodies), and was starting to say "there's a problem here". At this initial point, the patients did not have symptoms severe enough that warranted seeing their doctor. Unfortunately, in the vast majority of cases, no one is monitoring this early warning system. And so the body has to speak a little louder (more and different antibodies begin being produced)—no one is listening. And then a little louder—no one is listening. This continues for years until the body has to begin screaming. And how does the body scream? Pain. Have you ever stood under the telephone pole on the school playground when that Tuesday 1:00 PM siren went off? It rattles your brain. That's what is happening in the body when there eventually is enough damage that a diagnosis of an autoimmune disease becomes obvious-it can't be ignored. Researchers are telling us that autoimmunity appears to be a warning system that has gone beyond ‘early warning' to ‘take cover'. It takes years from the first identification of antibody presence to the point of ‘clinical onset'—when the symptoms are obvious that something is wrong, and a diagnosis is made. The levels of up to seven different antibodies may continue to rise for five years or more before the diagnosis. If patients were armed with such information, they could start fighting the ailment years before the threshold of damage has been passed and a diagnosis is evident, thereby preventing or delaying symptoms. One just has to look for the evidence. Arguably, the most common auto-immune disease is also the only one where the ‘cure' is known and uncontested. For some, gluten causes an ‘alarm reaction' in the immune system with a ‘call out the troops' type of attack response. (upregulating macrophage pro-inflammatory gene expression and cytokine production).(5,6) When this allergy to gluten (found in wheat, rye, barley and spelt) stimulates the production of auto-antibodies to the intestinal tissue (anti-transglutaminase or anti-endomysium antibodies), Celiac Disease is the diagnosis. And this auto-immune disease is readily put into remission and disappears with a life-long avoidance of gluten in any form.(4) Are there early warning signs of Celiac Disease? Yes, there are. We know that Celiac Disease-associated antibodies can be identified up to 5.2 years before a diagnosis of Celiac Disease can be made. (17) Numerous pain syndromes and auto-immune diseases have been associated with an ‘alarm response' to gluten. From peripheral neuropathies (numbness and tingling in the arms and legs) to crippling migraines and ataxia, from acute myocarditis (inflamed heart) to chronic pancreatitis, from vitiligo (loss of pigment-white spots-in the skin) to Primary Biliary Cirrhosis (Gall Bladder problems), from Multiple Sclerosis to Rheumatoid Arthritis, from Attention Deficit Hyperactivity Disorder (ADHD) to Epilepsy, in sensitive individuals, gluten may initiate this auto-immune response.(5,14) So which organ is vulnerable to this auto-immune attack, this calling out of the troops? The target tissue seems to be determined by one's genetics (the blueprint you were born with) and all of the mitigating factors (accumulated exposures we've had in our lives such as toxic chemical accumulation, repeated use of antibiotics or other drugs contributing to intestinal permeability, heavy metal toxicity, excess stress hormone production, poor food choices…).(7) This response may affect tissue throughout the body and has been identified with brain and peripheral tissue(8), liver epithelial cells, pancreatic beta-cells(8), thyroid tissue (9), bone cells(10), skin tissue(11), skeletal muscle(12), myocardium(13), and the brain and nervous system. And it does not require the production of auto-antibodies to the intestines-that is, gluten intolerance can occur and be associated with other autoimmune diseases without the diagnosis of Celiac Disease (14). As an example, 57% of patients with neurological dysfunction of unknown cause have elevated antibodies to gliadin (a protein in wheat). Only 35% of this group also have evidence of intestinal damage (Celiac Disease). The remaining 65% have gluten sensitivity and elevated antibodies to the brain (cerebellum) or the nerves in the arms and legs, a situation analogous to that of the skin in Dermatitis Herpetiformis.(14) It appears that wheat can directly stimulate an auto-immune attack on the brain and nervous system in sensitive individuals without the diagnosis of Celiac Disease. Elevated antibodies to gliadin and gluten (the protein in wheat) are the immune systems way of saying "this food is not good for me". Many researchers take the position that if there are elevated antibodies to wheat, but there is no evidence of Celiac Disease, there is no evidence of value to avoiding wheat. This position is historic and is in the process of changing. The idea that until the sirens are screaming, it's ok to eat wheat, even if the immune system is saying "this is not good for me", is a position that more and more doctors are realizing is causing unnecessary suffering. Many doctors and health care practitioners believe that even in the absence of indicators of outright Celiac Disease-that is with normal transglutaminase or endomysial antibodies, or a normal biopsy, we are best served by heeding the message our body is giving us, and avoiding these foods. The concern is that if we ignore the actions of our immune system (elevated antibodies to wheat), the auto-immune process of the body (attacking its own tissue), may years down the road leave us standing under that telephone pole with the siren going off rattling our brains, or thyroid, or pancreas, or heart… Dr. Thomas O'Bryan is a graduate of the University of Michigan and the National College of Chiropractic. He is a Diplomate of the National Board of Chiropractic Examiners, a Diplomate of the Clinical Nutrition Board of the American Chiropractic Association, and a Certified Clinical Nutritionist with the International and American Association of Clinical Nutritionists. He is a Certified Applied Kinesiologist. He is a Certified Practitioner in Functional Biomechanics from the Motion Palpation Institute. He is a member of the Institute of Functional Medicine, the International and American Association of Clinical Nutritionists, the American Chiropractic Association, the International Academy of Preventive Medicine and numerous other professional organizations. References: 1. National Institutes of Health. Autoimmune Diseases Coordinating Committee. Autoimmune Diseases Research Plan. Accessed 1/18/07. 2. Bland, J, Understanding The Origins and Applying Advanced Nutritional Strategies For Autoimmune Diseases. March 2006. 3. Notkins, A, Predictors of Disease, Scientific American, March 2007, 72-78. 4. Murray, J, The Widening Spectrum of Celiac Disease. Am J Clin Nutr 1999;69:354–65. 5. Betterle C., Update on autoimmune polyendocrine syndromes (APS), ACTA BIOMEDICA 2003; 74;9-33. 6. Zanoni,G, In Celiac Disease, a Subset of Antibodies against Transglutaminase Binds Toll-Like Receptor 4 and induces Activation of Monocytes, PLoS Med. 2006 Sep;3(9):e358. 7. Kumar,V,Celiac Disease-Associated Autoimmune Endocrinopathies, Clinical and Diagnostic Labortory Immunology,July 2001, p. 678–685. 8. Alaedini,A, Immune Cross-Reactivity in Celiac Disease: Anti-Gliadin Antibodies bind to Neuronal Synapsin 1,J Immunology,2007,178:6590-6595. 9. Freeman HJ. Hepatobiliary and pancreatic disorders in celiac disease. World J Gastroenterol 2006; 12(10): 1503-1508. 10. Moreno, M,The IL-1 gene family and bone involvement in celiac disease, Immunogenetics (2005) 57: 618–620 . 11. Abenavoli L, Cutaneous manifestations in celiac disease. World J Gastroenterol 2006;12(6): 843-852. 12. Kozanoglu, E, Proximal myopathy as an unusual presenting feature of celiac disease, Clin Rheumatol (2005) 24: 76–78. 13. Frustaci,A, Celiac Disease Associated with Autoimmune myocarditis, Circulation, 2002;105:2611-2618. 14. Hadjivassiliou, M, Gluten Sensitivity as a Neurological Illness. J Neurol Neurosurg Psychiatry, 2002;72:560-563. 15. Sategna-Guidetti C., Prevalence of Thyroid Disorders in Untreated Adult Celiac Disease Patients and Effect of Gluten Withdrawal: An Italian Multicenter Study, AJG—Vol. 96, No. 3, 2001. 16. Oderta G., Thyroid Autoimmunity in Childhood Coeliac Disease, . J Paediatr Gastroenterol Nutr, 2002 Nov;35(5):704-5. 17. Salmi,T., Immunoglobulin A autoantibodies against transglutaminase 2 in the small intestinal mucosa predict forthcoming coeliac disease Aliment Pharmacol Ther 24, 541–552

Celiac.com 02/05/2023 - If you have celiac disease symptoms, for example chronic diarrhea, anemia, bloating, abdominal pain, rashes, are in a higher risk group, etc., your doctor may order a blood test for celiac disease. Note that before doing any blood tests for celiac disease you must be eating gluten for a while beforehand, and the amount and length of time can vary, but is somewhere between 2 slices of wheat bread daily for 6-8 weeks and 1/2 slice of wheat bread or 1 wheat cracker for 12 weeks, otherwise you may end up with false negative results. For a celiac disease antibody test, a clinician collects a small amount of the patient's blood. The sample is then sent to a lab, where the blood cells are then removed, and the test is conducted. Celiac Disease Blood Tests Note that the accuracy and specificity of each test can vary depending on the laboratory performing the test, the specific method used, and the population being tested. Sensitivity refers to the ability of a test to correctly identify individuals with the condition (true positive rate), while specificity refers to the ability of a test to correctly identify individuals without the condition (true negative rate). tTG-IgA (tissue transglutaminase IgA) Blood Test for Celiac Disease This test measures the levels of IgA antibodies to tissue transglutaminase, an enzyme that is involved in the immune response to gluten in those who have celiac disease. The test is estimated to have a sensitivity of approximately 90%, which means that it correctly identifies 90% of people with celiac disease. It also has a high specificity of around 95%, which means that it correctly identifies 95% of people who do not have celiac disease. Other Names for the tTG-IgA Test: Tissue Transglutaminase IgA Test Anti-Tissue Transglutaminase IgA Test tTG-IgA Blood Test tTG-IgA Serology Test IgA-tTG Antibody Test Tissue Transglutaminase Antibody IgA Assay tTG-IgG (tissue transglutaminase IgG) Blood Test for Celiac Disease This test measures the levels of antibodies to tissue transglutaminase, but it specifically measures IgG antibodies rather than IgA antibodies which are produced in people who eat gluten and have celiac disease. It is not as sensitive or specific as the tTG-IgA test, but it may be useful in cases where a person has an IgA deficiency, which can occur in approximately 2-3% of people with celiac disease. In these cases, the tTG-IgG test may be positive while the tTG-IgA test is negative. However, the tTG-IgG test is not recommended as a first-line screening test for celiac disease. The sensitivity of the tTG-IgG blood test is generally high, ranging from 85% to 98%. This means that the test can accurately detect celiac disease in a significant percentage of people who have the condition. The specificity of the tTG-IgG blood test is also high, typically around 90% to 98%. This indicates that the test can effectively rule out celiac disease in individuals who do not have the condition. Other Names for the tTG-IgG Test: Tissue Transglutaminase IgG Test Anti-Tissue Transglutaminase IgG Test tTG-IgG Blood Test tTG-IgG Serology Test IgG-tTG Antibody Test Tissue Transglutaminase Antibody IgG Assay EMA-IgA (endomysial antibodies IgA) Blood Test for Celiac Disease This is a highly accurate test for celiac disease, that requires specialized expertise to perform and interpret, and it is more expensive than other blood tests. It is generally used as a last test to confirm celiac disease after a positive tTG-IgA test. The sensitivity of a test refers to its ability to correctly identify individuals with the condition. For the EMA-IgA blood test, the sensitivity is generally very high, ranging from 90% to 98%. This means that the test can accurately detect celiac disease in a significant percentage of people who have the condition. The specificity of a test refers to its ability to correctly identify individuals without the condition. For the EMA-IgA blood test, the specificity is also high, typically around 95% to 100%. This indicates that the test can effectively rule out celiac disease in individuals who do not have the condition. Other Names for the EMA-IgA Test: Endomysial Antibodies IgA Test Anti-Endomysium Antibodies IgA Test Endomysial Antibody IgA Assay EMA IgA Blood Test EMA-IgA Serology Test Endomysium IgA Ab DGP-IgA and DGP-IgG (Deamidated Gliadin Peptide) Blood Tests for Celiac Disease These tests measure the levels of antibodies in the blood, but specifically targets deamidated gliadin peptides, which are a type of gluten protein that can trigger an immune response in people with celiac disease. The tests are not always included in adults, but should be in cases with IgA deficiency. The tests should always be included when screening children, especially if they are under 2 years old. The DGP tests were created to detect celiac disease in those with IgA deficiency, and there are here is more information about them: DGP-IgA Test: This test measures the levels of IgA antibodies specific to deamidated gliadin peptide. IgA antibodies are produced by the immune system in response to gluten exposure. In individuals with celiac disease who produce normal levels of IgA, a positive DGP-IgA test result suggests the presence of ongoing immune response to gluten. DGP-IgG Test: The DGP-IgG test measures IgG antibodies against deamidated gliadin peptide. IgG antibodies are another type of immune response and may be elevated in individuals with celiac disease who have IgA deficiency (a common occurrence in celiac disease). The DGP-IgA test is considered to have high sensitivity and specificity. In general, the DGP-IgA test has been reported to have a sensitivity ranging from 75% to 95% and a specificity ranging from 90% to 100%. Overall, the DGP tests, including DGP-IgA and DGP-IgG, exhibit a sensitivity of approximately 85-95% and a specificity of about 95-98%. Other Names for the DGP-IgA Test: Gliadin Peptide Antibody IgG (Immunoglobulin A) Anti-Gliadin Antibody IgA (AGA IgA) Anti-Gliadin IgA Antibody (AGA IgA) Anti-Gliadin IgA (AGA IgA) Anti-Gliadin Immunoglobulin A Antibody (AGA IgA) Anti-Deamidated Gliadin Peptide IgA (DGP IgA) Anti-Deamidated Gliadin Antibody IgA (DGP IgA) The sensitivity of the DGP-IgG test is reported to range from 75% to 85%, which means it can correctly identify individuals with the condition in about 75% to 85% of cases. The specificity of the DGP-IgG test is reported to range from 75% to 95%, which means it can correctly identify individuals without the condition in about 75% to 95% of cases. Overall, the DGP tests, including DGP-IgA and DGP-IgG, exhibit a sensitivity of approximately 85-95% and a specificity of about 95-98%. Other Names for the DGP-IgG Test: Gliadin Peptide Antibody IgG (Immunoglobulin G) Anti-Gliadin Antibody IgG (AGA IgG) Anti-Gliadin IgG Antibody (AGA IgG) Anti-Gliadin IgG (AGA IgG) Anti-Gliadin Immunoglobulin G Antibody (AGA IgG) Anti-Deamidated Gliadin Peptide IgG (DGP IgG) Anti-Deamidated Gliadin Antibody IgG (DGP IgG) IgA Levels/Deficiency Blood Test This should always be included in any blood panel for celiac disease, but it does not test directly for celiac disease, and is done to determine the accuracy of the other blood tests. People who are IgA deficient may score lower, of have no measurable levels on certain celiac disease blood tests. This test measures the levels of Immunoglobulin A (IgA) in the bloodstream. IgA is an important antibody that plays a significant role in the immune system, particularly in protecting the body's mucosal surfaces (e.g., respiratory and digestive tracts). Low IgA levels can indicate IgA deficiency, a condition where the body does not produce enough IgA, leading to an increased risk of infections and other health issues. The IgA Levels/Deficiency Test helps healthcare providers diagnose and monitor IgA-related conditions. Other Names for the IgA Levels/Deficiency Test: Immunoglobulin A (IgA) Test Total IgA Test Serum IgA Test IgA Serum Levels Test IgA Blood Test IgA Quantitative Test IgA Antibody Test IgA Immunodeficiency Test Celiac Disease Blood Antibody Screening is ~98% Accurate in Adults Using the Mayo Clinic Protocol A celiac disease blood panel includes several tests to determine whether someone has celiac disease. These tests are very specific because certain antibodies only appear in those with gluten sensitivity, celiac disease and/or dermatitis herpetiformis. Testing begins with a test called Immunoglobulin A (IgA). If the results are normal, then a Tissue transglutaminase, antibody, IgA test is given. A weak positive should lead to the following tests: Endomysial antibodies (IgA) and; Gliadin (deamidated) antibody, IgA. If the initial Immunoglobulin A (IgA) test is lower than normal, then these two tests should be done: Tissue transglutaminase antibodies, IgA and IgG profle. Gliadin (deamidated) antibodies evaluation, IgG and IgA. If the initial Immunoglobulin A (IgA) test is below the level of detection (<1.0 mg/dL), then these two tests should be done: Tissue transglutaminase (tTG) antibody, IgG. Gliadin (deamidated) antibody, IgG. It sounds complicated, but it's pretty standard procedure now, and when blood screening is done this way the results for celiac disease are ~98% accurate. Many People Can Be Diagnosed Using Only Blood Tests and No Biopsy According to the latest research, if the blood test results are at certain high levels that range between 5-10 times the reference range for a positive celiac disease diagnosis, it may not be necessary to confirm the results using an endoscopy/biopsy: Blood Test Alone Can Diagnose Celiac Disease in Most Children and Adults TGA-IgA at or Above Five Times Normal Limit in Kids Indicates Celiac Disease in Nearly All Cases No More Biopsies to Diagnose Celiac Disease in Children! Biopsy Still Standard in Adult Celiac Diagnosis After positive blood tests some doctors still require a biopsy to confirm the diagnosis. However, this is changing, as new techniques allow doctors to accurately detect celiac disease in adults without a biopsy. Remember, nearly all tests and screening for celiac disease require the patient to be eating a gluten-containing diet before testing, usually you should be eating at least 1/2 slice of wheat bread or 1 wheat cracker daily for at least 2 weeks before the endoscopy. Be sure to check with your doctor for the latest protocol. Blood Tests for Follow Up Care Blood tests may also be useful in follow up care in those with celiac disease to confirm that their diet is indeed free of gluten. Also, because of the lack of standardization, keep in mind that blood test results may not be directly comparable from one lab to the next. More Celiac Disease Testing Resources What is a Gluten Challenge and How Long Must it Last? Interpretation of Celiac Disease Blood Test Results Ten Facts About Celiac Disease Genetic Testing Blood Test Questions on the Celiac Disease and Gluten-Free Forum Test results and question about gluten challenge How Long To Eat Gluten For Accurate Blood Test Read more at mayocliniclabs.com

Celiac.com 02/06/2023 - Typically, doctors diagnose celiac disease using serological markers, like anti-tissue transglutaminase antibodies (t-TGA), along with a biopsy of the small bowel (SBB) to spot mucosal damage in the gut. To get a better understanding of the connection between serological markers and changes to gut mucosa in children with celiac disease, a team of researchers recently examined the connection between serological markers, and changes of the intestinal mucosa in children with celiac disease. To do so, they used data from a national Spanish registry, called REPAC-2, that included children under 15 years old. The wanted to determine the potential connection between t-TGA levels and other factors, such as mucosal damage and clinical findings, based on gender, age, symptoms. The study included nearly 5,000 patients with celiac disease, nearly 3,000 of whom underwent both t-TGA and a SBB for diagnosis. The results showed that more than two-thirds of the patients with normal IgA values had a Marsh 3b-c lesion, which is a severe form of mucosal damage, and nearly as many had t-TGA IgA levels at or above 10 times the upper limit of normal (ULN). The study found a statistically significant association between t-TGA IgA levels and the degree of mucosal damage. The higher the t-TGA IgA levels, the more severe the mucosal damage. Among other things, the study found that patients who reported symptoms had more severe mucosal damage compared to those who did not. They also found a negative association between age and changes of the intestinal mucosa, which suggests that younger patients are more likely to suffer severe mucosal damage. But, the team found no connection between gender and changes to gut mucosa. The study included a subgroup of 18 IgA-deficient patients. The results showed that nearly half of these patients had t-TGA IgA levels at or above 10 times ULN, while nearly seventy percent had Marsh 3b-c lesions. The team found no significant connection between t-TGA IgG levels and changes to gut mucosa, including for factors like age, gender, or symptom type. The results of this study suggest a positive association between t-TGA IgA levels and the degree of gut mucosal changes in children with celiac disease. However, they found no association in IgA-deficient patients with positive t-TGA IgG results. These findings echo the recommendations of the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN), which advises SBB in IgA-deficient patients, even with high t-TGA IgG readings. The study reinforces the practice of factoring in both t-TGA IgA and IgG levels, as well as conducting a small bowel biopsy, when diagnosing celiac disease in children, especially in those with IgA deficiency, regardless of t-TGA IgG levels. Studies like this are helpful for getting clinicians and primary care physicians on the same page about best practices for celiac diagnosis in children. However, there is still much to be discovered about the relationship between serological markers and changes to gut mucosa in celiac patients. Stay tuned for more on this and related topics. Read more in the Journal of Pediatric Gastroenterology & Nutrition

Celiac.com 04/08/2017 - "Do not fear to be eccentric in opinion, for every opinion now accepted was once eccentric" – Bertrand Russell. I would like to introduce the term "zero" when we talk about eliminating gluten. Precise language leads to precise action. Zero means none, not some. Yes, my recommendation is to change the gluten-language that we have been using. The meaning of the phrase 'gluten-free' has been diluted, so it almost has the connotation of 'not-much-gluten'. It suggests that 'a-little-gluten-does-not-matter' or 'you-are-free-to-give-up-gluten-if-you-want-to'. A much stronger expression is needed. I am changing the term 'gluten-free diet' to 'gluten-zero-diet'. This should change how people think about gluten. I am a paediatrician, so I see lots of sick children, and many of them are gluten-affected. Happily, they get better much more quickly, after going off gluten, than gluten-affected adults. I am a strong believer in putting these children on a gluten-free diet well before they end up with substantial gluten-related harm, and to spare them from years or even decades of gluten- induced symptoms. This means making an early diagnosis. It also means putting them on a gluten-zero-diet before they get the severe gut damage of celiac disease. The big question for the children, their parents, and me is "how gluten-free does he need to be?" and "for how long does he have to be gluten-free?" If you read my early books, I talk about eating gluten to tolerance. But I have completely changed my mind about that. My stance now is firmly zero-gluten. This might seem a radical position to take in the face of the FDA and other groups talking about 20 ppm as the okay level of gluten contamination. So, how can I justify my gluten-zero-diet opinion? I'll explain a little background information first. Do I have to go gluten-free? I am often asked if a gluten-free diet is the only way to manage celiac disease. Many of my families are initially resistant to the idea. This is no surprise because gluten-foods are all they know about. Actually, all they know about gluten is that they are just living like everyone else, mostly on wheat-derived foods. They have a food habit. They do not think much about what they are eating. They just eat what is cheap and convenient - that means wheat. But the simplistic answer to this question is "Yes! a zero-gluten diet is the answer." However, this is a complex question. So to broaden the question I have included all gluten-related disorders. I repeat, "Yes! A gluten-free diet is the central management strategy for celiac disease and gluten-related disorders." But what does a 'gluten-free diet' mean? How free-of-gluten do you have to be? To me, a gluten-free diet means zero-gluten for life – with no exemptions. Certainly there are many who suggest that people can eat gluten to tolerance. (I used to say this as well.) But now I strongly disagree. Any gluten has the potential to cause you harm. Get your gluten antibodies down Going on a gluten-free diet is more than just the eradication of gluten from your diet. Surprisingly, it is also about reducing the gluten antibodies that your immune system is churning out. Gluten can harm you in more ways than by a direct, or an immune effect, in your gut. Did you know that gluten can also cause you harm through the gluten antibodies that your body produces? (See the chapter on neurological harm.) There is growing evidence that the gluten antibodies (AGA – anti-gluten-antibody) are damaging to us, particularly to our neurological system. The research work done by Hadjivassiliou (2012) needs to be heeded. Think about why you get vaccinated. Vaccination is to keep you protected from bacteria and virus throughout your life. For this purpose, once you have stimulated antibody production by your immune system, whenever your body comes in contact with the identical stimulant again, your immune system begins to produce much more of this same antibody again. Most people get vaccinated against illnesses. For instance, most people have had their tetanus shot. This comprises a tiny amount of tetanus protein (the allergen), which stimulates your body to produce antibodies against the tetanus bacteria. This then protects you from tetanus infection for years to come. The vaccine is intended to stimulate your body to produce the anti-tetanus-antibodies, lifelong. To ensure this happens you will need to get a couple of booster shots during your lifetime. This also happens in gluten sensitization. So when you think about gluten, and the antibodies against gluten that your body is continually making, you can now understand that every time you eat gluten, by error or design, this will stimulate more gluten antibody production. And that is a very bad thing for you. It is crucial to reduce gluten antibody levels. Even a tiny amount of gluten is enough to stimulate ongoing antibody production, which is potentially harmful for your nerves and brain. The goal should be to get and keep your gluten antibodies down. Antibody reduction rather than just the elimination of gluten Hadjivassiliou, in his 1998, paper says, "These results strengthen our contention that eliminating these antibodies through strict adherence to a gluten-free diet may have important therapeutic implications for patients with gluten ataxia." Here the focus is on antibody reduction rather than just the elimination of gluten. Surely there is a strong case for investigating for gluten-sensitivity in all people with the likelihood of gluten-related disorders. Is 20 ppm really okay? Does a gluten-zero-diet literally mean no-gluten-at-all? Definitely, "Yes!" But the question everyone is asking is, "what does a gluten-zero-diet mean in terms of every-day practicality?" There is ongoing debate about how many parts per million (ppm) of gluten is acceptable in food. Pragmatically, because it is so difficult to get rid of cross-contamination in food production and processing, the number of 20 ppm is now surfacing as a 'reasonable' level of gluten to be consumed (some countries have 200 ppm, and the FDA is recommending 20 ppm). When you first hear about this number, it seems to be a negligible amount. However, there are still concerns for some people who seem to be exquisitely sensitive to gluten. For me, a gluten-zero-diet means 'no-gluten-at-all'. This can be achieved if you eat fresh fruits and vegetables, unprocessed meat and fish, uncontaminated rice, corn and other alternate grains, eggs, nuts and unprocessed dairy foods. This means no packet or processed foods – I have called this the no-packet-food-diet. Gluten-free is more than removing gluten It is a lot more than 'just' going gluten-free. Yes, there are many more things to do when healing someone with celiac disease/ gluten-related disorders. The longer you have had gluten-symptoms, the worse your body will be. More healing will be required. You may need additional minerals, vitamins and probiotics. There are many routine health checks to take. You should also ensure that your gut has healed (via blood test and, maybe, a repeat endoscopy). Advocating ZERO gluten Yes! I am a zero-gluten man. I advocate a gluten-zero-diet. This is based on the concern that tiny amounts of gluten in your food are enough to stimulate your immune system. Even if you are not feeling unwell from this apparently trivial exposure, your body could be getting sick. What seems trivial to you may not be trivial to your highly tuned and sensitized immune system. By definition, 'zero gluten' means ZERO! In other words – it is undetectable gluten (say less than 1 ppm – gluten detection is now getting down to these very low levels). Consequently, any food in which gluten can be detected (between 5–20 ppm should not be labeled gluten-free. This is because it is NOT gluten-free. It does contain (an apparently) trivial amount of gluten. These foods that contain 5–20 ppm need to be labelled 'contains gluten at levels 5–20 ppm'. We need to know exactly what is in our food. We need this information to make informed, healthy food choices. The main opposition to zero-gluten labeling comes from the food manufacturing and processing industries – not from the gluten-free community. Food companies say it is not practical or economic to make zero-gluten products. They claim that a 20 ppm is a realistic compromise. They say that 20 ppm is close enough. But this is not what the gluten-free community want: we demand "no-gluten-at-all". That is zero-gluten. The gluten-contaminated food chain needs to be entirely cleaned up. The zero-gluten market is growing. The gluten-free community does not want any gluten traces in their food. Gluten labeling: a two-tier approach In New Zealand, "Coeliac New Zealand" runs a gluten-logo program to give "consumers a quick reference point when shopping and faced with uncertainty about the genuine gluten-free status of a product." They have, very sensibly, adopted a two-tier system of certification. Products carrying the 'Crossed-Grain-symbol' in addition to the words 'GLUTEN-FREE' adhere to the FSANZ standard of "No detectable gluten". Products carrying the Crossed-Grain-symbol without any other words (that is, not displaying the wording 'GLUTEN-FREE') adhere to the international Codex standard for 'gluten-free tested' and they have gluten levels of less than 20 ppm ( which is considered suitable as per the Codex standard for gluten content). This two-tier system: undetectable-gluten; and less-that-20-ppm-gluten, is simple. We know just what we are getting. How hard is this? Everyone is satisfied. So why does the FDA just want a single definition? If we, the gluten-free consumers, refuse to buy gluten-contaminated products, then food makers will have to change – or some may decide not to chase the gluten-free market. Refractory celiacs still gluten contaminated Another argument for zero-gluten is that not all celiac sufferers heal on an apparently gluten-free diet. Celiac disease does not heal when you are constantly exposed to gluten. Dewar and co-workers investigated 100 patients who had non-responsive celiac disease. They found the following: 45 (45%) of these patients were not adequately adhering to a strict gluten-free diet, of whom 24 (53%) were inadvertently ingesting gluten, and the remaining 21 (47%) admitted non-compliance. http://www.ncbi.nlm.nih.gov/pubmed/22493548. Cross-contamination I suggest that you look at the "Gluten-Free Certification Organization (GFCO)" website for detailed information on testing for gluten and gluten cross-contamination. gfco.org The GFCO is a program of The "Gluten Intolerance Group" (GIG). GFCO inspects products specifically for gluten. They say "Unless food is grown in your own garden in an airtight bubble, it is impossible to guarantee a 100% pure product." Measuring gluten contamination is difficult as there are so many factors to consider. For example: the raw materials and the possibility they were cross-contaminated; the process used in production (such as the movement of raw materials and equipment) that could increase cross contamination; cleaning and packaging processes. Also their testing procedures need to be robust but affordable. They have to take into account: what is being tested (raw materials, equipment or finished products); the type of laboratory technology that is appropriate; the appropriate frequency for testing samples. Companies rely on "their Good Manufacturing Practices (GMP), Hazard Analysis Critical Control Point (HACCP) programs, and standard operating processes and procedures to determine a corrective action plan." Living with cross contamination Terri says about cross contamination at school, "We have to be so careful. So we go with home lunches, because food preparation can be an issue. Just one spoon in the wrong dish, and then back again, contaminates everything … and have you ever seen the cloud of flour that emits when you turn on a food mixer? We deal with celiac disease for my girls and for me. It is just not worth the risk of cross contamination. We prepare homemade gluten-free pasta salads, make homemade gluten-free "Lunchables" with far healthier ingredients, homemade minestrone, gluten-free sandwiches, chili, and a thousand other foods. We make gluten-free granola and trail mix for snacks. It gets easier. The best thing you can do is to find some awesome recipes and make sure whoever has celiac disease learns how to cook! My daughters are 7 and 9, and both know how to read labels and search for hidden gluten. They can prepare several easy foods and snacks, and do not feel like they are missing out. It really does get better!" How much easier it would be if there was no gluten in the food chain! Yes, cross contamination is the big on-going issue that few gluten-outsiders understand. At a recent hotel breakfast, I asked if they offered gluten-free options. She said, "yes, we have gluten-free bread". This was sitting among the ordinary gluten-breads, and shared the same toaster – covered in crumbs. The staff had no understanding of the concept of cross contamination. Should the whole family go gluten-free? Yes, there is a huge benefit for the entire household when all adopt a gluten-free lifestyle. But there is always resistance due to the cost and the "inconvenience" – and dads who do not want not give up their beer. However, if there is gluten in the house, there will be cross-contamination. Also, it is poor role modelling when the parents eat gluten (a forbidden food for the child) but their child is denied foods that (from their child's perspective) might seem like a punishment or an arbitrary rule. (Children often do not understand the reason they were put onto a gluten-free diet.) Having said that, at least having their child on a gluten-free diet is a great start, and many children seem to manage with low levels of cross-contamination. By the way, the parents can eat gluten outside the house if they are prepared to play gluten-roulette. However, for their own health they should adopt the gluten-zero policy. If gluten is in the house, there is cross-contamination. A Day in the Life: Living in a Mixed House If you want to know how to avoid cross contamination on a day-to day basis, I recommend that you read this article by Al Klapperich (GIG, East Central WI). http://www.gigofecw.org/news/files/living_in_a_mixed_house.php Al says "This document draws upon my knowledge and experience I have acquired since going gluten-free in 2003. I have given you, the reader, a glimpse into how I personally carry out a gluten-free diet in a mixed house. I am not suggesting this is the only way or the best way; it's simply my way. My only intent is to help others that may be struggling with the gluten-free lifestyle. Not only do we have to be concerned about gluten ingredients that make up our food – we also have to be concerned about any gluten that may come into contact with our gluten-free food." Do you put gluten on your skin? Cosmetics, should they be gluten-free? Nancy asks: "Doctors in the USA state there is no need to avoid gluten-containing cosmetics & topical medications for those with celiac. What is your viewpoint on this?" This is a great question. I tell my patients to avoid any gluten on their skin. However, the answer depends upon where your focus is. If your focus is only on gut damage (that is, celiac disease), then the tiny amounts of gluten in these skin products is trivial and not enough to cause intestinal damage. But, if your focus is on the person and symptoms, then gluten on the skin often causes itch and irritability. For example, people complain of itchy hair if using a gluten-containing shampoo. Children using play-dough can develop a contact rash and become irritable. Swallowing gluten in lipstick causes some people a sore tummy. I recommend gluten-free cosmetics and topical medications. Gluten-free food not always healthy There is a not-so-subtle message promoted by many food-manufacturers, that gluten-free foods are, as of by right, healthy foods. This is definitely not true. Have you seen all those advertisements for gluten-free cookies and sweet treats? They are empty calories, full of fat and sugar, and lacking micronutrients. I was recently sent a message that was advertising the gluten-free benefits of a "Natural alternative healthy energy drink". This was misleading and dishonest. This drink was just a sugar (sucrose) water, with a few added vitamins. It is a terrible product. It cannot even be called a food. It would be much healthier to eat fruit and vegetables than drink this. It would be much better value to buy and eat healthy whole foods and drink water. Carrying the label "gluten-free" does not automatically mean that the product is either healthy or good for you. Often it is not. For example, Coca-Cola is both gluten-free and fat-free, however, few health professionals would recommend it. Lots of specialized gluten-free products are full of sugar and fat. They might taste great, and they are okay for a treat, but should not be eaten as a regular every-day food. When first confronted with the need to go on a gluten-free diet, most people feel overwhelmed. They also want to reject the whole notion of being gluten-free. They might be angry. They feel as though they are giving up a cherished food, and they certainly are. They have been used to eating gluten-foods for their whole lives. Suddenly, they have to start paying attention to what they are eating. This is very difficult. No wonder there is resistance to a gluten-free diet from so many people. Is gluten-free food safe to eat for everyone? Anna asks me by email: "Hi Dr Ford, I would like to know if people who are not gluten-free should eat gluten-free food? Can you provide any information of this topic please for me as to the pro's and con's of this? Many thanks." This is an interesting question, as it insinuates that gluten-free foods could be unhealthy for some people. Except for the gluten-grains of wheat rye and barley, all foods are naturally gluten-free. Gluten free foods are naturally healthy. It is only over the last 100 years that wheat has been added to more and more of our foods. There is nothing harmful about eating gluten-free foods. Can you live without gluten? Arthur wrote: "Your article about gluten causing nerve problems has touched a nerve, as you could see from the general round of applause and approval it received. Bravo! I have consulted dozens of doctors over 30 years (in USA and France) but not one had ever suggested gluten could be the culprit for my problems. Now, I wonder if more education is needed in the medical community on this problem. I've been gluten-free for nearly three months now, and all my symptoms have disappeared and I feel great." My question is 'Can humans get along without gluten?' and what role does gluten play in nutrition. Thanks. Best wishes, Art." Who needs gluten? Here is the dilemma. The world still needs gluten grains to feed the population. But this is creating ill health in at least 10% of the population. If so many people are getting ill from the foods that they are eating, then surely it would be better to shift to other food types to improve the health of the population. It turns out that gluten is not a necessary protein. The gluten grains are convenient and demanded - but they are not biologically essential. In fact, for perhaps a third of the population, gluten is biologically undesirable. (This is a controversial statement and needs a lot more research to back it up.) Are there risks when going gluten-free? It is my experience that for most families who go gluten-free, the quality of their diet actually improves. As they no longer rely on the easy-filling cheap breads, they are forced to branch out into vegetables, fruits, meats and other non-gluten grains. This greatly enhances their food variety, which, in turn, improves their health. Gluten is unnecessary for a well-rounded diet. Is the gluten habit easy to kick? Unfortunately, gluten has an addictive quality because one of its breakdown products has a morphine-like activity. As you know, foods crammed with gluten such as cakes, dumplings, steamed puddings and big hunks of bread are often referred to as "comfort foods". For some, this comfort is derived from this morphine-like sedation of gluten on the brain. Consequently, when gluten is suddenly removed from the diet, some people experience a withdrawal effect. This is one of the reasons a gluten-free diet is viewed as a horror story by so many people. Indeed, withdrawal effects from gluten during the first week of a gluten-free diet are not uncommon. Although this usually passes after a week or so, it can be difficult for children during the first few days. It is sensible to gradually go gluten-free over a week or so to avoid this reaction. To sum up, yes! You can you live a healthy life without gluten! Absolutely! Overall, your diet without gluten is a much more healthy, wholesome and packed with goodness. This will be good news to people who have embarked on their gluten-free journey. High-fat high-sugar. When deprived of gluten, people often feel that they deserve something to replace it. This yearning for some sort of compensation for being on a strict gluten-free diet leads to people over-indulging in these high-fat, high-sugar gluten-free specialty products. Although these foods are gluten-free, they are not disease-free. They have a high glycemic index, and you can eat too much. They are unhealthy. Weight gain, obesity and insulin resistance may catch up to you. Many people are also addicted to gluten. Therefore, as they go through the withdrawal phase, the pleasure of eating sweet-food can provide some compensation to them for being denied gluten. Going gluten-free is not an easy thing for most people. Gluten-free reluctance You would think that being diagnosed with celiac disease would be a big motivation factor to go onto a gluten-zero-diet. But a study in England (2011) found that over 40% of patients with celiac disease were dissatisfied with a gluten-free diet (jgld.ro). They said that they were keen to go back onto gluten if they could get some sort of vaccine or pill to change the way their gut processes gluten. They were willing to make unknown changes to their immune system just so that they could go on eating a toxic food. To me this shows: the massive ignorance of these people about the seriously harmful nature of gluten. the low level of family and community support for these people. Going gluten-free should be easy, healthy and enjoyable. Gluten-free does need assistance initially. the lack of knowledge about the neurological and autoimmune harm caused by gluten. This is a chapter from Dr Rodney Ford's new book "Gluten: ZERO Global."

Celiac.com 04/07/2014 - Histologically non-responsive celiac disease (NRCD) is a potentially serious condition found in celiac disease patients who suffer persistent villous atrophy despite following a gluten-free diet (GFD). Currently, the only way to monitor patient progress rely on invasive and costly serial duodenal biopsies. Looking for better options, a team of researchers recently set out to identify antibody biomarkers for celiac disease patients that do not respond to traditional therapy. The research team included B. N. Spatola, K. Kaukinen, P. Collin, M. Mäki, M. F. Kagnoff, and P. S. Daugherty. They are affiliated with the Department of Chemical Engineering, University of California, Santa Barbara in California, the Department of Gastroenterology and Alimentary Tract Surgery and the Center for Child Health Research at the University of Tampere and Tampere University Hospital in Tampere, Finland, with the Department of Medicine at Seinäjoki Central Hospital in Seinäjoki, Finland, and with the Laboratory of Mucosal Immunology in the Departments of Medicine and Pediatrics at the University of California San Diego in La Jolla, California. Using flow cytometry to screen bacterial display peptide libraries, the team was able to identify the epitopes specifically recognized by antibodies from patients with NRCD, but not by antibodies from responsive celiac disease patients. By comparing ELISA results for sera from 15 NRCD patients and 45 patients with responsive celiac disease, all on a strict GFD for at least 1 year, the team confirmed that deamidated gliadin was the antigen mimicked by library peptides. They identified the dominant consensus epitope sequence by unbiased library screening QPxx(A/P)FP(E/D). The epitope sequence was highly similar to reported deamidated gliadin peptide (dGP) B-cell epitopes. They also found that anti-dGP IgG measurement by ELISA discriminated between NRCD and responsive celiac disease patients with 87% sensitivity and 89% specificity. Most importantly, they found that dGP antibody levels correlated with the severity of mucosal damage, meaning that IgG dGP levels may be useful in monitoring small intestinal mucosal recovery on a GFD in NCRD patients. The team found that celiac patients with NRCD can be spotted by their increased levels of anti-dGP IgG antibodies even when the patients are following strict gluten-free diets Lastly, they feel that anti-dGP IgG assays may be useful for monitoring mucosal damage and histological improvement in celiac disease patients on a strict GFD. Source: Aliment Pharmacol Ther. 2014;39(4):407-417.

Celiac.com 09/03/2021 - Specially designed antibodies could help prevent development of celiac disease, according to new research. Monoclonal antibodies are basically lab-crafted immune cells that increase the body's defenses against infections and toxins, according to the Food and Drug Administration. A research team used a new method to specially modify monoclonal antibodies that prevent the human immune system from recognizing gluten as a toxin. This means that the body's T cells, will not respond to gluten, enabling the body to digest and process it without triggering classic celiac symptoms. T cells, like antibodies, help the immune system to fight off potentially harmful diseases or other foreign intruders. The researchers used the same method to prevent celiac disease in mice, though they still need to conduct human trials using the method. These drugs, which are tailored specifically to the target virus or toxin, are commonly used in the treatment of autoimmune diseases such as rheumatoid arthritis, psoriasis and multiple sclerosis, and most recently have been explored as a potential treatment option for COVID-19. According to co-author, Geir Åge Løset, the team's research shows "that a highly successful and well-recognized drug class, namely monoclonal antibodies also may find its place in the growing therapeutic toolbox under investigation in celiac disease." The team's findings open a path to drug development "that ultimately may blunt the unwanted immune reaction seen in celiac patients, thereby allowing these patients to adopt a more normal way of living," said Løset, founder and CEO of Nextera, the Oslo-based firm that makes the monoclonal antibody for celiac. For their study, Løset and his colleagues screened a human antibody library for antibodies that block immune cells that target gluten. Using information gathered in the process, they developed monoclonal antibodies that mimic this process. When inflamed gut tissue samples from patients with celiac disease were exposed to the modified antibodies, they blocked the immune response to gluten and did the same in lab mice, without interfering with other cell functions, according to the researchers. "We think our study points to an untapped potential which allows a clear path for drug makers to act upon building on well-recognized principles," added Løset. Read more in UPI Health News

Celiac.com 07/06/2021 - People who have celiac disease have to eat a gluten-free diet, otherwise, they risk physical discomfort, intestinal damage, and potentially increased risks for numerous related conditions, and even deadly types of cancer. Most tests that screen for celiac disease work by detecting the antibodies that indicate the presence of celiac disease. One of the big drawbacks about celiac disease blood screening is that people usually have to eat gluten for 6-12 weeks in order for the tests to be accurate, and sometimes wait a couple of weeks more before the final results are known. This is often followed by a biopsy where you need to continue eating gluten for even longer periods. That can mean weeks or months of feeling very bad, followed by weeks of uncertainty for many people who are trying to figure out if they have celiac disease. But what if we could screen for celiac disease in a quick, reliable and accurate way? That's been an elusive goal for researchers for many years. That may be set to change, with the recent discovery by Anna Nguyen, a biochemistry student from at Metropolitan State University of Denver. Ngyuen has discovered a faster, easier way to detect celiac disease. The discovery arose as part of Nguyen's 2016 undergraduate research project. “I was really passionate about learning nutrition and diet, but eventually I got to the point where I was more interested in the science behind nutrition,” Nguyen said. “And it led me down this biochemistry route and wanting to get my Ph.D., which requires you to do undergrad research.” The method developed by Nguyen, and her fellow undergraduate researchers, would be faster and easier, and require a simple finger prick. “What we wanted to do was just do make a quick blood test that, maybe just after a day of eating gluten, you could be able to go to your doctor, get a pinprick blood test, and it would just tell you immediately.” The only problem is that Ngyuen's test uses an electrochemical biosensor. Even though electrochemical biosensor technology is currently not laboratory approved, the team is hopeful that it can be developed into a fast, convenient, and reliable test that will be used widely by both clinicians and patients. Keep an eye out over the next few years for more on this and other improvements in celiac blood testing. Read more at: 9news.com

Celiac.com 02/08/2021 - Anti-tissue transglutaminase antibodies (tTG) are a strong indicator of celiac disease, but positive anti-tTG antibodies have also been reported in some non-celiac patients. A team of researchers recently set out to examine positive anti-tTG antibodies that are not related to gluten intake. The research team included Mónica Garcia-Peris, Ester Donat Aliaga, María Roca Llorens, Etna Masip Simó, Begoña Polo Miquel, and Carmen Ribes Koninck. They are variously affiliated with the Pediatric Service, Lluís Alcanyís Hospital, Xàtiva (Valencia), Spain; the Pediatric Gastroenterology Unit, Hospital Universitari i Politécnic La Fe, Valencia, Spain; and the Celiac Disease and Digestive Immunopathology Unit, Instituto de Investigación Sanitaria La Fe in Valencia, Spain. The research team performed a review and follow up of suspected celiac patients, who showed increased anti-tTG levels and gastrointestinal symptoms, but atypical blood screens, positive anti-tTG with gluten-free diet, along with decreased anti-tTG levels, independent of gluten intake. They reviewed cases for a total of 9 patients, all of whom were positive for HLA DQ2/DQ8. In 5 cases (Group A), patients showed Marsh 3 involvement in the initial biopsy, and were diagnosed with celiac disease. Cow's Milk Protein Raises anti-tTG Levels Study subjects began diets that were both gluten-free, and free of cow's milk protein. When cow's milk protein was re-introduced, anti-tTG increased, and returned to normal after it was withdrawn again. CMP-Free Diet Normalizes anti-tTG Levels Because the clinicians suspected a non IgE mediated CMP allergy in the other four patients with normal initial biopsy (Group B), that group did not eat a gluten-free diet, but did begin a cow's milk protein free diet. In this group, symptoms disappeared, and anti-tTG normalized on a non-gluten-free, cow's milk protein free diet. Consuming cow's milk protein after an exclusionary diet can elevate anti-tTG levels in some celiac patients. The elevation of anti-tTG levels by cow's milk protein can happen even without gluten ingestion. Researchers have seen this response in non-IgE mediated CMP allergy patients with positive HLA DQ2/DQ8. Discovering that consuming cow's milk protein after an exclusionary diet can elevate anti-tTG levels in some celiac patients gives clinicians one more thing to look for in their quest to diagnose and treat celiac disease. Read more at ScienceDirect.com

Celiac.com 12/14/2020 - The science behind celiac disease diagnosis has been moving rapidly away from biopsy. First, biopsy screening was eliminated for celiac diagnosis in most children. Then, the European Society for the Study of Paediatric Gastroenterology, Hepatology and Nutrition guidelines suggested that celiac disease can be diagnosed without taking duodenal biopsies. The latest diagnostic guidelines suggest that a 10-fold increase in IgA antitissue transglutaminase (tTG) antibody levels, in combination with EMA positivity, supports a diagnosis of celiac disease, without the need for a duodenal biopsy. However, this approach has not yet been widely adopted into clinical practice for diagnosing adults, mainly due to a limited international multi-center data, and testing in groups with low celiac disease rates. New research confirms that most adults do not require a biopsy for a reliable celiac disease diagnosis. A recent study by a team of researchers showed that a 10-fold increase in serum IgA antitissue transglutaminase (tTG) antibody levels has high predictive capacity and diagnostic reliability for detecting small intestinal injury diagnostic of celiac disease in adults. The research team included Hugo A Penny, Suneil A Raju, Michelle S Lau, Lauren JS Marks, Elisabeth MR Baggus, Julio C Bai, Gabrio Bassotti, Hetty J Bontkes, Antonio Carroccio, Mihai Danciu, Mohammad H Derakhshan, Arzu Ensari, Azita Ganji, Peter H R Green, Matt W Johnson, Sauid Ishaq, Benjamin Lebwohl, Adam Levene, Roxana Maxim, Hamid Mohaghegh Shalmani, Mohammad Rostami-Nejad, David Rowlands, Irene A Spiridon, Amitabh Srivastava, Umberto Volta, Vincenzo Villanacci, Graeme Wild, Simon S Cross1, Kamran Rostami, and David S Sanders. Their study looked at three different groups of people: Group 1 featured 740 patients assessed in the specialist celiac disease clinic at a UK center; Group 2 featured 532 patients with low suspicion for celiac disease referred for upper GI endoscopy at a UK centre; while Group 3 included 145 patients with raised tTG levels from multiple international sites. The team used Marsh 3 histology as a reference standard to determine the performance features of an IgA tTG titre of ≥10×ULN for a diagnosing celiac disease in adults. Across all three groups of adult patients, the data shows that nearly every person with IgA tTG levels of ≥10×ULN has small intestinal mucosal changes (Marsh 3 lesions) that are hallmarks of clinical celiac disease as diagnosed via the former "gold standard" of duodenal biopsy. The team's data reveal that IgA tTG levels of 10×ULN have 100% specificity at detecting Marsh 3 lesions in Group 2's 532 adults with low suspicion of celiac disease, for a disease rate of 3.2%. The team also found that an IgA tTG cut-off of 10×ULN was effective at spotting patients with Marsh 3 lesions using different tests at various international locations. However, the team feels that establishing test-specific thresholds and/or standardized tTG tests used with this pathway could help to refine this method for widespread clinical use. The results of this study show that IgA tTG levels of ≥10×ULN strongly reflect intestinal changes consistent with adult celiac disease diagnosis. As such, the results support the elimination of biopsy in the diagnosis of most cases of adult celiac disease, in favor of the no-biopsy approach. Read more, including detailed data, at Gut.bmj.com The researchers are variously affiliated with the Academic Unit of Gastroenterology, Royal Hallamshire Hospital, Sheffield, UK; the Medicine, Gastroenterology Hospital Dr C Bonorino Udaondo, Buenos Aires, Argentina; the Gastroenterology & Hepatology Section, Department of Medicine, University of Perugia Medical School, Perugia, Italy; the Department Clinical Chemistry, Amsterdam Gastroenterology and Metabolism and Infection and Immunity Institutes, Amsterdam UMC, Amsterdam, The Netherlands; the Department of Health Promotion Sciences, Maternal and Infant Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, Palermo, Italy; the Pathology Department, Grigore T. Popa University of Medicine and Pharmacy Iasi, Iasi, Romania; the Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK; the Department of Pathology, Ankara University Medical School, Ankara, Turkey; the Department of Gastroenterology and Hepatology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; the Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA; Gastroenterology, Luton and Dunstable Hospital NHS Foundation Trust, Luton, UK; the Department of Gastroenterology, Dudley Group NHS Foundation Trust, Birmingham City University, Birmingham, UK; the Gastroenterology Department, Grigore T. Popa University of Medicine and Pharmacy Iasi, Iasi, Romania; the Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran; the Department of Gastroenterology, Queen Elizabeth II Hospital, Hertfordshire, UK; the Pathology, Brigham and Women's Hospital, Boston, Massachusetts, USA; the Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy; the Department of Pathology, Spedali Civili, Brescia, Italy; and with the Department of Gastroenterology, MidCentral District Health Board, Palmerston North, New Zealand.

Celiac.com 08/12/2020 - The interaction between celiac disease and the liver is complex and not well understood. In some cases, isolated hypertransaminasemia is the only clear sign of celiac disease, while in other cases, liver diseases can occur with isolated tissue transglutaminase antibodies IgA (tTG IgA), but without the histologic markers that would indicate celiac disease. A team of researchers recently set out to assess the results of tTG IgA testing for chronic liver disease (CLD) or cytolysis, and to seek out biopsy-confirmed celiac disease in patients with existing liver disease. The research team included Lena Cvetkovic, Gabriel Bernard, Nathanaelle Galette, Pierre-Olivier Hétu, Catherine Vincent, Mickael Bouin, and Amelie Therrien. They are variously affiliated with the Department of Medicine - Division of Gastroenterology, Centre de recherche du Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada; the Department of Biochemistry, Centre de recherche du Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada; and the Department of Medicine, Division of Hepatology, Centre de recherche du Centre Hospitalier de l'Université de Montréal in Montréal, Québec, Canada. Their retrospective study used two groups. The first included 444 consecutive patients with no known celiac disease, for whom liver specialists had ordered tTG IgA testing. In this group, the team assessed the incidence of positive tTG and biopsy-confirmed celiac disease. The second group included 212 consecutive individuals with positive tTG IgA and subsequent duodenal biopsies. In this group, the team assessed the frequency and clinical features of patients without biopsy-confirmed celiac disease, both with and without liver disease. Tests conducted on the first patient group by a liver specialist turned up nine first time positive tTG IgA results. However, only six of these patients had biopsy-confirmed celiac disease. The second group included 33 individuals who also had liver disease, though nearly 43% showed no biopsy-confirmed celiac disease, compared with the 16% of patients who did not have liver disease. Nearly two-thirds of the patients without biopsy-confirmed celiac disease showed an increase below three times the upper limit of normal of tTG IgA. Cases of chronic liver disease without elevated transaminase levels showed no association with celiac disease. Testing liver disease patients for celiac disease can be helpful, but large numbers of patients may show positive celiac tests without any histological signs celiac disease. Read more at J Can Assoc Gastroenterol. 2020 Aug;3(4):185-193.

Celiac.com 07/23/2020 - Celiac disease is a common inflammatory autoimmune condition that is influenced by both genetic factors and environmental triggers. Researchers still don't know very much about the early genesis of celiac disease. A team of researchers recently set out to describe the interplay between type 2 transglutaminase (TG2), gliadin peptide 31-43 and anti-TG2 antibodies in celiac disease. The team included Stefania Martucciello, Silvia Sposito, Carla Esposito, Gaetana Paolella, and Ivana Caputo. They are variously affiliated with the Department of Chemistry and Biology; and the European Laboratory for the Investigation of Food-Induced Diseases (ELFID) at the University of Salerno in Fisciano (SA), Italy Gluten is a protein found in wheat, rye and barley, and is the main factor implied in the onset of celiac disease, which involves both innate and adaptive immune responses to gluten. The immune-triggering potential of some gluten sequences are increased by the deamidation of specific glutamine residues by type 2 transglutaminase (TG2), an enzyme whose expression is up-regulated in the intestine of celiacs. The α-gliadin peptide 31-43 is a short gluten chain that resists intestinal proteases, and which seems to modulate TG2 function in the gut. Interestingly, TG2 can also influence the biological activity of this α-gliadin peptide 31-43. A strong auto-immune response to TG2 is a classic sign of celiac disease. Auto-antibodies exert biological effects on multiple cells. These effects partly overlap with those caused by α-gliadin peptide 31-43. In their recent review, the team poses a scenario in which TG2, anti-TG2 antibodies and peptide 31-43 come together to synergistically trigger and promote celiac disease. If their hypothesis is correct, further study could help researchers better understand celiac development and potentially point the way to new measures of prevention and/or treatment for celiac disease. Stay tuned for more articles on the role of TG2, anti-TG2 antibodies and peptide 31-43 in the development of celiac disease. Read more at Int J Mol Sci. 2020 May; 21(10): 3673

Celiac.com 07/13/2020 - Celiac disease is a systemic disease that damages the small intestine and which, left untreated, can lead to numerous related health problems. The only treatment for celiac disease remains a gluten-free diet. Celiac disease is classified as an autoimmune disease in part because of the presence of anti-tissue transglutaminase 2 (anti-TG2) antibodies in the serum, as well as the presence of other autoimmune features. Anti-TG2 autoantibodies are produced in the intestines, and they show up there even before they begin to circulate in the blood. Researchers Mariantonia Maglio and Riccardo Troncone of the Department of Medical Translational Sciences and European Laboratory for the Investigation of Food-Induced Diseases at the University Federico II in Naples, Italy, recently set out to see what they might be able to learn about celiac disease autoimmunity by looking at intestinal anti-tissue transglutaminase2 autoantibodies. Exactly how these antibodies are generated is still poorly understood, but gliadin-specific T cells seem to play a significant role. The team noted some somatic mutations in VH and VL genes in TG2-specific plasma cells, along with a major reliance on a heavy chain encoded by the VH5 gene. However, previous studies on the effect of anti-TG2 antibodies on TG2 function have produced variable data. Anti-TG2 antibodies in the blood is a major indicator of celiac disease, but their role in the development of the celiac lesion remains unclear. Researchers have taken various approaches to detect and measure the production of intestinal celiac-associated autoantibodies. Anti-TG2 antibodies may predict full-blown enteropathy in potential celiac patients. They also show potential for revealing gluten-reactivity in patients without circulating celiac-associated autoantibodies. Celiac disease-specific autoantibody production in the intestine, in patients who test negative for the same antibodies, may be among the first signs of early gluten reactivity. Or, if not specific for celiac disease, it might be a result of intestinal inflammation. The importance of mucosal anti-TG2 antibodies in the development of celiac disease remains unclear. The presence of mucosal anti-TG2 antibodies, the way they are produced, and their dependence on gluten make them promising targets for studying autoimmunity. Read more at: Front Nutr. 2020; 7: 73

Celiac.com 05/09/2013 - Previous studies have shown an immunologic response primarily directed against transglutaminase (TG)6 in patients with gluten ataxia (GA). A team of researchers set out to see if Transglutaminase 6 antibodies could be helpful in the diagnosis of gluten ataxia. The team included M. Hadjivassiliou, P. Aeschlimann, D.S. Sanders, M. Mäki, K. Kaukinen, R.A. Grünewald, O. Bandmann, N. Woodroofe, G. Haddock, and D.P. Aeschlimann. They are variously affiliated with the Departments of Neurology (M.H., R.A.G., O.B.) and Gastroenterology (D.S.S.) at Royal Hallamshire Hospital in Sheffield, UK, the Matrix Biology & Tissue Repair Research Unit (P.A., D.P.A.) of the School of Dentistry at Cardiff University in Cardiff, UK, the Department of Paediatrics (M.M., K.K.) of the School of Medicine at University of Tampere in Finland, and the Department of Biological Sciences (N.W., G.H.) at Sheffield Hallam University in Sheffield, UK. For their prospective cohort study, the team looked at patients from the ataxia, gluten/neurology, celiac disease (celiac disease), and movement disorder clinics based at Royal Hallamshire Hospital (Sheffield, UK) and from the celiac disease clinic at Tampere University Hospital in Tampere, Finland. Patients were broken into groups that included idiopathic sporadic ataxia, gluten ataxia, celiac disease, and neurology, along with healthy control subjects. The team screened all subjects for TG6 antibodies, and conducted duodenal biopsies on all patients with positive blood screens. In addition, they analyzed biopsies from 15 consecutive patients with idiopathic sporadic ataxia and negative serology for gluten-related disorders for immunoglobulin A deposits against TG. They found TG6 antibodies in 21 of 65 (32%) patients with idiopathic sporadic ataxia, in 35 of 48 (73%) patients with GA, in 16 of 50 (32%) patients with celiac disease, in 4 of 82 (5%) neurological control subjects, and in just 2 of 57 (4%) healthy control subjects. The results showed that forty-two percent of patients with GA had enteropathy, as did 51% of patients with ataxia and TG6 antibodies. Five of 15 consecutive patients with idiopathic sporadic ataxia had immunoglobulin A deposits against TG2, 4 of which subsequently tested positive for TG6 antibodies. Follow-up screens showed that one year of gluten-free diet left TG6 antibody levels greatly reduced or undetectable. The study shows that antibodies against TG6 are gluten-dependent and that they seem to be a sensitive and specific indicator of gluten ataxia. Source: Neurology. 2013 Apr 10.