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Celiac.com 11/25/2024 - The relationship between intestinal diseases and anal diseases has long been observed in clinical settings. Many patients with intestinal diseases, such as Crohn's disease or ulcerative colitis, also suffer from anal complications like hemorrhoids or fissures. However, the exact causal connection between these conditions is still unclear, due to limitations in previous observational studies. This study sought to clarify these relationships using Mendelian randomization, a method that uses genetic data to help determine causal effects and reduce bias caused by other variables. Methodology and Data Collection In order to explore the link between different types of intestinal diseases and anal diseases, researchers used genome-wide association study data. Seven types of intestinal diseases were examined, including inflammatory bowel disease, Crohn's disease, ulcerative colitis, irritable bowel syndrome, colorectal cancer, celiac disease, and constipation. Five types of anal diseases were also investigated: anorectal abscess, hemorrhoidal disease, fissures and fistulas of the anal and rectal regions, benign neoplasm of the anus, and malignant neoplasm of the anus. Using the Mendelian randomization technique, genetic variations were analyzed to determine whether these intestinal diseases have a direct influence on the development of anal diseases. This approach allowed researchers to control for confounding factors and focus on potential causal relationships. Key Findings The results of the analysis showed a significant link between several intestinal diseases and anal conditions. Inflammatory bowel disease, Crohn's disease, and ulcerative colitis were all found to increase the risk of three anal conditions: anorectal abscess, fissures and fistulas, and hemorrhoidal disease. These findings reinforce what has been noted in clinical practice—patients with these chronic inflammatory bowel conditions often experience anal complications. For celiac disease, the study identified a significant association with an increased risk of malignant neoplasm of the anus, a rare but serious form of anal cancer. This suggests that people with celiac disease may need to be more vigilant about monitoring for anal cancers. Other interesting findings include a potential link between irritable bowel syndrome and hemorrhoidal disease, and between colorectal cancer and benign neoplasm of the anus. While these associations need further exploration, they provide new avenues for research and clinical attention. Implications for Celiac Disease The link between celiac disease and anal cancer is particularly noteworthy. Celiac disease is characterized by an autoimmune response to gluten, which can lead to chronic inflammation in the gut. This chronic inflammation could contribute to the development of cancerous conditions, including in areas beyond the intestines, such as the anal canal. While more research is needed to fully understand the connection, this study highlights the importance of regular monitoring and early detection efforts for patients with celiac disease, especially concerning malignancies. Conclusion This study is significant in that it provides robust evidence supporting the causal relationship between certain intestinal and anal diseases. The use of Mendelian randomization strengthens the findings by reducing potential biases that have complicated earlier studies. For patients with celiac disease, Crohn's disease, ulcerative colitis, or other intestinal conditions, these findings emphasize the need for regular screening for anal diseases. The ability to understand these risks better may lead to improved prevention strategies and tailored medical advice for individuals with these chronic conditions. Read more at: nature.com Watch the video version of this article:

Celiac.com 06/08/2024 - Gastrointestinal disorders, such as gastroesophageal reflux disease (GERD), inflammatory bowel disease (IBD), gastritis, peptic ulcer disease (PUD), and celiac disease, significantly affect individuals globally, influencing both health and economic stability. This comprehensive summary explores these conditions, focusing on their impact, underlying mechanisms, and current management strategies, with a particular emphasis on celiac disease. Understanding Gastrointestinal Disorders GERD involves the frequent backflow of stomach acids into the esophagus due to a malfunctioning lower esophageal sphincter (LES). This results in symptoms like heartburn and regurgitation, and can lead to complications such as erosive esophagitis and Barrett’s esophagus. Diagnosis often includes endoscopy and pH monitoring, while treatment involves lifestyle modifications and medications like proton pump inhibitors (PPIs). IBD encompasses Crohn’s disease and ulcerative colitis, both characterized by chronic inflammation of the GI tract. Crohn’s can affect any part of the GI tract, while ulcerative colitis is confined to the colon. Symptoms include abdominal pain, diarrhea, and weight loss. Diagnosis relies on endoscopy and biopsy, with treatment options ranging from anti-inflammatory medications to surgery. Gastritis involves inflammation of the stomach lining, often caused by Helicobacter pylori infection or NSAID use. PUD involves open sores in the stomach or upper small intestine. Symptoms include stomach pain and nausea. Treatment focuses on addressing the underlying cause, such as eradicating H. pylori with antibiotics or discontinuing NSAIDs. Celiac Disease: Beyond Gluten Intolerance Pathophysiology and Symptoms: Celiac disease is an autoimmune disorder triggered by gluten ingestion in genetically predisposed individuals. The immune response damages the small intestine's lining, leading to malabsorption of nutrients. Symptoms vary widely and can include diarrhea, weight loss, anemia, and fatigue. Diagnosis: Diagnosing celiac disease can be challenging due to its diverse symptoms. Blood tests for specific antibodies, such as anti-tissue transglutaminase (tTG), and intestinal biopsies are commonly used diagnostic tools. Confirming the diagnosis typically involves both positive antibody tests and evidence of intestinal damage. Management: The cornerstone of celiac disease management is a strict, lifelong gluten-free diet. This diet involves avoiding all foods containing wheat, barley, and rye. Despite the challenges of adhering to this diet, it is essential for managing symptoms and preventing complications. Emerging therapies, including enzyme supplements and immune modulators, are being researched to complement dietary management. The Role of the Gut Microbiome The gut microbiome, a complex community of microorganisms in the digestive tract, plays a critical role in overall health. It aids in nutrient absorption, immune regulation, and protection against pathogens. Dysbiosis, or an imbalance in the microbiome, is linked to various GI disorders. Modulating the microbiome through probiotics, prebiotics, and diet is a promising therapeutic approach. For instance, a diet rich in fiber can promote a healthy microbiome, while processed foods can disrupt it. Advances in GI Disorder Management Recent advancements in the treatment of GI disorders include personalized medicine approaches, such as using biologics that target specific inflammatory pathways in IBD. Technological innovations like high-resolution manometry and capsule endoscopy improve diagnostic accuracy. Additionally, fecal microbiota transplantation is emerging as an effective treatment for conditions like recurrent Clostridium difficile infection. Importance of a Multidisciplinary Approach Managing GI disorders requires a comprehensive, multidisciplinary approach. This includes collaboration between gastroenterologists, dietitians, mental health professionals, and primary care providers. Addressing psychological factors, such as anxiety and depression, which often accompany chronic GI conditions, is crucial. Patient education and lifestyle modifications, including dietary changes and stress management, play significant roles in treatment. Conclusion: Implications for Celiac Disease Patients This review highlights the complex nature of GI disorders and the importance of a holistic, patient-centered approach to management. For those with celiac disease, understanding the disease's immunological basis and adhering to a gluten-free diet are essential for symptom management and preventing complications. Continued research into the gut microbiome and emerging therapies offers hope for improved treatments. A multidisciplinary approach, integrating medical, dietary, and psychological care, is vital for enhancing the quality of life and health outcomes for individuals with celiac disease. Read more: cureus.com

Celiac.com 08/21/2020 - So who, exactly, should be screened for celiac disease? The guidelines and parameters for who and when to test for celiac disease change as new data becomes available. Based on recent study data, and recommendations by the three major celiac disease organizations, many doctors advise celiac screening for patients with any of the following twenty-two conditions or diseases: Anemia Unexplained iron, vitamin B12 or folate deficiency. A 2014 study showed that celiac disease is common in people with unexplained anemia. The study team recommends celiac screening for anyone with unexplained iron-deficient anemia, while the The U.K. National Institute for Health and Care Excellence recommend celiac screening for anyone with unexplained vitamin B-12 or folate deficiency. Aphthous stomatitis People with severe or persistent mouth ulcers (canker sores) should get screened for celiac disease. A 2020 study confirms that doctors should consider celiac disease in patients with severe or recurrent aphthous stomatitis. Autism People with autism have celiac disease at rates almost 20 times higher than in those without autism, reported lead investigator Daniel Karb, MD, a second-year resident at University Hospitals Case Medical Center in Cleveland. As such, many doctors now recommend celiac screening for people with autism. Autoimmune Thyroid Disease The The U.K. National Institute for Health and Care Excellence recommends celiac screening for anyone with thyroid disease. Dental Enamel Defects Certain types of dental enamel defects can be strong indicators of celiac disease. A 2018 study shows that non-specific tooth wear and enamel defects can be strong indications of celiac disease. Dermatitis Herpetiformis (DH) People with dermatitis herpetiformis, aka DH, or Duhring’s disease, suffer from a herpes-like rash. About 10% to 15% of people with celiac disease have DH. Anyone with DH should be checked for celiac disease. Most people with DH see major improvements on a gluten-free diet. Failure to Thrive and Persistent Diarrhea in Children The North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) and The American College of Gastroenterology recommends celiac screening for children with failure to thrive, especially with persistent diarrhea. Unexplained Fatigue Unexplained fatigue. People with persistent unexplained fatigue should consider screening for celiac disease, according to the U.K. National Institute for Health and Care Excellence. GERD Some studies show no link between Gastroesophageal Reflux Disease (GERD) and celiac disease. A 2015 study showed that celiac disease not a big factor in gastro-esophageal reflux disease. But a 2020 study showed that non-celiac gluten sensitivity is common in patients with refractory functional dyspepsia. Many doctors recommend celiac disease screening for patients with GERD. High Transaminase Levels High transaminase levels can be an indication of liver damage, heart damage, and are common in people with celiac disease. Down syndrome A 2020 study shows that people with Down syndrome have celiac disease at up to twenty times the rate of the general population. Celiac disease screening is important for anyone with Down syndrome. IgA Deficiency The North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition recommends testing for celiac disease in asymptomatic children who have conditions associated with celiac disease, including selective IgA deficiency. Irritable Bowel Syndrome in Adults Adults with irritable bowel syndrome should be screened for celiac disease, according to the The U.K. National Institute for Health and Care Excellence. Persistent Unexplained Elevated Liver Enzymes The U.K. National Institute for Health and Care Excellence recommends celiac screening for people with persistently elevated liver enzymes with unknown cause. Recurrent Miscarriages The U.K. National Institute for Health and Care Excellence recommends celiac screening for women who experience recurrent miscarriages. Immediate Relatives of Anyone with Celiac Disease First-degree relatives (mother, father, brother, sister, son, daughter) of anyone with celiac disease should get a celiac screen, according to Mayo Clinic. Short Stature A 2020 study shows that biopsy confirmed celiac disease affects about 1 in 14 patients with all‐cause short stature, and 1 in 9 patients with idiopathic short stature. Based on these results, doctors are recommending screening all patients with short stature should be screened for celiac disease. Thyroiditis Thyroiditis is an auto-immune condition associated with celiac disease. The North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) recommends celiac disease screening in children who have thyroiditis. Turner syndrome Turner syndrome is associated with celiac disease. The North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) recommends celiac disease screening in children who have Turner syndrome. celiac.comhttps://www.celiac.com/celiac-disease/who-should-get-screened-for-celiac-disease-r5201/ Type 1 diabetes More than 20% of people with Type 1 diabetes have celiac disease. The North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) recommends celiac disease screening in children who have Type 1 diabetes. Unexplained Infertility Women with infertility face higher rates of celiac disease. Many doctors do not screen for celiac disease in these women. However, for women experiencing unexplained infertility, especially repeatedly, a celiac disease screen is probably a good idea. Unexplained Neuropathy Patients with unexplained neuropathy, or small fiber neuropathy should be screened for celiac disease and gluten-sensitivity, according to researchers. Unexplained Weight Loss According to the U.K. National Institute for Health and Care Excellence, people who suffer from unexplained weight loss should be screened for celiac disease. Consider Celiac Screening for These Common Physical Complaints People with any of the ten most common complaints of celiac patients, or any of the below conditions that are associated with celiac disease, along with any obvious signs of celiac disease, including persistent diarrhea or stomach upset, should consider celiac screening. These include: Anemia Alternating bowel habit Bloating Constipation Cryptogenic hypertransaminasemia Diarrhea Gastroesophageal reflux disease Osteopenia/Osteoporosis Recurrent miscarriages Unexplained Infertility Other Conditions Associated with Celiac Disease The following conditions are not included in the official celiac screening recommendations by the above organizations. However, anyone with any of the following conditions, along with any obvious signs of celiac disease, including persistent diarrhea or stomach upset, should consider celiac screening. These include: Addisons Disease Alopecia Anxiety and Depression Ataxia Attention Deficit Disorder/ADHD Autism Autoimmune Hepatitis / Chronic Active Hepatitis Bird Fanciers Lung Brain White-Matter Lesions Cerebellar Atrophy Chronic Fatigue Syndrome (myalgic encephalomyelitis or ME, PVS, post viral fatigue syndrome or PVFS) Crohns Disease Congenital Heart Disease Cystic Fibrosis Dental-Enamel Hypoplasia Dyspepsia Epilepsy (with or without cerebral calcification) Farmers Lung Fibromyalgia and Celiac Disease Fibrosing Alveolitis Follicular Keratosis Gall Bladder Disease Gastroparesis Head Aches (Migraine) IBD - Irritable Bowel Disease Impotency Infertility Inflammatory Bowel Disease Lung Cavities Multiple Sclerosis and Celiac Disease Myasthenia Gravis Pancreatic Disorders / Exocrine Pancreatic Insufficiency Peripheral Neuropathy Polymyositis Polyneuropathy Primary Biliary Cirrhosis Pulmonary Hemosiderosis Recurrent Pericarditis Sarcoidosis Schizophrenia / Mental Problems and Celiac Disease Scleroderma Short Stature, Delayed Puberty Small-Intestinal Adenocarcinomas Spontaneous Abortion and Fetal Growth Retardation Systemic Lupus Erythematosus Thrombocytosis (Hyposplenism) Thrombocytopenic Purpura (ITP) Thyrotoxicosis Vasculitis Vitamin K Deficiency Celiac Disease Screening Recommendations by Organization The American College of Gastroenterology The North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) The U.K. National Institute for Health and Care Excellence

Celiac.com 02/28/2022 - Immune regulation is important for carcinogenesis; however, the cancer risk profiles associated with immune-mediated diseases, like celiac disease, are not well understood. A team of researchers recently set out to assess the profiles of cancer risk associated with 48 immune-mediated diseases with the risk of total and individual cancers. They also assessed the prospective association of organ-specific immune-mediated diseases with the risk of local and extra-local cancers. The research team included Ming-ming He, MD; Chun-Han Lo, MD, MPH; Kai Wang, MD, PhD; Georgios Polychronidis, MD; Liang Wang, MD; Rong Zhong, PhD; Markus D. Knudsen, PhD; Zhe Fang, MD; and Mingyang Song, MD, ScD. For their prospective cohort study, the team used data from the UK Biobank cohort study on adults aged 37 to 73 years who were recruited at twenty-two assessment centers throughout the UK between January 1, 2006, and December 31, 2010, with follow-up through February 28, 2019. After adjusting for various potential confounders using time-varying Cox proportional hazards regression, the team assessed the connection between immune-mediated diseases with risk of cancer with multivariable hazard ratios (HRs) and 95% CIs. They used the contrast test method to assess heterogeneity in the associations of organ-specific immune-mediated diseases with local and extra-local cancers. In this group study of nearly half a million participants, the team found that immune-mediated diseases were associated with an increased total cancer risk. Organ-specific immune-mediated diseases showed higher associated risk of local cancers than extra-local cancers, and many immune-mediated diseases were associated with increased risk for cancer in the near and distant organs or other systems. Organ-specific immune-mediated diseases had stronger associations with risk of local cancers than extralocal cancers. The associations for individual immune-mediated diseases were largely organ specific, but were also seen for some cancers in the near and distant organs or different systems. Their findings suggest that immune-mediated diseases are associated with risk of cancer at the local and systemic levels, which supports the role of local and systemic immunoregulation in the development of cancers. Read more in JAMA Oncology The researchers are variously affiliated with the Department of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China; the Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; the Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston; the Division of Gastroenterology, Massachusetts General Hospital, Harvard Medical School, Boston; the Department of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg, Germany; the Study Centre of the German Surgical Society, University of Heidelberg, Heidelberg, Germany; the Center of Gastrointestinal Surgery, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China; the Section for Colorectal Cancer Screening, Cancer Registry of Norway, Oslo, Norway; the Division of Surgery, Department of Transplantation Medicine, Inflammatory Diseases and Transplantation, Norwegian PSC Research Center, Oslo University Hospital, Oslo, Norway; and the Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.

Celiac.com 09/25/2020 - New research into the origin of our medical woes has revealed something startling: As it turns out, we are our own worst enemy. Yes, the Pogo quote of yesteryear found in the title of this article is quite accurate when applied to our medical lives. We love to discuss those things that we call “causes” of diseases even though we often have little knowledge of how these things really cause illness. Even medical professionals can have difficulty grasping the true cause-and-effect. But that becomes understandable once some insight is gained into the true nature of medical training. One would think that we are exposed to the gamut of current medical knowledge in medical school. But in fact, we gain limited knowledge as to the true workings of pathogens, parasites, and chemical insults. Sure, we are often taught which virus or bacteria causes a certain disease state and are then shown the established/accepted mode of therapy. But most of us never gain an appreciation for the circumstances that led to that illness or why one individual has the condition while the next person remains healthy. We are also not told why many of these “pathogens” are ubiquitous in the environment and yet only cause clinical syndromes in a relatively small percentage of individuals. We refer to “immunity” but don’t delve into the fine points of why one pet or person lives to a ripe old age while the next one develops cancer or some other catastrophic illness at a much earlier age. We usually point to the old standby of “genetics” for the explanation. As many of you know, I love to discuss “genetics”. Now, I do not claim to be an authority on the subject, but I do love kicking it around. I like to ponder the logic behind scientists’ referring to certain diseases as “genetic” without offering a good explanation for why these “genes” wait so long to manifest. Do genes wait? Do the genes that code for our brain, liver and kidneys to form properly wait for 6 months or 6-60 years to do what they do? I get a kick out of reading how genes “mutate”, as well. Certainly, we do get true genetic mutations at times (e.g. one arm, one kidney, two heads) but thankfully these are relatively rare when compared to the number of “genetic mutations” that have been reported to cause disease. Here’s a door-opening key: Researchers now estimate that up to 45% of the genetic information in our DNA is viral information, some active and some extinct. Have you grasped the importance of this yet in relationship to the preamble above? Think about it for a moment before proceeding. Got it? Can you now see that our DNA not only contains the information that makes you who you are phenotypically (outward, observable appearance) but also has information encoded in it that can govern the outcome of your medical life. Yes, your double-stranded DNA is a little virus hotel and the guests can get a bit rowdy. I love to tell people that if I could do a Star Trek type of scan on then and give them a print out of all of the viruses in their body, both “genetic” and acquired, then they just might take better care of themselves. But here is the good news...the really cool news...the new “medical gospel”. We have much better control over our medical lives than most think or have been told. In fact, it is phenomenal how much control we have over whether we live a long, healthy life or a brief, afflicted one. How can that be, especially if these “culprits” are in our very DNA? Ahhhh! There is the amazing thing to see. They are not culprits. Viruses are residing in our body for a purpose and a good purpose at that. Viruses are responsible for two critically important functions in nature: Variation and adaptation. Yes, it is the virus that is behind much of what is termed “evolution”. Many viruses can change in response to alterations in their environment, sort of like a chameleon or a flounder. (How do they do that, anyway???) How did we end up with soooo many variations of butterflies? As many of you know, I am a creationist and wholeheartedly believe in God. But I also see how He could have used viruses to facilitate the wide array of appearances among the different species of insects, animals and plants. There are numerous species of butterflies. However, they are all butterflies. In order to prove his theory of evolution, Darwin himself said that finding numerous inter-species would be required. Have we found them? Would he now believe in his original theory? But the focus of this medical discussion should be on the adaptability of the virus. Yes, they are quite adept at this maneuver. And that is to our benefit more than it is to our detriment. Viruses exist throughout nature and our individual bodies in order to facilitate our adaptation to this ever-changing environment. If we could snap our fingers and take all of the viruses out of nature, the entire ecosystem would collapse, including this amazing thing we call a body. They are busily working away to help us cope with daily challenges such as air pollution, malnutrition, hormonal variations, and other microorganisms. They sense the change in their surroundings and react- and appropriately, I might add. “But what about the ‘diseases’ they cause?” you might be asking. Well let’s use my favorite example called cancer—nearly everyone’s biggest fear. We have demonized the virus in those forms of cancer that have been publicized as being “caused” by the virus. (I believe that most of you will hear in your lifetime that all cancer is viral.) In reality, the virus would not have caused the cancer without being goaded into it by what we call carcinogens. And, the cancer would not have developed had the immune system not failed in its duty. So, we suddenly see that cancer, like so many other conditions, is a “syndrome”, with multiple factors coming together to produce the result. Now, let’s dissect that premise for a moment. Viruses are in situ, doing what they do, adapting to changes and insults that are thrown our way. Along comes a “carcinogen” and the virus forms a tumor. Now whose fault was that? I mean, can we blame the virus for making a cocoon for itself and the cell it was charged to protect? (Do you see how I tried to just quickly slip that past you?) But seriously, I now look at tumors as the ultimate adaptation of the virus that we know “causes” the cancer. Once the insults are bad enough, the viruses goes into survival mode, telling the cell to replicate itself in order to survive the caustic insult we call a carcinogen. Is that too far-fetched? Again, this process does not occur until one more thing of vital importance takes place, which is the failure of the immune system to do its job. Yes, as some love to point out at cocktail parties, we are all fighting cancer as we speak...hopefully. As long as we possess a competent immune system, we are successful in our battle to keep cells that are being challenged with carcinogens (that we face every single day) from turning into cancer. However, once our immunity wanes, we are subject to these ongoing processes. Thankfully, there is an intermediate stage called “immune-mediated disease” where the immune system does housecleaning to rid our bodies of these revolutionaries that are gaining an upper hand in the face of our deteriorating governor. A number of wise doctors have said that cancer is the end game of immune mediated diseases, meaning that cancer often follows long bouts with “autoimmune*” conditions (*a term I no longer use). And they are right IF we survive the immune mediated attack. But how do we treat “autoimmune diseases”? Yes, we use immune suppressing drugs. Oh,oh! The term “pretzel logic” comes to mind. This is in the same vein as using carcinogens to treat cancer. Kinda sorta doesn’t make good sense. So whose fault is it when we fail with our current mode of therapy in the treatment of autoimmune diseases and cancer? “Darn those viruses and carcinogens.” So why is there so much variation in the age of onset and severity of cancer? I think we should all be gaining some insight into this conundrum by now. Cancer, like so many diseases, is a spectrum disorder, meaning that we have individuals ranging from the “best of the best” to the “worst of the worst”. The best live to be over 100 years old and experience a relatively disease-free life. The worst don’t survive the time in the womb. We see brain tumors and leukemia in the very young and in the aged. We also see age spikes in the cancer rates that are quite logical, accompanying concurrent stresses such as adolescence and “the wall” at age 40, while observing a meteoric rise after age 65. I used to call cancer viruses “opportunists”, applying to them the connotation of being malicious or even “evil”. But now I see that categorization was inaccurate and downright unfair. They are not waiting around to cause cancer or other diseases; they are FORCED into it by us. We are the ones supplying the carcinogens. We are the ones eating diets that are filled with potentially damaging proteins (gluten, casein , soy, and corn), chemicals, trans fats, and food additives. We are the ones who are trouncing our immune systems through poor diets, lack of exercise, improper sleep, and crazy lifestyles. We are our own worst enemy! We are quite accomplished at the blame game when it comes to shirking our own responsibilities in this process. But, in all fairness, it is not completely the patient’s fault. Look at the current medical and pharmacological approach to the symptoms we experience. “Got a fever? Not anymore. We have a pill for that. (Forget that fever is essential in the proper immune response.)” “Got heartburn, IBS, headaches, fibromyalgia, insomnia, or depression? Not anymore. We have lots of pills for those. (And you no longer have to worry about what causes them because “these medications can be taken for life”.) So, whose fault is it when those symptoms go away and the next and more severe set arise? I tell people, “If you don’t like these warning signs, you’re really not going to like the next set. And if you don’t like those, you’re really not going to like what they are warning you of.” What’s the bottom line? We need to wake up! We need to realize that our bodies are an amazing entity with the ability to withstand serious insult- repeated, ongoing insults. But, there is a limit to what it can take. Thankfully, that limit is quite gracious. But there will come a time when our bodies and those incredible little viruses in them say enough is enough. The phenomenal thing to see is that we have the vast majority of the say in when that occurs. We simply have to stop doing the harm that we are doing to these downright miraculous vessels that we have been given. It is that simple. It is not necessarily easy, but it is that simple. Are we our own worst enemy? We don’t have to be. Now that’s great news!

Celiac.com 07/08/2020 - There are a number of medical, and genetic, conditions related to celiac disease. Those include a number of autoimmune other conditions. Associated Diseases Disorders Common Among Celiacs Having associated autoimmune or other diseases increases the likelihood of developing celiac disease. Associated diseases include: Addison's disease; Autoimmune thyroid disease; Chronic active hepatitis; Dermatitis herpetiformis; Down syndrome or Turner syndrome; Graves disease; Lupus erythematosus; Microscopic colitis (lymphocytic or collagenous colitis); Myasthenia gravis; Rheumatoid arthritis; Scleroderma; Sjogrens syndrome; Systemic lupus erythematosus; and Type 1 diabetes Certain Risk Factors Associated with Celiac Disease These are the ten risk factors most associated with celiac disease include: Age at First Gluten Consumption; Amount of Gluten Consumed; Antibiotics; Being Female; Courses of antibiotics before 2 years old; Ear Infection; Skim Milk consumption; Viral Infection; and Vitamin D Drop Exposure in Infancy. High Rates of Celiac Disease Among Close Relatives of Celiacs Among celiacs and their relatives, there appears to be a higher incidence of other disorders related to the immune system. Celiac Disease Common with These Disorders Other diseases are related in the sense that large numbers of people who have them also have celiac disease. Those include: Type 1 diabetes mellitus, autoimmune thyroiditis, Down syndrome, Turner syndrome, Williams syndrome, selective IgA deficiency, and first-degree relatives with celiac disease Celiac Screening Recommended for These Conditions Additionally, The U.K. National Institute for Health and Care Excellence recommends considering serologic celiac testing for persons with metabolic bone disorder (reduced bone mineral density or osteomalacia), unexplained neurologic symptoms (particularly peripheral neuropathy or ataxia), unexplained sub-fertility or recurrent miscarriage, persistently elevated liver enzymes with unknown cause, dental enamel defects, Down syndrome, or Turner syndrome. Consider Celiac Screening for Top Physical Complaints The ten most common physical complaints of people who have celiac disease are: Osteopenia/Osteoporosis; Anemia; Cryptogenic hypertransaminasemia; Diarrhea; Bloating; Aphthous stomatitis; Alternating bowel habit; Constipation; Gastroesophageal reflux disease and Recurrent miscarriages. People with any one or more of these symptoms might want to consider the possibility of celiac disease, look for any other celiac-related symptoms, and consult a doctor if they suspect celiac disease. Most Common Misdiagnosis for Celiac Disease Celiac disease is commonly misdiagnosed as one of these conditions: Allergies; Chronic fatigue syndrome; Colitis; Cystic fibrosis; Gallbladder disease; Gastro-esophageal reflux disease (GERD); Inflammatory bowel disease; Irritable bowel syndrome; Lactose intolerance; Parasitic infection; Psychological dysfunction; and Ulcers. These Disorders are Commonly Confused with Celiac Disease These twenty-one diseases commonly suspected or diagnosed before celiac disease is discovered. Gluten-Free Diet Can Help In addition, a gluten-free diet appears to have helped some individuals with autism, chronic fatigue syndrome (myalgic encephalomyelitis or ME, PVS, post viral fatigue syndrome or PVFS), attention deficit disorder (ADD), and ADHD. However, a gluten-free diet is is by no means a cure for any of these conditions. For more information on this topic visit the Related Disorders page.

Celiac.com 11/21/2014 - When most people think of celiac disease, they think about gastrointestinal symptoms. However, researchers have documented a number of other medical conditions that are associated with celiac disease, and which improve when patients follow a strict gluten-free diet. The recent case of a 75-year old man who experienced a dramatic recovery from Parkinson's disease after eliminating all forms of gluten from his diet for three months, has researchers thinking about the possibility that gluten sensitivity may be related to Parkinson's disease. In fact, there is some evidence that patients with epilepsy and other conditions may benefit from ketogenic low carb and gluten-free diets. The ketogenic diet is a high-fat, low-carbohydrate, and adequate protein diet developed 90 years ago at the Mayo Clinic. The high fat content creates ketosis, which appears to prevent seizures. In addition to the ketogenic diet, there are several other high-fat, low-carbohydrate diets for seizure control: low-glycemic-index, medium-chain triglyceride, and modified Atkins diets. All require medical supervision and vitamin and mineral supplements. In another example of food serving as medicine, high fat low carb ketogenic diets increasingly are being used to control seizures in epilepsy patients. As reported in Medscape, ketogenic diets made a significant difference for many patients with epilepsy who cannot control their seizures with medication. In one study, more than 20 percent of the patients used the traditional ketogenic diet, while the rest used a modified Atkins diet that included medium-chain triglyceride supplements. These patients saw dramatic improvements. In addition to reducing the number and severity of seizures, 65 percent of patients felt "more alert or brighter," while 35 percent had "more energy." Many of the patients also had shorter seizures when they occurred. Sources: Epilepsy Behav. 2014;37C:59-70. doi: 10.1016/j.yebeh.2014.05.031 J Neurol. 2014 Feb;261(2):443-5. doi: 10.1007/s00415-014-7245-7

Celiac.com 11/28/2014 - According to a new study, obesity plays a major part in triggering and prolonging autoimmune diseases, such as celiac disease, Crohn's disease and multiple sclerosis. The study appeared recently in Autoimmunity Reviews by Prof. Yehuda Shoenfeld, the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases at Tel Aviv University's Sackler Faculty of Medicine and Head of Zabludowicz Center for Autoimmune Diseases at Chaim Sheba Medical Center, Tel Hashomer. According to the research, obesity erodes the body's ability to protect itself, triggering a pro-inflammatory environment that promotes the development of autoimmune diseases, hastens their progression, and impairs their treatment. For some time now, says Professor Shoenfeld, researchers have been aware of the “negative impact of contributing disease factors, such as infections, smoking, pesticide exposure, lack of vitamins, and the like. But in last five years, a new factor has emerged that cannot be ignored: obesity.” According to the World Health Organization, about one-third of the global population is overweight or obese, nearly a dozen autoimmune diseases are now associated with excess weight, which now impact nearly 5-20% of the global population. That is why, according to Shownfeld, it is “critical to investigate obesity's involvement in the pathology of such diseases." The main culprit is not fat itself, but adipokines, compounds secreted by fat tissue, which impact numerous physiological functions, including the immune response. In tandem with their own study, Shoenfeld and his colleagues reviewed 329 studies from across the globe that focused on the connections between obesity, adipokines, and immune-related conditions like rheumatoid arthritis, multiple sclerosis, type-1 diabetes, psoriasis, inflammatory bowel disease, psoriatic arthritis, and Hashimoto thyroiditis. "According to our study and the clinical and experimental data reviewed, the involvement of adipokines in the pathogenesis of these autoimmune diseases is clear," says Shoenfeld. "We were able to detail the metabolic and immunological activities of the main adipokines featured in the development and prognosis of several immune-related conditions." One of the team’s more interesting findings was that obesity also promotes vitamin D deficiency, which, “once corrected, alleviated paralysis and kidney deterioration associated with the disorder… [and] improved the prognosis and survival of the mice.” Source: Science Daily, November 10, 2014

Celiac.com 10/08/2018 - A new population based study reveals that celiac disease is associated with a wide range of medical conditions, including liver disease, glossitis, pancreatitis, Down syndrome, and autism, according to a database study of more than 35 million people. Moreover, people with autism have celiac disease at rates almost 20 times higher than in those without autism, reported lead investigator Daniel Karb, MD, a second-year resident at University Hospitals Case Medical Center in Cleveland. That raises the question of whether people with autism should be screened for celiac disease, and whether they might benefit form a gluten-free diet. "If you have a patient who is autistic and they have all these unusual symptoms, you might want to screen them for celiac disease," Dr. Karb told the World Congress of Gastroenterology last year. It is known that there are unusual symptoms of celiac disease, which include anything outside the classic symptoms of malabsorption, steatorrhea, malnutrition, abdominal pain, and cramping after eating, "but this is putting numbers to it," said Dr Karb. For their study, Karb and his fellow researchers used the Explorys database to pull health record data from 26 major integrated healthcare systems in the United States. Their search covered the period from 2012 to 2017. Of 35,854,260 people in the database, they found 83,090 with diagnosed celiac disease. Overall, the age-adjusted prevalence of celiac disease in that group was 0.22%, which is much lower than the 1% to 2% range previously estimated. Those numbers are not unusual, said Dr. Karb says that the researchers “don't think there are fewer people with celiac disease, just that it may be under-diagnosed.” The rates are, he says, “what you might expect when you screen asymptomatic people." Overall, the team found a significant connection between celiac disease and 13 other autoimmune disorders, such as type 1 diabetes, Crohn's disease, and ulcerative colitis. Moreover, celiac disease is associated with every autoimmune disease the team looked at, except for primary biliary cholangitis, Dr Karb says. This is some pretty startling study data. We knew that celiac disease was linked to other autoimmune conditions, and there has been some surprising data about gluten-free diets helping patients with autism, but these numbers are enlightening. It seems that people with autism should definitely be screened for celiac disease, and placed a gluten-free diet, if tests confirm celiac disease. Stay tuned for more information on this important celiac disease topic. Source: World Congress of Gastroenterology 2017

Celiac.com 03/18/2017 - Do you have an autoimmune disease? Does someone you know? Did you know that the numbers regarding autoimmune rates are all over the place, and that incomplete or wrong information can result in delayed or missed diagnoses? Want to help researchers create a database that will help them understand exactly how many people are living with autoimmune conditions? Then behold the latest project from ARI, a 501c(3) nonprofit, with a mission "to create a hub for research, statistics, and patient data on all autoimmune illnesses." The project seeks to provide data that will help researchers nail down some basic answers about the numbers of people who live with one or more autoimmune conditions. The ARI website says that the company "operate a national database for patients who suffer from any autoimmune disease." ARI's mission is to "reduce the time of diagnosis, support research, compute prevalence statistics, and establish autoimmune disease as a major class of disease so that it receives the awareness of the public, the attention of healthcare providers, and the appropriate funding needed to improve upon existing treatment protocols and disease management strategies." This is one reason why Aaron Abend, the founder and president of ARI, decided to create the Autoimmune Registry after his mother was misdiagnosed for 10 years because, based on incorrect statistical data, "doctors thought Sjogren's syndrome was a rare disease with only 37,000 cases in the U.S." Today, researchers agree there are probably 3 million cases in the U.S., so not so rare at all. Researchers currently estimate that anywhere from 9 million to 50 million people in the United States have an autoimmune disease. That's quite a wide range. Pinpointing the actual prevalence is part of what ARI will try to do. So, they are reaching out directly to patients to information about diseases like rheumatoid arthritis (RA), lupus, psoriasis, diabetes, Crohn's, celiac disease, Sjogren's syndrome, multiple sclerosis (MS), and many others fall under the autoimmune umbrella. The registry is easy to join. It is free to sign up and consists of a simple survey that people with autoimmune diseases answer. The information that people provide to ARI remains secure. The data may be used to compile statistics and qualify them for research opportunities, but no identifying information will be shared without permission. The hope is that the registry can help researchers connect with people and the data. You can view the registry here.

Celiac.com 02/14/2017 - In 1999, Loren Cordain, the renowned professor of Exercise Physiology at Colorado State University who has since popularized the Paleodiet, published an extensive exploration of why our cultivation and consumption of cereal grains has been disastrous for the human race, resulting in many autoimmune, nutrient deficiency, and other modern diseases (1). Previously, in 1987, the famous physiologist, Jared Diamond characterized humanity's shift to agriculture as "The Worst Mistake in the History of the Human Race" (2). A year later, medical doctor and professor of Anthropology, S. Boyd Eaton and colleagues suggested a mismatch between the human genome and our current agricultural diet/lifestyle (3). And more than a decade prior to that, gastroenterologist, Walter L. Voegtlin, M.D., self published a book apparently asserting, based on his treatments and observations of patients, that dietary avoidance of cereal grains and sugars, offset by increased consumption of meats and animal fats, is an effective treatment regimen for a variety of intestinal ailments including Crohn's disease, colitis, irritable bowel syndrome, and indigestion (4). Each of these perspectives was informed by a different but solidly scientific approach to human health. The academic field of each of these authors varied from Exercise Physiology to Physiology, to Gastroenterology, to Anthropology. Yet each of these specialist researchers arrived at the very similar conclusion that cereal grains are not healthful foods for humans. Their strident declarations to that effect leave little room for doubt. Dr. Cordain acknowledges that the roots of some of his thinking lie with Dr. Eaton and his colleagues. Nonetheless, there is a convergence here, of ideas and insights drawn from separate bodies of data and investigative approaches. While there is some overlap between these scientific disciplines, they all lead to a clear indictment of cereal grains as little more than a starvation food for humans. These scientists point to myriad signs of illness that arise more commonly when populations make the transition to eating diets dominated by grains, especially when the grains are refined and when they are combined with sugar. One critic of this paradigm is the evolutionary biologist, Dr. Marlene Zuk of the University of California at Riverside. According to Alison George at New Scientist, Zuk asserts that the 10,000 years that humans have been cultivating and consuming cereal grains is an adequate time period for humans to evolve an adaptation to these foods (5). But surely this is a Eurocentric view. Simply because some Europeans have been cultivating and consuming cereal grains for ten or more thousands of years does not mean that the entire world's population, or even all Europeans, would or could have adapted to consuming these foods. Let's look back to see what we currently know about our human roots and how those early humans spread all over the world. A group thought to number about 200 humans left Africa sometime between 85,000 and 70,000 years ago, during a glacial maximum that lowered worldwide sea levels by about 300 feet below current levels. The enormous glaciers of the time so depleted the oceanic barriers we see today, that these bodies of water were made navigable even with very primitive flotation devices. The progeny of this relatively small group of early modern people multiplied and went on to parent almost all of today's non-African people of the world with some 1% to 4% of today's human, non-African genes having been derived from the Neanderthal branch of the hominid tree (6). This predominantly early modern human group's progeny would quickly find its way to Australia, the South Pacific, across Asia, to China, east to the Americas and west across India, finally arriving in Europe, where they would supplant the long-time Neanderthal residents who had survived some of Europe's harsh and inhospitable glaciations but apparently could not survive having our forebears as neighbors. While specific paths and dates for exiting Africa, and worldwide patterns and timing of human distribution remain controversial, most experts now accept that indigenous Australians had arrived there at least 60,000 years ago (6). A similarly recent finding places people in the Americas by at least 55,000 years ago, long prior to the date at which the Bering Land Bridge was thought to be available for human movement from Siberia into the Americas (8). This newer, admittedly controversial date raises the likely possibility that people arrived in the Americas, from Asia, by boats or rafts on which they followed the shoreline east to what is now Alaska, then south of the glaciated wastelands of much of what is now Canada. (Or perhaps they arrived by some other means that we have not yet imagined.) But only a small portion of these early Americans would eat wheat, rye, oats, or barley before the last 200 years or so, especially those living on the Great American Plains, or in the frigid north, the dense jungles or places that were otherwise isolated from the encroaching wave of "immigrants" from Europe and beyond. And none of those aboriginal peoples of the Americas were eating these grains prior to 1492. The epidemics of autoimmunity and obesity that may be seen among indigenous Americans are clear reflections of their recent shift to the gastronomic wonders of foods derived from these European grains. Further, even among Europeans, grain cultivation and consumption had not uniformly spread across most of Europe until, at most, less than half of the 10,000 years that Zuk says would be sufficient for human adaptation. In Britain, for instance, grain farming was only getting under way about 4,000 years ago, and availability of grains varied according to local geographies and economies. Also, in parts of Scandanavia, wheat bread was a rare treat until after World War II. Some Europeans are thought to have been cultivating grains for even longer than the 10,000 years ago suggested by Cordain, but the evidence is contradictory and accompanied by a range of expert opinions. Further, the health consequences of this nutritional path are consistently seen in the skeletal remains of those early farmers, many of which can now be seen reflected among indigenous peoples of the Americas, as they assimilate our grain and sugar dominated diet. Adaptation to eating grains is not a gentle, joyful process. Early farmers may have produced many more children than their hunting and gathering neighbors, but their lives were shorter, their bodies were less robust, with substantial reductions in stature, and they experienced widespread infectious diseases and ailments driven by nutritional deficiencies. By the time grains became a cash crop for many European farmers, cereals were disproportionately consumed by affluent urbanites. Those who were large consumers of cereal grains did not include all Europeans, even where yields were prodigious. In more remote, northerly, or mountainous areas, cereal grains, or foods made from them, were likely a rare treat rather than a daily staple. Jared Diamond points out, that in addition to "..... malnutrition, starvation, and epidemic diseases, farming helped bring another curse upon humanity: deep class divisions." He goes on to argue that only with farming and the storage and accumulation of food can Kings "and other social parasites grow fat on food seized from others". He also presents evidence that farming led to inequality between men and women. Conversely, contemporary hunter-gatherers have repeatedly been shown to be quite egalitarian, both regarding gender and political leadership (9). Roger Lewin is another critic of the health impact of European grain cultivation on humans. He points out that even in the very heart of the Fertile Crescent, where agriculture got its start, there was not a uniform adoption of farming. One agricultural center at Abu Hureyra, experienced two cycles of abandonment, one at 8,100 B.C.E., lasting about 500 years, and another at 5,000 B.C.E. These periods when agriculture at this locale was abandoned are "thought to be related to climatic change that became less and less conducive to agriculture" (10). Lewin also harkens to Mark Nathan Cohen's collation of "physical anthropological data that appear to show increasingly poor nutritional status coincident with the beginnings of agriculture.... " (10) suggesting, again, that grains were a starvation food. Eaton et al also approach grain cultivation from an anthropological perspective, suggesting that increased dietary protein and fats from animal/meat sources likely gave rise to increased stature of earlier humans, along with providing the necessary fatty acids for building larger brains, and allowing smaller gut sizes over the past 2.5 million years. It seems reasonable to assume that if it took our pre-historic ancestors that long to adapt to eating meats and animal fats, the very irregular adaptation period of between less than one hundred years and about 10,000 years that various world populations have been cultivating and consuming wheat, rye, barley and oats would be insufficient to allow full adaptation to eating these immune sensitizing cereal grains. Dr. Zuk's perspective might be tempered a bit if she considers that Europeans and their descendants do not comprise the entirety of the world's populations. There are several Asian populations that are not insignificant when compared with European populations and their progeny, including the residents of China, India, Pakistan, and South-East Asia. Even among those of us who appear quite European, there may be a mixture of genes derived from peoples of any of the other five populated continents. The approximately 10,000 year maximum period since humans began to cultivate cereal grains would have little adaptive impact on populations that have only been exposed to these grains for a period of somewhere between four or five centuries and seven or eight decades, as is the case among the indigenous people of the Americas, Australia, New Zealand, and much of Asia (6). Even if all humans had been cultivating and consuming cereal grains for the 10,000 years since this practice was first begun in the Middle East, the high frequency of intestinal, autoimmune, and other diseases that can be mitigated by a gluten free diet, even among descendants of Europeans, leaves little room to doubt that Dr. Zuk's projected adaptation simply has not occurred. The current prevalence of celiac disease and non-celiac gluten sensitivity identifies, at a bare minimum, between 7% and 12% of the American population that has not adapted to cereal grain consumption. While a few research projects suggest that molecular mimicry and the opioids from cereal grains contribute to autoimmunity, obesity, type 2 diabetes and cardio-vascular disease, current research does not provide any clear sense of how many cases or to what degree these health conditions are driven by gluten consumption. We know that foods derived from cereal grains are often laced with refined sugar, but the insulin stimulating properties of gluten alone are such that their role in these conditions cannot, reasonably, be denied. I feel vindicated by these many experts who decry the folly in humanity's embrace of the European grains. I wonder how long it will take for this information to filter into, and be acknowledged by, those who claim that science has led them to advocate cereal grain consumption for everyone without celiac disease and, more recently, non celiac gluten sensitivity? Sources: Cordain, Loren. Simopoulos AP (ed): Evolutionary Aspects of Nutrition and Health. Diet, Exercise, Genetics and Chronic Disease. World Rev Nutr Diet. Basel, Karger, 1999, vol 84, pp 19–73 http://thepaleodiet.com/wp-content/uploads/2012/08/Cerealgrainhumanitydoublesword.pdf Jared Diamond, "The Worst Mistake in the History of the Human Race," Discover Magazine, May 1987, pp. 64-66. http://www.ditext.com/diamond/mistake.html Eaton SB, Konner M, Shostak M. Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective. Am J Med. 1988 Apr;84(4):739-49. Voegtlin, Walter L. (1975). The stone age diet: Based on in-depth studies of human ecology and the diet of man. Vantage Press. ISBN 0-533-01314-3 George, A. " The Paleo Diet Is a Paleo Fantasy" New Scientist. April 7, 2013. http://www.slate.com/articles/health_and_science/new_scientist/2013/04/marlene_zuk_s_paleofantasy_book_diets_and_exercise_based_on_ancient_humans.single.html Oppenheimer, Stephen. The Real Eve: Modern Man's Journey Out of Africa. Basic Books, NY, NY. 2004 Fagan, Brian. Cro-Magnon: How the Ice Age Gave Birth to the First Modern Humans. Bloomsbury Press, New York. 2011 http://www.utep.edu/leb/Pleistnm/sites/pendejocave.htm Brody, Hugh. The Other Side of Eden: Hunters, Farmers and the Shaping of the World. Douglas 7 McIntyre Ltd., Vancouver, B.C., Canada. 2000 Lewin, Roger. A Revolution of Ideas in Agricultural Origins. Science. vol 240, May 20, 1988

Celiac.com 01/31/2017 - In my practice, I have had the pleasure and honor of helping hundreds of people reverse their diabetes and put their autoimmune diseases into remission. One of the many things that we test for is gluten reactivity. The research, much of which has been cited in our book on gluten, Lose the Gluten, Lose your Gut. Ditch the Grain, Save your Brain, clearly demonstrates the connection between gluten reactivity and most autoimmune diseases, including but not limited to: Hashimoto's thyroiditis, rheumatoid arthritis and psoriasis. I intentionally didn't mention celiac disease, because, although it is very well established and accepted that gluten triggers celiac disease, what most don't realize is that those with celiac disease represent only a small percentage of people with autoimmunity that are impacted by gluten reactivity. What's alarming and disappointing to me is how many doctors 'pooh pooh' the concept of gluten reactivity, especially among their chronically ill patients. Because of this disconnect, patients continue to suffer needlessly with chronic diseases that, with the removal of gluten from the diet, would in many cases, clear up or go into remission. Hundreds of my patients tell me that when they told their health practitioner they had eliminated gluten from their diet, the health care worker didn't believe gluten would make a difference, or that since they didn't have celiac disease, eliminating gluten wouldn't help them. All this was said in the face of autoimmune diseases going into remission, or diabetes reversing right before their eyes, following the elimination of gluten from their diet. The issue is that many health care practitioners are just not keeping current with the research. As such, they are inadvertently preventing their patients from truly getting healthy. The additional travesty with this is that so many people look to their health care practitioners as 'experts'. When these providers, who are not 'experts' in a particular subject, (in fact, many are completely ignorant of how dietary changes and supplement therapy can help people thrive) advise a patient against something that the research shows would likely help them, it becomes an issue of negligence and, quite frankly, laziness. One patient in particular comes to mind when I think of this disconnect. I had the pleasure of working with a retired nurse who, in her seventies, had come to me with several medical issues. For purposes of this article, I will refer to her as Mary. Mary suffered with hypothyroidism, which we quickly discovered through additional testing, was caused by an autoimmune disease called Hashimoto's thyroiditis. Interestingly, it is estimated that roughly 90% of the 26 million people in the U.S. that have hypothyroidism actually have Hashimoto's. This is an autoimmune disease in which your immune system attacks and destroys the thyroid gland. The research, and our clinical experience, has demonstrated that gluten will cause your immune system to flare-up and attack the thyroid. In addition to Hashimoto's, Mary also suffered with cardiac arrhythmia and she had a history of blood clots and strokes. She also had a long-standing issue with another autoimmune disease, called pleva, whereby her skin would rash up, itch and scab. Mary was very overweight, and exhausted all of the time. Mary had a full functional work-up in our office and she was confirmed, with testing, to be very gluten-reactive. After working with her for several months, with one very important instruction to go completely gluten-free, she easily lost over 40 lbs (with no additional exercise), her energy increased to the point where she stated she hadn't felt that good in decades, and her arrhythmia and pleva cleared up completely. Her cardiologist was ecstatic and her general practitioner told her to keep up whatever she was doing because she was so healthy now. I hadn't seen Mary for almost 6 months when she emailed me one day to update me on something that had happened with her. She went to a food class taught by a vegan. At the class the guests were told very directly that eating gluten-free was a 'billion dollar hoax' and that eating gluten-free could be dangerous and bad for your health. Mary, even after all of her success, in part from going gluten-free, was suddenly doubtful of her diet. She tested it, and for 3 days brought back gluten-containing foods. She told me she reacted very badly and felt horrible. For Mary, the point was driven home that gluten-reactivity was a very real issue regarding her health. The difference in how she felt was like night and day. Lucky for her, she observed this first hand and immediately went back on her gluten-free diet before her skin disease and arrhythmia flared-up. Whether one is a doctor, a nutritionist, or a regular Joe, making statements about any subject without having researched that subject in earnest, is unethical, and may even be harmful. We have done the research and have seen first-hand, with thousands of patients reversing everything from psoriasis to diabetes, that eating gluten-free, while very 'trendy' right now, is a trend that is solidly backed up by the evidence.

Celiac.com 02/06/2017 - People with celiac disease have higher rates of autoimmune thyroiditis, and vice versa. Both of these common autoimmune diseases share multiple aspects lodging at the two ends of the gut-thyroid axis where the cross-talks' pathways are still unrivaled. A team of researchers recently set out to better understand the parameters for effectively screening patients with either disease for the presence of the other. The research team included Aaron Lerner, and Torsten Matthias of the Rappaport School of Medicine, Technion-Israel Institute of Technology, Haifa, Israel, and with AESKU.KIPP Institute, Wendelsheim, Germany. Many clinicians recommend screening patients with thyroid autoimmunity for celiac disease associated antibodies. However, the wisdom of routinely screening of celiac patients for anti-thyroid antibodies is less certain. Despite the fact that the latter screening fulfills most of the criteria for screening a disease, the timing and cost-effectiveness remains undetermined. For now, in face of celiac disease, the researchers are recommending that clinicians and practitioners keep in mind the higher rates of autoimmune thyroid disease in the interests of making timely and accurate diagnosis. Read their full report. Source: International Journal of Celiac Disease. Vol. 4, No. 4, 2016, pp 124-126. doi: 10.12691/ijcd-4-4-10

Celiac.com 01/11/2017 - Researchers know that canonical Wnt/β-catenin signaling controls the homeostasis of intestinal epithelium by regulating the balance between intestinal stem cell regeneration and differentiation, but they really don't know much at all about the non-genetic mechanics of the process. One research team recently set out to test a hypothesis that the epigenetic regulator, Polycomb Repressive Complex-2 (PRC2), plays a role in Wnt-mediated epithelial homeostasis on the crypt-villus axis, and that defects in the process are implicated both in celiac disease and intestinal cancers. The research team included Mikko Oittinen, Alina Popp, Kalle Kurppa, Katri Lindfors, Markku Mäki, Minna U. Kaikkonen, and Keijo Viiri. They are variously associated with the Tampere Centre for Child Health Research, University of Tampere, Department of Pediatrics and Tampere University Hospital, Tampere, Finland, with the Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland, and with the University of Medicine and Pharmacy “Carol Davila” at the Department of Pediatrics and Institute for Mother and Child Care in Bucharest, Romania. Their study showed that PRC2 establishes repressive crypt and villus specific trimethylation of histone H3 lysine 27 (H3K27me3) signature on genes responsible for nutrient transport and cell killing in crypts and, proliferation and differentiation in mature villi, suggesting that PRC2 facilitates the Wnt-governed intestinal homeostasis. When celiac patients regularly consume gluten, PRC2 goes out-of-bounds active, and its target genes in the intestinal epithelium are negatively impacted. Colorectal adenomas, and carcinomas, also differentially express a significant set of effective intestinal PRC2 targets. This indicates that PRC2 initiates and maintains polar crypt and villus specific H3K27me3 signatures. Because H3K27me3 is a mark enriched in developmentally important genes, identified intestinal PRC2 targets are possibe imperative drivers for enterocyte differentiation and intestinal stem cell maintenance downstream to Wnt-signaling. This research also clarifies the mechanics driving crypt hyperplasia in celiac disease, and suggests that PRC2-dependent fostering of epithelial stemness is a common aspect of intestinal diseases marked by epithelial hyperplasia or neoplasia. Lastly, the team's research shows that in the gut, PRC2 represses genes having both pro-stemness and pro-differentiation functions, a fact that should be weighed when designing non-genetic therapies including PRC2 as a drug target. Source: Stem Cells 2016

Celiac.com 03/25/2015 - In what may prove to be a remarkable step in understanding human diseases, a team of scientists affiliated with Northeastern University has found a way to connect diseases based on their shared molecular interactions. A paper by the Northeastern team appears in the journal Science. The paper details their creation of a mathematical tool to analyze the map of the molecular interactions within cells, called the human interactome, and the discovery that over-lapping disease modules, or "neighborhoods" of disease-associated proteins, can give rise to some very unexpected relationships between diseases. Increasing amounts of research, says Albert-László Barabási, are making it very clear that "human diseases can be interpreted only in the context of the intricate molecular network between the cell’s components." Barabási is Robert Gray Dodge Professor of Network Science and University Distinguished Professor and director of Northeastern’s Center for Complex Network Research. The Northeastern researchers are based in the Center for Complex Network Research. The team comprises Barabási, Menche, postdoctoral researcher Maskim Kitsak, research assistant professor Amitabh Sharma, and graduate physics student Susan Dina Ghiassian, PhD’15. For their study, the Northeastern team analyzed 299 diseases that had at least 20 associated genes. They found that 226 of the diseases had their own specific "neighborhood" within the interactome. They noticed that diseases within the same neighborhood had more in common in terms of molecular functions or symptoms, while diseases that were far away from each other within the interactome had very little in common in terms of molecular functions or symptoms. Among their findings, they noted that asthma, and celiac disease are localized in overlapping neighborhoods, which suggests shared molecular roots, even though they have very different pathobiologies. This is the first study to show that the available network maps offer enough coverage and accuracy to provide valuable information about the molecular origins of disease-disease relationships, says Jörg Menche, a postodoctoral researcher and one of the authors on the paper. This is a very interesting and potentially promising discovery that may pave the way for a much deeper understanding of relationships between celiac and numerous other diseases. Stay tuned for more news. Source: Northeasternnews.edu